Student Study Guide for General Surgery

TABLE OF CONTENTS

Pages Topics
1 Table of Contents
2-8 Shock
9-12 Body and Solute Composition
13-16 Hematology
17-18 Tissue Injury & Response
19- Wound Healing
20-23 Surgical Nutrition
23-27 Thyroid
27-35 Benign Breast Diseases
35-41 Malignant Breast Diseases
41-47 GI Hemorrhage
48-53 Stomach
53-55 Acute Abdomen
55-61 Small Bowel Obstruction
61-62 Colon Polyps
62-65 Colon & Rectal Cancer
65-66 Acute Pancreatitis
66-68 Chronic Pancreatitis
68-70 Pancreatic Cancer
70-71 Acute Cholecystitis
71-73 Hernias
73-74 Pre-Operative Urinary Retention
74-80 Traumatic Brain Injury (TBI)
80-84 Penetrating Neck Injury
84-87 Pelvic Trauma
87-91 Blunt Thoracic Trauma
91-93 Blunt Abdominal Trauma
93-95 Penetrating Chest Trauma
95-97 Penetrating Abdominal Trauma
97-101 Peripheral Vascular Disease (PVD)

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 SHOCK
Definition:
• Physiologic state characterized by significant reduction of systemic tissue perfusion decreased tissue
oxygen deliveryimbalance between oxygen delivery and oxygen consumption.
o Oxygen delivery can be normal, but if it’s accompanied by a hypermetabolic state (as is seen
in sepsis), the normal supply may not be adequate to meet tissue demands
Pathophysiology
• Prolonged oxygen deprivation cellular hypoxia and derangement of critical biochemical processes at
cellular levelcan progress to systemic level
• The response to hypoperfusion/hypoxia is to preserve oxygen delivery to the heart and brain by
diverting blood flow from other tissues (i.e. skin, subcutaneous tissues and GI tract.)
• Gut dysfunction may be a manifestation of the effect of shock, but it can be an important cause of the
perpetuation of various shock syndromes
• As a result of circulatory redistribution in shock, splanchnic blood flow, which normally comprises 15-
20% of cardiac output, is reducedmucosal ischemia and cellular hypoxia ensue, leading to further
injury and deleterious systemic effects. For these reasons, the gut has been termed the motor of
irreversible shock and MODS
• The pathogenesis of gut injury involves at least 2 different mechanisms
(1) Those related to hypoxia  causes mucosal ischemiadisruption of the normal epithelial
barriercan lead to increase gut permeability, allowing for enteric flora or bacterial toxins to
translocate across the gut wall and invade the host through lymphatic or portal venous routes
(2) Those related to reperfusion injury once blood flow is reestablished accumulation of toxic
oxidants (superoxide anion, hydroxyl radical and hydrogen peroxide)may lead to cellular
injury by lipid peroxidation and disruption of cell membrane integrity.
• Additionally, the oxidants may have a chemotactic role, leading to granulocyte
infiltration, activation and release of cytotoxic proteases with further injury mediated
by the elaboration of proinflammatory mediators
Classification of Shock:
• Hypovolemic
• Cardiogenic
• Neurogenic
• Vasogenic: all of the following have a common mechanism involving vasomotor collapse
o SIRS and/or Sepsis
o Anaphylaxis
o Adrenocortical
o Traumatic
Measurements Used for Patient Assessment
• BP, HR, central venous pressure, hematocrit, arterial blood gases and urine output are somewhat
insensitive in diagnosing or evaluating the treatment of shock because abnormal values reflect
secondary effects of shock or tissue hypoxia
• Swan-Ganz catheter (placed in pulmonary artery), when used in conjunction with an indwelling arterial
cannula and blood gas analysis, can provide considerable hemodynamic and oxygen transport data that
are extremely useful in directing therapy aimed at optimizing cardiac function and oxygen delivery.
• Mixed Venous Oximetry: continuous measurement of mixed venous oxygen saturation (SvO2) is
possible via a pulmonary artery catheter:
o Normal SvO2 = 75%: indicates balance between oxygen delivery and consumption
o Decreased SvO2: suggests a reduction in oxygen delivery (owing to low cardiac output,
decreased hemoglobin concentration or decreased arterial oxygen saturation) or an increase in
oxygen consumption.
SvO2 monitoring can provide early warning signs of inadequate oxygen delivery or hemodynamic
compromise

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• Transcutaneous oxygen monitoring is a noninvasive technique of continuously measuring skin pO2
• Serum lactate concentration (lactic acidosis) is a metabolic monitor of shock
o Mild-moderate hyperlactatemia: may be seen in hypermetabolic states; not necessarily
associated with tissue hypoxia.
• In absence of O2, pyruvate is converted to lactate, yielding 2 ATP per glucose. Under
aerobic conditions, glucose results in the net production of 38 ATP
o Degree of hyperlactatemia has been correlated with patient outcome in studies that indicate
the probability of survival decreases markedly as blood lactate concentration increases beyond
the normal range of 0-2 mmol/L.
• Mild acidemia (pH>7.2): catechol stimulation may cause tachycardia, ↑ cardiac
output and vasoconstriction.
• Severe acidemia (pH <7.2): direct effects of acidosis predominate, causing decreased
responsiveness to the effects of circulating catechols, bradycardia, vasodilation, and
decreased cardiac output. A direct, negative inotropic effect is also observed.
o Other effects of metabolic acidosis include ↓ threshold for ventricular fibrillation and a
rightward shift of the oxyhemoglobin dissociation curve ↓ affinity of hemoglobin for
oxygen, (this is partially opposed by a ↓ in 2,3-diphophoglycerate in RBCs)
Diagnosis and Management of Shock: General Approach:
• Ultimate goals in the management of shock are to restore perfusion and adequate oxygen delivery to
tissue.
• To improve oxygen delivery, 3 parameters may be manipulated:
(1) Arterial oxyhemoglobin saturation (SaO2): SaO2 should be kept above 90%.
(2) Hemoglobin concentration: transfusions of pRBC’s should be considered in patients who do
not quickly respond to initial volume expansion measures. Hemoglobin concentration should
be maintained between 11-13.
(3) Cardiac output: parameter that is most effectively manipulated to increase oxygen delivery.
 Assessment of volume status (preload) is done early in the evaluation of a patient in
shock. Patients who have mild forms of shock may respond to volume administration
alone, without the need for invasive hemodynamic monitoring. Many patients,
however, will need a pulmonary artery catheter placed to optimize cardiac output and
oxygen delivery
 Reasonable initial resuscitation goals include
(1) Maintaining PCWP between 15-18 mmHg,
(2) Achieving a mean arterial pressure between 60-80 mmHg,
(3) Maintaining SVO2 > 65-70%
(4) Achieving delivery-independent oxygen consumption.
• Patients may require the use of pharmacologic agents to:
o Improve cardiac inotropy (dobutamine, dopamine, epinephrine)
o Decrease afterload (nitroglycerin, nitroprusside),
o Increase perfusion pressure (agents with α-adrenergic effects: norepinephrine, epinephrine,
and phenylephrine)
SPECIFIC SHOCK SYNDROMES
HYPOVOLEMIC SHOCK
• Most common shock syndrome in surgical patients.
Pathophysiology
• Loss of body fluidsintravascular volume depletioncompensatory mechanisms fail to restore
normal tissue perfusion
Causes:
• Whole blood loss is seen in hemorrhagic shock after trauma
• Plasma or free water losses is seen with extracellular fluid sequestration, unreplaced gastrointestinal
fluid loss, or excessive insensible fluid loss.

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Clinical Signs and Symptoms of Hemorrhagic Shock Based on Severity of Blood Loss
% Loss of Pulse Systolic Pulse Capillary Respirations Central Urine
Circulating Rate Pressure Pressure Refill Nervous Output
Blood System
Volume
<15% Normal Normal Normal Normal Normal Normal Normal
15-30% >100 Normal Decreased Delayed Mild Anxious 20-30
tachypnea ml/hr
30-40% >120, Decreased Decreased Delayed Marked Confused 20 ml/hr
weak tachypnea
>40% >140, Markedly Markedly Absent Marked Lethargic Negligible
non Decreased Decreased tachypnea
palpable
Compensatory Mechanisms: aim to restore homeostasis and preserve blood flow to the heart and brain.
• Baroreceptors in aortic arch and carotid sinus respond to a fall in BP by transmitting ↓ afferent stimuli
to the vasomotor center in the medulla↑ sympathetic neural output↑ sympathetic tonearteriolar
and venous constriction↑ systemic vascular resistance and ↑ venous return to the heart.
• Adrenal medullary output of norepinephrine and epinephrine  tachycardia and enhanced myocardial
contractility
• Cerebral ischemia, (when mean arterial BP<50 mmHg), is potent stimulus for sympathetic output
vasoconstriction and augmentation of cardiac contractility and heart rate.
• ADH is released by the posterior pituitary in response to hypovolemia vasoconstriction (particularly
in splanchnic circulation) ↑ water reabsorption in the distal tubule of the kidney.
• Renin secretion is stimulated by hypoperfusion of the juxtaglomerular apparatus in the kidney
formation angiotensin I (liver) formation of angiotensin II (lungs), a powerful vasoconstrictor, that
also causes aldosterone release by adrenal cortex.
o Aldosterone restores circulating blood volume by promoting reabsorption of sodium (↑Na+,
↓K+) in the renal tubules.
Diagnosis:
• Characteristic hemodynamic profile of hypovolemic shock:
o Low right and left sided filling pressures (low CVP and low PCWP),
o ↓ cardiac output
o ↓ SVO2
o ↑ systemic vascular resistance
Treatment:
• Assessment of airway, with determination of whether adequate ventilation and oxygenation are
present. Almost all patients with severe shock and circulatory collapse require tracheal intubation and
mechanical ventilation
• 2 large bore IV lines + fluid bolus (isotonic electrolyte solution, i.e. LR) should be administered.
o In severe shock with hypotension, an initial 1-2 liter bolus is rapidly infused.
o If the clinical situation is compatible with hemorrhagic shock, and there is no response to
crystalloid administration, blood transfusion must be considered.
• Placement of a central venous line to monitor CVP or a pulmonary artery catheter for more extensive
hemodynamic monitoring may be necessary.

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• In the absence of CVP or pulmonary artery catheter monitoring, initial end-points for volume
resuscitation include reestablishment of:
o Urinary output: rate of 0.5-1.0 ml/kg/hr
o Normal heart rate and blood pressure
o Adequate capillary refill
o Normal sensorium
• Continuing fluid replenishment should extend beyond the initial resuscitative phase.
o After hemorrhagic shock there is an initial extracellular fluid volume contraction that lasts
about 1 day. Volume of sequestered fluid is related to the severity of trauma and the degree of
tissue damage.
o Failure to accommodate this obligatory extravascular fluid sequestration results in an
exacerbation of the shock state, metabolic acidosis, multiple organ dysfunction and death.
o After sequestration phase, the diuretic phase begins; the sequestered extravascular fluid is
mobilized and diuresed to restore the body fluid compartments to their normal, preinjury
levels.

CARDIOGENIC SHOCK
Pathophysiology:
• Heart fails to generate an adequate cardiac output to maintain tissue perfusion; aka pump failure
Causes: Can be due to intrinsic or extrinsic causes:
o Intrinsic causes:
 Myocardial dysfunction 2º to ischemic heart disease
 Arrhythmias
 Myocarditis
 Cardiomyopathy
 Metabolic abnormalities
 Cardiodepressant drugs or toxins
 Valvular dysfunction
o Extrinsic causes of cardiogenic shock may be either obstructive or compressive.
 Obstructive cardiogenic shock: causes produce mechanical or functional obstruction
that results in ↑ LV or RV afterload and associated heart failure.
Increased LV Afterload and Left Heart Failure
• Coarctation of the aorta
• Malignant hypertension
Increased RV Afterload and Right Heart Failure:
• Pulmonary embolism
• Various other causes of pulmonary hypertension
 Compressive cardiogenic shock: disease processes that cause ↑ in external pressure
on the heart↓ diastolic filling, ↓ cardiac compliance and ↓ cardiac output
• Pericardial tamponade: Beck’s triad: (hypotension, distended neck veins,
muffled heart sounds) + Pulsus parodoxus (systolic pressure ↓ > 10 mmHg with
inspiration)
• Restrictive pericarditis
• Tension pneumothorax or massive hydrothorax
• Positive-pressure ventilation
• Diaphragmatic hernia
Diagnosis:
• Appearance of patient in cardiogenic shock is similar to that of the patient in hypovolemic shock in
that signs of adrenergic stimulation and of peripheral and end-organ hypoperfusion are present.
o Cardiogenic shock must be differentiated from hypovolemic shock because the treatment of
the two conditions are very different.

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• Patient may appear anxious, tachycardic, and tachypneic, with cool, clammy, mottled skin and
oliguria.
• There may be signs of increased preload, such as distended neck veins, the presence of an S3 heart
sound, pulmonary rales, and peripheral edema.
• Prior history of cardiovascular disease may be useful in establishing a diagnosis
• Lab data, particularly ABGs, serum electrolytes, and cardiac enzymes may be useful in diagnosis and
management of cardiogenic shock.
• CXR and EKG should be obtained in all cases of suspected cardiogenic shock to identify acute, as well
as chronic disease.
• If pulmonary embolism is considered, a ventilation-perfusion scan or pulmonary angiogram should be
obtained
• Invasive monitoring using a pulmonary artery catheter is frequently required to optimize cardiac
function and oxygen delivery in cases of cardiogenic shock. Typical hemodynamic findings in
cardiogenic shock include:
o Low cardiac output (<2.2 L/min/m2)
o Elevated systemic vascular resistance
o Elevated filling pressures
Treatment:
• Goal: optimize cardiovascular function, improve oxygen delivery and restore tissue perfusion
• Preload, afterload and cardiac contractility are manipulated to optomize myocardial supply-to-demand
ratio.
o Preload is adjusted until PCWP is 15-18 mmHg (via fluid administration to increase preload if
it is low, or with pharmacologic intervention (vasodilators like morphine or furosemide) to
decrease preload if it is elevated
o Cardiac Contractility: sympathomimetic inotropic agents commonly used include dopamine,
dobutamine and epinephrine
o Afterload: vasodilators (i.e. nitroprusside or nitroglycerin) reduce afterload in patients with
cardiogenic shock and should be instituted in patients with elevated filling pressures, low
cardiac output, elevated systemic vascular resistance and normal or raised BP.
If pharmacologic manipulations of preload, afterload and contractility fail to improve cardiac
function, the use of intra-aortic balloon pump (placed in descending thoracic aorta) may be
considered.
• It inflates during diastole and deflates before systole. The effects of IABP are
(1) to provide diastolic augmentation hence increased coronary artery perfusion;
(2) to reduce left ventricular afterload; and
(3) to reduce myocardial oxygen consumption.
• Supplemental O2 and mechanical ventilation should be instituted, if indicated
• Hemodynamic interventions aimed at correcting arrhythmias and optimizing preload.

NEUROGENIC SHOCK
Neurogenic Shock: occurs when sympathetic denervation produces an impairment in vasomotor tone.
Pathophysiology
• Loss of vasomotor tone in both the arteriolar and venous systems leads to:
o Decrease in systemic vascular resistance
o Large increase in venous capacitance
o Decrease in venous return to the heart
o Decrease in cardiac output
Causes:
• Severe head injury
• Spinal cord injury
• Pharmacologic sympathetic blockade (i.e. high spinal anesthesia)
Diagnosis

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 • Hypotension and bradycardia are classically seen in neurogenic shock, but tachycardia is frequently
observed as well.
• Patient’s extremities are warm and dry (unlike cardiogenic or hypovolemic)
Treatment:
• Mainstay of treatment is to improve cardiac filling by IV volume administration. Several liters of fluid
may be required to achieve adequate venous return because of the greatly expanded intravascular
volume. Placement of the patient in the Trendelenberg position may assist in increasing venous return
to the heart.
• α-adrenergic agonists (i.e. phenylephrine) are rarely indicated if intravascular volume has been
effectively restored

VASOGENIC SHOCK
Vasogenic Shock: Endogenous or exogenous vasoactive mediators cause a ↓ in arteriolar and venous
vasomotor tone
Pathophysiology:
• Current interpretations of shock view the syndrome as a continuum, ranging from subclinical deficits
in perfusion to multiple organ dysfunction syndrome (MODS) or frank organ failure.
Causes:
1. Systemic Inflammatory Response Syndrome (SIRS) and/or Sepsis
2. Anaphylaxis
Included under
3. Adrenocortical insufficiency
vasogenic shock
b/c of their 4. Traumatic injuries
common 1. SIRS and/or sepsis
mechanism of o Systemic Inflammatory Response Syndrome (SIRS): systemic inflammatory response to a
vasomotor collapse variety of severe clinical insults; characterized by 2 or more of the following:
1) Temperature > 38ºC (100.4ºF), or temp < 36ºC (96.8ºF)
2) Heart rate > 90 bpms
3) Respiratory rate > 20 breaths per min. or PaCO2 < 32 mmHg
4) WBC count > 12,000 or WBC count < 4,000 (or > 10% bands)
o Sepsis: SIRS in association with culture-proven infection
o Septic Shock: sepsis w/ hypotension despite adequate fluid resuscitation, + manifestations of
hypoperfusion (i.e. lactic acidosis, oliguria, Δ in mental status)
o Multiple Organ Dysfunction Syndrome (MODS): altered organ function in an acutely ill
patient, in which homeostasis can’t be maintained without intervention
2. Anaphylactic and Anaphylactoid Shock:
o Anaphylaxis: allergic response to antigens (i.e. insect venom, drugs, foods) mediated by IgE.
o Anaphylactoid reactions are not immunologically-mediated.
Pathophysiology
o Symptoms are due to activation and release of inflammatory mediators (i.e. anaphylotoxins
C3a and C5a, histamine, kinins, prostaglandins, etc)
o These mediators produce vasodilation, ↑ capillary permeability, bronchospasm, airway
edema, and circulatory collapse secondary to a sudden ↓ in systemic vascular resistance and a
↓ in cardiac output.
Treatment
o Initial management consists of ensuring adequate airway, providing supplemental O2 and
administering epinephrine.
o Secondary therapy may include the use of aminophylline, corticosteroids, antihistamines
3. Hypoadrenal Shock:
o Shock due to adrenocortical insufficiency (relatively uncommon).
o Should be considered in patients with history of glucocorticoid therapy or in patients who
develop severe shock refractory to volume and pressor resuscitation.

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o Patients with high metabolic stress due to trauma, operation, or serious medical illness may
not exhibit symptoms of adrenocortical insufficiency in the unstressed state; thus, a relative
glucocorticoid deficiency may manifest itself only under conditions of severe stress.
Diagnosis:
o Clinical features of acute adrenocortical insufficiency may be similar but more severe than
those of Addison’s disease, such as hyperpigmentation, weight loss and GI symptoms (all or
some of which may or may not be present)
o Hypoglycemia in a hypotensive patient may suggest the diagnosis, which may be supported
by the findings of hyponatremia and hyperkalemia
o Diagnosis should be established by performance of rapid ACTH stimulation test, but
institution of corticosteroid therapy should not be delayed in unstable patients while awaiting
laboratory results. Baseline serum cortisol levels should be drawn before and 30-60 minutes
after the IV administration of 250μg of synthetic ACTH (cosyntropin).
 Peak cortisol level > 20 μg/100 ml suggests normal adrenal function
 Peak cortisol level < 20μg/100 mL suggests abnormal adrenal function
Treatment:
o Administration of stress doses of corticosteroids + hydration (glucose-containing saline
solutions)
o IV Dexamethasone, 4 mg, should be given to unstable patients in whom the diagnosis is
suspected; it will not interfere with ACTH stimulation test.
o Hydrocortisone 100 mg IV q 6 hrs, should be substituted once the stimulation test is
concluded b/c dexamethasone does not have mineralocorticoid activity.

4. Traumatic Shock: type of vasogenic shock that begins as hypovolemic shock.

Pathophysiology
o Microcirculatory derangements are common, leading to increased microvascular permeability
and excessive fluid requirements.
Causes
o This form of shock, which may develop with large burns or devastating soft tissue injuries, is
particularly refractory to fluid replacement therapy.
Diagnosis:
o In contrast to simple hypovolemic shock, traumatic shock is associated with:
 Larger volume losses
 Greater fluid sequestration in the extravascular compartments
 Greater activation of inflammatory mediators
 Development of SIRS
Treatment:
o Patients frequently require mechanical ventilation, pulmonary artery catheter monitoring, and
cardiovascular support with inotropic agents such as dobutamine or dopamine
o Despite aggressive resuscitation efforts, multiple organ dysfunction is frequently observed.

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 BODY WATER AND SOLUTE COMPOSITION
Body Water Composition
• Total Body Water: 40-60% total body weight in adults. More fat = less water, more muscle = more
water
• 2 Major Body Water Compartments: Intracellular Fluid (ICF) and Extracellular Fluid (ECF)
o ICF: 55% TBW. K+ major cation, PO4-, HCO3- major anions
o ECF: 45% TBW. Na+ major cation, Cl-, HCO3- major anions. Includes interstitium,
lymphatics, plasma
 Interstitial compartment (2/3): space between cells
 Intravascular compartment (1/3): within vessels
• Control of Body Water Distribution Between ICF & ECF by Osmolality
o Osmolality: measure of total # of solutes per mass of water; clnically, mmol/kg H2O
o ICF: principle osmoles K+, HCO3-, DNA, RNA, Creatine, ATP, ADP, Phospholipids, glucose,
urea
o ECF: principle osmoles Na+, Cl-, HCO3-
o Water moves rapidly between compartments until osmolality is equal
o Renal function regulates ICF & ECF sizes; retain sodium  expand ECF; urine osmolality
ranges from 100-1200 mmol/kg H2O
 Concentration depends on ADH (synthesized in hypothalamus, stored in posterior
pituitary)
 As ADH increases, urine osmolality increases
 Urine specific gravity 1.010 or less is dilute; ADH is low
 Urine specific gravity 1.030 or greater is concentrated; ADH is high
o As osmolality increases, strong conscious desire to drink occurs
• Disorders of Body Water Balance: Due to changes in production/release of ADH, exogenous
overproduction of ADH, failure of renal tubular cells to respond to ADH
o Brain injured patients stop synthesizing ADH if hypothalamus or pituitary are injured
 Dilute urine > 1L/hr – Diabetes Insipidus; become hyperosmolar

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 o Excess ADH produces overhydration, ECF osmolality < 285 mmol/kg H2O w/ concentrated
urine.
Body Solute Composition & Electrolyte Composition of ECF & ICF
• Distribution of Solutes Between ICF & ECF
o Difference in electrolyte composition of ICF & ECF sustained by transport enzymes
 Na+ from ICWECW in exchange for K+ via ATPase; 3Na+ out, 2K+ in; net
negative intracellular charge = resting membrane potential
o ICF [Na+] = 10 mmol/L, [K+] = 150 mmol/L
o ECF [Na+] = 140 mmol/L, [K+] = 4 mmol/L
Sodium: Normal Serum [Na+] 138 – 145 mEq/L.
• Mild Hyponatremia: 130-138…Moderate Hyponatremia: 120-130
o Rarely have signs/symptoms; identified on lab testing; look for reversible causes.
o Moderate hyponatremia w/ coexisting brain injury, infection, or tumor are at risk for
deteriorated neurologic function
• Severe Hyponatremia: < 120 mEq/L. causes cellular swelling
o Intracranial cell swelling headaches, lethargy, progression to coma, seizures
• IV infusion D5W rapidly produces hyponatremia in patients who have hemorrhaged, had acute
diarrhea, pancreatitis, burn w/ inflammatory edema. Volume contraction makes it worse due to
increased ADH secretion (increases water retention and dilution)
• Menstruating females w/ small body stature at highest risk for post-op syndrome of hyponatremia
decreased responsiveness, seizures, respiratory arrest. Have elevated ADH despite low serum
osmolality.
• Acute hyponatremia can complicate diuretic-induced diuresis due to Na+ loss and increased ADH.
Also sustained hyperglycemia causes osmotic diuresis.
• Brain injury causes excessive release of natriuretic peptides  cerebral salt wasting
o High urine output, high sodium excretion. Must replace sodium! Enteral nutrition often low
in sodium, may need isotonic or 3% hypertonic IV
• Treatment for acute hyponatremia & [Na+] < 120: increase serum [Na+] no more than 0.25 mEq/L/h; if
corrected too fastcentral pontine myelinolysis
• Chronic Hyponatremia
o SIADH:
 Diagnosis can only be made in euvolemic patients; serum osmolality <270 mmol/kg
H2O w/ inappropriately concentrated urine
 ADH Secreting tumor – carcinoid, small cell carcinoma of lung
 Cerebral injury, infection, or tumor affecting hypothalamus
o Other causes: medullary cystic disease, polycystic kidney disease, analgesic nephropathy,
chronic pyelonephritis, obstructive uropathy, post-decompression syndromes
o Rapid correction may cause central pontine myelinolysis: permanent neurologic disorder w/
spastic quadriparesis, pseudobulbar palsy, depressed levels of consciousness
 Don’t correct faster than 0.25 mEq/L/hr, or 8 mEq/kg/day
o Compensatory mechanisms: depletion of ICF K+: must replace K+ also
• Hypernatremia & Syndromes of Hypertonicity
o Moderate hypernatremia 146-159; >160 is severe, life-threatening
 Altered LOC, seizures, coma, intracerebral hemorrhage, postural hypotension, dry
mucous membranes, decreased skin turgor
o Acutely, water loss is most common cause
o Nephrogenic Diabetes Insipidus: impaired capacity of renal tubules to respond to ADH
 Results in moderate hypernatremia
 Dx by giving ADH and seeing no response
 Caused by chronically obstructed ureters, sickle cell nephropathy, medullary cystic
disease, lithium, glyburide, demeclocycline, amphotericin B
• Treatment of Hypernatremia

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 o 2o to dehydration: Isotonic saline IV to restore ICF contraction, then electrolyte-free H2O
o 2o to Central Diabetes Insipidus: give Desmopressin (DDAVP)
Potassium: Normal serum [K+] 4.5 mmol/L; kidney regulation by aldosterone (increase
aldosterone=increase K+ excretion)
• Hyperkalemia: [K+] > 5.0 mmol/L… > 6 changes resting cell membrane potential
o [K+] 6-7: tall, peaked T waves; particularly bad if T > R.
o [K+] > 7: P wave amplitude decreases, PR increases, QRS widens
o [K+] > 8: lethal – asystole, V-fib, wide pulseless idioventricular rhythms
o Acute onset renal dysfunction/renal failure: MCC of rapid onset hyperkalemia
 Loss of over 80% renal function can’t respond to aldosterone
o Drugs: spironolactone, triamterene, β-blockers, cyclosporine, tacrolimus, succinylcholine (in
patients w/ muscle atrophy, neurogenic denervation syndromes, severe burns, direct muscle
trauma, rhabdomyolysis, prolonged bed rest)
o Treatment: IV Ca+2 (i.e. calcium gluconate) to reduce risk for arrhythmia; NaHCO3 to buffer
ECW & push K+ in, Insulin/glucose infusions, hemodialysis
• Hypokalemia: < 3.5 mmol/L
o Fatigue, weakness, ileus, rhabdomyolysis, flaccid paralysis, respiratory compromise, cardiac
rhythm disturbances (atrial tachycardia w/ or w/o block, AV-dissociation, V-Tach, V-Fib; risk
of arrhythmia highest in pts on digoxin), depressed T-waves, U-waves
o Seen in pts w/ persistent vomiting, diarrhea, large volume draining gastric tubes, high output
enteric or pancreatic fistulas, CHF on multiple Rx, long-term diuretic Tx,
• Treatment of Hypokalemia:
o Require correction w/ KCl – hypokalemia associated w/ ECW contraction, where Cl- is major
anion
o Also give KPO4 via IV, as K in foods is often linked to phosphate
o Correct promptly to > 4.0 mmol/L to avoid arrhythmias, but not faster than 0.3 mmol/kg/hr
o Infuse in central line – K+ may irritate peripheral veins
o Rarely need more than 200 mmol K in one day
o If also acidotic, correct hypokalemia first
o If diabetic in DKA, add K+ to resuscitation fluids – insulin will cause hypokalemia
o If on diuretics, give spironolactone or triamterine to limit K+ loss in urine
o Also give Mg2+ – cofactor for K+ and also reduces risk of arrhythmias
CALCIUM AND MAGNESIUM
• Ca+2: 8.5-10.5 mg/dL; protein bound, diffusible on anions, and ionized (iCa+2)
o Cofactor in coags, needed for regulation of neuronal, myocardial, renal cell function, 2nd
messenger
o iCa+2: biochemically active form, 45% total.
• Serum [iCa+2] controlled by PTH, Calcitonin, Vit D
o PTH (parathyroid cells) increases [iCa+2]: activates osteoclasts to release Ca+2 from bone,
stimulates tubule cells in proximal nephron to absorb Ca+2 and excrete PO4-, enhances
absorption from gut (w/ vit D)
o Calcitonin (C-cells of thyroid) decreases [iCa+2]: increases Ca+2 incorporation into bone
matrix
o Vit D: converted to 25-hydroxycholecalciferol (25D) in liver, 1,25D in kidney. Increases
transport of Ca+2 & P from bowel lumen into ECF, increases bone resorption
• Mg+2: 1.4-2.0 mEq/L, 20% protein bound, ,1% in ECF
o Low Mg: hyper-reflexia, spasticity, similar symptoms to hypocalcemia
Hypercalcemia
• Mild: 10.5-12 mg/dL… Moderate: 12-14.5 mg/dL… Severe: > 15 mg/dL
• Transient small elevations generally asymptomatic; Sustained: renal lithiasis

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• Severe hypercalcemia: weakness, stupor, CNS dysfunction. Renal defects polyuria, loss of Na+ &
H2O.
• Hypercalcemic crisis: > 17 mg/dL. Tachyarrhythmias, coma, acute renal failure, ileus
• Causes: Hyperparathyroidism (osteoclastic..see above), multiple myeloma, lymphoma, solid tumors w/
mets to bone (osteoclastic-i.e. breast), thiazides, vitamin A & D overdose, immobilization (in young
patients…high rate of bone turnover)
o Treat Underlying Cause
o Hyperparathyroidism: surgical removal of parathyroid tissue
o Tumors in bone: Bisphosphonates – reduce osteoclast activity (zolendronic acid, pamidronate
disodium, etidronate disodium)
o Giving calcitonin increases renal excretion of Ca+2 and suppresses osteoclasts
o IV Saline and Loop Diuretics - induces saline diuresis & increased calcium clearance
Hypocalcemia
• Acute Hypocalcemia – impaired membrane depolarization, CNS dysfunction, paresthesias, muscle
spasms/tetany, seizures, prolonged QT
• Tumor Lysis Syndrome: Hypocalcemia, hyperphosphatemia, hyperuricemia, hyperkalemia.
Associated w/ solid tumors & lymphomas. May cause ARF needing dialysis
• Resuscitation from shock, severe pancreatitis, rapid infusion of citrate during blood transfusion all lead
to hypocalcemia
• Treatment of severe hypocalcemia: IV 10 ml 10% CaCl2, gives 272mg Ca+2
o Infuse carefully; rapid shifts in calcium can cause arrhythmias, especially in patients on
digoxin
o In patients w/ high phosphate, rapid calcium infusion can cause precipitation of calcium
o Ca+2 preparations are caustic; give quickly in central line. Peripherally, causes
skin necrosis
Hypermagnesemia & Hypomagnesemia
• Hypermagnesemia mostly seen in patients w/ renal failure, exacerbated by Mg+2 containing drugs like
antacids
o Mg blocks shift of Ca into cardiac cellsheart failure
• Hypomagnesemia: chronic diarrhea, prolonged aggressive diuretic tx, heavy EtOH, DM w/ osmotic
diuresis. Magnitude of hypomagnesemia often parallels magnitude of hypocalcemia
o Give IV MgSO4… always give MgSO4 concurrently with Calcium (if needed)

Figure 5-7 Electrocardiographic (ECG) changes indicating hyperkalemia. The T wave is tall, narrow, and
symmetrical.B, ECG changes indicating acute myocardial infarction. The Twave is tall but broad-based and
asymmetric. (From Somers MP, Brady WJ, Perron AD, Mattu A: The prominent T wave:
Electrocardiographicdifferential diagnosis. Am J Emerg Med 20:243-251, 2002.)

