PEMBAHASAN TO1

BATCH 1 2013
dr. Himawan, dr. Cemara, dr. Dini,
dr. Yusuf, dr. Ratna, dr. Anshari

ILMU PENYAKIT DALAM

1. Komplikasi Kidney Failure

Pasien , 48 tahun
Sulit BAK
Kaki bengkak
Mual muntah
Riwayat kencing batu
Kadar ureum 115, kreatinin 5,8, glukosa 168

Jenis Pemeriksaan

Nilai Normal

Deskripsi

Blood Urea Nitrogen (BUN)

7-25 mg/dL

Urea dihasilkan dari metabolisme

protein, difiltrasi di glomerulus. Jika
GFR urea direabsorbsi , kembali
ke aliran darah

Kreatinin

0,6-1,5 mg/dL

Produk pemecahan keatinin fosfat dari

otot rangka

Glukosa sewaktu

65-110 mg/dL

Uremia Symptoms

Chronic renal failure

Elevated concentration of urea nitrogen

Bacteria produce urease to disintegrate

urea high-concentration nitrogen
Stimulate gastrointestinal mucous
membrane

Nausea & vomiting

2. HIV

Laki-laki dewasa mudah merasa lemas. Sulit tidur,

nyeri sendi dan otot selama 5 minggu yang lalu.
Nafsu makan baik tetapi merasa BB .
PF : TB 155 cm dan BB 39 kg (IMT = 16,2
Underweight). Luka-luka kecil yang menggaung
yang pada awalnya terlihat seperti jerawat.
Lab : CD4 575

Pathogenesis of HIV
Infection

How HIV
Infection
Become
AIDS

HIV Time Course

http://www.microbiologybytes.com

3. Ikterik

, 40 tahun
Kuning seluruh tubuh sejak 2 minggu yll
BAB dempul
Bilirubin direk , bilirubin indirek normal

Bilirubin direk = conjugated bilirubin

Bilirubin indirek = unconjugated bilirubin

Type of Jaundice

Wikipedia

Color Atlas of Pathophysiology

Color Atlas of Pathophysiology

Table of Diagnostic Test

Wikipedia

4. Serologi Hepatitis

, 35 thn
Kuning 4 hari yang lalu, mual, muntah, lemas
Riwayat menggunakan suntik narkotika
PF hepatomegali
SGOT : 100, SGPT : 350, alkali fosfatase 720,
bilirubin total : 8, bilirubin direct 6

5. Cirrhosis

, 39 tahun
Riwayat peminum alkohol
PF: tampak tidur lelap, kurus, spider nevi (+) di
dinding perut, terdapat bercak darah pada bibir
dan bau amandel, ransang nyeri (-)
Lab : ammonia darah meningkat

Color Atlas of Pathophysiology

www. wikimed.com

6. Hemostasis

, 61 tahun
Perdarahan sejak 2 jam yll setelah cabut gigi
Penderita jantung koroner dengan konsumsi aspirin
100mg selama beberapa tahun

Aspirin has an
antiplatelet effect by
inhibiting the production
of thromboxane, which
under normal
circumstances
binds platelet molecules
together to create a
patch over damaged
walls of blood vessels

Hemostasis (hemo=blood; sta=remain) is the

stoppage of bleeding, which is vitally important when
blood vessels are damaged.
Following an injury to blood vessels several actions
may help prevent blood loss, including:

Formation of a clot

Formation of
platelet aggregate

Injured blood vessel

releases ADP, which
attracts platelets (PLT)
PLT comming in contact
with exposed collagen
release: serotonin, ADP,
TXA2, which accelerate
vasoconstriction and
causes PLT to swell and
become more sticky

7. Anemia

, 40 tahun
Badan lemas, tidak
nafsu makan, demam(-)
Lab : WBC: 4000
gr/dl, Hb: 8 gr/dl, Ht
34% MCV: 114 fl.
Gambaran darah tepi:
netrofil hipersegmen,
makroovalosit