12
 Composition of Common Crystalloid Solutions
Solution Other Name [Na+](mmol/L) [Cl-](mmol/L) [Glucose](mmol/L) [Glucose](mg/dl)
D5W 5% Dextrose 0 0 278 5000
2/3D & 3.3% Dextrose
51 51 185 3333
1/3S / 0.3% saline
Half-normal
0.45% NaCl 77 77 0 0
saline
Normal
0.9% NaCl 154 154 0 0
saline
Ringer's Lactated
130 109 0 0
lactate Ringer

HEMATOLOGY

13
 NORMAL COAGULATION NORMAL ANTICOAGULATION

3 initial responses to vascular injury: Antithrombin III is the key to anticoagulation

Vascular vasoconstriction -binds and inhibits thrombin
Platelet adhesion -inhibits factors IX, X, XI
Thrombin generation -Heparin binds AT-III

Prothrombin complex X, V, Ca, platelet factor 3, Protein C – vitamin K dependent; degrades factors
and prothrombin V and VIII; degrades fibrinogen
-forms on platelets
-catalyzes the formation of thrombin Protein S vitamin K dependent; protein C cofactor

Factor X is the conversion point for both paths Fibrinolysis

Tissue factor pathway inhibitor inhibits factor X
Fibrin combines with platelets to for platelet plug
 hemostasis
Thrombin is the key to anticoagulation
-converts fibrinogen to fibrin and fibrin split
products
-activates factors V and VIII
-activates platelets
Tissue plasminogen activator released from
endothelium and converts plasminogen to plasmin
Plasmin degrades factors V, VIII, fibrinogen, and
fibrin  loose platelet plug
Alpha-2 antiplasmin natural inhibitor of plasmin,
released from endothelium

Factor VII shortest half life

Factor V and VII –labile factors, activity lost in stored blood, activity not lost in FFP
Factor VIII only factor not synthesized in liver

Vitamin K dependent factor –II, VII, IX, and X; protein C and S

Vitamin K takes 6 hours to take effect

FFP effect is immediate and lasts 6 hours

Factor II - prothrombin
Normal half life RBCs: 120 days, platelets: 7 days, PMNs: 1-2 days

Prostacyclin (PGI2) – from endothelium, decreases platelet aggregation and promotes

vasodialation

Thromboxane (TXA2) – from platelets, increases platelet aggregation and promotes

vasoconstriction
- triggers release of calcium in platelets  exposes GpIIb/IIIa receptor and causes platelet to
platelet binding, platelet to collagen binding
- activates PIP system to further increase calcium

COAGULATION FACTORS

Cryoprecipitate Contains highest concentration of vWF VIII, used in von Willebrand’s

disease and Hemophilia A; also contains fibrinogen
FFP has high level of all factors
DDAVP and conjugated estrogens cause release of VIII and vWFfrom endothelium

COAGUALATION MEASUREMENTS
PT measures II, VII, IX, and X, fibrinogen; best for lover synthetic function
PTT measures most factors except VII and XIII, also measures fibrinogen
Want PTT 60-90 for anticoagulation

14
ACT -activated clotting time; want ACT 150-200for routine anticoagulation, 400 for
cardiopulmonary bypass
INR>1.5 relative contraindication for performing surgical procedures
INR>1.3 relative contraindication for central line placement, percutaneous needle
biopsies and eye surgery

CONDITIONS CAUSING ABNORMAL BLEEDING

Incomplete hemostasis most common cause of surgical bleeding

Von Willebrand’s disease most common congenital bleeding disorder
Types I and II are autosomal dominant; type III is autosomal ecessive
PT normal, PTT can be normal or abnormal, have long bleeding time
Type I and III Tx: cryoprecipitate, DDAVP, conjugated estrogens
Type II Tx: cryoprecipitate
Hemophilia A (VIII deficiency)
Sex linked recessive
Needs levels 100% preoperatively, 30% after surgery
Prolonged PTT and normal PT
Factor VIII crosses placenta, newborns may not bleed at circumcision
Tx for hemophiliac joint: no aspiration, ice, keep joint mobile with range of
motion exercises, factor VIII concentrate or cryoprepitate.
Hemophilia B (IX deficiency) – Christmas tree disease
Sex linked recessive
Needs levels 50% preoperatively
Prolonged PTT and normal PT
Tx: factor IX concentrate of FFP
Factor VII deficiency prolonged PTT normal PT, bleeding tendency. Tx: FFP
Platelet disorders – causes bruising, epitaxis, mucosal bleeding, petechiae, purpura
Acquired thrombocytopenia can be caused by H2 blockers, heparin
Uremia inhibits GpIb receptors, GpIIb/IIIa receptors, and vWF
Ticlopidine decreases ADP in platelets, prevents exposure of GpIIb/IIIa
Dipyridamole inhibits cAMP phosphodiesterase, ADP induced platelet
aggregation
Heparin-induced thrombocytopenia (HIT) thrombocytopenia due to antiplatelet
antibodies, results in platelet destruction
Forms a white clot
Can occur with low doses of heparin
Low molecular weight heparin may decrease risk
Disseminated intravascular coagulation (DIC) decreased platelets, prolonged PT, PTT
Low fibrinogen, high fibrin split products, high D-dimer
Often initiated by tissue factor
ASA stop 7 days before surgery; will have prolonged bleeding time
Inhibits cyclooxygenase in platelets, decrease TXA2
Coumadin stop 7 days before surgery consider starting heparin while coumadin wears
off
Platelets keep >50,000 before surgery, keep >20,000 after surgery
Prostate surgery can release urokinase, activates plasminogen thrombolysis
Tx: Amicar (aminocaproic acid)
H & P best way to predict bleeding risk
Normal circumcision does not rule out bleeding disorders; can still have clotting factors
from mother
Abnormal bleeding with tooth extraction or tonsillectomy picks up 99% patients with
bleeding disorder
Epitaxis common with vWF deficiency and platelet disorders
Menorrhagia common with bleeding disorders
CONDITIONS CAUSING ABORMAL HYPERCOAGULABILITY

15
Leiden factor most common congenital hypercoagulability disorder, resistance to
activated protein C, defect in factor V. Tx: heparin, warfarin
Hyperhomocysteinemia 10% of spontaneous venous thromboses, Tx: folic acid, B12
Protein C or S deficiency 5% of spontaneous venous thromboses, Tx: heparin, warfarin
Anti-thrombin III deficiency 2-3% of spontaneous venous thromboses, heparin does not
work in these patients, can develop after heparin exposure. Tx: ATIII concentrate
or FFP followed by heparin or hirudin or ancrod, warfarin
Polycythemia vera defect in platelet function, usually have thrombosis, can have
bleeding; keep Hct <48 and platelets <400 before surgery. Tx: ASA
Lupus anticoagulant antiphospholipid antibodies, procoagulant yet prolonged PTT not
corrected with FFP. Tx: heparin, warfarin
Acquired hypercoagulability –tobacco – most common factor, malignancy,
inflammatory bowel disease, infections, oral contraception, pregnancy, rheumatoid arthritis,
myeloproliferative disorders.
Warfarin induced skin necrosis occurs when placed on coumadin without being
heparinized first. Due to short half life of protein C and S, patients with protein C
deficiany are especially susceptible. Tx: heparin

Key elements in development of venous thromboses (Virchow’s triad) – stasis,

endothelial injury, and hyoercoagulability
Key element in the development of arterial thrombosis – endothelial injury

DEEP VENOUS THROMBOSIS (DVT) PULMONARY EMBOLISM

Stasis, venous injury, hypercoagulability risk factors
Treatment:
1st warfarin for 6 months
2nd warfarin for 12 months
3rd or significant PE -warfarin for lifetime
Greenfield filters for contraindications to
anticoagulation, temporary filters can be inserted in
patients at high risk for DVT
If patient has coded and is in shock, go to OR
otherwise give heparin or suction catheter based
intervention.
½ of positive VQ scans have negative duplexes.
Most common from the ileofemoral region.

HEMATOLOGIC DRUGS

Anticoagulation agents
Warfarin prevents vitamin K decarboxylation of glutamic residues on vitamin K
dependent factors
Dextran inhibits platelets and coagulation factors
Sequential decompression devices improve venous return but also induce fibrinolysis
with compression (release of tPA)
Heparin activates antithrombin III, reversed with protamine (cross reacts with NPH insulin or previous
protamine reaction), half life is 60-90 minutes,
cleared by reticuloendothelial system
Hirudin leeches, irreversible direct thrombin inhibitor, also the most potent direct
inhibitor of thrombin
Argatroban direct thrombin inhibitor, metabolized in the liver, often used in
patients with HIT, half life is 50 minutes
Bivalirudin reversible direct thrombin inhibitor, metabolized by proteinase enzymes in
the blood, half life is 25-30 minutes
Ancrod Malayan pit viper venom, stimulates tPA relaease

Procoagulant agents (antifibrinolytics)

16
Aminocaproic acid inhibits fibrinolysis by inhibiting plasmin, used in DIC persistent
bleeding followed by cardiopulmonary bypass,thrombolytic overdoses
Aprotinin (Trasylol) acid inhibits fibrinolysis by inhibiting plasminogen activation

Thrombolytics
Streptokinase has high antigenicity ; irokinase, tPA. For thrombinolytics to work, a
guidewire must get passed the obstruction . fibrinogen <100 assocaited with increased risk and
severity of bleeding
BLEEDING PRODUCTS

All blood products carry a risk of HIV and hepatitis, except albumin and serum globulins

CMV negative blood use in low birth weight infants, transplant patients

Clerical error leading to ABO incompatibility number 1 cause of death from transfusion reaction

Stored blood is low in 2,3 BPG causes left shift (increased affinity for oxygen)

HEMOLYSIS REACTIONS OTHER REACTIONS

Acute hemolysis ABO incompatibility, antibody
mediated, back pain, chills, tachycardia, fever,
hemoglobinuria, can lead to ATN, DIC, shock.
Tx: fluid, diuretics, HCO3-
Delayed hemolysis antibody mediated against
minor antigens.
Tx: histamine blockers (Benadryl), supportive
Non-immune hemolysis from squeezed blood.
Tx: fluids, diuretics
Febrile non-hemolytic transfusion reaction most
common transfusion reaction. Usually recipient
antibody reaction against WBCs in donor blood
Tx: discontinue transfusion if patient had previous
transfusion, use WBC filter for subsequent
transfusion
Anaphylaxis bronchospasm, hypotension, uticaria.
Usually IgG against IgA deficient patient. Tx:
fluids, Lasix, pressors, steroids, epinephrine,
histamine blockers

Urticaria usually nonhemolytic, usually a reaction

against plama proteins or IgA in the transfused
blood. Tx: histamine blockers (Benadryl),
supportive

Transfusion related acute lung injury

Caused by antibodies to recipient WBCs, clot in
pulmonary capillaries

OTHER TRANSFUSION PROBLEMS

Cold poor clotting, can be caused by cold products or cold temperature, patient needs to
be warm to clot correctly
Dilutional thrombocytopenia occurs after ten units of PRBCs
Hypocalcemia occurs when massive transfusion – Ca is required for clotting cascade
Antiplatelet antibodies develop in 20% of patients after 10-20 platelet transfusions
Hetastarch ca use up to one liter without risk of bleeding complications

TISSUE INJURY & RESPONSE

17
• Wound repair: effort of injured tissues to restore normal function & structural integrity after injury
• Regeneration is perfect restoration of preexisting tissue architecture in absence of scar formation. Only
occurs in embryonic tissue, bone, liver
• Wound closure is primary, secondary, or tertiary
o Primary, AKA First-Intention: wounds are sealed immediately w/ simple suturing, skin
graft placement, or flap closure
o Secondary, AKA Spontaneous-Intention: no active intent to seal wound; associated w/
highly contaminated wound, closes by reepithelialization resulting in wound contraction.
o Tertiary, AKA Delayed Primary Closure: Contaminated wound initially treated w/
repeated debridement, systemic or topical antibiotics, or negative pressure wound therapy.
Once ready, surgical intervention such as suturing, skin graft placement, or flap design.
WOUND HEALING PHASES
• 3 phases: Inflammation, Proliferation, Maturation
o Inflammatory (reactive) phase: Immediate response. Limit amount of damage and prevent
further injury.
 Eschar, fibrinous exudate
o Proliferative (regenerative, reparative) phase: reepithelialization, matrix synthesis,
neovascularization
 Granulation tissue
o Maturational (remodeling) phase: Scar contraction w/ collagen cross-linking, shrinking, loss
of edema
 Contracting or advancing edge
• Inflammatory Phase: Increased vascular permeability, migration of cells into wound by
chemotaxis, secretion of cytokines & growth factors, & activation of migrating cells
1. Hemostasis & Inflammation: Acute injuryblood vessel damage, exposure of
subendothelial collagen (IV & V)platelet aggregation (vWF)/activation of coagulation
pathwayvasoconstriction (to limit bleeding), then vasodilation & increased
permeability
2. Increased Vascular Permeability: Platelet alpha granules have PDGF, TGF-β, IGF-I,
Fibronectin, Fibrinogen, Thrombospondin, vWF. Platelet dense bodies have vasoactive
amines (5-HT) which cause vasodilation and increased permeability. Mast cells release
histamine, 5-HT. Clotting cascade is activated, so are TXA2, Prostaglandin F2α
3. Polymorphonuclear Cells: Immediate
1. Histamine, 5-HT increase permeability. Complement C5A, Leukotriene B4
promote adherence & chemoattraction of neutrophils, enhanced by Leukotriene
C4, D4 also monocytes make IL-1, TNF-α. Neutrophils come in, release
elastases, proteases, chemotactic factors, attracting more neutrophils. Leads to
Rubor, Tumor, Calor, Dolor.
2. Integrins function in motility of PMN’s: activation of integrins, then spreading
of pseudopods, traction through binding of integrins, and retraction of
pseudopod during movement.
3. Activated neutrophils scavenge for necrotic debris, foreign material, bacteria, &
then generate free oxygen radicals. Superoxide dismutase catalyzes production
of H2O2
4. Neutrophils have receptors for IgG, C3b, C3bi
5. PMNs are for initial injury and migrate in until contamination is cleared; live 24
hours; once gone, then monocytes come in. Sterile incisions will heal normally
w/o PMN’s.
4. Macrophage: The one cell truly crucial to wound healing. Arrives w/in 24-48 hours
1. Chemotactic factors: bacterial products, C5a, thrombin, fibronectin, collagen,
TGF-β, PDGF-BB. Have receptors for IgG, C3b, fibronectin

18
 2. Macrophages mediate angiogenesis & fibrodysplasia. IL-2 increases release of
free radicals, potentiates them. Macrophages also produce NO, induce
phospholipase to release TXA2, Prostaglandin F2α. Additionally, macrophages
release LTB4, C4 , matrix metalloproteinases
3. Secrete IL-1: activates lymphocytes, stimulates hypothalamuspyrogenic.
Induces vasodilators & stimulates coagulation, increases collagenase production,
stimulates cartilage degradation & bone reabsorption, activates neutrophils,
promotes chemotaxis. Beneficial in 1st week, damaging beyond
4. Secrete TNF-α: chemotactic, hemostasis, increased vascular permeability,
enhanced endothelial proliferation, pyrogenic, increased collagenase,
reabsorption of cartilage and bone, releases PDGF, more IL-1. Excessive
production associated w/ multi-system organ failure, morbidity/mortality.
Essential early, damaging late.
5. Secrete IL-6: Stem cell growth, activation of B & T cells, regulation of synthesis
of hepatic acute phase proteins. Synergistic w/ IL-1, TNF-α
6. Secrete IL-8: increased PMN/mono chemotaxis, PMN degranulation, increase
endothelial adhesion molecules
7. Secrete INF-γ: T-cells secrete this also. Causes macrophage/PMN activation,
increased cytotoxicity, reduces local wound contraction & aids in remodeling.
Used to treat hypertrophic/keloid scars.
8. Release PDGF: specifically PDGF-BB, stimulates fibroblast, endothelial cell,
keratinocyte proliferation
9. Release TGF-α: stimulates epidermal growth, angiogenesis
10. Release TGF-β: stimulates monocytes to release TGF-α, IL-1, PDGF. Causes
fibroblast migration, maturation, extracellular matrix synthesis
5. T-Lymphocytes – 5th day. B-Lymphocytes down-regulate healing as wound closes
1. IL-2, Fibroblast-activating factor stimulate fibroblasts
2. TGF-β, TNF-α, IFN-γ. IFN stimulates macrophages to release cytokines, causes
decreased synthesis of prostaglandins, suppresses collagen synthesis, inhibits
macrophages from leaving injurymay be important in chronic wounds
• Proliferative Phase: angiogenesis, fibroplasia, epithelialization. Characterized by granulation
tissue (capillary bed, fibroblasts, macro’s, collagen/fibronectin/hyaluronic acid).
1. Angiogenesis: New blood vessel formation.
1. Activated endothelial cells degrade basement-membrane of postcapillary
venules, bring in migrating endothelial cells that form tubule/lumen, and new
basement membrane is deposited
2. Vascular Cell Surface Adhesion Molecule-1 (VCAM-1) upregulated, brings in
more blood cells. Matrix degrading enzumes are released, and the basement
membrane is degraded, brings in endothelial cells due to FGF, PDGF (family
includes VEGF), TGF-β, results in scaffolding.
2. Fibroplasia
1. Produce extracellular matrix, collagen. Takes 3-5 days for undifferentiated
mesenchyme to differentiate into fibroblasts – results in lag phase of wound
healing between injury and appearance of collagen.
2. Collagen synthesis declines after 4 weeks, and collagen matures in months to
years, new capillaries disappear; changes increase wound strength.
3. Epithelialization: Epidermis prevents fluid loss, bacterial invasion. Basement membrane
gives structural support, attachment between epidermis & dermis
1. Basement has lamina lucida (laminin, heparin sulfate), lamina densa (type IV
collagen), anchoring fibrils (type IV collagen)
2. Re-epithelialization begins hours after injury. Keratinocytes begin resurfacing
wound. Basement membrane gets repaired first.
3. Once completed, cells become columnar, then stratified

19
 4. Extracellular Matrix: Scaffold to stabilize structure
1. Cells within it make Glycosaminoglycans, collagen, elastin, fibronectin, laminin
2. Proteoglycan gives shock-absorption, diffusion medium. Collagen gives
organization and strength. Elastin gives resilience. Matrix proteins give
adhesion.
5. Collagen Structure: Proline & Glycine
1. Proline gives stability, glycine allows tight packing.
2. Connective tissue made of types I, II, III, V, XI. I = skin/bone, most common.
III = newborns, early wounds.
6. Collagen Synthesis: Occurs in ribosomes, ER
1. Proline & lysine are hydroxylated  hydroxylproline, hydroxylysine, forms
triple-stranded helix.
1. Scurvy prevents proline hydroxylation  fragile blood vessels, loose
teeth
2. Vit. C, TGF-β, IGF-I, IGF-II increase collagen synthesis
3. IFN-γ, Glucocorticoids decrease collagen synthesis
2. Cross-linking of lysine residues provides tensile strength
7. Elastic Fibers: provide resilience. Predominantly composed of elastin. Hydrophobic
8. Glycosaminoglycans & Proteoglycans:
1. GAG: polysaccharide chains w/ repeating dissaccharide units. Negative charge
attracts waterturgor to withstand compressive force.
1. Hyaluronan: especially prevalent in fetal tissues. Not attached to any
protein. Facilitates cell migration, reduces strength of adhesion of
migrating cells to matrix fibers
2. Chondroitin Sulfate, Dermatan Sulfate
3. Heparan Sulfate
4. Keratan Sulfate
2. Proteoglycans: Glycoproteins w/ protein core and GAG chains.
1. Provide space around cells, form gels to regulate proteins
1. Immobilize proteins, provide protein reservoir, alter proteins,
prevent protein degradation, block protein activity
9. Basal Lamina: Flexible, thin mats of ECM separating cells & epithelia from surrounding
connective tissue. Together w/ type IV collagen, forms basement membrane
1. Forms molecular filter (glomerulus), Selective barrier to some cells, Scaffold for
regenerating cells to migrate. Element in tissue regeneration where basal lamina
survives
10. Degradation of the ECM: By MMP’s, proteases, to help cells migrate
1. Clears a path, exposes binding sites, facilitates cell detachment, releases signal
proteins to promote migration
• Maturation
1. Wound Contraction: centripetal movement of whole thickness of surrounding skin;
reduces amount of disorganized scar
1. Fibroblasts in contracting wound become myofibroblasts. Have alpha smooth
muscle actin – Stress Fibers – appear at day 6
2. Matrix metalloproteinases; may be necessary to cleave attachment between
fibroblast & collagen.
2. Wound contracture: Physical constriction or limitation of function & results from wound
contraction. Ex: Scars traversing joints & prevent extension, or scars involving eyelid or
mouth
3. Remodeling: Fibroblast population decreases, dense capillary network regresses.
1. Wound strength increases w/in 1-6 weeks, plateaus up to 1 year.
2. Scar strength only 30% tensile strength compared to unwounded skin. Also is
more fragile than regular skin.

20
 3. Increase in breaking strength after 3 weeks.

ABNORMAL WOUND HEALING

• Amount of tissue lost or damaged, amount of foreign material or bacterial inoculation, length of
exposure to toxic factors all affect time to recovery
• Chemotherapeutic agents, atherosclerosis, cardiac/renal failure, location on body affect wound healing
• Blood supply in lower extremity is worst in body. Blood supply to hands & feet is best. Older patient,
slower healing.
• Hypertrophic Scars & Keloids: Proliferative scars
o Excessive collagen deposition vs degradation
 Stretched collagen bundles in same plane as epidermis (Normal scar has collagen
randomly arrayed, relaxed.
o Keloid: Scars that grow beyond borders of original wounds. Rarely regress w/ time.
 More prevalent in pts w/ darkly pigmented skin
 Genetic predisposition
 Above clavicles, on trunk, on upper extremities, on face.
 Can’t be prevented; refractory to medical & surgical treatment
 Thicker, more abundant collagen, paucity of cells in center
o Hypertrophic Scars: Raised scars that remain w/in confines of original wound & frequently
regress spontaneously.
 Anywhere on body
 Islands of cell aggregates in center
 Preventable; Scars perpendicular to underlying muscle fibers are flatter & narrower;
contraction approximates wound edges
• Chronic Non-healing Wounds
o Chronic wounds have derangements in various stages of healing, unusually
elevated/depressed levels of cytokines/growth factors/proteinases.
• Infection
o Most common cause of healing delays; if bacterial count > 105/g or if β-hemolytic strep
present, won’t heal by any means
o Increases inflammation and interferes w/ epithelialization, contraction, collagen deposition
o Accelerate expression or increase MMPs, growth factors, cytokines
• Hypoxia
o Oxygen critical for post-translational hydroxylation of prolyl & lysyl residues for triple-helix
formation & cross-linking of collagen fibers.
o Angiogenesis proceeds poorly when PO2 below 40mm Hg.
o Anemia, tobacco, limit O2 capacity in blood and causes poor healing
• Diabetes: Impairs all stages of wound healing. Prone to atherosclerosis, ischemia, repetitive trauma,
infection.
o Hypoxia: due to vascular disease (large vessel & microvascular)
o Repeated trauma, attenuated inflammatory response, impaired chemotaxis, inefficient
bacterial killing increases risk for infection, and infection increases metabolism locally,
increasing O2 requirements
o Increased collagen degradation
• Ionizing Radiation
o Causes endothelial cell injury w/ endarteritisatrophy, fibrosis, delayed tissue repair
o Angiogenesis isn’t initiated
• Aging: Elderly more likely to have surgical wound rupture, delayed healing

21
 o Collagen content decreases, has distorted architecture/organization
o Increased MMP’s, decreased reepithelialization, decreased collagen synthesis/increased
degradation.
o Decreased response to hypoxia
• Malnutrition
o Protein: Albumin <2.0 g/dL can cause wound healing delay or dehiscence
o Vitamin C deprivation delays wound healing – give 100-1000g/day to reverse it
o Vitamin A deficiency impedes monocyte activation, cellular adhesion, causes lysosomal
membrane destabilization, counteracts effects of glucocorticoids
o Vitamin K deficiency limits synthesis of factors VII, IX, X; Vit K metabolism impeded by
antibiotics
o Zinc deficiency in pts w/ large burns, severe multiple trauma, hepatic cirrhosis. Causes early
wound healing delays
• Drugs
o Nitrogen mustard, cyclophosphamide, methotrexate, bischloroethylnitrosurea, doxorubicin are
most potent wound inhibitors – Don’t Give Pre-Op!!
 Reduce mesenchymal cell proliferation, reduce number of platelets, inflammatory
cells, growth factors.
o Tamoxifen: decreases cell proliferation, dose-dependent decrease in wound-breaking strength
o Glucocorticosteroids impair fibroblast proliferation, collagen synthesis, decrease granulation
tissue formed
o Steroids stabilize lysosomal membranes (give Vitamin A) and decrease breaking strength
o NSAIDS at supratherapeutic levels delay healing

FETAL WOUND HEALING

• Fetal skin wounds heal rapidly, without scarring & inflammation

• Adult skin has no regeneration of dermal appendages – hair follicles, sweat glands, sebaceous glands
• Normal skin: Reticular collagen pattern. Healed skin: Densely packed collagen perpendicular to
wound surface

WOUND DRESSINGS
• Nonsurgical Wounds – Dressings should…
o Protect wound from trauma & contamination, absorb wound exudates, obliterate dead space,
provide compression, all while not adhering to the wound, provide immobilization.
o Not every dressing provides every function, and not every wound needs it to.
• Types of dressings: Occlusive
o Provides mildly acidic pH, low O2 tension; good for fibroblasts & granulation tissue
o Also provides moisture retention, mechanical protection, barrier to bacteria
o Biologic dressings: Allograft, xenograft, amnion, skin substitutes
• Types of dressings: Absorptive
o Beneficial for wounds w/ lots of exudates or high bacterial counts.
o Lyofoam, Allevyn, Curafoam, Flexzan, VigiFOAM
o Slower healing than w/ occlusive dressings
• Types of dressings: Non-Adherent
o Fine-mesh gauze w/ supplementation to augment occlusive or antibacterial properties
o Scarlet Red (anti-microbial) or Xeroform (occlusive, hydrophobic, anti-bacterial)
• Negative Pressure-Assisted Wound Closure
o Removes chronic edema, increases local blood flow, stimulates granulation tissue
o Faster healing with fewer complications

22
o May result in increased bacterial counts

23
CYTOKINE CELL SOURCE BIOLOGIC ACTIVITY
Proinflammatory Cytokines
TNF-α Macrophages PMN margination and cytotoxicity, with or without collagen synthesis; provides
metabolic substrate
IL-1 Macrophages Fibroblast and keratinocyte chemotaxis, collagen synthesis
Keratinocytes
IL-2 T lymphocytes Increases fibroblast infiltration and metabolism
IL-6 Macrophages Fibroblast proliferation, hepatic acute phase protein synthesis
PMNs
Fibroblasts
IL-8 Macrophages Macrophage and PMN chemotaxis, keratinocyte maturation
Fibroblasts
IFN-γ T lymphocytes Activates macrophages and PMNs, retards collagen synthesis and cross-linking,
stimulates collagenase activity
Macrophages
Anti-inflammatory Cytokines
IL-4 T lymphocytes Inhibition of TNF, IL-1, IL-6 production; fibroblast proliferation, collagen
synthesis
Basophils
Mast cells
IL-10 T lymphocytes Inhibition of TNF, IL-1, IL-6 production; inhibition of macrophage and PMN
activation
Macrophages
Keratinocytes
From Rumalla VK, Borah GL: Cytokines, growth factors, and plastic surgery. Plast Reconstr Surg
108:719-733, 2001.
IFN-γ, interferon-γ; IL, interleukin; PMNs, polymorphonuclear leukocytes; TNF, tumor necrosis factor.

24
 Table 8-2 -- Cytokines That Affect Wound Healing
CYTOKINE ABBREVIATION SOURCE FUNCTIONS
Platelet-derived growth factor PDGF Platelets, macrophages, Chemotactic for PMNs, macrophages, fibroblasts,
endothelial cells, and smooth muscle cells; activates PMNs,
keratinocytes macrophages, and fibroblasts; mitogenic for
fibroblasts, endothelial cells; stimulates
production of MMPs, fibronectin, and HA;
stimulates angiogenesis and wound contraction;
remodeling
Transforming growth factor-β TGF-β Platelets, T lymphocytes, Chemotactic for PMNs, macrophages,
(including isoforms β1, β2, macrophages, endothelial lymphocytes, and fibroblasts; stimulates TIMP
and β3) cells, keratinocytes, synthesis, keratinocyte migration, angiogenesis,
fibroblasts and fibroplasia; inhibits production of MMPs and
keratinocyte proliferation; induces TGF-β
production
Epidermal growth factor EGF Platelets, macrophages Mitogenic for keratinocytes and fibroblasts;
stimulates keratinocyte migration
Transforming growth factor-α TGF-α Macrophages, T Similar to EGF
lymphocytes,
keratinocytes
Fibroblast growth factor-1 and FGF Macrophages, mast cells, Chemotactic for fibroblasts; mitogenic for
-2 family T lymphocytes, fibroblasts and keratinocytes; stimulates
endothelial cells, keratinocyte migration, angiogenesis, wound
fibroblasts contraction, and matrix deposition
Keratinocyte growth factor KGF Fibroblasts Stimulates keratinocyte migration, proliferation,
(also called FGF-7) and differentiation
Insulin-like growth factor IGF-I Macrophages, fibroblasts Stimulates synthesis of sulfated proteoglycans,
collagen, keratinocyte migration, and fibroblast
proliferation; endocrine effects similar to those of
growth hormone
Vascular endothelial cell VEGF Keratinocytes Increases vasopermeability; mitogenic for
growth factor endothelial cells
Modified from Schwartz SI (ed): Principles of Surgery, 7th ed. New York, McGraw-Hill, 1999, p 269.
HA, hyaluronic acid; MMPs, matrix metalloproteinases; PMNs, polymorphonuclear leukocytes; TIMP,
tissue inhibitor of matrix metalloproteinase.

Factors That Inhibit Wound Healing

Infection
Ischemia
Circulation
Respiration
Local tension
Diabetes mellitus
Ionizing radiation

25
Advanced age
Malnutrition
Vitamin deficiencies
Vitamin C
Vitamin A
Mineral deficiencies
Zinc
Iron
Exogenous drugs
Doxorubicin (Adriamycin)
Glucocorticosteroids

Surgical Nutrition
Sangeetha Kolluri
- Subjective Global Assessment
o Based on history, intake, unintentional weight loss > 7-10 lbs, disease, functional status
o Low serum albumin: < 3 g/dL
o PE – temporalis muscle wasting, fat wasting, edema or ascites, glossitis, skin lesions
o Mild/moderate malnutrition = >10%, severe = > 20%, pre-morbid = > 30%
- Biochemical Indicators
o Albumin
 Visceral protein, indicates malnutrition in the absence of other causes of low
albumin (hepatic insufficiency, protein-losing nephropathy, enteropathy)
 Half-life = 21 days, so can’t tell short term nutrition status
o Acute phase reactants – CRP, complement C3 and C4; also, see low albumin and pre-
albumin because the body uses up the proteins trying to make APRs
o Rapid Turnover Proteins
 Transferrin – half-life = 8 days, but can be seen with anemia; < 220 mg/dL
 Thyroxin-binding pre-albumin – half-life = 2 days
 Retinol-binding protein (RBP) – half life = 12 hrs
o Nitrogen balance
o Total N loss (g/day) = 24 hr urinary urea nitrogen (UUN) + 4 g/day fecal and non-urinary
N loss
 To do this: 24 hr urine collection, figure out how many g N given daily, and amt
of carb needed to utilize the N (calorie:nitrogen ratio)
- Immunologic Function
o Delayed cutaneous hypersensitivity – anergy can also be seen with cancer, severe
infection, renal or hepatic failure, after chemo or radiation
o Total lymphocyte count < 1500 cells/mm3
o Check complement levels, neutrophil function, opsonic index – not widely used
- Nutrition and Stress
o Normally…
 Carbs – 4 kcal, dextrose – 3.4, protein – 4, fat – 9
 Carbs + fat = 85% of daily energy expenditure, protein = 15%
 1 gram nitrogen = 6.25 g protein
 What you need: 30-35 kcal/kg/day
• Protein – 0.8-1 g/kg/day
• Adequate calorie intake to utilize nitrogen effectively (the ratio)

26
 • Brain, RBC, WBC and renal medulla all need glucose; others can use
fat as an energy source
• Basal Energy Expenditure (BEE), via the Harris-Benedict Equation:
use weight, age and height to figure out a baseline energy need, after
which you can add onto it depending on the pt’s stress level
First Calculate BMR (Basal Metabolic Rate)
o Women: BMR = 65 + ( 4.35 x weight in pounds ) + ( 4.7 x
height in inches ) - ( 4.7 x age in years )
o Men: BMR = 66 + ( 6.23 x weight in pounds ) + ( 12.7 x
height in inches ) - ( 6.8 x age in year )
o Then plug in BMR value into the Harris Benedict Formula
which varies based on the appropriate activity factr
 Sedentary (little or no exercise) :
Calorie Calculation = BMR x 1.2
 Lightly active (light exercise/sports 1-3 days/week) :
Calorie Calculation = BMR x 1.375
 Moderately active (moderate exercise/sports 3-5
days/week) :
Calorie-Calculation = BMR x 1.55
 Very active (hard exercise/sports 6-7 days a week) :
Calorie-Calculation = BMR x 1.725
 Extra active (very hard exercise/sports & physical job
or 2x training)
Calorie-Calculation = BMR x 1.9
o In stress
 Calorie:nitrogen ratio = 100-150:1
• Uremics: 300-400:1
• Septics: 100:1
• Minor surgery = 20% increase
• Trauma = 35%
• Sepsis = 60%
• Thermal injury = 110%
• Confined to bed – 20%
o Indirect Calorimetry – measure the pt’s O2 consumption and CO2 production
 Index of fuel utilization: Resp Quotient (RQ) = VCO2 / VO2, in which V = vol of
the gas consumed
 Normal RQ = 0.8-1.0; < 0.7 = underfeeding, > 1.0 = overfeeding
 By diet type, carbs RQ = 1, mixed = 0.8, lipids = 0.7, lipogenesis = > 1.0,
ketogenesis = < 0.7
- Indications for Nutritional Support
o Age and starvation tolerance: < 60 years tolerates up to 10 days, 60-70 tolerates 7 days, >
70 years tolerates up to 5 days
o Prior health status – DM, COPD, renal, cardiac or hepatic insufficiency
o Current condition (septic, trauma, etc)
o Pre-op nutritional supplementation: anticipated duration of dietary deprivation (ex:
surgery + NPO time)
o Post-op: needed until tolerated oral intake is enough
 Functional GI tract – enteral nutrition preferred, use an NG tube
 Prolonged support needed – feeding gastrostomy or jejunostomy
- Enteral Nutrition
o Prolonged period without caloric intake
o Functional GI tract

27
 o Inadequate oral intake
o Situation where you want to avoid gut mucosal atrophy (ie, trophic feeds)
o Major burns and trauma, to decrease hypermetabolism
o Short Term – NG tube
 Alert pt with intact gag reflex
 Adequate gastric emptying
 Naso-intestinal comes with higher risk of aspiration
o Long term, > 6 weeks
 Gastrostomy – placed operatively or percutaneously, intermittent bolus or
continuous infusion
 Jejunostomy – placed operatively, continuous infusion only
o Oral Products
 High calorie – 2 kcal/mL, like Magnacal; hyperosmolar, so can cause diarrhea
 Polymeric – 1 kcal/ml, like Isocal: complete diet, well tolerated
 Monomeric – like Vivonex or Criticare: no digestion needed, complete SB
absorption, hyperosmolar
 Disease-specific (ex: renal, hepatic, etc) – unproven benefit
 Glutamate – used in formulas to feed intestinal mucosa
o Administration
 All tube feedings should be iso-osmolar (300 mOsm) for the start
 Elevate the head 30°, check gastric residuals q 4 hrs
 Use Reglan to aid gastric emptying
 Confirm tube placement with x-ray prior to starting feeds
o Major Complications
 Aspiration pneumonia – minimized by jejunal feeds
 Feeding intolerance – vomiting, abdominal distention, cramping, diarrhea;
decrease infusion rate or dilute feedings
 Diarrhea: > 5 stools/day
 R/O antibiotic-associated colitis
 Give kaolin pectate, diphenoxylate, immodium or Metamucil
 Metabolic complications
• Treat hyperglycemia with short-acting insulin, R/O sepsis for new-
onset hyperglycemia
• Hyperosmotic non-ketotic coma – due to too many calories w/o enough
free water to excrete the obligatory renal osmotic load
- Parenteral Nutrition
o Indications: Prolonged period without caloric intake, enteral feeding not tolerated,
malnutrition
o Primary Therapy - Efficacy of TPN Demonstrated In…
 GI Fistula – allows for total bowel rest; incr rate of spontaneous closure, but
overall mortality not changed
 Short bowel syndrome – maintain nutrition until the remaining bowel can
undergo hypertrophy (non-operative strategy)
 Acute tubular necrosis – decreased mortality rate; meet hypercatabolism of renal
failure by the TPN
 Acute on chronic hepatic insufficiency – normalize the amino acid profiles;
improve recovery from encephalopathy
o Primary Therapy - Efficacy NOT established in…
 IBD – Crohn’s disease limited to small bowel responds best
 Ulcerative Colitis – course not affected, but improved post-op course when
given prior to ileo-anal pull-through procedure

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  Anorexia Nervosa
o Supportive Therapy
 Established for radiation enteritis, acute GI toxicity from chemotherapy,
hyperemesis gravidarum
 Not established for pre-op malnourished pts, cardiac cachexia, pancreatitis, resp
insufficiency with prolonged vent support, prolonged ileus (> 5 days), nitrogen-
wasting wounds

o Composition of Formulas
 Carbs – dextrose, 15-47% concentration
 Amino acids
 Lipid emulsion
 Available as 10% or 20% solution (1 kcal or 2)
 Often, have minerals, vitamins and electrolytes added
 Central Formula – standard has 15-25% dextrose
 Peripheral Formula
• Standard has 3% amino acids in 10% dextrose
• Give 500 mL 10% lipid emulsion to maintain the calorie:nitrogen ratio;
monitor lipid profile
• Increased cost, phlebitis from long-term use
• Eliminate risks associated with central venous catheterization
• Also, use when central venous catheterization is contraindicated:
candida sepsis, blood dyscrasia, thrombosis
o Administration
 Always via a new central line when you start it
 Catheter tip has to be inside the innominate vein, or preferably the SVC
 Stable, well-hydrated and without serious coagulopathy – giving nutrition is
NEVER an emergency!
 Infusion: start at 40-50 ml/hr, increase to calculated pt’s needs
 Fingerstick glucose Q 6 hrs, maintain glucose at 100
 I/O monitoring
o Complications
 Pneumothorax
 Thrombosis of subclavian vein or SVC: silent in 35% of pts, treat with local
heat, catheter removal and heparinization
 Catheter sepsis
 Hyperglycemia
 Hypoglycemia – rare; if TPN is suddenly d/c, give 5% dextrose
 Liver dysfunction – fatty liver due to excess carbs being stored in liver as fat
The Thyroid
Sangeetha Kolluri
- General
o 3 categories: hypo, hyper and enlargements (diffuse goiter vs nodule)
o Normally, weighs 15-20 g
o Blood Supply:
 Superior thyroid arteries (from external carotid)
 Inferior thyroid arteries (from thyrocervical trunk),
• Branches of thyrocervical trunk are:
o Inferior thyroid artery
o Suprascapular artery

29
 o Transverse cervical artery
 (“Thyroidea ima”-vessel directly off the aorta-not always present)
o Nerves:
 Recurrent laryngeal nerve – 70% have it running in the tracheo-esophageal
groove, 60% posterior to inferior thyroid artery  important to always ID!
• Unilateral damage results in a hoarse voice.
• Bilateral damage presents as laryngeal obstruction on removal of the
tracheal tube and is a surgical emergency: an emergency tracheostomy
must be performed
 Superior laryngeal nerve – near superior thyroid arteries
• Injury results in altered speaking/singing voice (loss of high octaves)
o Hypothyroidism: autoimmune thyroiditis (Hashimoto’s), thyroidectomy, iodine
deficiency, dishormonogenesis
o Surgeons get called to manage 3 types of disease: enlargement causing compression,
certain hyperthyroidisms, thyroid nodules
- Thyroid Function Tests
o Get the TSH, T4, T3, radio-iodine uptake (T3RU)
o Free T4 index = T4 x T3RU, which tells you the level of circulating T4 corrected for
changes in transport protein levels
o Can also do US of thyroid to check out nodules
- Compression
o Dyspnea, dysphagia, tracheal or esophageal deviation, either clinically or
radiographically
o Get TFTs, chest and neck x-rays
o Compression symptoms suggest substernal extension of the thyroid, so get CT neck and
chest
- Hyperthyroidism
o Causes: Graves disease, toxic solitary nodule, multi-nodular goiter
o In all 3, you need to medically control the thyrotoxicosis if you want to avoid a thyroid
storm. (A rare but serious complication of hyperthyroidism. It may occur when patient
becomes very sick or physically stressed or undergoes general anesthesia. Symptoms
include increase in body temp >104°F or 40°C, tachycardia, arrhythmia, vomiting,
diarrhea, dehydration, coma and death).
 Propylthiouracil (PTU) – 300-600 ng/day, 6-8 weeks pre-op
 Propranolol
 SSKI or Lugol’s – 1-2 drops TID 1 week pre-op
o Graves Disease
 Pathogenic thyroid-stimulating antibodies
 Dx: diffusely enlarged gland with autonomous thyroid function  low TSH,
high thyroid hormones
 Total thyroidectomy is curative, but 100% hypothyroidism afterwards; can leave
6-8 g behind and only 20-30% will be hypothyroid.
o Toxic Multi-Nodular Goiter/Plummer’s Disease
 Multiple nodules secreting TH, independent of TSH
 Milder symptoms than graves, palpable nodules
 Tx: bilateral subtotal lobectomies
o Toxic Solitary Nodule
 Single autonomously functioning nodule, palpable
 Tx: lobectomy
o Thyroid Storm – life threatening, can be induced in any hyperthyroid pt by stress, esp
surgery!

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  Hyperpyrexia, tachycardia, numbness, irritability, vomiting, diarrhea, proximal
muscle weakness
 Die due to high-output cardiac failure
 Tx: prevention is best
• Mechanical cooling, oxygen, volume resuscitation
• Hydrocortisone IVPB to prevent adrenal insufficiency
• Propranolol for symptom control
• D-50 for glucose management
• PTU should be started
- Nodules
o 4-8% of people in the US
o Differential Dx: adenoma, cyst, thyroiditis, Graves, teratoma, mets to thyroid (breast,
lung, kidney, melanoma), thyroid carcinoma
o PE: stand behind pt, have them swallow water to palpate masses (move due to tracheal
attachment); note size, consistency, tenderness, nodularity
o Don’t rely on TFTs to tell you benign vs malignant
o Thyroid scanning with 123I – functional activity of nodule; cold nodules have 10-25%
malignancy chance, hot = 1% chance
o US – find non-palpable nodules, and differentiate solid from cystic
o Fine Needle Aspiration (FNA) – best test for evaluating nodules
 20 or 22 gauge needle
 7% are non-diagnostic, intermediate lesions are 20-60% malignant
 20% false-negative rate, so if you suspect malignancy clinically, go to excision
 Reliable for all cancers except follicular (adenoma vs carcinoma look the same,
so you need a biopsy to tell you about capsular vs vascular invasion)
 Drain all cysts completely, which is curative in 75%
- Thyroid Cancer
o 20-30% of nodules are malignant
o Most common endocrine malignancy, 1/25,000
o Risk Factors
 Male, over 15 y and under 60
 History of head and neck radiation or thyroiditis
 Family history of thyroid cancer
 Rapidly enlarging nodule
 Hard single nodule and/or nodules fixed to surrounding structure
 Hoarseness
 Cervical lymphadenopathy
o Frequency and Types
 Papillary Carcinoma – 70%
• Popular (most common type)
• Psamomma bodies
• Palpable lymph nodes: spread via lymphatics (50% have positive nodes
at dx), but does not affect prognosis
• Slow growing, 60% are multicentric
• 80-90% of post-radiation thyroid cancers
• Males:females = 1:3
• Positive (good) 131I uptake
• Usually, do lobectomy
• Tumor > 3 cm, male > 40, female > 50, distant mets or angio-invasion
 total thyroidectomy indicated
• 10 year survival: 85%

31
 Follicular Carcinoma – 10%
• More aggressive, unifocal, rubbery, encapsulated
• Male : female = 1:3
• Spreads hematogenous route, more aggressive than papillary
• Angioinvasive, mets to lung and bone (MC)
• Good 131I uptake
• Diagnosis can NOT be made by FNA, tissue structure is needed for
differentiation between follicular adenoma and follicular carcinoma;
capsular and blood vessel invasion are grounds for diagnosing
carcinoma
• Do total thyroidectomy
• 10 year survival: 40%
 Mixed papillary-follicular carcinoma – behaves like and is treated like papillary
 Hurthle cell tumor – 5%
• Unifocal, spreads by lymphatics
• Male:female = 2:1
• Do a thallium scan for mets localization
• Does not take up 131-I, so have to do total thyroidectomy to cure it
• 10 year survival: 60%
 Lymphoma – 5%
• Intermediate, can have history of Hashimoto’s thyroiditis
• Usually female
• Rapid enlargement and compressive symptoms common
• Chemo + radiation sensitive
• 10 year survival: 40-50%
 Medullary thyroid cancer – 7%
• Very aggressive
• 90% sporadic, 10% in association with MEN-II (autosomal dominant,
screen ALL pts for pheochromocytoma so you can resect it first)
o MEN I (Wermer syndrome): 3 P’s
 Pituitary adenoma
 Parathyroid hyperplasia
 Pancreatic islet cell tumors: Insulinoma, Gastrinoma,
VIPoma
o MEN 2a (Sipple syndrome):
 Medullary thyroid cancer
 Parathyroid hyperplasia
 Pheochromocytoma
o MEN 2b:
 Medullary thyroid carcinoma
 Pheochromocytoma
 Multiple mucosal neuromas
 Marfanoid body habitus
• aMyloid stroma, 95% make calcitonin, 85% make CEA
• Sporadic: Unifocal, 45 years old, worse prognosis
• Familial: 35 years, multifocal, not as bad; see C-cell hyperplasia as
precursor
• Secretes calcitonin, therefore, appropriate test is: Pentagastrin (causes
an increase in calcitonin)
• Diagnosis: FNA

32
 • Does not concentrate 131-I
• Total thyroidectomy and median lymph node dissection (modified
neck dissection if lateral nodes are positive)
• Localize mets when you see calcitonin rising – thallium, MIBG,
DMSA
• 10 year survival: 30-40%
 Anaplastic – 3%
• Undifferentiated carcinoma
• Women > Men
• Associated findings: Giant cells, spindle cells
• Very aggressive, 30% develop in a well-differentiated carcinoma and
have to be distinguished from lymphoma
• Differential diagnosis: Thyroid lymphoma (much better prognosis)
• Possible debulking thyroidectomy, chemo and radiation may slightly
improve chances
• 10 year survival < 2%; mean survival = 2-4 months
- Post-Op Care
o Elevate head of bed, cool misted oxygen
o Check calcium post-op, then q 8 x 24 hrs, then q daily.
o Pts may have tingling and numbness around lips and fingers, and (+) Chvostek sign (sign
of hypocalcemia- spasm of the facial muscles elicited by tapping the facial nerve in the
region of the parotid gland.)
o Hypothyroidism – give synthroid to replace TH and suppress TSH (growth factor for
well-diff cancers)
o Keep trach tray ready in case of airway compromise
- Complications
o Vocal cord paralysis due to recurrent laryngeal nerve damage – 1% if nerve is visualized,
4% if it’s “avoided”
o Hypoparathyroidism – 1-2% permanent, 10-20% temporary
o Hypothyroidism – 100% in total thyroidectomy (obviously)
o Pneumothorax
o Wound hematoma – if at bedside and pt has resp distress, open the wound up right there
BENIGN BREAST DISEASE
Cyndy Gitler
• The vast majority of breast lumps and breast complaints are caused by benign
breast disease
• Initial step in the assessment of breast lumps is history and physical
examination. The majority of women will need further testing (mammography,
ultrasound, fine needle aspiration, and core needle biopsy).
o Histologic exam of the excised lump is the "gold standard" test
• The challenge of diagnostic evaluation is to be as sure as possible that the
breast lump does not contain cancer, while minimizing pain, emotional trauma,
invasiveness of the biopsy procedure, and cost incurred in the evaluation of
breast lumps.
o Benign lesions are found in 80%of the 1.4 million breast biopsies
performed in the United States each year.
History:
• A complete history in women with a breast lump includes:
o The precise location
o How it was first noted (accidentally, by breast self-examination, clinical
breast examination, or mammogram)
o How long it has been present

33
 o Presence of nipple discharge
o Any change in size
o Whether the lump waxes and wanes at times in the menstrual cycle.
(Benign cysts may be more prominent premenstrually and regress in size
during the follicular phase.)
• Clinicians should also ask about a past history of breast cancer or breast
biopsy, and history of risk factors for breast cancer
Risk and Protective Factors for Breast cancer
Low Risk High Risk Relative Risk
Risk Factors
Deleterious BRCA1/BRCA2 genes Negative Positive 3.0-7.0
Mother or sister with breast cancer No Yes 2.6
Age 30-34 70-74 18.0
Age at menarche >14 <12 1.5
Age at first birth <20 >30 1.9-3.5
Age at menopause <45 >55 2.0
Use of contraceptive pills Never Past/current 1.07-1.2
use
HR (estrogen + progestin) Never Current 1.2
Alcohol None 2-5 drinks/day 1.4
Breast density on mammography 0 >75 1.8-6.0
(%)
Bone density (portion of population) Lowest ¼ Highest ¼ 2.7-3.5
History of a benign breast biopsy No Yes 1.7
History of atypical hyperplasia on No Yes 1.7
biopsy
Protective Factors
Breast feeding (months) >16 0 0.73
Parity >5 0 0.71
Recreational exercise Yes No 0.70
Postmenopausal BMI (kg/m2) <22.9 >30.7 0.63
Oopherectomy before age 35 years Yes No 0.3
Aspirin > Once/week Nonusers 0.79
for 6 months

Physical Exam:
• Breast tissue in healthy women is often lumpy; first goal of the PE is to
determine whether a dominant mass is present.
• If a dominant mass is detected, PE should concentrate upon factors that help
differentiate breast cancer from benign lesions. “Classic" characteristics of
cancerous lesions include:
o Single lesion
o Hard
o Immovable
o Irregular borders
o Size ≥2 cm
• Other symptoms and physical findings to note include:
o Lump contour: smooth, well-demarcated lumps are usually benign.
o Breast pain: although usually painless, breast cancer can be
accompanied by pain.

34
 o Nipple discharge: discharge is uncommon in cancer and, if present, is
unilateral. Bloody discharge should warrant further workup.
o Lymph node examination: careful examination of the axillae and
supraclavicular area for nodal involvement is necessary.
Clinical Follow-Up
• In women < 35 years who present with a breast lump with no suspicious
physical findings suggesting malignancy, it is often advised that the patient
return 3-10 days after the onset of the next menstruation to determine if the
lump regresses. If the lump remains palpable after next period, further
investigation is indicated.
Mammography
• Diagnostic mammography is part of the evaluation of any woman age 35 or
older who has a breast mass, primarily to search for other lesions that are
clinically occult, but also to evaluate the mass in question.
• Certain mammographic features suggest malignancy:
o Increased density
o Irregular margins
o Spiculation
o Accompanying clustered irregular microcalcifications
• Mammography misses 10-20% of clinically palpable breast cancers. Thus, a
negative mammogram should not stop further investigation if a suspicious lump
is felt on clinical examination.
• Diagnostic mammography is not ordered routinely in women under age 35.
Breast tissue in younger women is often too dense to evaluate the lump, and
breast cancer is too rare to search for it elsewhere in the breasts. Routine
mammography is neither cost-effective nor clinically beneficial for this younger
group with breast complaints unless there is a high suspicion of cancer.
Ultrasonography
• Ultrasonography can determine whether a breast mass is a simple or complex
cyst or a solid tumor and is most useful in the following circumstances:
o Women under age 35
o Evaluation of a non-palpable mass detected on screening
mammography
o Patient declining aspiration of a mass
o Mass that is too small or deep for aspiration
Fine Needle Aspiration Biopsy
• FNAB is especially valuable in evaluating cystic breast lesions and can be
therapeutic if all of the fluid is removed. There are three possible sample findings
with FNAB:
1. Non-bloody fluid: does not need to be sent for analysis; the mass
should disappear with the removal of fluid and the patient can be reassured
and checked in 4-6 weeks to ensure that the cyst has not reappeared;
recurrence suggests the need for surgical referral.
2. Bloody fluid: should be sent for pathological analysis; cancer is found
in approximately 7%. The patient should be checked in 4-6 weeks to ensure
that the cyst has not reappeared. If cytologic examination is suspicious, or if
there is a residual mass after aspiration, the patient should be referred to a
breast surgeon.
3. No fluid: when mass turns out to be solid, cells can be obtained for
cytologic analysis with FNAB by aspirating cells from the solid mass.

Core Needle Biopsy

35
 • Uses a larger needle (14 to 18 gauge, compared with 22 to 24 gauge) than
FNA, and thereby provides histologic material.
• Often performed using stereotactic mammographic equipment or ultrasound
guidance to evaluate non-palpable breast lumps.
• Because it obtains surrounding tissue, core biopsy is useful in distinguishing
atypical hyperplasia and ductal carcinoma in situ from invasive disease.
Triple Diagnosis:

• Triple diagnosis refers to the concurrent use of

physical examination, mammography, and skilled
Triple Diagnosis FNAB for diagnosing palpable breast lumps,
especially solid lumps. Very few breast cancers are
missed using triple diagnosis.
• Recommendations for follow-up with the triple
diagnosis approach are:
o Women in whom all three tests suggest
benign disease are followed with thorough
physical examination every three to six months
for one year to make sure the mass is stable or
regresses.
o Women in whom all three tests suggest
malignancy are referred for definitive therapy.
o Women with any one of the tests
suggesting malignancy should undergo core
biopsy and excisional biopsy, according to local
expertise.

Guidelines for Breast Lump Evaluation:

• Age cutoffs: Because of the increasing risk of breast cancer with age, most
groups distinguish recommendations for younger and older women, but vary in
defining cut points, which range from 30 to 40 years old. Mammography,
ultrasound and tissue sampling are generally recommended earlier in the
evaluation process for older women, compared to younger women.
• Mammography in younger women: Most expert groups do not recommend
diagnostic mammography on a routine basis for breast lump evaluation in women
younger than 35 years.
• Role of ultrasound: Some guidelines recommend ultrasonography in
conjunction with mammography in women over age 35 and ultrasound alone in
women under age. Other guidelines recommend skipping ultrasonography
altogether and moving straight to fine needle aspiration.
Approach to the Patient
• In general, the older the woman, the higher the degree of suspicion and the
more aggressive the evaluation should be. Compared to younger women, older
women are both at greater risk for cancer and more likely to delay presenting
with a breast complaint.
• Reasonable diagnostic approaches for dominant breast masses are
summarized in the figures below:
American Cancer Society Mammography Guidelines
• Women age 40 and older should have a screening mammogram every year
and should continue to do so for as long as they are in good health.
• Women in their 20s and 30s should have a clinical breast exam (CBE) as part
of a periodic (regular) health exam by a health professional, preferably every 3

36
years. After age 40, women should have a breast exam by a health professional
every year.
• Breast self exam (BSE) is an option for women starting in their 20s. Women
should be told about the benefits and limitations of BSE. Women should report
any breast changes to their health professional right away.
• Women at high risk (greater than 20% lifetime risk) should get an MRI and a
mammogram every year.
High Risk Factors: women who
o Have a known BRCA1 or BRCA2 gene mutation
o Have a first-degree relative (parent, brother, sister, or child) with a
BRCA1 or BRCA2 gene mutation, and have not had genetic testing themselves
o Have a lifetime risk of breast cancer of 20% to 25% or greater,
according to risk assessment tools that are based mainly on family history
(see below)
o Had radiation therapy to the chest when they were between the ages
of 10 and 30 years
o Have Li-Fraumeni syndrome, Cowden syndrome, or Bannayan-Riley-
Ruvalcaba syndrome, or have one of these syndromes in first-degree relatives

37
Flow Diagram for Evaluation of a Dominant Breast Mass

OVERVIEW OF BENIGN BREAST DISEASES

Classification of Benign Breast Lesions:
• Benign epithelial breast lesions can be classified histologically into three
categories; categorization is based on the degree of cellular atypia:
1. Non-proliferative: do not increase a woman’s risk of developing breast
cancer
• Example: simple cysts
2. Proliferative without atypia: confer a modest increase in risk of developing
breast cancer (relative risk 1.6-1.9)
• Example: fibroadenomas, usual ductal hyperplasia, intraductal papillomas

38
 3. Atypical hyperplasias: confer a moderate increase in the risk of subsequent
breast cancer (relative risk 3.7-5.3).
• Example: atypical ductal hyperplasia, atypical lobular hyperplasia
1. Non-Proliferative Breast Lesions:
• Generally NOT associated with an increased risk of breast cancer
• Includes fibrocystic changes, fibrocystic disease, chronic cystic mastitis,
and mammary dysplasia.
• The most common non-proliferative breast lesions are breast cysts (fluid
filled, round or ovoid masses derived from the terminal duct lobular unit)
• Found in up to 1/3 of women between 35-50 years old.
• Acute enlargement may cause severe, localized pain of sudden onset.
• Includes both simple and complicated cysts (complex cysts are also discussed
but are much more likely to be malignant):
i. Simple cysts
o On ultrasound, simple cysts are circumscribed, anechoic, with posterior
acoustic enhancement, lack of Doppler signal, and absence of solid
components.
o Benign by definition and no intervention is necessary
o Aspiration is often performed to relieve pain. Bloody fluid is sent for
pathology, clear fluid can be discarded.
o Cyst should disappear with removal of the fluid, if it recurs, a second
aspiration is reasonable. With a third recurrence, excision can be considered
ii. Complicated cysts
o Cysts that meet most, but not all, criteria for simple cysts on
ultrasound examination; including, lesions with internal echoes, fluid or
debris levels, thin septations, a perceptible wall, or lack of posterior acoustic
enhancement.
o These lesions are rarely malignant (0.4 percent) but should be
aspirated to confirm diagnosis or followed with imaging.
iii. Complex cysts
o Also referred to as complex masses, contain mixed cystic and solid
components or an intracystic solid mass.
o Require biopsy! Core needle biopsy is utilized, if possible, and a clip
must be placed to ensure that the lesion can be localized to allow excision if
the core biopsy is positive.
o These lesions have a relatively high rate of cancer, (20-43%).
2. Proliferative Breast Lesions Without Atypia:
• Associated with a slightly increased risk of developing breast cancer (1-2x
that of the general population)
• As the risk of subsequent breast cancer in this population is modest,
chemoprevention is not indicated.
a. Fibroadenomas
• Benign solid tumors containing glandular and fibrous tissue.
• Present as a well-defined, mobile mass. In 20% of cases, multiple
fibroadenomas occur in the same breast or bilaterally.
• Etiology is unknown; hormonal relationship likely since they persist during the
reproductive years, tend increase in size during pregnancy or with estrogen
therapy, and regress after the menopause.
• Most commonly found in women between 15-35 years.
• Diagnosis of fibroadenoma is best confirmed with core (MC) or excisional
biopsy.
• Ultrasound alone or fine needle aspiration (FNA) cannot differentiate between
a fibroadenoma and a phyllodes tumor.

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 o Phyllodes tumors appear similar to fibroadenoma on ultrasound and
physical exam; they are unusual fibroepithelial tumors characterized by
rapid growth. They require more extensive surgical resection and in some
cases radiation treatment as well.
• If a biopsy proves a lump to be a fibroadenoma and the patient is
asymptomatic, then it can be left in place. After confirming the pathologic
diagnosis, short-term follow-up (six months) with ultrasound is recommended to
assure stability.
• Most fibroadenomas get smaller over time and can be left in place unless they
increase in size, are symptomatic, or the patient desires excision.
o Disadvantages of excisional surgery include scarring at the incision
site, dimpling of the breast from the removal of the tumor, damage to the
breast's duct system, and mammographic changes (including architectural
distortion, skin thickening, increased focal density).
• Cryoablation is an alternative to surgical excision of fibroadenomas.
Cryoablation under ultrasound guidance causes the lesions to progressively
disappear. Transient side effects of cryoablation include ecchymosis, local
swelling, and discomfort.
• Percutaneous vacuum-assisted ultrasound-guided excision is another
alternative to open excision technique for removal of fibroadenomas, but is be
less effective for lesions >2 cm.
• Subtypes of fibroadenomas:
i. Giant fibroadenomas
o Refers to fibroadenomas over 10 cm in size. Excision is recommended.
The primary challenge is to differentiate these from phyllodes tumors.
ii. Juvenile fibroadenomas
o Variant of fibroadenoma found in women between the ages of 10-18.
o Vary in size from 5-20 cm in diameter and are usually painless,
solitary, unilateral masses that grow rapidly.
o Juvenile fibroadenomas are distinguished from adult fibroadenomas by
exhibiting more glandularity and greater stromal cellularity.
o Excision is recommended as these tumors can cause discomfort,
anxiety, and breast asymmetry.
iii. Complex fibroadenomas
o Complex fibroadenomas contain other proliferative changes, such as
sclerosing adenosis, duct epithelial hyperplasia, epithelial calcification, or
papillary apocrine changes.
o Associated with a slightly increased risk of cancer when multicentric
proliferative changes are present in the surrounding glandular tissue.
o Appropriate management is controversial. Some believe that complex
fibroadenomas warrant complete removal for histological examination,
others suggest that they can be managed conservatively following core
biopsy.
b. Usual Ductal Hyperplasia
• Ductal hyperplasia without atypia is characterized by an increased number of
cells within the ductal space; although the cells vary in size and shape, they
retain the cytological features of benign cells.
• No additional treatment is needed for ductal hyperplasia. Chemoprevention is
not indicated
• Risk of subsequent breast cancer in usual ductal hyperplasia is modest
c. Papilloma
• Solitary intraductal papillomas may present as a breast lump, a nodule on
ultrasound, or may be the cause of nipple discharge and can be seen on
ductography

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 • Consist of a monotonous array of papillary cells that grow from the wall of a
cyst into its lumen.
• Can harbor areas of atypia or ductal carcinoma in situ (DCIS).
• Standard recommendation for management of papillomas is that they be
excised whenever they are diagnosed by core needle biopsy
• Once the diagnosis of solitary papilloma is confirmed by excisional biopsy, no
additional treatment is needed. Unless there is associated atypia, there is no
increased risk of subsequent breast cancer.
d. Multiple Papillomas (Diffuse Papillomatosis)
• Minimum of 5 papillomas within a localized segment of breast tissue.
• No additional treatment is needed for diffuse papillomatosis.
• Risk of subsequent breast cancer is modest and chemoprevention is not
indicated.
e. Sclerosing Adenosis
• Lobular lesion with increased fibrous tissue and interspersed glandular cells.
• Can present as a mass or a suspicious finding on mammogram
• No additional treatment is needed
• Risk of subsequent breast cancer in this population is modest and
chemoprevention is not indicated.
f. Radial Scars
• Usually discovered incidentally when a breast mass is removed for other
reasons; occasionally they are large enough to be detected by mammography,
which cannot reliably differentiate between these lesions and spiculated
carcinoma.
• Characterized microscopically by a fibroelastic core with radiating ducts and
lobules.
• When radial scars are found on core biopsy, the entire lesion must be excised
b/c there is a chance of finding an unrecognized in situ or invasive component.
There is also some evidence that radial scars are premalignant lesions that can
slowly progress from scarhyperplasiacarcinoma over time.
• No additional treatment is needed for radial scars. Risk of subsequent breast
cancer is modest and chemoprevention is not indicated.
3. Atypical Hyperplasias
• Proliferative lesions with atypia include atypical ductal hyperplasia (ADH) and
atypical lobular hyperplasia (ALH)
• Patients with this diagnosis on core biopsy need excisional biopsy to confirm
the diagnosis.
• They are counseled about risk reduction strategies, including close screening,
avoidance of adjuvant hormone use, avoidance of heavy alcohol use, and
consideration of chemoprevention of breast cancer with tamoxifen or raloxifene.
a. Atypical Hyperplasia
• Specific lesion of either ductal or lobular elements with uniform cells and loss
of apical-basal cellular orientation.
• Relative risk of invasive breast cancer associated with AH ranges from 3-6x.
• Multifocal lesions, especially those associated with calcification, increase risk
10x.
• AH is associated with an increased risk of contralateral breast cancer and thus
provides evidence of underlying breast abnormalities that predispose to breast
cancer
• Atypical hyperplasia on core biopsy always requires surgical excision. Analysis
of tissue removed at the time of surgery results in an upgrade in diagnosis to
ductal carcinoma in situ (DCIS) in up to 20%.

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 • Risk reduction strategies: ongoing surveillance with yearly mammography and
2x yearly breast exams; cessation of birth control pills or hormone replacement
therapy (if applicable); tamoxifen or raloxifene may be considered in women
with AH for breast cancer risk reduction
b. Flat Epithelial Atypia (aka columnar cell change with atypia or clinging
carcinoma)
• Usually diagnosed on breast biopsies done for calcifications.
• When diagnosed on a core needle biopsy specimen, excision should be
performed b/c 1/3 of cases will show a more advanced lesion.
• Data suggest that the risk of local recurrence or progression to invasive
cancer is low
c. Lobular Carcinoma In Situ
• Women with lobular carcinoma in situ (LCIS) have a significantly increased risk
of breast cancer
4. Miscellaneous Benign Lesions of the Breast
a. Lipoma
• Benign, usually solitary tumors composed of mature fat cells.
• Present as soft, non tender, well circumscribed masses. Diagnosis can be
confirmed with a core or excisional biopsy.
• Lipomas should be surgically excised if they cause diagnostic confusion,
continue to enlarge or grow rapidly.
• For smaller lesions, excisional biopsy is often preferable.
• There is no increased risk of subsequent breast cancer associated with
lipomas.
b. Fat Necrosis
• Benign condition that most commonly occurs as the result of breast trauma or
surgical intervention.
• Can be confused with a malignancy on physical exam and may also mimic
malignancy on radiologic studies, therefore biopsy is sometimes necessary to
confirm the diagnosis
• Mammographic and ultrasound findings consistent with fat necrosis include oil
cysts.
• Once diagnosis is established, excision is not necessary and there is no
increased risk of subsequent breast cancer.
c. Diabetic Mastop/athy
• Most commonly seen in premenopausal women with longstanding type 1
diabetes
• Typical presentation is a suspicious breast lump with a dense mammographic
pattern.
• Core biopsy is/ recommended for diagnostic confirmation.
• Pathology shows dense keloid-like fibrosis and periductal, lobular, or
perivascular lymphocytic infiltration.
• Once diagnosis is established, excision is not necessary and there is no
increased risk of subsequent breast cancer.
d. Galactocele (aka milk retention cysts)
• Cystic collections of fluid, usually caused by an obstructed milk duct.
• At mammography, may appear as an indeterminate mass, unless the classic
fat-fluid level is seen. Ultrasound may show a complex mass.
• Diagnosis can be made on the basis of the clinical history and aspiration,
which yields a milky substance.
• Once diagnosis is established, excision is not necessary and there is no
increased risk of subsequent breast cancer.
e. Hamartoma (aka fibroadenolipoma, lipofibroadenoma, or adenolipoma)

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 • Benign lesions that have varying amounts of glandular, adipose, and fibrous
tissue.
• Present as discrete, encapsulated, painless masses or are found incidentally
on screening mammography.
• Diagnosis can be difficult to make with limited tissue as hamartomas do not
have specific diagnostic features.
• Coincidental malignancy can occur; excision is recommended for this reason.
f. Adenoma
• Pure epithelial neoplasms of the breast; distinguished from fibroadenomas by
their sparse stromal elements.
• Divided into 2 main groups: tubular and lactating adenomas (lactating
adenomas occur commonly in pregnancy; they are well circumscribed and
lobulated. They may require excision because of their size, but they do not have
malignant potential)
g. Idiopathic Granulomatous Mastitis
• Inflammatory mass in the breast. Patients typically present with a firm breast
mass, often associated with inflammation of the overlying skin.
• Nipple retraction, peau d'orange like changes, and axillary adenopathy may
be present.
• Symptoms may be mistaken for non-puerperal mastitis, a breast abscess, or
most often, carcinoma.
• Radiologic findings of IGM, like the physical findings, are worrisome for
malignancy
• Biopsy is necessary to make a diagnosis and IGM is a diagnosis of exclusion,
as there are several processes, such as sarcoidosis or tuberculosis of the breast
that may also induce a granulomatous mastitis.
o When IGM is suspected, the biopsy specimen should be sent for acid
fast bacilli and fungal stains in addition to pathology.
• While antibiotics are often initiated during the work-up, they will have little
impact on true cases of IGM.
• For the asymptomatic patient, excision is not necessary; observation alone is
a reasonable option.
• For symptomatic patients with localized disease, excision is a reasonable
option if the entire area can be excised with minimal cosmetic impact.
• Steroid therapy is sometimes considered for symptomatic patients, based on
idea that this is an autoimmune disease
• There is no increased risk of subsequent breast cancer associated with IGM.
h. Pseudoangiomatous Stromal Hyperplasia (PASH)
• May present as a mass on physical exam or radiologic studies.
• Benign stromal proliferation is found as an incidental microscopic finding in as
many of 25% of breast biopsy specimens.
• Histologic appearance is characterized by anastomosing slit-like empty spaces
lined by spindle cells.
• Benign, but should be distinguished from a malignancy and is often confused
with mammary angiosarcoma. If there are any suspicious features on imaging,
the diagnosis of PASH on a core biopsy should not be accepted as a final
diagnosis and excisional biopsy should be performed. In absence of suspicious
imaging characteristics, a diagnosis of PASH at core biopsy is considered
sufficient, and surgical excision is not always necessary. There is no increased
risk of subsequent breast cancer associated with PASH.
i. Sarcoidosis
• Breast symptomatology in sarcoidosis is rare and seen primarily in patients
with systemic involvement.

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 • Sarcoidosis of the breast presents as firm hard masses, mimicking carcinoma.
• Mammographic appearance is suspicious with irregular ill defined, spiculated
masses that are solid on ultrasound.
• Biopsy is needed for confirmation of diagnosis
• There is no increased risk of subsequent breast cancer associated with
sarcoidosis of the breast.
Complex Masses
• Masses with mixed cystic and solid components or an intracystic solid mass
• Require biopsy! Core needle biopsy is utilized, if possible, and a clip is placed
to ensure that the lesion can be localized to allow excision if the core biopsy is
positive.
• These lesions have a relatively high rate of cancer, ranging from 20-43%
Nipple Discharge
• Discharge is considered pathologic if it is spontaneous, persistent, or arises
from a single duct or if the discharge contains gross or occult blood.
Breast Pain
• Classified as cyclical (ie, related to the menstrual cycle), noncyclical, or
extramammary.
• Breast cancer may present as breast pain, thus full evaluation is indicated.
• Simple reassurance that the patient most likely does not have breast cancer
provides adequate relief for most women.
• Symptomatic relief also may be achieved with use of a soft bra with good
support, acetaminophen, and/or NSAIDs.
Prognosis:
• Following establishment of a benign diagnosis, treatment in general is aimed
at symptomatic relief and patient education.
• Some benign breast disease such as atypical hyperplasia, does confer a
moderate increase in the patient's future risk of developing breast cancer, and
should lead to counseling about screening recommendations and risk reduction
strategies.

Malignant Breast Disease

Sangeetha Kolluri
- Epidemiology
o 12% of cancers in women develop it during lifetime, making it the most common non-
skin cancer
o 30% of all cancers in women
o Leading cause of death in women 40-55
- Risk Factors
o 100-150x more likely in women than men
o Increasing age  screen starting at age 40 for normal-risk women
o Relatives
 1st degree relative  2-3x increased risk
 Decreases with more distant relatives
 Overall risk depends on number of 1st degree relatives with breast cancer, and
whether it was unilateral vs bilateral
• Pre-menopausal with unilateral breast cancer = 20-30%
• Pre-menopausal with bilateral breast cancer= 50%
o Genetic predisposition (ex: BRCA): < 3% of all breast cancerss
 Li-Fraumeni – mutation in p53
 BRCA1 gene on chr 17q – early-onset/familial breast camcer

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 o Prior history of breast cancer – 5x increased risk
o History of breast biopsy, regardless of underlying pathology
o Atypical ductal or lobular hyperplasia on biopsy: 5x increased risk
o Coexistence of positive family history of breast cancer and atypical ductal or lobular
hyperplasia – 9x increased risk
o DCIS or LCIS
o Early menarche < 12 years, or late menopause > 55 years
o Cumulative duration of menstruation > 30 years
o Nulliparity, or > 30 years at first birth
o Post-menopausal estrogen replacement – 40% increase
o Oral contraceptive use
o Exposure to low-dose ionizing radiation between ages 13 and 30
o Alcohol consumption, especially before age 30
o Induced abortion (controversial!!)
- Presentation
o Non-palpable lesion identified on mammo (microcalcifications)  do needle localization
biopsy or FNA
o Palpable mass: most common presentation, usually non-tender, firm, irregular, relatively
immobile, upper outer quadrant (50%); may be multifocal, multicentric or bilateral
o Skin changes – dimpling (cooper’s ligaments tethering), nipple retraction or inversion,
erythema, warmth, edema, peau d’orange (dermal lymphatic invasion), ulceration,
eczema or excoriation of nipple epidermis (Paget’s)
o Nipple discharge – bloody, most often due to intraductal papilloma (but need to r/o
invasive papillary carcinoma)
o Mets to lungs, bone, brain, liver, LNs  classic cancer wasting, bony pain (especially
vertebral), pathologic fractures
- TNM Classification
o Primary Tumor
 T0 – no evidence of primary tumor
 T1S – carcinoma in situ; ductal, lobular, paget’s of nipple without tumor
 T1 – 2 cm or smaller
 T2 – between 2 and 5 cm
 T3 - > 5 cm
 T4 – any size, + direct extension into chest wall or skin
• T4a – chest wall extension
• T4b – edema (including peau d’orange), breast skin ulceration, satellite
skin nodules confined to same breast
• T4c – both T4a and b
• T4d – inflammatory carcinoma – diffuse, brawny skin induration,
erysipeloid edge, without underlying mass
o Regional Lymph Nodes (N)
 N0 – no LN mets
 N1 – to moveable ipsilateral axillary LNs
 N2 – mets to ipsilateral axillary LNs fixed to something
 N3 – Mets to ipsilateral internal mammary LNs
o Distant Metastases (M)
 M0 – no distant mets
 M1 – supraclavicular, cervical, contralateral internal mammary LNs; brain,
bone, lungs, etc
- Staging
o 0 – Tis N0 M0
o 1 – T1 N0 M0

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 o 2a
 T0 N1 M0
 T1 N1 M0
 T2 N0 M0
o 2b
 T2 N1 M0
 T3 N0 M0
o 3a
 T0 N2 M0
 T1 N2 M0
 T2 N2 M0
 T3 N1/N2, M0
o 4 – any T, any N, M1
- Pathology
o Growth patterns
 Epithelial tumors from duct or lobule linings
 Non-epithelial tumors from supporting stroma (ie, sarcomas)
 Non-invasive (DCIS or LCIS, not through basement membrane) or invasive
 Multifocal (in same quadrant), multicentric (distant quadrant, same breast) or
bilateral
o Histological Types
DCIS
 Completely contained within breast ducts
 More common than LCIS
 Average age = 50’s
 80% are non-palpable and found by microcalcifications on mammogram
 35% are multicentric
 Occult invasive carcinoma co-exist in 11-21%
 Subsequent risk for invasive ductal = 25-30%, happens within 10 years of
diagnosis
Infiltrating Ductal Carcinoma
 80% of breast malignancies
 Comes from ductal epithelium, infiltrates supporting stroma
 Subtypes: medullary, colloid, tubular, papillary
 Usually, palpable mass or mammographic abnormality
LCIS
 Completely contained within breast lobules
 Average age = 44-46, 80% of cases in premenopausal women
 Estrogen plays a role in pathogenesis
 No palpable mass or mammogram findings!  find it incidentally on biopsy for
something else
 60-80% of cases are bilateral and multicentric
 LCIS found in contralateral breast 25%
 7-10x increased risk for subsequent invasive carcinoma (usually ductal), in
either breast
 1% risk of breast cancer development per year
 Invasive carcinoma happens > 15 years after diagnosis
Invasive Lobular Carcinoma
 5-10% of invasive breast malignancies
 From lobular epithelium, infiltrates supporting stroma

46
  NO microcalcifications!
 Similar prognosis to invasive ductal carcinoma
 Presents as palpable mass or mammographic abnormality
Paget’s Disease of the Nipple
 1-3% of breast malignancies
 Associated with DCIS or invasive, just below the nipple
 Tumor cells invade across the epithelial – epidermal junction, and enter the
nipple skin
 Presentation: erythema, mild eczematous changes that become eroded and
ulcerated
 Diagnosis: scrape cytology, shave biopsy, punch biopsy or nipple excision
 Rapid, lethal malignancy that gets treated by mastectomy or excision of nipple +
areolar complex (if limited to retro-areolar area)
Inflammatory Breast Carcinoma
 1-4% of breast cancers, the most rapidly lethal one
 Poorly differentiated, dermal lymphatic invasion
 Presentation: diffuse induration, erythema, warmth, edema, peau d’orange,
possible palpable mass, axillary lymphadenopathy (almost always)
 17-36% already have distant mets at time of diagnosis  staging more
important than histology for prognosis
 Other prognostic factors: nuclear/histologic grade, (+) ER/PR, DNA content and
proliferative fraction (# cells in S phase)
 Induction chemo with combined-modality therapy gets you a 40-70% 3 year
survival rate
o Breast Cancer During Pregnancy
 2 per 10,000 gestations, 2.8% of all BCs
 Harder to diagnose, and often delayed, due to breast engorgement, tenderness
and increased nodularity
 Suspicious masses should get FNA or excisional biopsy
 If malignant, treat based on the trimester
• Termination of pregnancy, in hopes of reducing hormonal tumor
stimulation, has no added benefit
• 1st and 2nd trimesters – MRM but no immediate breast reconstruction
because you can’t tell what the other breast will look like post-partum
• Breast conservation surgery
o Complicated by the fact that you can’t do adjuvant radiation
therapy due to pregnancy contraindication
o In 3rd trimester, you can do WLE and axillary node dissection,
and delay radiation until after delivery
• Chemo can be done during 2nd and 3rd trimesters without risk of fetal
malformation, but 1st trimester has increased risk of spontaneous
abortion and congenital malformation
o Male Breast Cancer
 1/100 the incidence of BC in women
 Increased risk with hyperestrogenic states: klinefelter’s, liver disease, exogenous
estrogen use (metastatic prostate cancer, transvestites on hormone therapy); low
dose radiation also implicated
 Average age at diagnosis = 60-65, delayed diagnosis results in more advanced
stage and worse prognosis
 Most common: infiltrating ductal carcinoma

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  Since have much less breast tissue, pectoralis major is more often involved  if
so, radical mastectomy (if not, MRM is best)
 Node-negative disease has same prognosis as women, but node-positive has far
worse prognosis
 Treatment
• Post-op radiation – improves local control but doesn’t affect survival
• Adjuvant chemo or hormone therapy for node-positive or high-risk
node-negative pts
• > 80% are hormone receptor positive, so tamoxifen is important
- Surgical Treatment Options
o Breast Conserving: wire loop excision (WLE), lumpectomy, segmental mastectomy
 Goals: complete tumor excision with clear margins, good cosmetic result
 Do axillary node dissection + radiation therapy to entire breast (50 Gy over 5
weeks, starting 2-4 weeks after surgery), with a radiation boost to the tumor bed
 Eligibility
• Tumor < 4 cm
• Good tumor size : breast size ratio
• Tumor not fixed to muscle or chest wall, no skin involvement
• No fixed or matted axillary nodes
• No multicentric cancer (unless it’s right next to the main tumor)
• Pt can tolerate and reliably stick to chemo regimen
o Contraindications to breast conservation surgery
 Absolute
• >= 2 primary tumors in separate quadrants
• Diffuse malignancy with mini-calcifications
• History of breast irradiation > max total dose allowed
• Pregnancy
• Persistently positive surgical margins
 Relative
• Collagen vascular disease
• Tumors > 4 cm
• Multiple tumors in same quadrant
• Large breast size
o Subcutaneous mastectomy
 Takes breast tissue only, spare the nipple-areolar complex, skin and nodes
 NOT a cancer operation!  leaves 1-2% of breast tissue behind
o Simple Mastectomy
 Removes breast tissue, nipple-areolar complex and skin
 No axillary node dissection
 Indication: DCIS, LCIS
o Modified Radical Mastectomy (MRM)
 Removes breast tissue, pectoralis fascia, nipple-areolar complex, skin, axillary
LNs  spare the pectoralis major
 Patey modification – preserve the pectoralis major, but sacrifice the pectoralis
minor to remove levels 1-3 of axillary nodes
 Auchincloss modification – save both muscles, so you’re limited to only level 3
axillary node dissection  not clinically significant in most cases
o Radical Mastectomy
 Removes breast tissue, nipple-areolar complex, skin, pectoralis major and
minor, axillary nodes
 Leaves bare chest wall with significant cosmetic and functional deformity

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  MRM vs radical: clinical trials show no difference in disease-free survival
- Chemotherapy and Hormonal Therapy
o Goal: systemic control of breast cancer
o Adjuvant therapy
o Palliation for metastatic disease: base decision on extent and rate of progression,
hormone receptor status, degree and progression of symptoms, pt ability to tolerate
therapy
o Chemotherapy
 Time to response = 4-6 weeks, response rate = 40-60%, duration of action = 8-
12 months, increased toxicity
 Indicated for pts with hormone negative tumors, high s-phase ratio, aneuploidy,
aggressive mets, ability to tolerate toxicity  premenopausal pts have better
response
 Combination chemotherapy more effective
o Hormonal therapy
 Time to response = 8-12 weeks, response rate = 25-35%, duration of action =
14-18 months, lower toxicity
 Indicated for pts with hormone responsive tumors, palliatively for relatively
indolent metastatic disease, node (+), high risk node negative pts, post-
menopausal pts
 Tamoxifen is treatment of choice
• Binds to the ER and prevents estrogen from binding  competitive
antagonist
• Take for at least 2 years
• As effective as any other form of hormone therapy, including
oophorectomy
• If chemo is started, pt should start tamoxifen before the chemo is
finished
• ER+ / PR+ = 78% response rate; ER+ only = 34%, PR+ only = 45 %,
neither = 10%
 Alternatives to tamoxifen
• Progesterone agents (progestins)
• Luteinizing hormone-releasing analogs
• Aminoglutethimide – aromatase inhibitor; decreases circulating levels
of estrogen by blocking the peripheral conversion of androstenedione
 estrogen (ie, medical adrenalectomy)
• Anti-progestins
• Oophorectomy – only indicated for mets of BC in premenopausal,
hormone receptor (+) pts; tamoxifen should be tried first!
- Treatment by Staging
o Stage 0
 DCIS – total ipsilateral mastectomy vs WLE + radiation, both without axillary
LN dissection; 95-100% 5 year survival
 LCIS – bilateral total mastectomy vs tamoxifen 20 mg daily x 5 years; no
axillary LN dissection
 Clinically occult invasive carcinoma – MRM vs WLE with axillary LN
dissection + radiation
 Paget’s – total mastectomy vs MRM
o Stage 1 and 2
 85% of breast cancers

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  MRM vs WLE with axillary LN dissection and radiation
 Both have same outcome, but WLE has to have tumor-free margins to work
 Adding radiation to WLE improves disease-free survival but doesn’t improve it
in the long run, or overall survival in node-negative pts
 Adjuvant chemo for node-positive pts, and high risk node-negative pts; can do it
pre-op to make breast conserving surgery possible
 Factors in Recurrence
• Age < 35 years
• Tumor size > 2 cm
• Poor histological and nuclear grade, , aneuploid DNA content, high S-
phase ratio
• Absence of ER/PR, over-expression of EGF receptor -1, (+) cathepsin
D, amplified c-erb-b2 oncogene
 Lobular carcinoma – use mirror-image biopsy or total mastectomy for
contralateral breast is controversial
 5 year survival for stage 1 and 2 = 80% and 60%
o Stages 3 and 4
 Total or MRM, radiation, systemic therapy
 Goal of therapy: control of loco-regional and distant disease
 Unfortunately, most pts will die of distant mets disease anyways
 5 year survival for stage 3 and 4 = 20% and 0%, respectively
 Pre-op chemo and local radiation being investigated as an option for
inflammatory breast carcinoma
- Breast Reconstruction Following Mastectomy
o Does not delay diagnosis of recurrence or interfere with chemo
o Significantly improves pt’s concept of body image
o Can be done immediately, or delayed until completion of chemo and radiation
o Types of Surgery
 Prosthetic breast implant – filled with silicone or saline, inserted under the
pectoralis
 Myocutaneous Flap Reconstruction
• More complicated, but better long term cosmetic results
• Transverse Rectus Abdominus after Mastectomy Flap (TRAM Flap)
o Based on the SMA and SMV blood supply
o The entire contralateral rectus abdominis muscle is transposed,
along with transverse ellipse of skin and sub-Q tissue from the
lower abdomen
• Latissimus Dorsi flap – based on thoracodorsal artery and vein
• Free rectus abdominis flap – thoracodorsal or anterior serratus vessels
are anastomosed to the inferior epigastrics  maintain blood supply to
the flap!
• Greater omentum pedicle flap, covered with a skin graft
• Gluteus maximus free flap
 Nipple Areolar reconstruction – secondary procedure, after breast reconstruction
(6-12 weeks) – pucker the skin, tattoo areolar coloration
o Complications of Breast Reconstruction
 Infection
 Tissue loss – especially, the flap loss due to vascular compromise
 Poor cosmetic result
 Slippage of prosthetic implant, or capsular contraction
Gastrointestinal Hemorrhage:
Cyndy Gitler

50
Epidemiology:
• Annual incidence of GI hemorrhage: 100 per 100,000 population
Age Stratification:
• Young patients: diagnosis frequently includes IBD, Meckel's diverticulum, and juvenile polyps
• Middle-aged patients: polyps, hemorrhoids, and diverticula
• Elderly patients: angiodysplasia, malignancy, ischemia, diverticulosis, and polyps
Classification
• Upper GI tract bleeding: proximal to ligament of Treitz
• Lower GI tract bleeding: distal to ligament of Treitz
• Bleeding can be acute, with hematemesis, melena, and hematochezia, or chronic, presenting as iron-
deficiency anemia or guaiac-positive stool.
Physical Exam
• The patient's general appearance is also important; skin turgor and jugular venous pressure supplement
vital signs in determining the level of volume depletion.
o Cachexia, lymphadenopathy, and abdominal masses suggest malignancy
• The abdominal examination should evaluate for tenderness, masses, hepatosplenomegaly, ascites, and
bowel sounds.
• A rectal examination provides valuable information on the color and consistency of the stool (e.g.,
maroon vs. bright red, melena vs. occult blood).
• Cutaneous stigmata may suggest the etiology of GI hemorrhage.
o Jaundice, spider nevi, palmar erythema, and ecchymoses suggest liver disease
o Orofacial telangiectasias suggest Osler-Weber-Rendu syndrome (hereditary hemorrhagic
telangiectasia).
o Café au lait spots suggest neurofibromatosis
o Erythema nodosum is associated with inflammatory bowel disease (IBD).
Initial Approach
• The primary initial objective of the clinical evaluation is to assess the patient's severity of hemorrhage
by determining hemodynamic status. Vital signs are monitored frequently, including BP, pulse, and
postural changes
o Initial hematocrit (Hct) determination can be misleading at presentation because vascular fluid
redistribution requires 24 to 72 hours to equilibrate
• The key to the successful management is the rapid institution of fluid resuscitation to maintain organ
perfusion and tissue oxygenation.
• Resuscitation of the patient is initiated concurrently with the clinical assessment.
• Blood should be sent to the laboratory for determination of the complete blood count (CBC),
coagulation profile, and serum chemistries, including blood urea nitrogen (BUN), creatinine, and liver
function tests. Blood is also sent to the blood bank for typing and crossmatching.
• 2 large-bore (14-to 18-gauge) intravenous (IV) catheters should be placed for the administration of
fluids and blood products.
Hemodynamic Parameters:
• The use of rigid transfusion guidelines, such as maintaining Hct above 30%, should be avoided. A
hemoglobin (Hb) level greater than 7 to 8 g/dl is generally acceptable if the patient is young and not
actively bleeding and if fluid resuscitation has achieved a near steady-state value
o In elderly patients or those with known cardiovascular disease, a Hb level of approximately
10 g/dl should be maintained.
• Platelet counts less than 80,000/dl are associated with increased bleeding and, in the setting of active
GI bleeding, should be corrected with transfused platelets. If existing platelets are dysfunctional, as
with recent aspirin or NSAID use, platelet replacement should be considered for the actively bleeding
patient even when platelets are quantitatively normal.
Localization of Gastrointestinal Hemorrhage
• The initial challenge after stabilization of the patient is to determine whether the hemorrhage is
emanating from above (upper intestinal) or below (lower intestinal) the ligament of Treitz.

51
 • The presence of hematemesis is virtually always indicative of an upper gastrointestinal (UGI)
hemorrhage; however, epistaxis or oropharyngeal bleeding may infrequently simulate a UGI bleed.
• Melena usually indicates UGI bleeding and occurs as a result of bacterial degradation of Hb to
hematin and other hemochromes as blood traverses the small bowel and colon.
o Melena can result from as little as 50 to 100 ml of blood introduced into the UGI tract.
o Rarely,melena will occur during a lower GI bleed, but only when bleeding is slow and is
localized to the right colon or small bowel.
• Other clinical findings suggestive of UGI hemorrhage include hyperactive bowel sounds and
elevated BUN out of proportion to serum creatinine.
• The passage of red blood (hematochezia) from the rectum usually indicates a lower GI bleed. (A brisk
upper GI bleed can present similarly, however, patients with hematochezia from UGI bleeding usually
have evidence of volume depletion from the history and physical exam
Nasogastric Aspiration
• NG aspiration should be considered in patients with suspected UGI hemorrhage when
esophagogastroduodenoscopy (EGD) will be delayed in order to:
(1) Confirm the upper tract nature of bleeding when melena or hematochezia is
present rather than hematemesis
(2) Provide prognostic information, and
(3) Cleanse the stomach to facilitate endoscopic examination.
• NG findings:
o The presence of gross blood or “coffee grounds” on gastric aspirate confirms an UGI source.
o A clear aspirate does not exclude an upper bleed, however, since bleeding may be episodic or
the lesion may be distal to the stomach, with a competent pylorus preventing duodenogastric
reflux of blood.
o Bile in a nonbloody aspirate makes an upper source less likely, although this can be
misleading because the visual appearance of the aspirate does not reliably discriminate
between the presence and absence of bile.
Upper GI Bleeding
Epidemiology
• Most common causes of upper GI bleeding are peptic ulcers and esophagogastric varices (which
occurs in setting of portal hypertension).
• Less common causes include Mallory-Weiss tears, malignancy, erosive disease, vascular
abnormalities.
• Mortality from acute upper GI bleeding requiring hospitalization remains ~4% for young patients and
~15% for elderly.
• 75-80% of upper GI bleeds resolve without intervention
Lesion Prevalence (%) Comments
Account for up to 50% of all UGI bleeds.
Classic feature: epigastric pain relieved by food suggests PUD
21 (gastric ulcer) (usually gastric ulcers are made worse with food, duodenal
Peptic ulcer disease (PUD) 24 (duodenal ulcer) ulcers are made better)
2 (anastomotic ulcer) Up to 40% may lack dyspeptic symptoms before bleed.
Any age, but more common in elderly persons.
Mortality rate of 5%.
Bleeding usually self-limited and treated similar to PUD.
Multiple etiologies: stress, drugs (NSAIDs, alcohol, iron,
Erosive gastritis 5-25
potassium chloride), corrosives, ischemia, vasculitis, radiation,
mechanical causes, portal hypertension.
Responsible for a high proportion of severe hemorrhage.
Esophageal varices 9-21
Secondary to portal hypertension

52
Lesion Prevalence (%) Comments
Arterial bleeding from longitudinal mucosal lacerations.
Retching followed by hematemesis should suggest a Mallory-
Mallory-Weiss tear 11-14
Weiss tear
Bleeding stops spontaneously in up to 90%.
Most cases are a primary nonspecific form, but some result from
Erosive duodenitis 5-9 stress, alcohol, NSAIDs, ischemia, infection, inflammatory
bowel disease, or renal failure.
Clinically significant bleeding in UGI neoplasms is uncommon.
Malignancy ˜3 If bleeding occurs, endoscopic therapy is usually temporizing
measure before definitive surgery.
Occult more common than overt blood loss.
Most respond to conservative medical therapy.
Esophagitis 2-8
Multiple etiologies: gastroesophageal reflux, infection, pills,
corrosives, radiotherapy, nasogastric trauma.
Emergency Evaluation/Treatment:
• Initial focus for any patient with significant blood loss should be evaluation and restoration of
intravascular volume, which begins with careful evaluation of blood pressure and pulse, including
special attention to any orthostatic changes.
• Hemoglobin and hematocrit are unreliable markers of acute blood loss, but are helpful as baseline
values
• IV access and vigorous volume replacement (with isotonic electrolyte solutions) decreases the
morbidity of acute upper gastrointestinal bleeding.
Assessing Level of Bleeding:
• Endoscopy is method of choice to establish site of gastrointestinal bleeding.
• An upper GI source can be assumed when there is a history of hematemesis with frank blood or coffee
grounds-like material
• History of melena alone is suggestive but not pathognomonic of a bleeding source proximal to the
ligament of Treitz. (Hematochezia is more suggestive of a bleeding site in the lower GI tract), but in as
many as 10%, it may also result from vigorous upper GI bleeding
• When acute bleeding source is thought to be in the upper GI tract, nasogastric aspiration is 80%
sensitive for the presence of an actively bleeding lesion, and evidence of blood in a nasogastric aspirate
suggests bleeding proximal to the ligament of Treitz. Suction of bile (without blood) suggests that the
bleeding source is distal to the ligament of Treitz or that the bleeding has ceased.
• Nasogastric suction is also useful to determine whether bleeding is persistent or recurrent and to
estimate the rapidity of bleeding.

Diagnostic Endoscopy
• Endoscopy has a sensitivity of 92% for identification of the site of upper gastrointestinal bleeding, with
a specificity that approaches 100%.
• Endoscopy has the added advantage of guiding biopsies to test for Helicobacter pylori infection and to
diagnose malignant disease.
o Barium radiography has a lower sensitivity (54%) is contraindicated in acute upper
Endoscopic
gastrointestinal bleeding because it interferes with subsequent triage in
endoscopy, acute upperorgastrointestinal (GI)
angiography,
surgery. bleeding. (Flow chart for the cost-effective use of
endoscopic triage to determine the level of care required
• Careful endoscopic examination not only identifies the source of upper gastrointestinal bleeding but
for patients with acute upper gastrointestinal bleeding).
also is the most accurate predictor of prognosis (probability of rebleeding, morbidity, and mortality).
• Patients who have no clinical risk factors for
• Clinical risk factors for higher morbidity and mortality include older age, shock, volume of bleeding,
rebleeding and who have ulcers with low-risk
need for transfusion, onset of bleeding in the hospital, and presence of comorbid clinical conditions.
stigmata (clean base, flat pigmented lesions) may be
treated as outpatients.
• Patients with high-risk lesions (active bleeding, a
nonbleeding visible vessel) and clinical risk factors
53 should receive endoscopic therapy and
hospitalization in a unit on the basis of their
individual risk.
Non-Ulcer Causes of Acute Upper Gastrointestinal Bleeding
• Variceal bleeding is the most common cause of nonulcer upper gastrointestinal hemorrhage.
• The approach to variceal bleeding is a combination of pharmacologic (octreotide- synthetic
somatostatin), endoscopic (band ligation, sclerotherapy), and mechanical (balloon tamponade)
approaches:
o Octreotide (aka synthethic somatostatin) is efficacious because it inhibits the secretion of
many hormones, including digestive enzymes (i.e. gastrin, cholecystokinin, secretin,
pancreatic polypepetide, VIP, etc), and more importantly it causes vasoconstriction in the
blood vessels which limits blood loss
• The most common cause of non-peptic ulcer, non-variceal bleeding of upper GI tract is a tear at the
gastroesophageal junction, called a Mallory-Weiss tear, which accounts for 5 to 14% of upper
gastrointestinal bleeding.
o Mallory-Weiss bleeding usually stops spontaneously, but persistent bleeding should be treated
in a manner similar to bleeding from peptic ulcers.
• Dieulafoy's lesion, which is an aberrant submucosal artery that erodes into the lumen of the stomach,
is a rare cause of recurrent vigorous upper gastrointestinal bleeding.
• Tumors also are rare (<1%) causes of acute upper gastrointestinal bleeding.
• Vascular lesions may rarely present as acute bleeding, but more commonly they cause chronic, low-
grade blood loss.
• Bleeding from diffuse gastric erosions, which can occur in critically ill patients, does not respond to
endoscopic therapy but can usually be prevented by prophylactic treatment.
Treatment
Medical Therapy.
• Theoretically, by slowing or halting bleeding, pharmacologic agents may be useful in the resuscitative
phase of management and in enhancing the visualization of lesions during endoscopy.
o Iced saline gastric lavage has been a time-honored treatment considered essential for
controlling UGI hemorrhage; however, the therapeutic value of lavage has since been refuted.
• Pharmacologic agents that act as antifibrinolytics (e.g., tranexamic acid), reduce gastric acid (e.g.,
histamine receptor antagonists [H2RAs], proton pump inhibitor [PPIs], and prostaglandin analogs), act
as mesenteric vasoconstrictors (e.g., vasopressin ), or both reduce acid and act as vasoconstrictors (e.g.,
somatostatin or octreotide) have been studied in an attempt to control actively bleeding ulcers.
Although a few studies have reported benefit, most have found these agents to be ineffective, and at
present, no medical therapy can be strongly recommended for the acute treatment of nonvariceal UGI
bleeding.
• Data from in vitro studies suggest that clotting occurs more effectively and that lysis of clots by
proteolytic enzymes occurs more slowly at high intraluminal pH levels. This forms the basis for
regimens designed to reduce gastric acidity in patients with intestinal bleeding.
Endoscopic Therapy.

54
• In the 20% of patients with nonvariceal upper GI bleeding who have persistent or recurrent bleeding as
determined by nasogastric lavage or endoscopy, endoscopic therapy reduces both morbidity and
mortality
• The most common endoscopic interventions used are thermal coagulation, injection therapy (saline or
diluted epinephrine), and mechanical compression (hemostatic clips, rubber band ligation). Hemostasis
is achieved in 90% of patients with active bleeding using these methods
• Endoscopic therapy should be limited to patients at high risk for persistent or recurrent bleeding and
death.
o This group includes those with clinical evidence of significant blood loss and endoscopic
evidence of active bleeding or a nonbleeding visible vessel.
o Ulcers with minor signs of recurrent hemorrhage or a clean base have a much lower rate of
rebleeding and do not benefit from endoscopic therapy.
o Other nonulcer lesions amenable to endoscopic therapy include select vascular malformations,
Dieulafoy's lesion, and Mallory-Weiss tears.
• The two major complications of endoscopic therapy are the induction of bleeding (0.5%) and intestinal
perforation (0.3%).
Angiographic Intervention.
• Angiographic therapy should be considered only for severe, persistent bleeding if surgery confers a
high risk and endoscopic therapy is not available or has been unsuccessful.
• Arterial embolization with absorbable gelatin sponge (Gelfoam) and autologous clot or with
nonabsorbable polyvinyl alcohol and sponge-wire coils may control bleeding identified
angiographically in 75% to 80% of patients, although recurrent bleeding may occur in more than half.
• Alternatively, selective intraarterial vasopressin infusion may temporarily stop bleeding in up to 50%
of patients.
• Complications of angiographic therapy include allergic reactions, renal insufficiency, ischemia, and
perforation in target and nontarget organs.
Emergency Surgery.
• All patients with UGI bleeding severe enough to cause significant hemodynamic instability that
requires ICU admission warrant evaluation by a surgeon.
• Criteria for emergency surgery include
(1) Failure to control bleeding with nonoperative means;
(2) Severe rebleeding despite two attempts at endoscopic hemostasis;
(3) A lesion inaccessible to endoscopy because of prior surgery, anatomic anomaly, or pyloric
stenosis;
(4) Severe shock when emergent surgery may prevent exsanguination; and
(5) Severe complication of endoscopic therapy (e.g., perforation, worsening bleeding lesion).
Lower GI Bleeding:
Epidemiology
• Incidence of lower gastrointestinal bleeding is 20 per 100,000 population (1/5 as frequent as upper GI)
• Lower gastrointestinal bleeding is most commonly a disorder of the elderly, with a dramatically
increased incidence with advancing age.
Symptoms/Signs
• Hematochezia, which is the most common presenting symptom for lower gastrointestinal hemorrhage,
can be variously described as bloody diarrhea, blood and clots per rectum, maroon-colored stool, or
blood mixed with the stool.
o Hematochezia can occur from bleeding anywhere in the gastrointestinal tract. 10% of patients
who present with hematochezia have an upper gastrointestinal source of bleeding.
• With lower GI hemorrhage the presence or absence of abdominal pain is important:
o Diffuse abdominal pain can suggest inflammatory bowel disease or ischemic bowel
o Painless bleeding is common with diverticula, angiodysplasia, malignancy, polyps, and
Meckel's diverticulum.

55
• Bloody diarrhea may indicate infectious (e.g., Clostridium difficile) colitis or IBD, or recent antibiotic
use; whereas recent constipation suggests anorectal sources, such as hemorrhoidal bleeding, anal
fissure, or solitary rectal ulcer syndrome
Pathophysiology:
• The most common causes of lower gastrointestinal bleeding are colonic diverticula, vascular ectasias
(angiodysplasia), and tumors, all of which increase in prevalence with age.
Age and Clinical Presentation of Lower Gastrointestinal Bleeding
Clinical presentation Child Young adult Middle-age adult Elderly
IBD,
Abdominal pain IBD IBD Ischemia
intussusception
Angiodysplasia,
Meckel's juvenile Meckel's Diverticulosis,
Painless bleeding diverticulosis, polyp,
polyp diverticulum polyp, malignancy
malignancy

Diarrhea IBD, infection IBD, infection IBD, infection Ischemia, infection

Hemorrhoids,
Hemorrhoids, Malignancy,
Constipation/dyschezia Fissures fissures, rectal
fissures hemorrhoids, fissures
ulcers
Common Causes of Lower Gastrointestinal Bleeding
Prevalence
Lesion Comments
(%)
Diverticular disease 17-40 80% are self-limited.

Frequency varies widely in clinical series. Source

Colonic vascular ectasia 2-30
tends to be proximal colon in acute bleeding.

Ischemic colitis often presents with pain and

Colitis (ischemic, infectious), IBD, limited hematochezia.
9-21
radiation proctopathy Bloody diarrhea is most common symptom of
infectious colitis and IBD.

Colonic neoplasia, postpolypectomy Postpolypectomy bleeds are usually self-limited

11-14
bleed and tend to occur 7-14 days after polypectomy.

Anorectal causes 4-10 Proctoscopy can be helpful in initial evaluation.

Although bilious nasogastric aspirate makes UGI
UGI source 0-11 source unlikely, it cannot totally eliminate UGI
tract as source.
Small bowel source (Crohn's ileitis,
Diagnosis is often made by radiologic studies and
Meckel's diverticulum, vascular ectasia, 2-9
enteroscopy after acute bleed has resolved.
tumors)
Evaluation of Lower GI Bleed
• After initial evaluation and volume resuscitation, further management depends on the results of an NG
tube aspirate.
o About 1000 ml or more of blood is required to cause hematochezia from an upper source, and
hemodynamic compromise is typically an accompanying feature.
o If copious nonbloody bile is seen on NG aspiration, the physician should proceed directly to a
colonoscopy.

56
 o In all other cases, however, the colonoscopy should be preceded by an EGD because as many
as 10% to 15% of patients with suspected lower GI bleeding have a UGI source.
• The initial approach to the patient should be the same as in upper gastrointestinal bleeding, with
careful assessment of vital signs and vigorous volume replacement.
• A history of prior bleeding, inflammatory bowel disease, radiation therapy, and NSAID use may be
helpful but does not identify the bleeding lesion.
• When obtaining a history, questions should address prior episodes of bleeding, family history of GI
diseases (e.g., hereditary hemorrhagic telangiectasia), known illnesses (e.g., ulcers, cirrhosis, cancer,
bleeding diathesis), and previous abdominal surgery Workup of Lower GI Bleeding:
• Nasogastric aspiration is indicated to exclude an
upper gastrointestinal source.
• The optimal diagnostic approach is rapid colonic
lavage followed by colonoscopy, which can also be
therapeutic.
• When colonoscopy does not reveal the bleeding
lesion and bleeding persists at a brisk volume,
angiography may identify and control the bleeding
vessel.
• In the absence of vigorous bleeding, a radionuclide
red blood cell (RBC) scan may identify the site of
more slowly bleeding lesions and guide further
evaluation and therapy.
• Close observation is indicated in patients whose
bleeding has stopped spontaneously without a
definitive diagnosis.
• Surgical consultation early in the course is
indicated. Surgical therapy, however, should be
reserved for patients with an identified lesion or
those with exsanguinating bleeding that cannot be
controlled any other way.
Diagnosis
FIGURE 137-4 Approach to acute lower gastrointestinal (GI)
• Identification and treatment of the bleeding lesion should be attempted after the patient is
hemodynamically stable.
• Early colonoscopy identifies lesions, facilitates treatment, and decreases hospital stay. The diagnostic
yield from colonoscopy ranges from 60% to 80%. Endoscopy should be performed as soon as possible
in patients with continuous hematochezia. Patients who have stopped bleeding can undergo
examination on a semielective basis.
o The three outcomes to colonoscopy are source identification, negative examination, or
incomplete colonoscopy secondary to severe bleeding.
• When urgent colonoscopy does not identify a bleeding source or if bleeding is too rapid to permit
colonoscopy, angiography may identify the bleeding site.
o The yield of angiography ranges from 40 to 80%, but to be successful, angiography requires a
bleeding rate of at least 1 mL/min.
• In settings in which bleeding is not rapid enough for angiography, nuclear scintigraphy may be helpful
in identifying the site but not the cause of the lesion.
o The bleeding rate required for identification is at least 0.1 mL/min. In optimal conditions, the
sensitivity of scintigraphy is 85%, and its specificity is 70%. One advantage of tagged red
blood cell scintigraphy is the ability to detect intermittent bleeding by serial scans performed
over the lifetime of the radionuclide
• There is no role for barium enema in the setting of acute lower gastrointestinal bleeding because it is
unlikely to provide a definitive diagnosis and prevents or delays more accurate diagnostic modalities
with potential therapeutic benefits.

57
Treatment
• Endoscopic therapy for these lesions, similar to the methods described earlier for upper gastrointestinal
bleeding, reduces the rate of rebleeding and the need for surgery.
• Vascular lesions can be treated with injection, contact thermal methods, or endoscopic laser therapy.
• Surgical consultation and comanagement are appropriate in all cases of gastrointestinal bleeding and
are most critical in the setting of severe lower gastrointestinal bleeding.
• Vigorous efforts should be made to diagnose the bleeding lesion or, if that is not possible, at least the
involved segment of the colon to guide surgical therapy.
• Surgery directed at a lesion identified endoscopically or radiographically is often curative.
• Empirical total colectomy or right hemicolectomy should be reserved for life-threatening bleeding that
cannot be localized and has not responded to available therapeutic approaches.
Stomach
I. Embryology
a. The stomach is derived from the embryonic foregut
b. At the 5th gestational week, a caudal dilatation of foregut become the future stomach
c. Ventral mesentery becomes falciform ligament, lesser omentum, gastrohepatic, and
hepatoduodenal mesenteries
d. The celiac artery passes through the dorsal mesentery
i. Branches of the Celiac artery:
1. Left gastric artery:
a. Esophageal branch
b. Hepatic branch
2. Common hepatic artery:
a. Hepatic artery proper
b. Right gastric artery
c. Gastroduodenal artery
3. Splenic artery
a. Dorsal pancreatic artery
b. Short gastric arteries
c. Left gastro-omental artery
e. Dorsal mesentery forms the gastrocolic, gastrosplenic, and gastrophrenic ligaments
f. In the 6th to 7th week of gestation, the left gastric wall (greater curvature) growth is
accelerated in comparison to the right gastric wall (lesser curvature)
II. Anatomy
a. Anatomy of the Stomach
i. Gross Anatomy
1. Cardia is region just distal to the GE junction
2. Fundus is the region superior and to the left of the GE junction
3. Corpus (body) of the stomach encompasses the area between the
fundus and antrum
4. Antrum compromises the distal stomach and ends at the pylorus
ii. Vascularization
1. Arterial supply
a. Left gastric artery - branch of celiac artery and supplies a large
portion of lesser curve and GE junction
b. Right gastric artery - branch of the common hepatic artery
from the celiac artery and supplies the distal lesser curve
c. Short gastric and left gastroepiploic arteries – branches of the
splenic and supply the greater curvature and fundus
d. Right gastroepiploic artery – a branch of the gastroduodenal
artery and supplies the greater curve of the stomach
2. Venous drainage via the portal system, paralleling the arterial supply

58
 iii. Innervation
Parasympathetic/vagal
1. Vagal trunks pass through the esophageal hiatus along the anterior and
posterior esophagus
2. After the GE junction, the anterior vagus nerve divides and the hepatic
branch sends fibers to the liver and gallbladder
3. Distal to the hepatic branch, the anterior vagus becomes the nerve of
Latarjet
Sympathetic
1. Sympathetic fibers originate from spinal nerve roots T5 to T10, and
pass via gray rami communicantes to enter prevertebral ganglia
2. Presynaptic fibers then follow the greater splanchnic nerves to the
celiac plexus
3. Postsynaptic fibers enter the stomach with the blood vessels
iv. Lymphatic drainage
1. The proximal stomach near the lesser curve initially drains lymph into
the superior gastric lymph nodes that surround the left gastric artery
2. The distal stomach near the lesser curve drains into the suprapyloric
nodes
3. The proximal greater curvature drains to the subpyloric and omental
lymph nodes
4. Secondary drainage from these lymph nodes basins passes on to the
celiac axis node
III. Histology. The gastric mucosa is composed of simple columnar epithelium with surface
mucus cells.
a. Oxyntic glands are located in fundus and body of stomach
i. Glands contain parietal cells that are responsible for acid and intrinsic factor
production
ii. The contain chief cells that produce and secrete pepsinogen
iii. Mucus cells produce mucus and bicarbonate that protects the lining of the
stomach from damage by luminal acid
iv. Enterochromaffin-like cells (ECL) are also found in oxyntic glands. ECL cells
produce histamine, and are a major regulator of gastric acid production
b. Antral glands are located in the distal stomach and pyloric channel
i. Most secrete mucus, but many also contain G-cells that produce gastrin
ii. D-cells produce the inhibitory hormone somatostatin
iii. Chief cells are also found in pyloric glands
IV. Physiology
a. Gastric peptides
i. Gastrin
1. Meals stimulate release of gastrin via intragastric breakdown of
proteins
2. Gastric distension contributes to cholinergic activation, and subsequent
gastrin release
3. Somatostatin decreases gastrin release
4. Acidification after a meal also inhibits gastrin release when luminal pH
falls below 3.0
ii. Somatostatin
1. Inhibits acid secretion and gastrin release
2. A decreased intragastric pH stimulates its release, and an increased pH
will inhibits its release
iii. Ghrelin
1. Produced by oxyntic glands
2. Is a orexigenic hormone, and it stimulates food intake
iv. Pepsins are a group of proteolytic enzymes secreted by gastric chief cells

59
 1. Cholinergic stimulus is the most important secretagogue
2. Pepsins initiate protein digestion
v. Intrinsic factor is secreted by parietal cells. It functions by binding cobalamin
(Vit B12), which is subsequently absorbed in the terminal ileum
V. Benign Disorders
a. Peptic Ulcer Disease (PUD)
i. Epidemiology
1. Peak incidence in the 6th and 7th decades of life
2. PUD tends to occur in lower socioeconomic classes
3. Each year, approx 300,000 to 500,000 new cases of PUD occur
4. 3-4 millon patients are self-medication for symptoms of PUD, and
30,000 surgeries are performed annually for PUD
ii. Etiology. Causes of ulceration are multifactorial. Predisposing conditions
include:
1. Age > 40
2. Use of nonsteroidal anti-inflammatories
3. Pepsin and acid secretion abnormalities
4. Delayed gastric emptying
5. Bile reflux
6. Coexisting duodenal ulceration
7. Helicobacter pylori infection
iii. Pathophysiology
1. Mucosal H. pylori infection contributes to ulcer formation in most
cases
a. H. pylori is a helical gram-negative rod with flagella that
resides beneath the mucus layer of stomach
b. Production of the enzyme urease allows H. pylori to survive in
the acidic environment of the stomach
2. There are 5 types of gastric ulcers
a. I – Lesser curve
b. II – Body and duodenum (excessive acid secretion)
c. III – Prepyloric (excessive acid secretion)
d. IV – Lesser curve near GE junction
e. V – Anywhere induced by NSAID
3. The majority of ulcers are type I and aren’t associated with excessive
acid secretion
iv. Clinical presentation
1. PUD may occur intermittently, with relapsing episodes
2. Often, it’s difficult to differentiate PUD from gastric cancer
3. Abdominal pain, bleeding obstruction and perforation are all symptoms
of PUD
v. Diagnostic tests
1. PE often reveals epigastric abdominal pain. Peritoneal signs suggests
perforation
2. Upright chest radiography is useful to evaluation for the presence of
free intra-abdominal air, signaling perforation
3. Contrast radiography can diagnose PUD, but it may miss some
malignant disease presenting as PUD
4. Flexible endoscopy is the mainstay in the diagnosis of PUD. Biopsy of
all gastric ulcers is mandatory to rule out the presence of a gastric
cancer presenting as PUD
5. Test for H. pylori include serology, urea breath test, and biopsy with
rapid urease testing (CLO test), or histological analysis
vi. Medical treatment

60
 1. Eradication of H. pylori with regimens that include a PPI in
combination with two antibiotics for approximately 14 days
2. Histamine receptor antagonists
3. PPIs
4. Sucralfate (an aluminum salt of sulfated sucrose that polymerizes, and
becomes viscous to adhere to gastroduodenal mucosa and ulcer bed)
5. Bismuth compounds for H. pylori
vii. Surgical Treatment
1. Indications include bleeding, perforation, obstruction, and intractable
PUD resistant to medical therapy
2. Truncal vagotomy involves the division of vagal trunks at the
esophageal hiatus and is usually combined with a pyloroplasty
(denervation results in delayed gastric emptying)
3. Truncal vagotomy and antrectomy have lowest recurrence rate for PUD
4. Proximal gastric vagotomy , where only the nerves to acid-secreting
cells are divided. The hepatic and celiac branches as well as fibers to
antrum and pylorus (nerves to Latarjet) are spared
5. Increasingly, treatments have involved addressing the acute problem,
such as repairing a perforation, controlling the hemorrhage with
nonresective surgical procedures, or managing the PUD medically with
acid reduction and H. pylori
VI. Benign Tumors
a. Hyperplastic polyps
i. Polyps are usually small in size, and less than 2 cm in diameter
ii. Typically they arise in the setting of chronic atrophic gastritis
iii. Most resolve with H. pylori treatment
iv. Malignant transformation is unusual to rare, at 1% to 3%
v. Endoscopic polypectomy is the treatment of choice
b. Fundic gland polyps represent hyperplasia of normal fundic glands
i. They can be associated with familial polyposis syndromes
ii. They harbor no malignant potential
c. Adenomatous polyps
i. Polyps may be tubular, tubulovillous, or villous
ii. The risk of malignant transformation increases with larger size and villous type
iii. Gastric adenocarcinoma may be found in approximately 20% of cases
iv. Endoscopic polypectomy is effective if the entire polyp is removed and no
invasive carcinoma is found on review of the histologic specimen
v. Surgical resection is indicated for sessile lesions greater than 2 cm, polyps with
invasive tumors, or polyps causing symptoms such as bleeding or obstruction
d. Ectopic pancreas or pancreatic rests
i. These occur during embryonic development while the dorsal and ventral fuse
ii. The majority of cases involve the stomach, duodenum, and jejunum
iii. Most patients are asymptomatic
iv. Symptoms include abdominal pain, discomfort, nausea, vomiting, and bleeding
v. Diagnosis is made via endoscopy. Endoscopic ultrasound may be helpful for
location and biopsy
vi. Treatment of symptomatic lesions is by surgical resection
VII. Other Gastric Lesions
a. Hypertrophic gastritis (Menetrier disease) is an acquired rare premalignant disorder
characterized by massive gastric folds involving the fundus and body
i. On evaluation, the mucosa has a cobblestone appearance
ii. Histologic analysis reveals foveolar hyperplasia and the absence of parietal cells

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 iii. Menetrier disease is associated with protein loss from the stomach, excessive
mucus production, and achlorhydria. It is linked with CMV in children and H.
pylori infection in adults
iv. Presenting symptoms are epigastric pain, weight loss, vomiting, and peripheral
edema
v. Medical treatment involves anticholinergics, acid suppression, octreotide, and
H. pylori eradication
vi. Surgical treatment is via total gastrectomy and is reserved for patients with
massive protein loss despite adequate medical therapy or for the development of
dysplasia or carcinoma
b. Zollinger-Ellison Syndrome
i. Caused by the uncontrolled secretion of abnormal amounts of gastrin by a
pancreatic or duodenal neuroendocrine tumor (i.e., gastrinoma)
ii. 80% are sporadic, 20% are inherited (associated with MEN I – parathyroid,
pituitary, pancreatic tumors)
iii. Most common symptoms are epigastric pain, GERD, and diarrhea
iv. Average age is 50 years, and over 90% of patients with gastrinoma have peptic
ulcer
v. Most ulcers are in proximal duodenum, but atypical locations including distal
duodenum, jejunum, or multiple ulcers should prompt an evaluation for
gastrinoma
1. Hypergastrinemia in the presence of elevated BAO suggests gastrinoma
2. Diagnosis of ZES is confirmed by the secretin stimulation test
a. IV bolus of secretin is given and gastrin levels are checked
before and after injection
c. Dieulafoy gastric lesion
i. Pulsations of an abnormally large artery coursing through the submucosa lead to
erosion of the mucosa, followed by exposure to gastric contents and
hemorrhage. The vessel is usually located along the lesser curve within 6 cm of
the GE junction
ii. Peak incidence is in the fifth decade of life and is more common in men
iii. Classic presentation is with sudden recurrent massive hematemesis and
hypotension
iv. Endoscopy is used for diagnosis and treatment. Endoscopic control of
hemorrhage may be therapeutic
v. Treatment is surgical and includes laparotomy or laparoscopy with wedge
resection that incorporates the offending vessel
d. Gastric varices
i. These may occur with esophageal varices with portal hypertension or secondary
to sinistral hypertension from splenic vein thrombosis
ii. Treatment
1. Splenectomy is the treatment of choice for splenic vein thrombosis
2. Those associated with portal hypertension are treated in a similar
manner as esophageal varices
e. Gastric bezoars are collections of nondigestible substances within the lumen of the
stomach
i. Phytobezoars are made of cellulose from ingestion of vegetables
ii. Treatment is with enzymatic therapy with papain
1. Papain administration is followed by gastric lavage or endoscopic
fragmentation
2. Failure of enzymatic digestion leads to surgical removal
iii. Trichobezoars are formed from the ingestion of hair
1. Small lesions can be removed via endoscopy, lavage, or enzyme
treatment

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 2. Large casts require surgical removal

VIII. Malignant Disease

a. Adenocarcinoma of the stomach
i. Epidemiology
1. The 2nd most common cancer worldwide, adenocarcinoma of the
stomach is the 10th most common cancer in the US
2. In the US, it’s more common in black males, and men are more likely
to be affected than women, with a ratio of 2:1
3. In Japan and in South America, incidence rates are higher
4. Site of gastric cancers has shifted from the distal stomach to the more
proximal gastric cardia
ii. Risk factors
Diet
1. Salted meat or fish
2. Nitrate consumption
3. Complex carbohydrates
Medical
4. H. pylori infection
5. Adenomatous polyps
6. Pernicious anemia
iii. Clinical presentation
1. Symptoms include vague epigastric discomfort and indigestion
2. More advanced disease is associated with anemia, anorexia, weight
loss, fatigue, or vomiting
b. Gastric lymphoma
i. Epidemiology
1. The stomach is the most common site for lymphoma in the
gastrointestinal tract
2. More than 50% of affected patients have anemia
3. Peak incidence is in the 6th and 7th decades
4. The disease is more common in males
ii. Mucosa-associated lymphoma tissue (MALT)
1. Gastric submucosa does not normally contain lymphoid tissue
2. H. pylori infection is believed to be a causal factor for MALT
3. Low-grade MALT resembles Peyer patches
iii. Gastrointestinal stromal tumors of the stomach (GIST)
1. These account for 3% of gastric malignancies, because these tumors
arise in the mesenchymal portion of the gastric wall
2. Patients present at a mean age of 60, and after the 6th decade
3. Lesions with more than 5 to 10 mitoses per 10 high-powered fields
demonstrate an increased potential for metastasis
4. Metastasis occurs via the hematogenous route and lymphatic
involvement is rare
5. Surgical resection is the treatment of choice
iv. Carcinoid
1. Gastric carcinoids are uncommon and account for only 3% to 5% of
gastrointestinal carcinoids
2. They appear as reddish-pink to yellow submucosal nodules
3. Invasion is rare but occurs more frequently in tumors greater than 2 cm
in size
4. Curative resection is indicated in most cases
Acute Abdomen
Trisha Fertig

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 • Refers to a sudden, severe abdominal pain that is less than 24 hours in duration and is so intense
that the patient seeks medical treatment.
• Some causes require urgent surgery, while many do not require surgical treatment. There is a
wide differential diagnosis.

Peritoneal signs:
• Extreme tenderness, voluntary guarding, rebound tenderness, percussion tenderness, patient lying
motionless
• Order of abdominal exam: inspection, auscultation, palpation, percussion
Lab tests:
• CBC w/diff, CMP, LFT, UA, amylase, B-hCG
Differential Diagnosis by Quadrants:
• RUQ: appendicitis (especially pregnant patients), cholecystitis, choledocholelithiasis, cholangitis,
hepatitis, peptic ulcer disease, perforated ulcer, pancreatitis, inferior wall MI
• RLQ: appendicitis, Meckel’s diverticulum, intussusception, cecal diverticulitis, mesenteric
lymphadenitis, UTI, pyelonephritis, GYN causes (ectopic, PID, endometriosis, ovarian cyst, ovarian
torsion)
• LUQ: peptic ulcer disease, perforated ulcer, dissecting aortic aneurysm, hiatal hernia, Mallory-
Weiss tear, splenic disease/rupture, Boerhaave’s syndrome (rupture of the esophageal wall)
• LLQ: diverticulitis, sigmoid volvulus, perforated colon, colon cancer, SBO, UTI, pyelonephritis,
GYN causes (ectopic, PID, endometriosis, ovarian cyst, ovarian torsion)
Other Etiologies:
• Endocrine causes: DKA, Addisonian crisis
Most Common Causes
• RUQ: cholecystitis
• RLQ: appendicitis
• LLQ: sigmoid diverticulitis
Classic Referred Pain Syndromes:
• Appendicitis: early- periumbilical; later localizes to RLQ
• Cholecystitis:: right subscapular pain (Boa’s sign)
• Pancreatitis: back pain
• Nephrolithiasis: flank pain
• Small bowel: periumbilical
Surgical Acute Abdomen
Small Bowel Obstruction (SBO)
• Accounts for approximately 4% of all patients presenting with an acute abdomen.
• Diagnosis of SBO is made when dilated small bowel and collapsed small bowel loops seen on CT
• If obstruction is present, try to identify its cause and location (adhesion, tumor, volvulus,
intussusception, inguinal hernia).
• Adhesions account for 60-80% of all cases and are the likely cause when a smooth transition from
dilated to collapsed small-bowel loops is noted
• Treatment: ex-lap

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Volvulus
• A life-threatening bowel obstruction in which a loop of bowel has abnormally twisted on itself.
• Most commonly in the sigmoid colon, accounts for 8% of SBO cases,
• Most common in middle-aged and elderly men, also in patients with Duchenne Muscular
Dystrophy
• Causes bowel obstruction and ischemia
• Can lead to necrosis, acidosis, death
Intussusception
• A blockage of the small intestine that occurs when one part of the small intestine invaginates, or
telescopes, into another section of intestine
• Nausea, vomiting, red currant jelly stool
• Tx: barium/air insufflation enema, or surgical reduction if enema does not work
Bowel Perforation
• The presence of free intraperitoneal air is proof of bowel perforation, and indicates a surgical
emergency
o Seen best on upright abdominal xray
o Can also see it on lateral decubitus x-ray if patient can’t stand up
• A pneumoperitoneum has only two frequent causes:
o Perforation of a gastric ulcer
o Perforation of colonic diverticulitis
• Treatment: ex-lap
Mesenteric Lymphadenitis.
• Common mimicker of appendicitis
• Second most common cause of right lower quadrant pain after appendicitis
• Self-limiting inflammation of right-sided mesenteric lymph nodes without an identifiable
underlying inflammatory process, occurring more often in children than in adults
• Diagnosis can only be made confidently when a normal appendix is found, because adenopathy
also frequently occurs with appendicitis
Ruptured Aneurysm
• Most abdominal aortic aneurysms rupture into the left retroperitoneum
• Clinically this may simulate sigmoid diverticulitis or renal colic due to impingement of the
hematoma on adjacent structures
• Most patients present with the classic Beck’s triad: hypotension, a pulsatile mass and back pain
• Continuous leakage will lead to rupture into the peritoneal cavity and eventually death
• Imaging: abdominal CT or ultrasound
• Treatment: emergency surgery
Appendicitis
• 250,000 cases per year in USA
• Incidence highest in 10-19 years of age, higher in men
• Anatomy review:
o Appendix is connected to cecum, located at McBurney’s point (1/3 distance laterally of
line joining ASIS and umbilicus)
o Appendix is displaced towards RUQ in pregnant patients
• Blood supply: appendicular artery, branch of ileocolic artery
• Venous: ileocolic vein, tributary of superior mesenteric vein
• Nerves: superior mesenteric ganglia
• Early: poorly localized, periumbilical pain, due to stimulation of visceral nociceptors, pain
becomes localized when inflammation reaches parietal peritoneum Mc Burney’s tenderness
• Obstruction of appendiceal lumen is most common mechanism

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 • Presentation: malaise, periumbilical pain, poorly localized pain, nausea and vomiting, fever,
leukocytosis,
• Rovsing’s sign: RLQ pain when LLQ palpated
• Obturator sign: pain with internal rotation of hip
• Iliopsoas sign: RLQ pain when hip extended
• Treatment: hydration, correction electrolyte imbalances, antibiotics, and appendectomy
Small Bowel Obstruction
Adam Litroff
Anatomy of the Small Intestine
• Extends from pylorus to ileocecal valve
• 200cm in length in the newborn
• 4-7m in length in the adult
• 3 segments: Duodenum, Jejunum, Ileum
 Duodenum
◦ Most proximal portion of small intestine; 25cm
◦ Begins at pylorus, extends through retroperitoneal space, and ends at the
Ligament of Treitz in the peritoneal space
◦ Can determine where second portion of duodenum is based on the fact
that the ampulla of vater (from pancreas) attaches to the 2nd part of the
duodenum
◦ End of duodenum is signified by ligament of treitz, GI tract proximal to this
ligament receives blood supply from celiac artery and nerve supply from
celiac plexus; distal to the ligament of treitz and down to 2/3s of the
transverse colon, blood supply is superior mesenteric artery and the
superior mesenteric ganglion
 Jejunum
◦ Begins at the Ligament of Treitz; no obvious endpoint
◦ Proximal 2/5 of small intestine
◦ Larger circumference, thicker mucosa, prominent plicae circulares
◦ One or two arcades with long, straight vasa recta
 Ileum
◦ No obvious beginning; ends at ileocecal valve
◦ Distal 3/5 of small intestine
◦ Smaller circumference, thinner mucosa, less prominent plicae circulares
◦ Multiple separate arcades with short vasa recta
Vascular Supply
 Vascular, neural, and lymphatic supply travels through the mesentery
◦ Base of mesentery attaches to posterior abdominal wall, left of L2, extends
to the right and inferiorly to the right SI joint
◦ Proximal duodenum supplied by branches of celiac artery
◦ Remainder of small intestine supplied by superior mesenteric artery
Neural Supply
 Parasympathetic fibers from Vagus nerve
◦ Affect secretion, motility, all phases of bowel activity
 Sympathetic fibers from three sets of splanchnic nerves
◦ Derived from plexuses around the SMA
◦ Send fibers to myenteric plexus and the plexus of the submucosa
◦ Affect blood vessel motility, gut secretion & motility, general visceral
afferent fibers for pain
Lymphatic Supply
 Peyer patches in distal small bowel (ileum)
 Nodes adjacent to bowel in the mesentary

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  Regional nodes adjacent to mesenteric arterial arcades
 Nodes at base of SMA/V
 Cysterna chyli
 Thoracic ducts
Etiology of Small Bowel Obstruction
 3 Main Categories
◦ Extraluminal Causes
◦ Causes Intrinsic to the Bowel Wall
◦ Intraluminal Obturator Obstruction
 Extraluminal Causes
◦ Adhesions*
◦ Hernia* (External or Internal)
◦ Neoplasia* (Carcinomatosis, Extraintestinal neoplasia)
◦ Intra-abdominal Abscesses
 Obstruction Intrinsic to Bowel Wall
◦ Congenital defects (Malrotation, Cysts)
◦ Inflammation (Crohn’s, Infections)
◦ Neoplasia* (Primary or Metastatic)
◦ Trauma (Hematoma, Ischemic stricture)
◦ Miscellaneous (Intussusception, Endometriosis, Radiation enteropathy or
stricture)
 Intraluminal Obstruction
◦ Swallowed foreign bodies
◦ Bezoars
◦ Parasites (A lumbricoides)
◦ Gallstones
◦ Food Bolus
◦ Inspissated meconium in cystic fibrosis
Adhesions
 Most Common Cause of Obstruction Overall
 Account for > 60%
 Particularly after pelvic operations
◦ GYN, Appendectomy, Colorectal Resection
◦ Bowel in lower abdomen more mobile than in upper abdomen
Malignancy
 Account for 20% of obstructions overall
 Most are metastatic with intra-abdominal primaries
Hernias
 Most common cause of obstruction in patients without history of previous surgery
 Third leading cause overall – 10%
 Most commonly are ventral, inguinal, or internal hernias
Pathophysiology
 Initially, intestinal motility & contractile activity increase both above & below
obstruction
◦ Diarrhea in early stages of partial or complete SBO
◦ Later, bowel fatigues, dilates – water & electrolytes accumulate in lumen &
within the bowel wall
◦ “Third-spacing” – accounts for dehydration, hypovolemia
◦ Constipation/Obstipation
 Proximal obstruction
◦ Hypochloremia, Hypokalemia, Metabolic Alkalosis, Increased emesis
 Distal obstruction

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 ◦ Less dramatic changes in electrolytes
 Dehydration may lead to
◦ Oliguria
◦ Azotemia
◦ Hemoconcentration
◦ Hypotension
◦ Shock
 Hypovolemia exacerbated by
◦ Increased Intra-luminal pressure
 Decreased mucosal blood flow, especially in closed-loop obstruction
◦ Decreased venous return
◦ Elevation of the diaphragm
Types of Obstructions
 Simple obstruction
◦ Mechanical blockage without compromising intestinal wall
 Strangulation obstruction
◦ Usually involves closed-loop obstruction
◦ Vascular supply compromised  infarction
Clinical Presentation and Diagnosis
 History
◦ Colicky abdominal pain
 Less frequent with distal obstruction
◦ Nausea, vomiting
 More common with proximal obstruction
 Becomes feculent with late and established obstructions
◦ Abdominal distension
 Increased dilation of proximal intestine
◦ Obstipation
 Late development – early stages may have diarrhea
 Physical Exam
◦ Tachycardia & Hypotension
◦ Fever
◦ Distended abdomen
◦ Surgical scars
◦ Observable peristaltic waves
◦ Borborygmi vs Absent bowel sounds
◦ Tenderness
◦ GUIAIC
 Radiology: Abdominal X-Ray
◦ Plain abdominal radiographs – accuracy of 60%
◦ Supine: Dilated loops of S.I. w/o colonic distension
◦ Upright: Multiple air-fluid levels, stepwise pattern
◦ May be able to discern cause
 Radiology: Abdominal CT
◦ Sensitive for complete or high-grade SBO & determining location & cause
◦ Helpful in extrinsic causes
◦ Provides evidence of strangulation
◦ Less sensitive for PSBO
◦ May be necessary in 20-30% of cases
◦ Particularly useful when
 Hx of abdominal malignancy

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  Postsurgical patients
 No Hx of abdominal surgery but symptomatic
 Radiology: Barium Contrast – Enteroclysis
◦ Oral insertion of tube into duodenum to instill air & barium directly
◦ Definitive study in low-grade, intermittent SBO
◦ Precisely demonstrate level, possibly cause
◦ Disadvantages
 Needs Nasoenteric intubation
 Slow transit of contrast
 Needs radiologist with expertise in procedure
◦ Recommended use
 Hx of recurring obstruction
 Defining obstructed segment and degree in low-grade mechanical
obstruction
 Radiology: Ultrasound
◦ Useful for evaluation of pregnant patients
 Radiology: MRI
◦ No advantage over CT
Treatment
 Conservative Management
◦ Fluid Resuscitation and Antibiotics
◦ Tube Decompression
 Operative Management
Treatment: Fluids and Electrolytes
 Dehydration and electrolyte imbalance must be corrected
◦ Replace with isotonic saline such as Lactated Ringer’s
◦ Monitor urine output (foley); add KCl, if needed, once outputs are stable
◦ Serial CBC, BMP to monitor response
 Broad-spectrum antibiotics prophylactically
Treatment: Tube Decompression
 NGT for suction
 Reduces risk of aspiration of vomitus
 Minimizes intestinal distension
Treatment: Conservative Management
 May be sufficient for PSBO
◦ 60-85% have resolution of Sx and D/C w/o surgery
 Clinical deterioration or increasing distension during decompression requires
operative intervention
Treatment: Operative Management
 Required for complete SBO
◦ Incidence of strangulation, other complications increases after 12-24 hours
 Management tailored to cause of obstruction
◦ Adhesions
◦ Hernia
◦ Malignancy
◦ Crohn’s
◦ Intra-abdominal Abscess
◦ Radiation Enteropathy
 Adhesions
◦ Lysis of adhesions
 Hernia

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 ◦ Herniorrhaphy
 Malignancy
◦ Consider stage, prognosis when formulating plan
 Crohn’s Disease
◦ Acute: conservative management
◦ Chronic: bowel resection or strictureplasty
 Intra-abdominal Abscess
◦ CT to determine specific cause and location
◦ Percutaneous drainage prior to OR
◦ Radiation Enteropathy
◦ First manage w/ Tube decompression, corticosteroids
◦ Laparotomy with resection or bypass
 If strangulated, bowel viability must be assessed
◦ Segment should be released & placed in warm, saline-moistened sponge
for 15-20 minutes
◦ Re-examine for color, peristalsis
◦ “Second-Look” laparotomy 18-24 hours after initial procedure
 Always indicated if patient deteriorates
 Laparoscopic Treatment Criteria
◦ Mild abdominal distension with adequate visualization
◦ Proximal obstruction
◦ Partial obstruction
◦ Anticipated single-band obstruction
 Laparoscopic Treatment – Most Beneficial for:
◦ Less than 3 previous operations
◦ Seen early after symptom onset
◦ Adhesive bands most likely cause
 Laparoscopic Treatment – Not Indicated:
◦ Advanced, complete, or distal obstructions
◦ Matted adhesions
◦ Carcinomatosis
◦ Distension after NGT placement

Other Issues: Recurrent SBO

 Initially, treat conservatively, but most require surgical intervention
 Internal Fixation, Stenting, Gastrostomy, Jejunostomy
◦ Complications may require further surgery
 Most common cause of recurrence: Adhesions
◦ Good surgical technique essential

Other issues: Acute Post-Op Obstruction

 Presents with abdominal pain, N/V
 Correct electrolyte deficiencies (K+) to rule out ileus
 Enteroclysis to determine presence and level of obstruction

Other Issues: Ileus

 Intestinal distension & slowing or absence of passage of luminal contents without
mechanical obstruction
 Presentation
◦ Abdominal distension without colicky pain
◦ Nausea & Vomiting +/-

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 ◦ May pass flatus & stool (diarrhea)
◦ Radiology
◦ Plain Abdominal X-Ray: distended small & large bowel
◦ Barium studies for difficult cases to differentiate from SBO
 Drug Induced
◦ Anti-ACh, Anti-H, Psychotropics, Opiates
 Metabolic
◦ Hypokalemia, hyponatremia, hypomagnesemia, uremia, diabetic coma,
hypoparathyroidism
 Neurogenic
◦ Post-Op Ileus, Spinal injury, retroperitoneal irritation, orthopedic
procedures on spine/pelvis
 Infections
◦ Pneumonia, peritonitis, generalized sepsis
 Treatment is supportive
◦ Nasogastric decompression
◦ IV fluids
◦ Aggressive treatment of sepsis
◦ Aggressive correction of metabolic & electrolyte imbalances
◦ Discontinuation of medications
Colonic Polyps-Lindsey McPhillips
Protuberance into the lumen from the normally flat colonic mucosa.

Non neoplastic
1. Hyperplastic – most common; composed of normal cellular components
a. Have a characteristic saw tooth pattern; doesn’t exhibit dysplasia
b. Typically located in rectosigmoid
c. Measure less than 5mm
d. Rarely develop into colorectal cancer
e. Hyperplastic Polyposis Syndrome –
i. Criteria: at least 5 hyperplastic polyps proximal to the sigmoid colon two of
which are greater than 1cm; or any hyperplastic polyps proximal to the sigmoid
colon in a pt with a positive family hx of hyperplastic polyposis; or greater than
30 hyperplastic polyps throughout the colon
ii. Median age of onset: 44 y/o
iii. Treatment: Surveillance every 1-3 yrs and removal of polyps in the proximal
colon
iv. Increased risk of colorectal cancer
2. Mucosal polyps
a. Less than 5mm
b. Histologically made of up normal mucosa
c. No clinical significance
3. Inflammatory pseudopolyps
a. Irregularly shaped colonic mucosa resulting from ulceration and regeneration found in
IBD
b. Multiple, filiform and scattered throughout the colon
c. Not dysplastic and not a risk factor for CRC
4. Submucosal Polyps
a. Lymphoid aggregates, lipomas, carcinoids, leiomyomas, hemangiomas, fibromas,
metastatic lesions

Hamartomatous Polyps
1. Juvenile Polyps

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 a. Consist of a lamina propria and dilated cystic glands
b. High likelihood of bleed
c. Familial juvenile Polyposis
i. Associated with increased risk of CRC and gastric cancer
2. Peutz-Jegher polyps
a. Glandular epithelium supported by smooth muscle cells contiguous with muscularis
mucosa
b. Polyps are usually benign but may progress to malignancy
c. Increased risk of GI and nonGI cancers
3. Cronkhite Canada Syndrome
a. Rare, nonfamilial d/o
b. Assoicated with alopecia, cutaneous hyperpigmentation, GI polyposis, onychodystrophy,
diarrhea, weight loss, abd pain
c. Polyps include myxoid expansion of lamina propria and increased eosinophils
d. 5-year mortality is 55% with most deaths due to GI bleed, sepsis, and CHF
e. Treatment: nutritional support, corticosteroids, acid suppression, ABX

Adenomatous Polyps
2/3 of colonic polyps are adenomas defined as dysplastic with malignant potential
Nearly all CRC arise from adenomas but only a small number of adenomas progress to cancer (1/20).
Average time progression from adenoma to cancer is 7 yrs
Polyps do not contain invasive malignancy and are not associated with mets
a. Tubular – 80% of colonic adenomas; c/ized by branching epithelium; the tubular component
is at least 75%
b. Villous – 5-15%; c/ized by glands that are long and extend straight down to the surface; the
villous component is at least 75%
c. Tubulovillous – 5-15% of adenomas; 26-75% villous component
d. Sessile – base is attached to colonic wall; tend to be histologically advanced
e. Pedunculated – contains a mucosal stalk
f. Depressed – likely to harbor high grade dysplasia or malignancy

Presentation
Generally asx but can present with a bleed and positive FOBT

Risk Factors
a. Villous histology
b. Increasing polyp size
c. High grade dysplasia
d. Older age

American College of Gastroenterology

1. If a polyp is detected by barium enema, perform a colonoscopy to establish histo, remove the polyp
and search for synchronous lesions
2. Follow up colonoscopy 3-6 months after polypectomy with a lg sessile polyp (>2cm), an incomplete
polypectomy, or if numerous adenomas (>10) are removed

Techniques for Removal - 28% recur or persist and 17% degenerate to carcinoma
1. Cold bx
2. Hot bx forceps
3. Cold snare excision – used for polys 5-10mm; offers most complete removal of adenomatous tissue
4. Standard snare excision - used for polys 5-10mm; offers most complete removal of adenomatous tissue
5. Piecemeal excision

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Surveillance
Small rectal hyperplastic polyps – f/u in
10 yrs
1-2 small tubular adenomas with low-
grade dysplasia – f/u in 5-10 yrs
3-10 adenomas, size >1cm, adenoma
with villous features, or high grade dysplasia
– f/u in 3 yrs then 5 yrs
More than 10 adenomas – f/u in less
than 3 yrs (clinical judgement)
Sessile adenomas removed by
piecemeal – f/u in 2-6 months
More intense surveillance with Fhx of
HNPCC
Colorectal Cancer-Lindsey McPhillips
95% adenocarcinoma (5% risk of synchronous lesion; 10% risk of metachronous)
Incidence: 3rd most common cancer for both males (70,000/yr) and females (68,000/yr)
Rectal ca: 41,000/yr
Mortality: 2nd highest mortality amongst cancer (57,000 deaths/yr)
Cancer arising at or below the peritoneal reflection has a worse 5-yr-survival rate
Within the rectum the distal cancers have a worse prognosis
Location: 30% right side; 25% sigmoid; 20% rectal; 15% descending; 10% transverse
Men more common on left side and females more common on right side

Screening Polyps and Cancer – Average Risk starting at 50 y/o

1. Colonoscopy every 10 years
2. Flexible sigmoidoscopy every 5 years (if positive perform a colonoscopy)
3. Double Contrast Barium Enema every 5 years (if positive perform a colonoscopy)
4. Virtual colonoscopy every 5 years
Detection of Cancer
1. Fecal Occult Blood Test every year (if positive perform a colonoscopy)
2. Fecal Immunochemical Test every yr (if positive perform a colonoscopy)
3. Stool DNA Test every yr (if positive perform a colonoscopy)
Screening for Increased Risk Pts
1. Hx of colon polyps – repeat colonoscopy 3 yrs after polypectomy; if negative f/u colonoscopy in 5 yrs
2. Hx of CRC – repeat colonoscopy at 6 and 12 months after resection; if negative f/u colonoscopy in 3
years
3. UC – colonoscopy every 1-2 years after having UC for 10 yrs
4. FHx of CRC – colonoscopy 10 yrs younger than the age the family member was diagnosed; f/u
colonoscopy in 3 years

Genetics
1. Hereditary Nonpolyposis Colorectal Cancer (HNPCC)
► Autosomal Dominant Disorder with few polyps present
► Most common form of genetically inherited colon cancer (3-6%)
► Earlier age of onset compared to sporadic cases (45 y/o)
► Presence of primary extracolonic cancers
► Presence of germ-line mutations: hMLH1 and hMSH2 (found in 90% of cases)
► 70-80% risk of developing colon cancer
► Recommendations are to begin annual colonoscopies between 20-25 years old
2. Familial Adenomatous Polyposis
 Autosomal Dominant Disorder with thousands of polyps present
 Represents about 1% of colon cancer
 Mutation of the APC gene (tumor suppressor)

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  100% risk of colon cancer by 50 y/o
 Screening begins at puberty with annual or biannual colonoscopies
 Treatment is total colectomy
Others: Peutz-Jehgers syndrome, Cronkhite-Canada Syndrome, or Juvenile Polyposis

Risks
1. Medical Conditions: UC, Crohn’s, Schistosomal Colitis, obesity, radiation exposure
2. Diet: Increased saturated fat and red meat, increased caloric intake, decreased calcium, and decreased
fiber (prophylaxis: dietary fish oil and high fiber diet)
3. Hormonal imbalance: estrogen and progesterone
4. Social: Cigarette smoking
Signs + Sx: (Left colon has smaller lumen than right colon)
Right Colon Left Colon
-Unexplained weakness or fatigue -Change in bowel habits
(microcytic, hypochromic anemia) -Gross blood in stool
-Persistent post prandial abd discomfort -Obstructive sx
-Palpable abd mass (10% of cases) -Pencil shaped stool
Rectal Cancer
-Rectal bleed
-Change in bowel habits
-Sense of rectal “fullness”
-Pain with defecation
-Tenesmus

Diagnosis:
-At diagnosis: 44% of rectal cancers are localized; 40% LN involvement; 16% mets
-Colon ca at Dx: 40% localized; 37% LN involvement; 19% mets
Imaging
1. Barium Enema – Left sided cancer has apple core configuration and Right sided cancer has
constriction or mass
2. CT/MRI – extramural spread
3. PET – recurrence or mets
4. Colonoscopy – screening and pre-op
5. EUS – best for visualizing the rectal walls and better determining the depth of transmural invasion
and perirectal nodal involvement
6. DRE and Rigid sigmoidoscopy – rectal cancer
Staging
T: invasion of intestinal walls N: regional lymph nodes M: metastasis
Tx cannot assess Nx cannot assess Mx cannot assess
T0 no evidence of tumor N0 no LN involvement M0 no mets
Tis carcinoma in situ N1 1-3 LN involvement M1 distant mets
T1 submucosa N2 4+ LN involvement
T2 muscularis propria
T3 into subserosa, nonperitonealized pericolic tissue
T4 perforates visceral peritoneum or directly invades organs

Stage 0: Tis
Stage I: T1 and T2
Stage II: T3 and T4
Stage III: T1-4 N1-2 M0
Stage IV: T1-4 N0-2 M1

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Prognosis
Colon Cancer
Stage I 93%
Stage II 80%
Stage III 60%
Stage IV 8%
Rectal Cancer – 5yr survival rates are lower
Stage I 92%
Stage II 73%
Stage II 56%
Stage IV 8%

Treatment for Colon Cancer

1. Resection of colon
a. Cecum or ascending colon – right hemicolectomy
b. Hepatic flexure – extended right hemicolectomy
c. Transverse colon – transversectomy or extended right hemicolectomy
d. Splenic flexure – extended left hemicolectomy
e. Descending colon – left hemicolectomy
f. Sigmoid – rectosigmoid resection
2. Adjuvant therapy
a. Stage I – no radiation or chemo
b. Stage II – controversial; discuss risks and benefits with pt
c. Stage III – systemic chemo for 6 months (FOLFOX): Folinic Acid, Fluorouracil,
Oxaliplatin
d. Stage IV – same as stage III
Serum levels of CEA should be followed to determine the progression of the disease after treatment

Treatment for Rectal Cancer

1. Neoadjuvant chemo for all stages – similar survival rates but a lower rate of pelvic relapse; perservation
of sphincter function
2. Local excision – superficial rectal ca (T1, T2)
3. Ano-perineal resection – for invasive rectal ca of the lower 1/3 of the rectum; removal of primary tumor
and a complete proctectomy with the need for a permanent colostomy
4. Low anterior resection – for invasive rectal ca of the upper 2/3 of the rectum; dissection and
anastomosis below the peritoneal reflection with preservation of the sphincter
5. Coloanal anastomosis – very low-lying rectal ca that does not invade the sphincter muscles and whom
standard LAR is not an option; primary anastomosis between the colon and the anus sparing the
sphincter

Acute Pancreatitis-Lindsey McPhillips

Incidence: 4.9-35/100,000
Race: 3 times higher in blacks than whites
Sex: Affects men more than females; (males:alcohol; females:gallstones)
Causes: I GET SMASHED!
I-Idiopathic (30%)
G- Gallstones (35-40%)
E- Ethanol
T-Trauma
S- Steroids
M-Mumps and other viruses
A-Autoimmune
S-Scorpion
H-Hypercalcemia, Hyperlipidemia, Hypertriglyceridemia (1.3-3.8%)
E-ERCP (2-9%)

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 D-Drugs (AIDS therapy, Antimicrobial, Diuretics, IBD drugs, Immunosuppressive, Neuropsychiatric, Anti-
inflammatory, calcium, estrogen, tamoxifen, etc)
Signs and sx
1. Epigastric pain + guarding w/ band-like radiation to the mid-back for several days
2. Nausea and vomiting
3. Low grade fever
4. Tachycardia
5. Hemorrhagic Complications: Grey Turner’s (flank), Fox (groin), Cullen’s (umbilical) sign
6. Rare: panniculitis (subq fat necrosis), thrombophlebitis or polyarthritis
Differential Diagnosis
1. Cholangitis 5. IBS 9. Duodenal ulcer
2. Cholecystitis 6. Pancreatic cancer 10. Gastric ulcer
3. Choledocholelithiasis 7. Chronic pancreatitis 11. Colon cancer
4. Cholelithiasis 8. Pneumonia
Labs
1. Serum amylase: 3-5 times the upper limit of normal (nonspecific)
Amylase returns to normal in 72 hours
2. Increased serum Lipase; remains elevated 7-14 days
3. Increased serum ALT suggests gallstone pancreatitis (above 150 IU/L)
4. Leukocytosis (15-20,000)
5. Hyperglycemia – due to a decrease in insulin release
6. Hypocalcemia – fat necrosis binds the calcium known as fat saponification
7. Abnormal LFTs – hyperbilirubinemia, elevated AST and alkaline phosphatase
8. Elevated LDH
Radiographic Studies
1. Abd Plain film: sentinel loop (localized ileus) or colon cut-off (air distal to the splenic flexure due
to spasm 2˚ to pancreatic inflammation)
2. MRI/CT scan C+: identifies areas of pancreatic necrosis, obstruction, fluid collections, abscess,
hemorrhage, and pseudocysts

Balthazar Severity Scale based on CT scan

Grade A: Normal pancreas consistent with mild pancreatitis
Grade B: Focal/diffuse enlargement of the gland with contour irregularities but without peripancreatic
inflammation
Grade C: Grade B plus peripancreatic inflammation
Grade D: Grade C plus a single fluid collection
Grade E: Grade C plus two or more peripancreatic fluid collection or gas in the pancreas or retroperitoneum

Complications
1. Pancreatic Necrosis: sterile or infected
2. Pseudocyst: typically develops in 2-3 weeks; collection of pancreatic enzymes, fluid and tissue debris
without an epithelial lining diagnosed by CT scan. If the pseudocyst is less than 5cm than you observe;
if greater than 5 cm than drainage is needed.
3. Hemorrhagic Pancreatitis
4. ARDS
5. Pancreatic Ascites
6. Pleural Effusion
7. Ascending Cholangitis
8. Pancreatic Abscess
Ranson Criteria
0 Hours (G. LAAW) 48 Hours (C. HOBBS)
Age >55 HCT Fall by 10%
WBC >16,000/mm3 BUN Increase by >5mg/dl
Blood Glucose >200 mg/dl Serum Ca <8 mg/dl

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 Lactate Dehydrogenase >350 U/L pO2 <60mmhg
AST >250 U/L Base Deficit > 4meq/L
Fluid Sequestration >6000 ml
G lucose C alcium
L actate Dehydrogenase H ematocrit
A ge O (pO2)
A ST B ase deficit
W BC B UN
F luid Sequestration

Mortality
< 3 Criteria 1%
3-4 Criteria 15%
5-6 Critera 40%
> 7 Criteria 100%

Treatment
1. Mild acute pancreatitis: NPO, IV fluids, analgesics (Demerol); if caused by gallstones then a
cholecystectomy is performed
2. Severe Pancreatitis: patients should be placed in the ICU, hydrated with a several liter bolus followed
by 250-500cc/hr, imipenem/cilastatin prophylaxis (controversial) to prevent intra-abdominal infection,
ERCP if caused by gallstones with stone extraction and sphincterotomy, total parenteral nutrition
3. CT guided needle aspiration: if pancreatic necrosis is present w/ possible I&D
Chronic pancreatitis-Lindsey McPhillips
Chronic irreversible inflammation (monocytes and lymphocytes) leading to fibrosis and calcifications
Incidence: 87,000 new cases/yr; mean age 45 y/o
Race: 3 times higher in blacks than whites
Sex: Men > women; men: alcohol abuse; females: idiopathic, hyperlipidemia
Causes
1. Alcohol abuse (70%)
2. Idiopathic (15%)
3. Intraductal plugging and obstruction (10%) (congenital, stones, tumors)
4. Direct toxins or metabolites: act on pancreatic acinar cells to release cytokines that stimulate
collagen, fibrosis and inflammation
5. Recurrent acute pancreatitis – heals with necrosis and fibrosis
6. Autoimmune (<1%) – associated with Sjogrens, primary biliary cirrhosis, renal tubular acidosis,
primary sclerosing cholangitis, SPINK1 mutation, cystic fibrosis
7. Hypercalcemia - hyperparathyroidism
8. Hyperlipidemia (Type I and IV)
9. Trauma
Signs and Sx
1. Intermittent attacks of severe mid or RUQ abd pain radiating to the mid back lasting for several
hours
2. Diarrhea/Steatorrhea – pancreatic insufficiency
3. Weight loss
Physical Exam
1. C/istic position – lying on left side, flexing the spine, drawing knees to the chest
2. Fundoscopic exam – milky white hue in retinal blood vessels if hyperlipidemia is the cause
3. Tender fullness or mass in the abdomen with advanced disease – suggests pseudocyst or
inflammation
4. Advanced disease with steatorrhea – decreased subq fat, temporal wasting, sunken supraclavicular
fossa and physical signs of malnutrition
Labs

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 1. Amylase and Lipase – increased during an acute on chronic attack; normal with atrophy of the
parenchyma; decreased with advanced disease and significant fibrosis
2. Low serum trypsin levels
3. Hypercalcemia
4. Hyperlipidemia
5. Qualitative and Quantitative fecal fat analysis – only positive with loss of 90% of pancreatic
function found late in the disease
6. Direct Test – early detection
a. Duodenal aspirate – intubate the duodenum and measure amylase, lipase, bicarbonate and
protease
b. Determination of pancreatic juice with ERCP – measures lipase, amylase, protease and
bicarb
7. Indirect Test – detects moderate to severe chronic pancreatitis
a. Oral ingestion of complex substance when hydrolyzed by pancreatic enzymes releases a
marker measured in serum or urine

Imaging – morphological abnormalities are not present until mod-to-severe disease

1. Abd X-ray – pathognomonic are calcifications within the ducts (30%)
2. CT abdomen
3. ERCP – gold standard – most accurate visualization of the pancreatic ductal system
Histology
1. Early Stages: increase in connective tissue around the ducts and lobules with patchy minimal
to moderate necrosis
2. Middle stage: increasing connective tissue extends to the acini which become distorted.
3. Late stage: fibrous tissue replaces the acini and the pancreas becomes contracted, small and
hard; islets of langerhans are spared until this stage
Plugs of precipitated protein will develop within the ductal system throughout the stages. Calcium
will form deposits on these plugs and form calculi. The periductal connective tissue may encroach
on the lumen and cause ductal stenosis irregularly distributed throughout the ductal system.
“Chain of lakes” pattern on a pancreatogram

Treatment
1. Behavior Modification
a. Stop drinking and smoking
b. Reduce fat intake and increase protein and carbohydrates
2. Pain Relief
a. CCK-antagonist
b. Exogenous pancreatic enzymes with a meal
c. Analgesics
d. Celiac-ganglion block
3. Digestion/Absorption
a. Exogenous pancreatic enzymes
b. Supplements of fat soluble vitamins
4. Surgical Intervention
a. Endoscopic therapy – extraction of stones, dilation of pancreatic duct strictures, dilation
of papillary sphincter
b. Pancreatic duct drainage - Roux-en-Y side-to-side pancreaticojejunostomy
c. Pancreatic resection – Whipple procedure (if limited to the pancreatic head), subtotal or
total pancreatectomy (if intractable pain, diffuse disease with nondilated ducts)
d. Total pancreatectomy with islet autotransplantation – prevents development of diabetes

Pancreatic Cancer-Lindsey McPhillips

o 4th leading cause of cancer related death in the US

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 o Incidence: 33,700 new cases/yr; rarely before 45y/o w/ incidence increasing sharply after
o Mortality: 32,300 deaths/yr
o Sex: 30% higher in men
o Race: 50% higher in blacks
o Presentation: 7% present with localized disease; 26% with regional disease; 50% with mets
o Risk factors
1. Non-hereditary chronic pancreatitis
2. Smoking – risk is 1.5x, increases with the amount of cigarettes consumed
3. DM/insulin resistance – consequence or cause?
4. Hereditary (5-10%) – hereditary chronic pancreatitis (mutation of cationic trypsinogen gene); pts
with BRCA1 and BRCA2; Peutz Jegher syndrome; ataxia telangiectasia; familial atypical
multiple-mole melanoma
5. Obesity/physical inactivity – BMI at least 30
6. Diet – diet high in fat and red meat; coffee and alcohol
7. Hx of partial gastrectomy or cholecystectomy – 2-5 fold increased risk of pancreatic cancer in 15-
20 yrs due to elevated CCK
8. Hx of H pylori infection
History
1. Pain – 80-85%; pain is located in upper abd as a dull ache radiating to the back
2. Weight loss – may be associated with anorexia, early satiety, diarrhea, steatorrhea
3. Jaundice – accompanied by pruritus, acholic stool, dark urine
a. Painful jaundice – 50% with locally unresectable dz
b. Painless jaundice – 50% of pts with potentially resectable and curable lesion
4. Based on Location
a. Tumors in pancreatic body or tail – present with pain and weight loss
b. Tumor in pancreatic head – present with steatorrhea, weight loss, jaundice
5. New-onset atypical DM
6. Thrombophlebitis
Physical Exam
1. Abdominal mass or ascites – 20% of pts at presentation
2. Nontender, palpable gallbladder – Courvoisier’s sign/law: in the presence of a palpable gall
bladder, painless jaundice is unlikely to be caused by gall stones.
3. Virchow Node – left supraclavicular lymphadenopathy from metastases
4. Sister Mary Joseph node – perumbilical node from mets
5. Blummer’s Shelf – palpable rectal shelf from mets
6. Pancreatic panniculitis – subcutaneous areas of nodular fat necrosis
7. Trousseau’s Syndrome – hypercoagulable state with high incidence of thromboembolic events
Diagnosis and Staging
Labs
1. Elevated serum bilirubin, alkaline phosphatase, mild anemia
2. CA 19-9 - serum concentrations above 37 U/ml is most accurate cutoff for differentiating
pancreatic cancer from benign pancreatic disease; serum levels above 1000 U/ml are associated
with surgically unresectable lesions; serial monitoring is used to follow potentially curative
surgery (rising levels represent disease progression)
Radiology
1. Abdominal Ultrasound – dilated bile ducts or presence of a mass in the head
2. CT and CT angiography – bile and pancreatic duct dilation; mass lesion within pancreas; ascites;
extrapancreatic spread to liver, lymph nodes; major blood vessel involvement which determines
respectability
3. ERCP – “Double duct” sign: superimposable strictures or obstruction of the CBD and pancreatic
ducts, pancreatic duct stricture in excess of 1cm in length, pancreatic duct obstruction, absence of
chronic pancreatitis changes;

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 4. EUS – best at tumors smaller than 2-3cm; evaluates nodal and major vascular involvement
(besides the SMA and SMV)
5. MRI, MRCP – may emerge as the preop imaging procedure of choice; better at defining the
anatomy of the biliary tree and pancreatic duct, evaluates the bile ducts above and below a
stricture, identifies an intrahepatic mass
6. PET with tracer 18-FDG – differentiates benign masses from proliferative lesions
Biopsy
1. Percutaneous biopsy – risk of disseminating tumor cells intraperitoneally or along needle path
2. EUS-guided biopsy – less likely to cause intraperitoneal spread b/c extracting thru bowel wall
Screening
• American Gastroenterological Association recommends screening at 35 y/o for those with hereditary
pancreatitis and 10 yrs before the age at which pancreatic cancer was first diagnosed with positive
family hx. Recommends spiral CT and EUS
Unresectable
1. Extrapancreatic involvement of lymphatics or distant mets
2. Encasement or occlusion of the SMV or portal vein
3. Involvement of the SMA, IVC, aorta, celiac
Treatment – only 15-20% of pts are candidates for a pancreatectomy
Stage 0-IB is resectable
1. Tumors of the pancreatic head –
a. Whipple procedure - removal of pancreatic head, duodenum, first 15cm of jejunum,
CBD, and gallbladder with a partial gastrectomy; biliary and pancreatic anastomosis is
placed 45-60 cm proximal to the gastrojejunostomy
b. Total Pancreatectomy – results in exocrine insufficiency and DM
c. Regional pancreatectomy
2. Tumors of the pancreatic tail and body – rarely are candidates for surgery because pt does not
present until later in the course when the cancer is locally advanced or has mets
a. Distal pancreatectomy with a combined splenectomy
b. Palliative treatment
3. Radiation –external beam radiation vs. brachytherapy vs. intraoperative radiation
4. Chemotherapy – injected or oral
Palliative Treatment
Obstructive Jaundice – stents placed endoscopically or percutaneously
Gastric Outlet Obstruction – gastrojejunostomy
Pain – celiac plexus block
Staging
Tx cannot assess Nx cannot assess Mx cannot assess
T0 no evidence of tumor N0 no LN mets M0 no mets
Tis in situ carcinoma N1 regional LN mets M1 distant mets
T1 limited to pancreas less than 2 cm
T2 limited to pancreas greater than 2 cm
T3 extends beyond pancreas w/o involving celiac or SMA
T4 involves celiac or SMA

Stage 0 – Tis, N0, M0 Stage IIB – T1-3, N1, M0

Stage IA – T1, N0, M0 Stage III – T4, any N, M0
Stage IB – T2, N0, M Stage IV – any T, any N, M1
Stage IIA – T3, N0, M0
Prognosis
Stage IA – 41% Stage IIB – 14%
Stage IB – 35% Stage III – 11%
Stage IIA –24% Stage IV – 5%
ACUTE CHOLECYSTITIS
Katie Pare
Pathogenesis

80
 - Inflammation of the gallbladder usually associated with a gallstone impacted in the cystic duct
causing painful distention of the gallbladder
- Prognosis is good with treatment
- 5% of cases acalculous obstruction are found
- Obstruction leads to thickening of the bile, bile stasis, and finally secondary infection sets in from
gut organisms – primarily E. coli and Bacteriodes.
General Presentation
• Charcot’s Triad: Unrelenting RUQ pain, fever, jaundice
• Leukocytoisis – a WBC >15,000 may indicate perforation or gangrene
• Low-grade fever
• Boas’ sign (referred pain in the right subscapular region)
• Epigastric discomfort
• Nausea/vomiting and discomfort frequently after meals rich in fats
• Palpable gallbladder in 1/3 of cases
• If chronic - nausea, vague abdominal pain, belching, and diarrhea
• Suppurative cholangitis – Reynold’s Pentad: Charcot’s triad + mental status changes +
sepsis/shock
Causes
- Exact cause unknown, but abnormal metabolism of cholesterol and bile salts is likely
Risk factors
• Gallstones – seen primarily in: fat female, fertile, forty, fair
• High calorie, high cholesterol diet associated with obesity
• Elevated estrogen levels from oral contraceptives, postmenopausal therapy, and pregnancy
• DM, ileal disease, TPN (due to bowel stasis), hemolytic disorders, liver disease, pancreatitis,
NPO
Diagnosis
• Cholelithiasis
• Murphy’s sign
• Sono and HIDA are best
• HIDA to indicate if cystic duct is blocked (feed the pt hours before the study so that the
gallbladder empties)
• RUQ Sono
- Thickened gallbladder wall of 3-4mm, pancreatic duct of 3-4mm, common bile duct size
greater than 4mm on sono is suspicious with a size >11mm highly suggestive.
- Note that duct size is age dependent.
- Sonogram may also show pericholecystic fluid, distended bladder, gallstones
present/cystic duct stone, and patient may display sonographic Murphy’s sign involving
reaction when the ultrasound probe is placed over gallbladder.
• If a CT is done, a CBD >8 is suggestive
Labs:
• Leukocytosis, possible slight elevation in alkaline phosphatase and/or amylase, LFTs, elevated
total bilirubin (although this could indicate choledocholithiasis), elevated C-reactive protein. The
degree of elevated levels may be directly related to the acute process.
• Also, ALT/AST and Alk Phos are more suggestive of CBD stones where as an increase in amylase
may be gallstone pancreatitis.
Treatment
• Cholecystectomy
• Fluid resuscitation
• Antibiotics: primarily broad spectrum  piperacillin-tazobactam (Zosyn concentrates well in
bile), ampicillin-sulbactam (Unasyn), ticarcillin-clavulanate (Timentin), or a cephalosporin. Also a

81
 drug against anaerobic bacteria such as metronidazole. If patient is allergic to penicillin try
aztreonam or clindamycin.
Complications of acute cholecystitis
- Ascending cholangitis
- Abscess
- Perforation
- Rupture
- Gallstone ileus (fistula forms through to diverticulum to ileocecal valve – leads to intestinal
obstruction)
- Choledocholelithiasis
- Rokitansky-Aschoff sinuses (entrapped epithelial crypts) which are diverticula or pockets in the
wall of the gallbladder
- Cholecystenteric fistula formation
Complications from abscess formation, perforation, or ascending cholangitis usually present with high
fever, jaundice, and shock.

Associated disease
Acute acalculous cholecystitis
• If there is no evidence of stones – acute acalculous cholecystitis – findings are usually
sludge in the gallbladder from biliary stasis and disuse. This could be secondary to lack of
cholecystokinin stimulation (decreased contraction of gallbladder).
• Diagnosis – ultrasound visualizing sludge and inflammation or HIDA scan showing a
non-filled bladder.
• Risk factors are prolonged fasting, TPN, trauma, multiple transfusions, dehydration, post-
op or ICU patients are most susceptible.
• Management is the same – cholecystectomy or cholecystostomy tube if the patient is
unstable.

Gallstone ileus:
• A small bowel obstruction caused by a large gallstone, 2.5cm or > lodged in the lumen. The stone
usually travels through a fistula between the gallbladder and the small bowel. It often lodges at the
ileoceccal valve.
• Symptoms include: absent bowel sounds (in complete bowel obstruction), intermittent colicky pain
over several days, nausea/vomiting, abdominal distention.
• Treatment: laparoscopy of obstructed stone through the small enterotomy. The gallbladder is usually
untouched however in 30% of cases patients complain of chronic gallbladder symptoms and an
elective cholecystectomy is performed.
Choledocholithiasis
Choledocholithiasis is the presence of stones within the bile ducts of the biliary tree, most often the
Common Bile Duct (CBD). Almost all biliary tract stones are derived from the gallbladder, although both
cholesterol and pigmented stones can form de novo anywhere in the biliary tree. Complications of CBD
stones include:
• Cholangitis
o bacterial infection of the bile ducts, can result from any lesion that creates obstruction to bile
flow, but most commonly from choledocholithiasis
• Obstructive jaundice
• Acute pancreatitis
• Biliary colic
o pain associated with irritation of the viscera secondary to cholecystitis and gallstones
• Biliary cirrhosis
o slow progressive destruction of the small bile ducts (bile canaliculi) within the liver. Bile
build-up in the liver (cholestasis) damages the tissue, leading to scarring, fibrosis, and
cirrhosis.

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Clinical features
Patients may be asymptomatic for years. When present, symptoms include RUQ or epigastric pain and
jaundice. Patients with CBD stones may be asymptomatic for years; however, the onset of symptoms in
choledocholithiasis can signal the development of life-threatening complications such as cholangitis and
acute pancreatitis. When symptomatic, signs and symptoms include:
• Right upper quadrant (RUQ) pain
• Jaundice with or without pain
• Fever
• Nausea
• Vomiting
• Anorexia
Diagnosis
Endoscopic cholangiography is the gold standard for diagnosing common bile duct stones. That being said,
as cholelithiasis is most commonly the initial cause of CBD stones, RUQ ultrasonography is usually
performed to confirm the presence of stones. A dilated common bile duct (>8 mm in diameter) on
ultrasonography in a patient with gallstones, jaundice, and biliary pain is highly suggestive of common
bile duct stones. US is not sensitive enough study to rule out choledocholithiasis. The gold standard for
diagnosing CBD stones is endoscopic cholangiography. This procedure has the distinct advantage of
providing a therapeutic option at the time of diagnosis. ERCP showing dilated CBD and presence of single
or multiple CBD stones is diagnostic of choledocholithiasis. The most common complication of ERCP is
pancreatitis. Percutaneous transhepatic cholangiography (PTC) is an alternative to ERCP in patients with
contraindications to ERCP.

Laboratory tests reveal Total Bilirubin equal to or greater than 1.5, increased direct bilirubin levels, and
alkaline phosphatase levels equal to or greater than 150.

Treatment
• ERCP with sphincterotomy and stone extraction with stent placement is successful in treating 90% of
patients.
• Laparoscopic choledocholithotomy (preferred when cholangitis present or if pancreatitis does not
resolve)
• Percutaneous transhepatic cholangiography and stone extraction if ERCP unsuccessful and cholangitis
present

HERNIAS
Katie Pare
• A protrusion of a structure through a wall of muscle or membrane that normally contains it. The
hernia has three parts: the orifice through which it herniates, the hernial sac, and its contents.
Inguinal: Direct and Indirect
Direct (Acquired):
• More common in older men than younger men (b/c it’s a mechanical breakdown over years).
Incidence is 1% of all men.
• Abdominal contents herniate directly through a weakness in the fascia of the abdominal wall to the
inguinal canal.
• The hernia is within the floor of the Hesselbach’s triangle (epigastric vessels, inguinal ligament, and
lateral border of the rectus sheath). Meaning the hernia does not traverse the inguinal ring.
• If large enough, it can descend through the external ring and into the scrotum. A sliding direct hernia
involves the bladder most commonly.
Indirect (Congenital)
• MC hernia in both men and women - ~5% of all men.
• Primary population is infants/children, and young adults.

83
• A protrusion through the internal inguinal ring of the internal canal, traveling down towards the
external ring.
• A complete hernia means it enters the scrotum upon exiting the external ring.
• Think of the hernia sac traveling indirectly through the abdominal wall from the internal ring to the
external ring.
• It is caused by the failure of embryonic closure of the processus vaginalis – therefore it can be referred
to as a “persistent patent processus vaginalis”. Indirect hernias primarily descend into the scrotum –
may not easily reduce.
Symptoms/Signs on Physical Examination
• Most hernias produce no symptoms until a groin swelling is noticed. Some pts may report a sudden
pain and a bulge that occurred while lifting/straining.
• Generally, direct hernias produce fewer symptoms than indirect and indirect are more apt to become
incarcerated or strangulated.
• Many pts with indirect hernias also report a dragging sensation with radiation of pain into the scrotum.
If direct, a more symmetric, circular swelling at the external ring is seen; swelling appears when
patient is supine.
• Pt should be examined both supine and standing and also with coughing/straining in order to elicit a
response from smaller hernias.
• To differentiate between indirect and direct, have the patient cough or strain while you compress over
the internal ring – a direct hernia bulges forward through Hesselbach’s triangle but the opposite hand
can maintain reduction of an indirect hernia at the internal ring.
Differential Diagnosis
• Lipoma of the cord
• Femoral hernia that has extended above the inguinal ligament (if the examining finger is placed on the
pubic tubercle, femoral hernia sac lies lateral and below while inguinal hernia sac lies above)
• Undescended/ectopic testis
• Inguinal/femoral lymphadenopathy
• Psoas abscess
Treatment
• Emergent herniorrhaphy if strangulated – which has a higher risk with indirect but highest in femoral
hernias above all
• Complications of incarceration, obstruction, and strangulation are greater risks than that of operating in
most patients. The elderly generally tolerate this elective procedure well while emergent repairs carry
a greater risk for this population.
• Inguinal hernias should always be repaired as they carry a high risk of incarceration. Due to the
possibility of strangulation, any incarcerated, painful, or tender hernias need emergency repair.
• If leukocytosis, peritonitis, or if hernia sac contains dark/bloody fluid, the abdomen should be explored
in the OR.
• Truss can be used if pt not willing to go to OR. A Truss is applied to the groin after a spontaneous or
mechanical reduction to maintain reduction and prevent enlargement
Complications
• Risks of urinary retention and URI are high in pts with prostate obstruction therefore if prostatic
hyperplasia is present address this prior to the OR.
• Scrotal swelling
• Pain/numbness in groin area – up to 1 year!
• Recurrent hernia within months to a year if inadequate sac reduction or internal ring closure. This is
reduced if a mesh is used.
INCISIONAL (VENTRAL) HERNIA
• Results from 10% of abdominal operations.

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• Weak surgical scar causes the defect near or directly along a prior surgical incision due to improper
healing or increased tension along the scar site. Most likely to occur in people who are obese or
pregnant due to an increase in strain on the abdominal wall or in people who may be prone to poor
wound healing due to use of steroids or chemotherapy. Most common cause is a wound infection.
• Factors for postoperative wound failure include:
- Poor surgical technique (poor fascial bites, tension on fascial edges, tight closure)
- Postoperative wound infection
- Age (due to poorer wound healing therefore think of other conditions that preexist which may lead
to this – cirrhosis, cancers, chronic wasting disease)
- Conditions which compromise nutrition can increase incisional breakdown
- Obesity – increases intra-abdominal pressure
- Vigorous coughing – therefore smokers and those pts with COPD
- Placement of drains or stomas in the primary operative wound
Symptoms/Signs on Physical Examination
• Pt may first notice pain at incision site – months or even years after surgery
• Bulge/mass at or near surgical site although this is not needed for pt to have pain
Treatment
• Early repair to prevent bowel obstruction with mesh
• Taxis to move abdominal contents back into cavity with rocking motion while patient is in
trendelenberg position.
• The tension-free method involves the permanent placement of surgical (prosthetic) steel or
polypropylene mesh patches well beyond the edges of the weakened area of the abdominal wall. The
mesh is sewn to the area, bridging the weakened area beneath it. As the area heals, the mesh becomes
firmly integrated into the inner abdominal wall membrane (peritoneum). This method creates little or
no tension and has a lower rate of hernia recurrence, as well as a faster recovery with less pain.
• Incisional hernias recur more frequently when staples are used rather than sutures to secure mesh to the
abdominal wall. Autogenous tissue (skin from the patient's own body) has also been used for this type
of repair.
The alternatives to first-time and recurrent incisional hernia repair begin with preventive measures such as:
• Maintaining suitable weight for age and height.
• Strengthening abdominal muscles through regular moderate exercise such as walking
• Reducing abdominal pressure by avoiding constipation and the buildup of excess body fluids, therefore
eat a high-fiber, low-salt diet.
• Learning to lift heavy objects in a safe, low-strain way using arm and leg muscles.
• Controlling diabetes and poor metabolism with regular medical care and dietary changes
• Eating a healthy, balanced diet including whole grains, fruits and vegetables, limited meat and dairy,
and eliminating prepared and refined foods.

Urinary Retention Post Op

Katie Pare
Common urinary problems post op
• Urinary retention: common immediate postoperative complication that can often be dealt with
conservatively with adequate analgesia. If this fails pt may need to be catheterized.
• UTI: very common, especially in women, and may not present with typical symptoms. Treat with
antibiotics and adequate fluid intake.
• Acute renal failure: may be caused by antibiotics, obstructive jaundice and surgery to the aorta. Often
due to episode of severe or prolonged hypotension. Presents as low urine output with adequate
hydration. Mild cases may be treated with fluid restriction until tubular function recovers. In severe
cases may need hemofiltration or dialysis while function gradually recovers over weeks or months.
Urinary Retention (Ischuria) Causes
• Neuropathy or neurological damage – neurogenic bladder

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• Anticholinergic medications: antiparkisonian agents, antispasmotics, antipsychotics (primarily older
ones), tricyclic antidepressants
• Calcium channel blockers and narcotics: may cause retention when given with other anticholinergics
• Diuresis with sudden bladder over distention: use of diuretics, alcohol toxicity, hyperglycemia
• Vitamin B12 deficiency
• Opiates
Specific Surgical Causes:
• Abdominal/bladder/anorectal/pelvic/genital/prostate surgical procedures
• Anesthetics
• Peri-operative fluid volume
• Constipation
• Reduced mobility
Patients most at risk for urinary retention
• Elderly; detrussor hyperactivity with impaired contractility
• Bladder outlet obstruction: BPH, prostate cancer, uterine or bladder prolapse, impaction
• Trauma: spinal cord/pelvic injury
• Neurological disease: MS, Parkisons, diabetic neuropathy, chronic alcohol use
• Iatrogenesis: radiation, medication, anaesthetics, large volume replacements
Detection with a post void residual (PVR) - it is best to measure when pt has a natural urge to void and
when they are voiding in a more “natural” position for them. Measure the void and then measure residual
no more than 15-30mins post-void (can use catheter or ultrasound).
• Bladder capacity norm 400-600mL
• Desire to void at 250-300 mL
• 300-400mL per void normally
• <50mL residual normally (<100mL normal for elderly)
• 1/3 voided volume at night
• No straining, hesitation, pain, or post-void dribble normally
• >100mL indicates inadequate emptying
• If >400mL requires In and Out catheter – foley is more likely to cause infection but could consider
foley for 7 days for bladder decompression
• In/Out Cath purpose= to retrain bladder/restore bladder capacity after foley. Goals= to maintain total
bladder vol (void + residual) <500mL
Prevention of urinary retention post op
• Prevent/resolve constipation
• Prevent/resolve bladder infection
• Get pt mobile asap and have pt use toilet/commode – avoid bedpan
• Adequate fluid intake (min 1500mL)
• Encourage pt to void with urge – discourage voiding requests
• D/c anticholinergic asap – effects of which can last up to 2-3weeks
---------------------------------------------------------------------------------------------------------------------------------
Traumatic Brain Injury
Lydia Kasper (+ Emma)
1. Etiology
• Trauma is the leading cause of death for persons under 45 years, with TBI a major contributor
• Men: Women ratio is 2.8:1
• Most common cause: Falls 28%
• MVA 20% (however it is the largest source of serious TBI , hospitalization, and death)
• Assault with firearm 11%

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• As patient gets older, risk of TBI increases due to falls and pedestrian struck after 7th decade.
• Most TBI are not life threatening but induce lifelong sequelae

2. Initial Assesment/Clinical Findings

• Initial general trauma assessment focus on ABCs (airway, breathing, circulation)
• Stabilize the patient hemodynamically
• Quick assessment brain, brainstem, and spinal cord function, via mental status, Cranial Nerve
Reflexes, and Motor function respectively.
• Glasgow Coma Scale – most widely used neurotrauma scale used
o Eye Opening (out of 4)
 4 – Eye open to ambient stimulus
 3 – Directed to verbal stimulus
 2 – Directed to pain
 1 – No eye opening at all
o Verbal Response (out of 5)
 5 – Normal speech with normal content
 4 – Normal speech with inappropriate content
 3 – Words without sentence structure
 2 – Sound without words
 1 – Absence of verbal output
o Motor Response (out of 6) – Most sensitive indicator of neurologic dysfunction and
predictor of outcome
 6 – Follows verbal commands
 5 – Localize to pain
 4 – Withdraw from pain
 3 – Flexor/decorticate posturing
 2 – Extensor/decerebrate posturing
 1 – No response to pain
o All 3 components are added up for composite score 3-15
o Coma is technically 8 or less – severe injury (3-8)
o Airway protection via Rapid Sequence Intubation for GCS of 8 or less
o Moderate injury (9-12), Mild injury (13-15)
• Cranial Nerve Exam – Used in comatosed patients who cannot follow commands, entire brainstem
function can be determined
o Pupillary Reflex – Midbrain, CNII (afferent) and CNIII (efferent)
 Unilateral dilated/fixed pupil indicates transtentorial herniation of ipsilateral
temporal uncus due to supratentorial intracranial hypertension
o Corneal Reflex – Pons, CNV (afferent) and CNVII (efferent)
o Gag reflex – Medulla CNIX (afferent) and CNX (efferent)
 Loss of Gag Reflex indicates severe brain stem trauma
• Motor Exam – initially may be movement of all 4 extremities, more detailed exam (sensation,
deep tendon reflexes, coordinatin) can wait until after initial resuscitation efforts
o However, DRE is mandatory in acute period - assessment of rectal tone
• Vital Signs
o Hypotension with Tachycardia – hypovolemic shock (MC) or high to mid thoracic spinal
cord injury
o Hypotension with normal or bradycardia – cervical injury or cardiac pathology (sick
sinus syndrome, junctional rhythm)
o Hypertension and bradycardia (Cushing’s Reflex) – indicates the presence of intracranial
hypertension, even trends towards this must alert neurosurgeon
• Imaging Studies
o Head CT without contrast – fast (>2mins), sensitive to bleeds and fractures

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 o Angiography if vascular injury is suspected is petrous carotid hard to visualize from
basilar skull fracture is difficult to visualize on CT
o MRI – severity of pathologic process not clearly visualized by CT, however takes much
longer than CT, so not optimal for hemodynamically or neurologically unstable patients,
(also no metal in head, chest)

3. Mechanism of Injury
• Acceleration/Deceleration Injuries
o Tentorium holds brainstem and cerebellum tight in posterior fossa within the skull;
therefore these structures do not move readily.
o Cerebral hemispheres not fixed rigidly within the skull causing mechanical forces
transmitted onto underlying brain to compress or lacerate the surface, don’t forget about
shock waves! Sagittal, side to side, or swirling motions. Coup/contra-coup injuries
o Think MVA, shaken baby
o Shearing injury to neuronal axons and blood vessels
o Neuronal axons shearing leads to Diffuse Axonal Injury (DAI)
o Blood vessel shearing leads to Subdural Hematomas (see intracranial hemorrhages)
o Brain impacts intracranial bony irregularities - floor of frontal fossa, sphenoid wing,
petrous ridge
• Impact Injuries
o Often S/P assault bats, pipes, etc.
o Skull absorbs much of object’s kinetics force  skull fractures; therefore severity of
injury to brain is not as severe
o Brain often absorbs enough to cause a concussion
o Skull Fractures:
 Simple: break in bone without damage to skin
 Linear or hairline: break in cranial bone resembling a thin line, without
splintering, depression, or distortion of bone
 Depressed: Break in cranial bone with depression of bone towards the brain
 Compound: break in or loss of skin and splintering of the bone. Along with the
fracture, brain injury, ie epidural hematoma may occur
 Basilar skull fracture: Raccoon sign (periorbital ecchymosis) and Battle sign
(mastoid ecchymosis) both a result of blood tracking from skull fracture pooling
in the dependent portions behind eyes and ears. Hemotympanum – blood
pooling in middle ear tympanic cavity. Also CSF leaks from damage to
meninges leading to CSF otorrhea, and CSF rhinorrhea
• Penetrating Injuries
o Causing damage to structures along path of entry, don’t forget about shock waves!
o High velocity – kinetic energy is absorbed and slowed by skull as it penetrates the skull,
causes similar injury as acceleration/deceleration ie conventional firearms vs military
assault weapons
o Low velocity – most do not penetrate skull but can enter via orbitocranial window, ie
pens, chopsticks, arrows, darts, brances, etc

4. Intracranial Hemorrhages and Contusions

• Indications for evacuation of space occupying hematomas are based up on amount of midline shift
(>5mm), location of the clot (posterior fossa can cause brain stem compression and herniation),
and the patient’s ICP
• With subdural and epidural hematomas morbidity is often associated with the midline shift
resulting in brainstem herniation, not damage to the brain tissue itself; therefore surgical
evacuation of the clot and control of the hemorrhage can significantly improve outcome
• Subdural hemorrhage

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 o Origin of blood is from injury to the bridging cortical veins before they penetrate the
dural sinuses (often shearing injury from acceleration/deceleration)
o Lesion originates in the space between the dura and the arachnoid meningeal layers
o Drain into 6 typical locations: frontal pole, frontoparietal junction, occipital pole,
sphenoparietal sinus at the temporal pole, transverse sigmoid junction, superior petrosal
sinus
o Atrophy of the brain often occurs in the elderly; therefore the bridging veins are
stretched, more room for the brain to move, thus causing elderly people to be more
susceptible to subdural hematomas with a more mild/trival head trauma, or no history of
trauma elicited
o Raise intracranial pressures and compress the brain, however venous bleeds create a time
interval between the trauma and onset of symptoms
o Cresenteric Shape

o Mobidity due to rapid onset of mass effect as well as injury to the brain parenchyma
beneath the subdural hemorrhage.
o Presentation may be initial LOC and then period of lucency may be prolonged period
of time (unlike Epidural which lucency is usually a shorter period of time)
o Treatment with craniotomy, hemostasis to stop active bleeding, the ventriculostomy
passed into the lateral ventricle and subdural drain placed, both tunneling through the
skin to the outside
• Epidural hematoma
o Dura is strongly adhered to the inner table of the skull therefore the hematoma forms in a
potential space created between the skull and dura
o Skull fracture most commonly causes epidural hematoma
o Most common fracture is of the thin squamous portion of the temporal bone most
commonly results in the laceration of the middle meningeal artery
o Less common location include frontal and parietal convexity as well as occipital and
infratentorial compartments
o Venous sinus resulting in epidural hematoma rare but can occur at superior sagittal sinus
and transverse sinuses
o Hematoma occurs most often at the dural sinuses in low parieto-occipital region along the
convexity
o Morbidity occurs most frequently due to the arterial bleed resulting in large extent of
mass effect and resulting herniation
o As the hematoma accumulates, the temporal lobe is forced medially compressing the
third nerve and eventually the brain stem
o Sequence: initial loss of consciousness  awakening and lucid interval  recurrent loss
of consciousness with unilateral fixed and dilated pupil  cardiac arrest
o Identification and removal of hematoma via craniotomy is the treatment, hemostasis
ensured making sure to repair the dura as thoroughly as possible
o If no neurosurgeon present, ipsilateral (to dilated pupil) burr holes can evacuate the clot
to decompress the clot not control the hemorrhage and then transfer to hospital with
neurosurgeon
o Lens shape

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 o

• Subarachnoid Hemorrhage
o Rupture of corticomeningeal vessels and hemorrhagic contusions of the brain (think
circle of willis and its branches)
o Usually more diffuse and does not always exert localized pressure
o Blood tracks into the ventricles and is diluted by the CSF, which prevents clotting until it
is massive
o Raises intracranial pressure, impairs cerebral perfusion, thus causing hypoxic-ischemic
encephalopathy
o Blood within the ventricles and surrounding spinal cord is extremely irritating and can
also incite fibrosis of the arachnoid membrane further impairing CSF circulation 
hydrocephalus
o Hemoglobin released from the RBCs in subarachnoid space triggers arterial vasospasm
appearing around Day 3-4 reaching peak incidence and severity on Day 7-10

5. Pathobiology and Secondary Injury

• Secondary Brain Injury
o Initial impact leads to biochemical alterations involving unregulated release of
neurotransmitters simultaneously
o Glutamate (excitatory NT) released in greatest quantity causing cytotoxic cascade
mediated through NMDA glutamate receptors
• Resulting in alterations of cellular energy, metabolism, cerebral blood flow,
transmembrane ion concentration gradients, free radical production, and
cytokine release
o Gross changes include: intracranial hematomas, cerebral edema, and hydrocephalus
o Systemic problems further neurologic injury such as hypotension, seizures, infections,
and hypoxia

• Goal of management of TBI is focused on maintaining cerebral perfusion pressure (CPP) rather
than solely lowering intracranial pressure (ICP)
• CPP = MAP – ICP

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• Cerebral blood flow (CBF) is lowest in the hours following injury (1/3 of patients, even if
normotensive, have ischemic levels of cerebral blood flow)
• Prevention of secondary brain injury include optimizing oxygenation and regulation of
carbon dioxide; therefore, early definitive airway control is critical in directly controlling
oxygenation and ventilation (GCS <8)
• Hypoxia must be avoided! – apnea, cyanosis, O2 sat <90%, partial pressure of O2 <60mmHg
• Avoidance of hypercarbia is also critically important
o Hypercarbia results in cerebral vasodilatation  increasing intracranial blood volume 
elevating intracranial pressure
• Since intracranial volume is fixed, volume changes in brain parenchyma, CSF, and intracranial
blood affect ICP exponentially
• Intracranial hypertension may cause cerebral herniation and brain death
• Signs of intracranial hypertension include: decline of GCS of 2 points or more, hemiplegia or
hemiparesis, Cushing’s phenomena
• Autoregulation is the brain’s ability to maintain constant blood flow over a range of perfusion
pressures, however, this may be lost  CBF to passively change with perfusion pressure
o Metabolic Autoregulation: alters local cerebral blood flow to match changes in local
cerebral metabolism
o Pressure Autoregulation: keep constant cerebral blood flow over a wide range of
systemic blood pressures
o Osmotic Autoregulation: keeps blood flow constant with changes in blood viscosity
• All Autoregulation essentially work through tissue pH as means of detecting ischemia
o As tissue pH drops, autoregulatory mechanisms see this as the tissue becoming hypoxic
and respond by vasodilating upstream arterioles  increase local blood flow 
increasing ICP
o Conversely, increasing tissue pH leads to vasoconstriction .: lowering ICP
o Cerebral vasoconstriction can be achieved through decreasing serum PCO2 by
mechanical hyperventilation (↑tissue pH causes ↓ICP) by fooling the brain into believing
that local cerebral blood flow is too high
o However! Hyperventilation below a PCO2 of 30 leads to worse neurological outcome b/c
too much vasoconstriction can lead to cerebral ischemia!!
• As long as Autoregulation remains intact, systemic hypertension transiently increases cerebral
blood flow causing brain to respond by vasoconstriction .: lowering ICP
• Initial issues of concern are: airway management, cervical protection, control of ICP, and choice
of IV fluids, and anesthetic agents
• First hemodynamically stabilize the patient with rapid and aggressive volume resuscitation with
crystalloid solution, PRBCs for blood loss, FFP for coagulopathies
• Dextrose-free isotonic crystalloid solution are treatment of choice to maintain intravascular
volume and CPP ie: 0.9% NaCl solution, Lactated Ringers solution
o Keeping patient mildly hypernatremic (serum Na 146-148) raises seizure threshold, and
helps control intracranial hypertension
o Dextrose is converted to lactate within cells, producing intracellular acidosis.
Hyperglycemia is assoc with poor outcome.
• Pressor agents: Neo-Synephrine, dopamine, norepinephrine must be used, never before
intravascular volume has been repleted
• Seizure control: intraparenchymal contusions, subdural hematomas, epidural hematomas all are
at risk for posttraumatic seizures
o Phenytoin, Fosphenytoin used IV
o For status epilepticus: Benzodiazepams
o In absence of seizure activity for 7 days, may remove anticonvulsant
o If seizure activity develops after d/c, reinstitute for 6 months

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 • Decreasing ICP can be achieved by: sedation, paralysis, cerebrospinal fluid drainage, osmotic
diuresis, head-up positioning, modest hypothermia, and barbiturate coma
• Anesthetic agents should decrease cerebral O2 consumption (CMRO2), maintain CPP, and not
increase ICP (Neuromuscular blockade can also prevent bucking/coughing which increase ICP)
o Barbituates, benzodiazepines, propofol, all decrease CMRO2 but when associated with
hypovolemia also likely reduce CPP (b/c they decrease cardiac activity).
o Etomidate is the anesthetic of choice b/c of its cardiac stability in presence of
hypovolemia so does not decrease CPP.
• If ICP fails to decrease by these therapies, brief periods of hyperventilation may be necessary
when there is acute neurologic deterioration; however, prophylactic hyperventilation should be
avoided
• ICP monitors/ventriculostomy include:
o drainage placed into ventricle, subarachnoid, or subdural space to give info on ICP, but
can also be used to drain ventricular CSF to lower ICP
o non-drainage monitor placed directly into brain parenchyma (but can’t drain CSF for
therapeutic lowering of ICP)
• Brain Volume
o Lobectomy is only used in emergency situations in order to buy extra space for the brain
to swell, avoid if at all possible
o Medical Management: IV mannitol
 Mannitol does not cross the BBB, so it is a powerful osmotic diuretic that draws
water out thereby decreasing ICP
 Monitor for herniation
6. Outcome
• Rehabilitation is ongoing process
• Depends primarily on initial severity of injury and correlates fairly well with postresuscitation
GCS
o Mild TBI: GCS 13-15 generally do well
 Postconcussive symptoms: Headache, fatigue, dizziness, nausea, blurred vision,
diplopia, memory difficulties, tinnitus, irritability
 Most are resolved but persistent symptoms are less severe and less frequent with
time
o Moderate TBI: GCS 9-12 – depends upon age, abnormality on initial CT,
progressive changes on CT
 60% good recovery
 26% moderately disabled
 7% severely disabled
 7% vegetative or dead
o Severe TBI: GCS 8 or less (paying close attention to motor score). Group often
hemodynamically or neurologically unstable, and have significant secondary brain injury
 Initial papillary response, papillary size, midline shift, ICP
• Most common cause of death leading to cadaveric solid organ transplant donation in which early
recognition is key to this success
Penetrating Neck Injury-Trisha Mahabir

► Refers to neck injuries caused by guns, knives, impaling objects (ie; shrapnel, glass)
► Makes up 5-10% of traumatic injury in adults
► Mortality 3-10%
► Most commonly occurs in young males, 21-30 yrs old age group
► The faster the velocity of an object the greater chance of multiple structures involvement
► Risk Significant injury: 50% with gun shot, 10-20% with stabbings
► Penetrating neck trauma compared to blunt trauma has a higher incidence of simultaneous injuries
with 30% of PNI having multiple structural involvement

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 ► Low calibler gun shots and knives are less likely to break bone as oppose to shot guns or military
weapons because of they have higher velocity

Anatomy

Layers of the neck are skin- subcutaneous tissue-superficial fascia-platysma-deep cervical fascia

The neck can be divided into triangles and zones. In penetrating neck injury the zone classification is
often used.

Zone I is called the upper thoracic it goes from clavicle to cricoid cartilage. It contains structures such
as Subclavian, Jugular, Common Carotid, thyroid, brachial plexus trunks, esophagus midline.

Zone 2- Cricoid cartilage to cephalad angle of mandible. It is the most frequently involved zone in
penetrating injury and is managed differently from the other zones. It contains structures such as CN
X, XI, XII, INTERNAL AND EXTERNAL CAROTID, esophagus midline

Zone 3- Angle of mandible to base of the skull, CN VII and IX.

Clinical Presentation

A person with PNI has a history of trauma, the findings on exam and symptoms depend on which
structures are involved.

 If the trachea is involved the person can present with respiratory distress change in voice,
hoarseness, dypsnea, tachypnea, cyanosis, stridor, tracheal deviation, etc.
 Esophageal injury
 Dysphagia, odynophagia, hematemesis
 Most common presentation in esophageal injury is asymptomatic, physical exam is not
useful in ruling out the presence of injury, b/c many patients lack symptoms but if they
do have any of the 3 symptoms above its 80% sensitive for injury.
 Pharynx
 Drooling, bleeding from mouth

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  Vascular Injury
 Sure signs- bruit, expanding hematoma, hemorrhage, pulse deficits
 Hypotension, shock, neurologic deficit
 Brachial Plexus Injury
 Horner’s Syndrome- carotid injury or structures along sympatheic chain
 Injury to trunks can lead to Erb Palsy or Klumpke Palsy

Due to the deep cervical fascia internal neck hemorrhage does not bleed out of the body leading to and
expanding hematoma which can lead to airway compression.

Management

ATLS-primary survey, resuscitation, secondary survey

► Primary Survey
► Primary survey is intended to find life threatening problems that must be fixed before
preceding to next step

► A- airway with cervical spine immobilization

 A-if a person is speaking the airway is usually patent, individuals with
penetrating neck injury with internal bleeding can lead to airway
compression b/c the necks fascial layers prevent external bleeding
forming a hematoma, damage to the airway can present as tachypnea,
hoarseness,dypsnea, cough, cyanosis, or tracheal deviation. If GCS <8,
altered mental status should be lyrangoscoped or intubated

► B- Breathing and Ventilation
 Tension pneumothorax, open pneumothorax,flail chest, massive
hemothorax, cardiac tampodane
 All patients should receive supplemental oxygen with pulse ox
monitoring

C-Circulation- Here get blood pressure, palpation of peripheral pulses, HR, IV
access with initial fluid resuscitation and control of external hemorrhage. For extremities
Manual compression and clamps are adequate, for head, neck, groin digital control may
be needed, never probe a neck wounnd
D- Disability- neurologic exam using the glasgow coma scale – which looks at
motor, verbal, and eye opening response.

E- Exposure AND Environment- check persons temp, prevent hypothermia

► Secondary survey
 Done once all life threatening events is addressed or excluded
 Patient is examined from head to toe looking for injury, rectal exam, foley or ng tube may
be placed, radiographs obtained
 History obtained
Radiographs to get are -Routine Anterior and Lateral, Neck and Chest Radiographs to look for foreign
body, free air which can signify damage to larynx and trachea, look for PTX and Pneumomedatinum

After patient is stabilized, access whether the injury penetrates platysma. If it doesn’t then treatment is
simple wound closure with observation and eventual discharge.

If it does penetrate platysma assess whether the patient has these “hard signs”- respiratory distress, stridor,
bruit, expanding hematoma, subcutaneous emphysema, active bleed. Then go straight to surgery.

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If none of these hard signs then management varies by which zone of the neck is injured

Zone I and III- is selective management. This means you do studies first, if studies abnormal can do
surgery if symptomatic or observe if asymptomatic

For Zone I you have to do an angiography to look for vessel injury and an esophagram, because injury at
this level is usually asymptomatic until sepsis or mediastnitis, by then its usually to late. Symptoms for
mediastnitis are fever, chest pain, tachy, widening
mediastinum

Zone II mandatory angiography

 Zone II management is controversial, initially any zone II injury went straight to open
neck exploration to look for any injuries, regardless of if the individual is symptomatic or
not. Current EAST guidelines state that open neck injury is still justifiable and safe
leading to Lead to less mortality, and has been shown to find structural damage in a
significant number of asymptomatic patients. However a recent study in the Journal of
Trauma has found CTA to be safe and reliable in managing penetrating neck injury
including Zone II injury CTA has been shown to be the greatest imaging modality to rule
out vascular, trachael, and esophageal injury.

So if person is asymptomatic you can do selective management which involves CTA, if symptomatic go
straight to surgery.

► Vascular Injury
► Normal auscultation does not rule out vascular injury
► Injuries to the vascular system occur in 25-56% of penetrating neck wounds, and injuries to the
carotid and subclavian arteries are the most common cause of mortality
► Physical exam is unreliable, abnormal auscultation of carotids is >95% sensitive for abnormality ,
pts with vascular injury may develop pseudoaneurysms and neurologic events
► Diagnosis of vascular injury

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 ► Duplex ultrasound or CT angiography can be used to rule out arterial injury –
EAST Level 2
► CT of neck can be used to rule out vascular injury if trajectory of object is
remote from vital structures – EAST Level 3

Reconstruction of artery has better outcome than ligation, and regardless of neurologic status carotid injury
should be repaired

► Esophageal Injury
► Generally no physical exam findings, esophageal perforation undetected after 24
hrs have high mortality and infectious rate
► Contrast esophagraphy or esophagoscopy can be used to rule out perforation
► TX
► Suture, if large sternocleidomastoid flap with drainage for 7-10 days
► Injury inferior to arytenoid cartilage require drainage

Anatomy

Triangles of the neck are used mainly when looking at masses, depending on the triangle Ddx can change.
There two triangles of the neck formed by the sternocleidomastiod, and anterior and posterior triangle

► Anterior Triangle
► Midline of the neck-lower border of the mandible-anterior
portion of sternocleidomastiod
► Carotid artery, Internal Jugular Vein, Vagus Nerve, thyroid,
layrnx, trachea and esophagus
► Posterior Triangle
► Middle third of clavicle-trapezius-posterior border of
sternocleidmastoid
► Subclavian artery, brachial plexus, CN XI

Pelvic Trauma

• Most common cause is Motor vehicle collisions 57-71%, followed by motorcycle, peds struck 13
to 18, falls 4 to 9%
• Pelvic ring fractures with hemorrhage and shock have a mortality rate of 50%

Anatomy
• Pelvis is made up of 2 bony innominated bones, sacrum, and coccyx
• Innominate is made of three bones fused at the acetabulum-ischium, pubis, ilium
• Sacrospinous, sacrotuberoud, ileiolumbar and SI ligament which provide mechanical support and
stability
• Vascular supply is from the internal iliac artery
• In posterior arch fractures the superior gluteal artery a branch of internal iliac is often injured
• In pubic rami fracture the artery often injured is the obturator and the internal pudendal
• The veins in the pelvis form a collateral like the arteries but lack valves allowing bidirectional
flow, and this is a reason why massive hemorrhage can occur

Type of fracture

• Stable- can withstand normal physiologic forces without being disrupted

o Fractures that do not disrupt pelvic ring or have anterior displacement less than 2.5 cm
are stable

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 Unstable- widening of the symphysis pubis or displacement of pubic rami fractures greater than
2.5 cm. Superior translation of a hemipelvis through fractures of the sacrum or ilium plus
disruption of the sacroiliac joint by more than 1 cm constitutes vertical instability

Open-book fracture — Open-book pelvic fracture is a common term used to describe pelvic ring
disruptions. This fracture encompasses an anterior injury, either widening of the pubic symphysis
or rami fractures or both, and a posterior pelvic fracture or ligamentous injury. Lateral
compression, anteroposterior compression, and vertical shear injuries may all be termed open-
book based upon the extent of injury and anterior widening. When the anterior pelvic ring widens
more than 2.5 cm, the posterior pelvis (especially the anterior portion of the sacroiliac ligamentous
complex) is frequently injured, increasing the risk of hemorrhage.

Clinical Features/ Physical Exam

History of Trauma, check for external bleeding, signs of eccymosis, palpate iliac crests, pubic
symphysis, sacrum, sacroiliac joints, and greater trochanters, look at how extremities lie, ask verbally if pt
has any pain.
Due to location high incidence of urinary tract injury, if pt unable to void, has blood at urethral
meatus, elevated bladder high riding prostate worry about injury to bladder or bladder rupture. It prostate is
misplaced or there is blood at urethral opening must do retrograde urethrogram before foley placement.
Most ruptures heal by 10 days def. by 3wks.
Rectal exam- look for rectal bleeding, feel for any fractures, r/o high riding prostate and look for
mucosal lacerations
. These are signs of bladder injury
Check if hypotensive can be a sign of retroperitoneal bleed

Management

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 Figure 21-15 Algorithm for
resuscitation after pelvic disruption.
C spine, cervical spine; ER,
emergency room; Fx, fracture; IVs,
intravenous lines; OR, operating
room; PASG, pneumatic antishock
garment; RPH, retroperitoneal
hematoma; R/O, rule out.
Follow ATLS

Can do FAST exam in an ustable patient, if FAST negative but patient unstable do DPL. In pelvic
fractures DPL must be done SUPRAUMBILICAL this is oppose to DPL in non-pelvic trauma b/c its
usually done with incision underneath the umbilicus. The reason for supraumbilical is to prevent going into
a pelvic hematoma. If > 5 cc of blood or enteric content do lap.

X-rays often show injury do an AP pelivis with inlet and outlet view

CT is good to look at sacroiliac joint, acetubular fracture, and sacral fracture. The gold standard for
diagnosing pelvic injuries is multidetector computed tomography (MDCT) due to its high sensitivity and
detailed delineation of fractures. MDCT can determine concomitant injuries, areas of arterial bleeding, and
the extent of retroperitoneal hemorrhage

In unstable patient with know pelvic fracture do external fixation first even before surgery, "Wrapping" the
pelvis reduces pelvic volume (creating a tamponade effect), stabilizes fracture fragments (reducing
hemorrhage from the fracture sites), and improves patient comfort. External fixation can be done by
having a sheet wrapped circumferentially around the greater trochanters and held in place with towel
clamps, or binders like Military antishock trousers.

Positive DPL a laporatomy can be done with packing placed, its found that after this procedure the patient
has an increase in BP. If patient still unstable after lap do embolization with angiography. If
retroperitoneum is found to be ruptured and actively bleed during lap, pack and then do angiography.
Angiography should be done in patients with active bleed in which all other non-pelvic bleeds is rules out,
Patients with evidence of arterial extravasation of intravenous contrast in the pelvis by computed
tomography should be considered for pelvic angiography and possible embolization. Indications for
angiography are recurrent hypotension after initial resuscitation attributable to the pelvic fracture or
transfusion requirements exceeding 4 to 6 units within the first 2 hours after injury.

Stable fractures or injury patterns usually require no more than restricted weight bearing

-with an open fracture patient should be placed on prophylaxis antibiotics for at least 3 days, can use
Cefuroxime. Also a tetanus shot should be given

FYI

Lateral compression– and vertical shear–type fractures are associated with intra-abdominal and head
injuries.
Anteroposterior compression–type injuries have the greatest risk for retroperitoneal hemorrhage

Young and Burgess classification9, 12

Young and Burgess proposed a classification system based on Tile's classification. In this classification,
they determined the injury pattern in relation to different mechanisms of injury. The 4 subtypes are
anterior-posterior compression (APC), lateral compression, vertical shear (VS), and combined mechanisms
(CM). These subtypes have been found to correlate with the resuscitation needs of the patient.

• APC injury results from an anteriorly directed force applied directly to the pelvis or indirectly via
the lower extremities (see Image 1). The result is an external rotation force on the innominate

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 bones and an open-book type injury. This classification delineates the severity of the injury by
quantifying the amount of ligamentous damage present with radiographs.
o APC-I injuries result from low- to moderate-energy forces. They result in slight (<2 cm)
widening of the pubic symphysis. The sacroiliac joint (SIJ) is ligamentously intact.
o APC-II injuries are higher-energy injuries that result in tearing of the anterior SI
ligaments, as well as tearing of the sacrotuberous and sacrospinous ligaments. The
posterior SI ligaments are intact. The pubic symphysis diastasis usually measures greater
than 2 cm. These fractures are rotationally unstable and are more likely to be associated
with neurovascular injuries, soft tissue complications, and hemorrhage.
o APC-III injuries are a result of high-energy injuries. The hemipelvis continues to rotate
externally until the posterior sacrospinous ligaments are also disrupted. Thus, these
injuries result in complete ligamentous dissociation of the involved hemipelvis to the
axial skeleton. These injuries are associated with the highest rate of neurovascular
complications and blood loss.
• Lateral compression injuries result from lateral impact of innominate bone, with internal rotation
of the pelvis toward the midline. The sacrotuberous, sacrospinous, and internal iliac vessels are
shortened rather than stretched. The injury sustained to the anterior ring in these injuries is not
critical to the weight-bearing function of the pelvis. Because of this, lateral compression injuries
are further classified into 3 subsets based on the nature of the injury to the posterior ring.
o Lateral compression-I injuries are the most common type of lateral compression injury.
They result in a transverse fracture of the anterior ring and a cancellous impaction
fracture of the sacrum posteriorly. This impaction fracture often goes unidentified.
Generally, these injuries are low-energy and stable. They are commonly observed in the
elderly population.
o Lateral compression-II injuries are usually the result of a greater laterally applied force.
This fracture pattern often results in a posterior fracture dislocation of the SI joint, which
is referred to as a crescent fracture.13 This injury involves a combination of ligamentous
disruption of the inferior portion of the SI joint and a vertical fracture of the posterior
ilium that extends from the middle of the SI joint and exits the iliac crest. The posterior
superior iliac spine remains firmly attached to the sacrum via the superior portion of the
posterior ligamentous complex. The remaining anterior fragment is more mobile to
internal rotation but remains relatively stable to external rotation and vertical forces.
o Lateral compression-III injuries usually occur when an individual receives a laterally
directed force on one side of the pelvis and is trapped against an immobile object on the
contralateral side. This results in a lateral compression injury pattern on the side of the
laterally directed force and an external rotation injury on the contralateral side. The
ligamentous injury pattern observed on the contralateral side is the same as that in the
APC injuries, with disruption of the sacrospinous, sacrotuberous, and anterior SI
ligaments. Most hemorrhages observed in these fractures occur on the side contralateral
to the injury force, where tensile forces are acting.
• A vertical shear injury results in vertical translation of the hemipelvis (see Image 2). The typical
mechanism for this injury involves a fall from a height and landing on an extended limb.
Anteriorly, the injury usually involves the pubic symphysis, but fractures through the pubic rami
are not uncommon. Posteriorly, the force is directed through the SI joint, causing a complete
disruption of this joint.
• Combined-mechanism injuries have features of at least 2 of the above-mentioned categories. The
most common is the combined lateral compression and VS injuries

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 Blunt Thoracic Trauma
Lydia Kasper (+ Emma)
Epidemiology
• MVA most common cause of major thoracic injury
• MVA Risk Factors: high speed, no seatbelt, front seat occupancy, extensive vehicular damage
(intrusion), steering wheel deformity, fatality at the scene, ejection
• Increased mortality and morbidity associated with multiple rib fractures, increased age (>60
years), high injury severity scores
• Abrupt deceleration
• Blunt aortic injury is the most lethal thoracic injury
• Up to 20% MVA with thoracic injuries are blunt cardiac injuries
• Pneumothorax (PTX) most common complication
Prehospital Management
• ABCs always first
• Rapid transport, intervention delaying transport should be avoided
• Cervical spine immobilization, high flow O2 and monitoring
• IV lines and endotracheal intubation can be performed while en route
• Hypotension important indicator of significant injury
Initial Management
• ABCDE
• Rapid Sequence Intubation (RBI) for respiratory distress, marked hemodynamic instability or
severe injury
• Assess for life threatening injuries: aortic injury, tension PTX, hemothorax with active bleeding,
pericardial tamponade, tracheobronchial disruption, flail chest, large open wounds.
• Imaging: Trauma series: CXR-AP, cervical x-ray, pelvic x-ray
o FAST exam – Ultrasound exam to assess for pericardial effusion, pneumothorax,
hemothorax, fluid in abdomen and pelvis
o Chest CT: detailed evaluation of pulmonary and mediastinal structures, can detect small
pneumothorax, pulmonary contusions and laceration, reconstructs aorta
• If a patient is in respiratory distress due to tension PTX needle decompression and chest tube
thoracostomy before intubation b/c postitive pressure ventilation will exacerbate PTX
• Needle Decompression and Tube Thoracostomy
o Needle decompression used for suspected tension PTX with distress, desaturation,
hemodynamic instability
o No Needle decompression with simple PTX  must obtain CXR first
o Needle Decompression: 14-guage IV catheter, mid-clavicular in the 2nd or 3rd intercostal
space
o Tube Thoracostomy:
 Mid-axillary line
 5th or 6th intercostal space (above diaphragm and thinnest chest wall
musculature)
 Ipsilateral arm raised above patient’s head
 Inject with lidocaine
 2cm incision above rib to avoid VAN
 finger inserted through opening and chest wall explored
 ~36 french tube placed and directed posteriorly and superiorsly
 Tube is then connected to water seal and negative suction
 obtain CXR for tube placement confirmation
 For hemothorax larger chest tube necessary for blood and clot drainage (>36
French)

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 • Bleeding exceeding 1000-1500 mL of blood or hemodynamic
instability is an indication for emergency thoracotomy.
• Pericardial Tamponade/Pericardiocentesis
o Detected by FAST (Focused Assessment with Sonography for Trauma)
o Performed on patients with pericardial effusion and significant hypotension
o EKG used to guide
o Head elevated 30-40 degrees
o 10 cm long 18 guage needle
o Left sternal border through 5th or 6th intercostal space or L side infrasternal/subxyphoid
o Emergent Thoracotomy: patients who lose vital signs in ED and appear to have no
obvious non-survivable injury (massive head trauma, multiple severe injuries)
 Rarely successful means of resuscitation
Specific Injuries:
• Aortic Injury
o Mechanism of Injury: Fall from >10feet, MVA at speeds >40mph
o 80% cause immediate death from aortic transection
o Prompt ED Dx is crucial, no clinical signs to Dx with sufficient sensitivity therefore,
CXR
 Widened mediastinum (CXR supine >8cm, upright CXR >6cm)
 Obscured aortic knob, abnormal aortic contour
 Left “apical cap” pleural blood above apex of L Lung
 Large left hemothorax
 Deviation of NGT rightward
 Deviation of trachea to the right and right mainstem bronchus deviation
downward
 Wide left paravertebral stripe
o Abnormality in CXR, or strong suspicion should prompt Chest CT
o Management:
 Prevent propagation of adventitial dissection into free wall rupture
 Control wall stress and shearing forces by
• Beta Blockers to decrease HR (ie esmolol). Calcium channel blockers
(diltiazem) if Beta blocker contraindicated
• IV Nitroprusside or Nitroglycerine to lower BP
• Thoracotomy with open repair, or graft and endovascular stenting, or
percutaneous stenting
• Cardiac Contusion
o Obtain ECG
 Pain/tenderness directly over mid-anterior chest
 Sternal Fracture
 History or active symptoms of cardiac disease
 Major mechanism of injury (rollover, high speed, fatality at scene)
o Signs: unexplained tachycardia, new BBB, dysrhythmia, multiple PVCs
• Myocardial Rupture
o Most do not reach ED alive
o Hypotension may have reduced the pressure on myocardium so as ED physicians
administer fluid resuscitation subsequent rupture may take place killing patient
o Mimic signs of tamponade: hypotension, distended neck veins, muffled heart sounds
o Unexplained shock out of proportion to apparent injuries
o Immediate US for diagnosis
o ED thoracotomy not pericardiocentesis
• Myocardial infarction

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 o LAD most often
o Rapid EKG
o Cardiac cath with stenting best approach

• PTX
o Most common complication of blunt thoracic trauma
o Often sustained from rib fracture
o Signs: tachypnea, hypoxia, unilateral diminished or absent breath sounds, unilateral
hyperresonance to percussion
o CXR, follow up with Chest CT
o Management: see above
• Hemothorax
o Massive secondary to aortic rupture, myocardial rupture, hilar structures
o Lung parenchyma, intercostals vessels, mammary blood vessel damage
o 300 mL necessary for Dx on upright CXR
o Management Tube thoracostomy using >36 French chest tube
o Immediate bloody drainage of >20ml/kg, shock, persistent bleeding are considered
indications for surgical thoracotomy
• Pulmonary contusion
o Develop over 24 hours and resolve within 1 week
o CXR hallmark: Irregular, nonlobular opacification of pulmonary parenchyma, may not be
evident on 1st CXR
o Pain control, and sometimes fluid resuscitation with crystalloid to euvolemia
o Complication: pneumonia and ARDS
• Tracheobronchial injury
o Less than 1% of thoracic blunt trauma, most die at scene
o Trachea protected by mandible, sternum, and vertebral column so injury is difficult –
often follow fracture of 1st 3 ribs
o R main bronchus most injured within 1-2 cm from carina then L main
o Hallmark sign: significant air leak, PTX, pneumomediastium that reaccumulates despite
tube thoracostomy
o Signs: retained secretions, recurrent pneumothoraces, obstruction, dyspnea, hoarseness,
subcutaneous emphysema
o Definitive Dx in OR or bronchoscopy, (CT sensitivity is unknown)
o Treatment: OR primary repair or with possible lung resection
• Diaphragm Rupture
o L side rupture > R side rupture due to L posterolateral aspect of hemidiaphragm is
weaker and Liver is more protective than bowel and stomach
o Increased diaphragm (gasp)  stretch/avulsion, direct laceration, fractured ribs penetrate
o L sided rupture  bowels enter thoracic cavity
o Serial CXR: atelectasis, pleural effusion, loss of hemidiaphram contour
o CT improved sensitivity
o Surgical repair
• Esophageal rupture
o Lacks specific symptoms
o Blood in NGT, subcutaneous cervical air, neck hematoma
o CXR pneumomediastinum, pleural effusion, mediastinal contour changes,
tracheoesphageal communication
o Dx: endoscopy, CT may show subtle leaks
• Sternal Fracture
o Result of high-energy direct blow to anterior chest wall often steering column, seatbelt
o Associated injuries include rib fractures, myocardial contusion/rupture, hemopericardium

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 o AP/lateral CXR, CT but no gold standard
o EKG and cardiac monitoring is warranted
o Operative fixation may be necessary
• Scapular fracture
o Significant force necessary raising concern for further injuries
 Clavicle fractures, rib/spine fractures, spleen and liver injuries
o CT and look for concominant injury
o No additional concern for analgesia, comorbidities, social circumstances, patients may be
discharged
• Rib Fracture
o 3 or more rib fractures are at significant risk for complications
 Pulmonary contusion, pneumonia
o Supplemental O2, analgesia (intercostal nerve block, narcotics), treat complications
• Flail Chest
o 3 or more adjacent ribs fractured in 2 places  creating one floating segment of ribs and
soft tissue beneath
o Paradoxical motion – moves in opposite direction of normal-functioning chest wall
o Significant morbidity from pulmonary contusion
o O2, monitor for respiratory compromise, some necessitate intubation

Blunt Abdominal Trauma

Lydia Kasper (+ Emma)
Epidemiology
• Most common MVA 75% (including pedestrian vs automobile)
• Assault 15% (including child abuse and domestic violence)
• Fall 6-9%
• Most common injury is of the liver and spleen
• Deceleration can create shearing forces and laceration of both solid and hollow organs at points of
attachment to peritoneum  create stretching/tears at vascular pedicles  infarction
• Fractured ribs and pelvis can lacerate intraabdominal tissue
• MVA risk factors: fatality at scene, size/speed of vehicles, roll over, intrusion, steering wheel
deformity, seat belt use, expulsion
• Pedestrian struck triad of injury: leg, torso, cranium
Initial Assessment
• ABCDE
• Initial presentation may be benign despite significant intraabdominal injury, absence of physical
findings doesn’t preclude serious pathology
• Be aware of distracting extraabdominal injury that may mask signs of abdominal injury, including
head trauma
• Hypotension can result from hemorrhage of solid organ or vascular injury
• Signs: “seatbelt sign:” abdominal wall ecchymosis, abdominal distention, decreased bowel sounds
(peritoneal irritation  ileus) pneumoperitoneum, hemoperitoneum
• Rectal exam: tone for spinal cord integrity, and palpation of high riding prostate suggests urethral
injury
• Diagnostic Tests:
o Type/Screen and crossmatch for transfusion
o Hematocrit: baseline, will not be low initially despite large blood volume loss
o Base deficit – hemorrhagic shock may create metabolic acidosis with a base deficit or
increased serum lactate
o LFTs – may elevate serum transaminase levels but can’t distinguish minor from major
contusions, or alcohol-induced liver disease

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 o UA: gross hematuria indicates serious renal injury, microscopic hematuria and abdominal
tenderness with CT is 94% specific for injury
o β -HCG
• Imaging
o CXR/Pelvis x-ray can ID rib, pelvic, vertebral body, transverse process fractures but
limited in assessing blunt abdominal trauma
o CT: fast, noninvasive, detects presence/source/amount of hemoperitoneum,
retroperitoneum can be assessed
o FAST exam: US that is used to identify fluid in peritoneum at sites:
 Hepatorenal space (Morrison’s pouch)
 Splenorenal recess
 Inferior portion of intraperitoneal cavity (including pouch of Douglas) and
bladder
 Pericardium also evaluated
 Advantages: Fast, portable, sensitive 65-95% in detecting 100ml of
intraperitoneal fluid, inexpensive
 Disadvantages: injury to solid parenchyma, retroperitoneum, or diaphragm not
well seen, body habitus, not sensitive for bowel injury
o Angiography: unstable patients with pelvic fracture patients benefit b/c can embolize
bleeding retroperitoneal pelvic vessels
o Diagnostic peritoneal lavage – DPL
 Physician attempts to aspirate free intraperitoneal blood
 If 10 mL of blood is aspirated stop and perform laparotomy
 If no blood, can perform lavage of peritoneal cavity with NS and effluent is sent
to lab (>100,000/mm3 is positive)
 Advantages: unstable multi-system trauma can reveal or exclude intraperitoneal
hemorrhage, and can detect small amounts of blood in stable patient that
otherwise may be missed
 Disadvantages: local/systemic infection, injury to intraperitoneum, false positive
results (pelvic fracture, dissection of hematoma)
• Subsequent Management
o Hemodynamically unstable: primary survey  FAST exam  if limited FAST then DPL
 if either FAST or DPL is diagnostic then emergent laparotomy
o Hemodynamically stable: FAST + CT then observe or Ex-Lap
• Clinical Indications for Emergent Exploratory Laparotomy:
o Unexplained signs of blood loss or hypotension who can’t be stabilized or intraabdominal
injury is strongly suspected
o Clear and persistent signs of peritoneal irritation
o Radiologic evidence of pneumoperitoneum consistent with viscus rupture
o Evidence of diaphragmatic rupture
o Persistent, significant GI bleed in NGT or vomit
• Pelvic Fracture
o Risk for life-threatening retroperitoneal hemorrhage (can have negative US and negative
DPL)
o Treatment is angiography for embolization of active bleeding vessels
o External fixation placed in OR
• Splenic Injury
o Contusion, subcapsular hematoma, laceration, rupture
o Immediate fluid and blood product resuscitation  surgical exploration
o Diagnosis: CT
o Ex-lap splenic repair or splenectomy

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 o Splenectomy can lead to immune deficiency with polysaccharide-encapsulated bacteria
(Streptococcus pneumoniae, Hemophilus influenza, Neisseria meningitides)
• Liver Injury
o Contusion, subcapsular hematoma, laceration, rupture, disruption of ductal system
o Immediate fluid and blood product resuscitation  surgical exploration
o Liver laceration:
 Typically involves R lobe secondary to proximity to ribs and spine
 L Lobe injury associated with pancreatic and duodenal injuries
o Massive bleeding intracapsular or into peritoneal cavity  shock, anemia, tachycardia,
hypotension
 Several days later: vomiting, abdominal distension, abdominal tenderness with
rigidity, absent bowel sounds
o Ex-Lap

• Pancreatic Injury
o Organ edema from contusion, laceration usually in body of pancreas as it overlies the
spine, ductal laceration, pseudocyst formation, complete transection, acute pancreatitis
o Symptoms: vomiting, abdominal pain radiating to back, epigastric tenderness, peritonitis,
hypovolemia
• GI perforation
o Uncommon injury
o Acceleration-deceleration shearing tear of the bowel from its point of attachment to
posterior abdominal wall
o Most common site is duodenum, jejunum, and duodenojejunal junction
o Signs: Tachycardia, unexplained fever, abd pain, decreased bowel sounds, decreased
urine output, peritoneal signs
o CT: pneumoperitoneum, fluid in gutters
o Ex-Lap
• GI Hematoma
o Compression of intestinal wall against vertebral column  intramural hematoma
o Most frequent location is duodenum
o Signs: gastric distension, abdominal pain, anorexia, bilious vomiting, proximal bowel
obstruction signs, anemias
o Ex-Lap
Penetrating Chest Trauma-Tricia Fertig
• Thoracic trauma accounts directly for OR is a contributing factor in 50% of deaths due to trauma.
• Early deaths are commonly due to
(1) airway obstruction,
(2) flail chest,
(3) open pneumothorax,
(4) massive hemothorax,
(5) tension pneumothorax,
(6) cardiac tamponade.
• Later deaths are due to respiratory failure, sepsis, and unrecognized injuries.

ATLS protocols:
1- Primary survey (ABCDE) and correct life-threatening problems
2- Secondary survey
3- Definitive care
Primary survey chest injuries
• Airway obstruction

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• Tension pneumothorax
• Open pneumothorax
• Massive hemothorax
• Pericardial tamponade
Secondary survey chest injuries
• Pulmonary contusion
• Myocardial contusion
• Aortic disruption
• Traumatic diaphragmatic hernia
• Tracheobronchial disruption
• Esophageal disruption
Management of the Ustable Patient
Indications for emergency room thoracotomy
• Acute pericardial tamponade unresponsive to cardiac massage
• Exsanguinating intra-thoracic hemorrhage
• Intra-abdominal hemorrhage requiring aortic cross clamping
• Need for internal cardiac massage
Indications for Thoracotomy
• ED Thoracotomy (from SBH clinical practice guidelines)
Anterolateral Thoracotomy through an inframammary incision (4th – 5th ICS).
o May include opening of pericardium longitudinally.
o May include cross clamping of thoracic aorta.
o May include cross clamping of hilum if source of bleeding.
• When ED thoractomy is performed:
o Penetrating Thoracic Trauma
o Any signs of life (SOL) in the ED:
o Palpable Pulse or Pressure
o Spontaneous Motion
o Spontaneous Respiration
o Reactive Pupils
o Non-Agonal cardiac rhythm
o Gag with Intubation
o Loss of SOL en route or documented by EMS as a loss of SOL in field of less than 20 minutes
duration.
o Hypotension refractory to resuscitation.
o Massive blood loss over 1500 cc’s and continuous from a chest tube.
o Massive air leak from a chest tube and inability to oxygenate the patient.
Indications for urgent thoracotomy
• Chest drainage >1500 ml or >200 ml per hour
• Large unevacuated clotted hemothorax
• Developing cardiac tamponade
• Chest wall defect
• Massive air leak despite adequate drainage
• Proven great vessel injury on angiography
• Proven esophageal injury
• Proven diaphragmatic laceration
• Traumatic septal or valvular injury of the heart
Hemothorax
• Common after both penetrating and blunt trauma
• Pleural cavity can hold up to 3 liters of blood
• One liter may accumulate before apparent on chest x-ray
• 90% due to injury to internal mammary or intercostal vessels

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• 10% from pulmonary vasculature
• Bleeding usually stops when lung re-expanded
• Most require no more than simple chest drainage
Pericardial tamponade
• Major complication of penetrating chest trauma
• Hemopericardium prevents diastolic filling of the heart
• Classic signs are Beck's triad:
o Hypotension
o Venous distension
o Muffled heart sounds
May be associated with pulsus paradoxus (pulse weaker with inhalation, stronger with exhalation,
but exaggerated)
• Chest x-ray shows a globular heart
• Unstable patient requires urgent thoracotomy
• In stable patient diagnosis can be confirmed by
o Echocardiography
o Pericardiocentesis
• Subxiphoid pericardiotomy is both a diagnostic and therapeutic procedure

Cardiac Stab Wounds

• Right side of the heart is more commonly injured
• Patients with right ventricular wounds are more like to survive than with left sided injury
• Atria, inflow and outflow tracts may also be damaged
• Patients usually present with pericardial tamponade
• Treatment consists of resuscitation and pericardiocentesis
• Stab wounds can be accessed via a median sternotomy
• Can be directly repaired without cardiopulmonary bypass
• Proline sutures are generally used
Injuries to the Great Vessels
• Suspect possibility of injury from the mechanism or site of penetrating injury
• Usually present with shock or pericardial tamponade
• Chest x-ray may show:
o Widening of the mediastinum to greater than 8 cm
o Depression of the left main bronchus to greater than 140°
o Hematoma in the left apical area
o Massive left hemothorax
o Deviation of esophagus to the right
o Loss of aortic knob contour
o Loss of paraspinal pleural stripe
• Requires emergency thoracotomy or sternotomy
• Injuries to descending thoracic aorta require left anterior thoracotomy
• Injuries to proximal aorta and proximal carotid arteries require median sternotomy
Flail Chest
• Flail chest is associated with multiple rib fractures on the same side (3+ consecutive ribs)
• Flail segment does not have continuity with remainder of thoracic cage
• Results in paradoxical chest wall movement with respiration
• Often associated with underlying pulmonary contusion
• Paradoxical movement results in impaired ventilation
• The work of breathing is increased
• Ventilation perfusion mismatch and arterio-venous shunting occurs
• Chest x-ray will show

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 o Multiple rib fractures
o Underlying lung contusion
o Hemopneumothorax
o Other associated injuries
• Treatment requires
o Adequate ventilation
o Humidified oxygen
o Adequate analgesia
o Usually intubation with PEEP required
• Operative fixation is not normally required
Diaphragm Injuries
• Diaphragmatic lacerations occur in 10–15% of cases of penetrating wounds to the chest and in as many
as 40% of cases of penetrating trauma to the left chest. The injury is rarely obvious and is frequently
missed. These injuries rarely heal spontaneously.
• Herniation of abdominal viscera into the chest can occur with major complications
• Signs and symptoms include: abdominal tenderness, dyspnea, shoulder pain, or unilateral breath
sounds.
• Chest x-ray, CT scan are good studies but often miss the injury
• The most common finding is ipsilateral hemothorax
• Treatment involves suturing the laceration with non-absorbable sutures via thoracotomy

Abdominal Trauma
Evaluation of Penetrating Abdominal Trauma
Tricia Fertig
Penetrating Abdominal Injury
• Anatomy: abdomen extends from nipples to groin crease anteriorly, scapulae to gluteal creases
posteriorly.
• Any penetrating injury to this area is a potential abdominal injury.
1-Primary Survey (ABCDE)
• Airway
• Breathing
• Circulation
• Disability (GCS)
• Exposure
2-Adjuncts
• DRE
• Chest x-ray
• Ddiagnostic peritoneal lavage
• FAST scan, 4 locations:
o Pericardium - to visualize the heart
o Perihepatic- to visualize Morrison's pouch and paracolic gutter (Morrison's pouch is the
potential space between Glisson's capsule of the liver and Gerota's fascia surrounding the
kidney. Morrison's pouch along with Douglas' pouch are the MOST SENSITIVE areas for
detection of free intraperitoneal fluid.)
o Perisplenic - to visualize the spleno-renal recess and paracolic gutter
o Pelvis - to visualize pouch of Douglas.
• Nasogastric catheter
• Urinary catheter
3-Secondary survey
• Complete exam, head to toe, front and back
• Priorities: Patients with significant penetrating abdominal injury tend to fall into 3 major categories:

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 Presentation Injury Type Management priority

Pulseless Major vascular injury Emergency laparotomy

Hemodynamically unstable Vascular and/or solid organ Identify & control

injury hemorrhage
AND/OR
Hemorrhage from other sites

Hemodynamically Normal Hollow viscus injury Identify presence of

Pancreas or renal gastrointestinal,
diaphragmatic or
retroperitoneal injury
1- Pulseless (but had recent vital signs or PEA)
Immediate ex-lap
(Resuscitation efforts should continue prior to surgery)
2- Hemodynamically Unstable
Immediate ex-lap if wound clearly in abdomen
If unclear about cavity injured, FAST scan or DPL to determine if
abdomen is source of bleeding
3- Hemodynamically Normal
a) Clinical signs of peritonitis or evisceration of bowelstraight to OR
b) Further diagnostic testing and routine physical examination
Adjuncts to the initial evaluation of the trauma patient can provide clues to significant intra-peritoneal
injury:
• Chest X-ray (to identify sub-diaphragmatic air)
• NG Tube (blood drained from the stomach will identify gastric injury)
• Urinary catheter (Macroscopic hematuria indicates renal or bladder injury, microscopic injury suggests
ureteric injury)
• Rectal examination (rectal blood indicates rectal or sigmoid penetration)
Options for Evaluation
• Further evaluation requires the use of one or more of the following diagnostic modalities:
o Serial Physical Examination (PE)
o Local Wound Exploration (LWE)
o Diagnostic Peritoneal Lavage (DPL)
o Ultrasound (FAST)
o CT Scan
o Laparoscopy
o Laparotomy
• Organs injured: Small bowel > colon > liver (order of most commonly injured)
P eripheral Vascul ar Di seas e
Ryan Bendl
1. Aneurys mal vascul ar dis ease
I. General Princi ples
i. True aneurysm : enl argement com posed of all three l ayers (tuni cs )
of the ves sel wal l
ii. F als e aneurys m: al so known as ps eudoaneurysm s, they lack at
l east one, and sometim es all t hree, layers of the ves sel wal l.
Bl ood is cont ai ned by perivas cular connect ive tis sue and if
present , the tunica advent iti a. (P uls at ing Hematoma)
ii i. Aorti c diss ecti on: pass age of bl ood from the arteri al l umen i nto
t he art erial wal l, t hereby creat ing a fal se lumen

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 i v. Dis sect ing aneurysm : aort ic dis sect ion with aneurys mal
dilatati on of the fal se lumen. Thes e can be prone to rupture.
v. Infrarenal aneurys m: aneurysm with a norm al -cali ber aort a
bet ween the renal arteri es and the aneurys m
vi. The mos t comm on cause of fal se aneurysm s is trauma to t he
blood ves sel. Thi s includes i at rogeni c ins ult s.
vii. In m al es older than 50 years of age, t he normal abdom inal aorti c
cal iber i s between 15 and 24 mm .
2. Abdom inal Aorti c Aneurys ms
I. Anatomy. The abdom inal aorta is a di rect continuati on of the
t horaci c aort a as it pass es through the aort ic hi at us i n the di aphragm.
It lies in t he retroperit oneum , and sl ightl y to the l eft of midl ine. It
bifurcates i nto t he right and left com mon ili ac arteri es at L4 .
II. Epi demi ology
i. Abdom inal aorti c aneurys ms (AAAs ) affect about 1% to 3% of
t he general population. Agi ng of t he popul at ion and increasi ng
use of routi ne radi ographic studi es has result ed in an increas e in
t he prevalence of AAAs .
ii. AAAs are the 13th l eadi ng cause of death in all age groups .
iii. 3rd leading caus e of sudden deat h i n males >70YO
i v. Rupt ured AAAs account for 15,000 deaths per year in the Unit ed
St at es .
III. Ri sk factors for AAAs
i. Age: nat ural tis sue degenerati on, and atheros cl eros is , increas e
wit h age and predis pose to t he formati on of aneurysm s. Most
pat ient s are 65 years of age and older.
ii. S ex: M:F at l east 4:1
iii. Sm oki ng: Preval ence of AAAs in sm okers i s 4x that of
nonsmokers .
i v. Connecti ve ti ss ue dis orders : i ndi vi dual s wit h Marfan syndrome
and Ehlers –Danlos
IV. Ri sk factors for rupt ure of AAAs —whi ch pat ient s need elect ive
s urgery?
i. Generall y, aneurys ms 5 cm or great er should be repai red.
ii. Hypertens ion can res ul t in rapid enlargem ent of the aneurys m
iii. Sm oki ng: es peci al ly if there i s as soci at ed C OPD, sm oki ng is an
i ndependent ris k fact or for rapi d enl argement and event ual
rupture of AAAs .
iv. S ex: females 3x more li kely to rupture
v. F ami ly hi story: 25% of pat ient s wit h AAA rupt ure have a first -
degree rel at ive wit h a h/o of a ruptured AAA.
V. Cli ni cal features and di agnosi s
i. M ost AAAs are as ym pt omati c and are dis covered i ncidentall y.
ii. Sympt om s can be due to mass effect and i rritati on of regional
s ensory nerves or due to showering of clots dist al ly
(thromboembol ism ).
VI. Abdom inal s onography i s a good s creeni ng and s urveil lance tool.
VII. Computed t omography (CT) s cans wit h int ravenous cont rast and hi gh
res ol ut ion serve as confirmatory evi dence
VIII. M anagem ent
i. Aneurys ms sm all er than 5 cm can be fol lowed by survei ll ance
s onography or C T scans.

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 ii. Aneurys ms that are t ender to pal pati on and those that are rapidly
enl argi ng (great er t han 5 mm/ 6 months) shoul d be repaired
elect ivel y.
ii i. Three different techni ques : t he open t rans peri toneal , open
ret roperi toneal, and endovascul ar aneurys m repai r (EVAR ).
IX. Rupt ured AAAs
i. M ost feared complicat ion of AAA
ii. C arri es an overall mortali ty rat e of m ore t han 80%
ii i. P resent s with acute abdom inal pai n, back pain, and hypot ensi on
3. F em oral and Poplit eal Aneurys ms
I. Epi demi ology and et iol ogy
i. Alm ost 90% of t he peri pheral aneurys ms are found in the fem oral
and poplit eal arteri es .
ii. Popli teal aneurysm s alone m ake up about 70% of the peripheral
aneurys ms . The m ajori ty are s econdary to degenerati ve
atheros cl eroti c di seas e, and are predom inantl y in m en.
II. Cli ni cal features. Accumulati on of throm bus, dist al propagat ion, and
li mb-t hreateni ng is chem ia can often be t he pres enti ng catast rophic
features. Ot her sym pt oms incl ude pain s econdary to nerve
com pres si on or edem a, and venous t hrom bosis s econdary to venous
out fl ow obs tructi on.
III. Diagnos is
i. 50% of poplit eal aneurys ms are bi lateral, and 30% have an aorti c
aneurys m as soci at ed with t hem.
ii. Duplex ul tras onography can be us ed to confirm the anat om ic
confi gurati on as well as t he fl ow dynam ics of the aneurys mal
s egment .
4. Aortoili ac Occlusi ve Dis ease
I. General Princi ples
i. R es tricted to t he dis tal aort a and the bi lateral comm on and
ext ernal ili ac arteri es .
ii. Dis ease of the aorta and the ili ac arteri es is referred to as
"i nflow" dis ease, and diseas e di st al to t he groi n is referred to as
" out fl ow" di seas e.
ii i. Inflow dis ease affect s the m ajor m uscle groups of the pelvis and
l ower ext remi ties, and can res ul t in di sabl ing sym ptoms .
II. Anat om y
i. The abdomi nal aort a enters the diaphragm at ic hiatus at t he l evel
of the t welfth thoraci c vertebra, and bi furcat es at the level of the
fourt h lumbar vert ebra.
ii. The int ernal iliac suppl ies the pel vi c vi scera. The ext ernal ili ac
cours es ant eriorl y al ong the ps oas muscle under the ingui nal
li gament , formi ng t he com mon femoral artery.
ii i. The proxim al aorta is dist ingui shed from the dis tal aort a by
presence of the renal vess el s.

III. P at hophysi ology

i. The dis rupt ion in normal laminar flow at the level of the
bifurcati on res ul ts in t he form at ion and organizat ion of plaque.
Furt her plaque deposi tion result s in the augment at ion of
col laterals around t he occl us ive s egment s.
ii. These col laterals are not al ways s uffi ci ent t o provide flow to the
pel vi c vi scera or lower extrem it ies. When unabl e to m eet the
m et abol ic demands of the lower extrem it ies or pelvis , impotence,

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 butt ock claudicat ion, and s evere disabl ing lower extrem it y pain
occurs.
IV. Ri sk factors . Incl ude smoki ng, hypert ensi on, hyperli pi demi a,
diabetes m el lit us type 2, m al e s ex, ol der age (age 50–60), and
genet ic di sposi tion.
V. Cl audi cati on. This denot es an extrem el y dis abli ng condi tion wi th
characteris ti c exerci se- i nduced, cramping pain, when oxygen suppl y
does not meet demand in act ive m uscles. Rest rel ieves pain.
VI. Cl as si fi cati on
i. Type I dis ease: confined to t he dist al aort a and bil at eral iliacs
(10%). Thi s often present s in young females wi th claudicat ion of
t he butt ocks and hi ps .
ii. Type II dis ease: more extens ive (80%) and invol ves the aorta, the
il iacs , and often the com mon femoral artery. Type II di seas e is
t he m ost com mon.
ii i. Type III: invol ves the fem oropopli teal and ti bial s egment s (10%).
P ati ents wit h type III diseas e usuall y pres ent wi th cri ti cal lim b
is chem ia.
VII. The sym pt om cons tell at ion cons is ting of lower ext remi ty
claudicat ion, gl uteal atrophy, im pot ence, and dimi nis hed fem oral
puls es result s in "L eriche syn drome. "
VIII. Dis ease s everit y: type III>t ype II>type I.
IX. Di agnosi s
i. Phys ical Exam inat ion
1. P resence of gangrene
2. Tiss ue at rophy, es peci al ly in t he calf
3. Dermal changes such as livedo ret icul aris s uggest
proxi mal occl us ive dis ease wit h showeri ng of di stal
mi croembol i
4. P resence/ abs ence of pul ses in the groin and al ong the
l ower ext remi ty
5. P resence of bruits i n the abdomen and groi n
X. Noninvasi ve vascul ar testi ng
i. S egment al press ure m easurement s: ankle-brachi al index (ABI) in
a pati ent wi th claudicat ion ranges from 0.5 to 0.9, whereas
pat ient s wi th res t pain and tis sue l oss have AB I less t han 0.5 .
ii. In s ome scenarios, t he ABI at res t m ay be normal, but wit h
exercis e t he AB I may decrease.
iii. A drop of 15% in the AB I aft er exerci se is cons idered
si gnificant .
iv. Als o real ize that pati ents with m edial calcinos is may have fal sely
elevated AB I.
XI. Duplex s canning. Alt hough thi s can be us ed t o ident ify occlusi on,
utili ty is lim ited by such fact ors as the pati ent's body habit us and
operator experti se.
XII. Art eriography. Thi s techni que i nvolves the us e of radio-opaque dye
t o delineate t he vascul ar anatomy/abnormali ti es of the lower
ext remi ty. The pat ient requires a palpable puls e (eit her in the
fem oral art ery or an upper extrem it y artery) t o cannul at e the vess el
for the angiogram .
XIII. M anagem ent
i. M edical Management

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 1. Sm oki ng ces sati on: the m ost im port ant modi fi able ri sk
factor that has been s hown i nnumerabl e tim es to improve
claudicat ory sympt om s.
2. Vigorous exercis e program : m ust be emphasi zed in
pat ient s who are abl e t o exerci se. It is thought t hat
exercis e i ncreas es the anaerobic tol erance i n ischemi c
m uscle tis sue.
3. Aspirin
4. Hypertens ion, di abet es , and hyperli pi demi a control : this
approach m ay not revers e the diseas e but cert ai nl y may
prevent it s progress ion.
ii. Surgical m anagem ent
1. Endovas cular t echniques
a. P ercutaneous acces s foll owed by balloon
angiopl as ty wit h a st ent has s hown s ome prom is e
for short segm ent, nonocclusi ve di seas e in the
il iacs .
b. Compl icat ions i nclude perforati on, dis sect ion,
t hrom bosis , and di st al emboli sm .
2. Aortoili ac endarterect om y: The procedure i nvolves an
art eriotomy, wit h careful di ss ecti on to remove t he plaque
from the aorti c wall .
3. Art erial recons tructi on wit h anat om ical ly placed
prost hesi s: graft from the proxim al aorta t o the ili acs or
fem oral s.

5. F em oropoplit eal and Tibial Occl us ive Di seas e

I. General Princi ples
i. Leads to claudicat ion, res t pain, and crit ical ischemi a, res ul ting
i n gangrene .
ii. Increas ed ri sk of cardiovas cular mortali ty.
ii i. Limb l oss rat es can be as hi gh as 1% to 5% as a res ul t of
i nfrainguinal dis ease.
II. Anatomy
i. Out fl ow dis ease i s defi ned as bei ng dist al to the inguinal
li gament .
ii. Hunter canal (adductor hi at us ): as the s uperfi ci al fem oral art ery
cours es t oward the knee, it pass es via the adduct or canal . This is
t he m ost com mon sit e of occl us ion bel ow the ingui nal ligam ent .
ii i. It is im port ant to identi fy the coll at erizat ion in the lower
ext remi ty via the profunda fem oris , and the geni culate branches
at the l evel of t he knee.
III. Diagnos is
i. Hist ory. Pts oft en wit h exerci se- i nduced lower extrem it y pain,
nonheal ing ul cer, and muscle wast ing. 80% have a hist ory of
sm oking.
ii. Phys ical exam inat ion. Puls e exam. Identi fy trophi c changes,
m uscle was ti ng, thi nni ng of the s ki n and nail s, and los s of hair.
Ischemi c ul cerati ons begi n as small dry ulcers of the toes or heel,
and progress to frank gangrene.
ii i. Noninvasi ve testi ng. Check ABI, s egment al pres sures, and pul se
vol ume recordings . Magnet ic res onance angi ography and C T
angiography are bei ng increas ingl y us ed to identi fy dis ease and
plan int ervent ion.

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 i v. Diabetes and renal fai lure m ake pat ient s more sus cept ible to
art erial insufficiency.
IV. In bl ue toe syndrome, atheroembol ic dis ease moves from an
aortoil iac or fem oropopli teal source t o the di stal microvascul ature,
res ul ti ng in digi tal is chem ia.
V. M anagem ent
i. Ri sk factor modificat ion
1. Sm oki ng ces sati on
2. Dietary modi fi cati on
3. St ruct ured exercis e program
ii. M edical management : us e of HM G CoA reductase inhibitors ,
aspirin, and pentoxi fylli ne
ii i. Surgical m anagem ent
1. P ercutaneous angioplast y
2. Other operati ve t echniques
a. Aut ol ogous vei n bypas s. The ipsil at eral or
contral at eral s aphenous vein i s harves ted for
bypas s around t he occluded segm ents . The vein is
revers ed to al low flow through the venous valves .
b. In-s itu vei n bypass . The saphenous vei n is
i denti fi ed in it s nati ve l ocat ion. The venous valves
are dis rupt ed usi ng a valvul otome, and t he bypass
is carri ed out around the occluded segm ents .
3. P rosthet ic bypass .
6. Amput ati ons
I. Mortality rates range from 5% to 30%
II. 67% morbidity rate
i. Generally highest in patients undergoing above-knee amputations since these
patients are the least functional and most ill
ii. Perioperative myocardial infarction is the most common cause of death
iii. Deep venous thrombosis occurs in 10–15% of patients and may be present prior
to amputation because of the sedentary state of these patients both
preoperatively and postoperatively.
III. Indications for surgical amputation
i. The removal of all diseased tissue—but this is not always achieved with the
initial amputation, particularly when performed for ischemic or infectious
disease.
ii. The relief of pain is critical—but this may not be achieved because of healing
failures and chronic pain syndromes (eg, phantom limb pain and reflex
sympathetic dystrophy).
1. Primary healing of the amputation wound is desirable but may not be
accomplished because of infection or efforts to maintain limb length.
2. Construction of a stump that will permit the most useful function with
or without prosthetic fitting is most consequential in functional
patients.
IV. Many minimally functional elderly patients develop breakdown and pressure
necrosis of their distal lower extremities primarily from inactivity in combination
with ischemia. Amputations in these patients are often performed more proximally to
ensure healing.
7. Additional info on vascular testing techniques

Ankle Brachial Index

• Normally >1.0 and a value <0.9 indicates some degree of arterial obstruction
• 0.5 to 0.7 Claudication
• 0.3 to 0.5 rest pain

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 • <0.3 Gangrene

PVR (Pulse Volume Recording)

Using cuffs similar to those involved in segmental pressure testing, PVR cuffs are inflated, but only a little.
Instead of temporarily stopping the blood flow to determine your blood pressure, the PVR cuff allows the
blood to continue flowing through your leg. As blood pulses through your arteries, your blood vessels
expand causing an increase or decrease in the volume of air within the cuff.

A recording device displays these pulse volume changes as a waveform. The shape of the waveform gives
the doctor useful information about the blood flow in your legs. This test often is more informative for
patients with diabetes or whose arteries have become stiff and hard to compress due to calcification.

Arteriogram
Diagnostic angiography has represented the gold standard in vascular imaging prior to an intervention. The
imaging system and the contrast agent are used to opacify the target vessel. Complications can occur from
angiography, or more commonly with interventions such as angioplasty and stenting. Local complications
include groin hematoma, pseudoaneurysm, and traumatic arteriovenous fistula. Catheters can enter the wall
of an artery, producing dissection, rupture, or thrombosis. One of the most dangerous complications is
retroperitoneal hematoma, in which blood leaking from the puncture site tracks superiorly into the
retroperitoneum. Frequently the groin examination is totally normal, and the patient presents with
hypotension. Diagnosis is established by CT scan, and the hole in the femoral or external iliac artery should
be surgically repaired.
S

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