Anemias are defined based on cell size (MCV) and

amount of Hgb (MCH).
MCV less than lower limit of normal: microcytic
anemia
MCV within normal range: normocytic anemia
MCV greater than upper limit of normal:
macrocytic anemia
MCH less than lower limit of normal:
hypochromic anemia
MCH within normal range: normochromic
anemia
MCH greater than upper limit of normal:
hyperchromic anemia

Pernicious
anemia (megaloblastic
anemia due to vitamin B12
deficiency)
Disturbance of proliferation
and differentiation of stem
cells

Anemia of prematurity
(premature infants at 2 to 6
weeks of age)

Impaired RBC production

Disturbance of proliferation
and maturation
of erythroblast

ANEMIA

Anemia of folic acid

deficiency (megaloblastic
anemia)

Iron deficiency anemia

(deficiency of heme
synthesis)

Intrinsic

Thalassemia(deficiency
of globin synthesis)

Extrinsic

Congenital
dyserythropoietic anemias

Increased RBC destruction

(hemolytic anemias)

Blood loss
Anemia of renal failure
Fluid overload

MEGALOBLASTIC
ANEMIA

Anemia (of macrocytic classification) Laboratorium Findings:

Decreased red blood cell (RBC) count
that results from inhibition of DNA
synthesis in red blood cell production and hemoglobin levels[
MCV >95 fl
Pathopgenesis
Increased MCH
Folate and vitamin B12
Normal MCHC, 3236 g/dL
deficienciesdefective RNA and Decreased Reticulocyte count
DNA syntheses
destruction of fragile and
continuing cell growth without
abnormal megaloblastic erythroid
division
precursor

Erythrogenic precursorslarger Blood smear:

hypersegmented neutrophils
than mature red blood cells
macroovalocytes macrocytes with oval
(RBCs)
shape RBC

http://emedicine.medscape.com/article/
http://en.wikipedia.org/wiki/Megaloblastic_anemia

Anisocytosis (increased variation in RBC

size) and poikilocytosis (abnormally
shaped RBCs).

Glucose-6-phosphate
dehydrogenase deficiency

an X-linked recessive hereditary disease

characterised by abnormally low levels of glucose6-phosphate dehydrogenase
Blood smear: Heinz body in RBC

http://www.diseaseaday.com/wpcontent/uploads/2009/05/g6pddeficiencyprocess.png

http://en.wikipedia.org/wiki/Glucose-6phosphate_dehydrogenase_deficiency

8. Kelainan Katup Jantung

, 16 tahun
Sesak napas saat beraktivitas sejak 3 bulan yll
PF: Auskultasi P2 mengeras, opening snap saat diastolik
dengan nada rendah pada apikalis, hepatomegali (-)

Opening Snap
High-frequency early diastolic sound
(occurs 50-100 msec after A2) associated
with mitral stenosis; sound due to abrupt
deceleration of mitral leaflets sound with
associated murmur

 Loud P2 (pulmonic) component of the

(S2) pulmonary hypertension
secondary to severe mitral stenosis
An opening snap heard after the A2
(aortic) component of the (S2)
correlates to the forceful opening
of the mitral valve
The mitral valve opens when the
pressure in the left atrium is
greater than the pressure in the
left ventricle
This happens in ventricular
diastole (after closure of the
aortic valve), when the pressure
in the ventricle precipitously
drops

Pathophysiology of
Mitral Stenosis

The sounds waves

responsible for heart sounds
are generated by vibrations
induced by:
valve closure,
abnormal valve opening,
vibrations in the
ventricular chambers,
tensing of the chordae
tendineae,
turbulent or abnormal
blood flow across valves
or between cardiac
chambers

 closure of the
mitral and
tricuspid valves
at the beginning
of isovolumetric
ventricular
contraction

closure of the
aortic and
pulmonic valves
at the beginning
of isovolumetric
ventricular
relaxation

When audible,
occurs early in
ventricular filling
may represent
tensing of the
chordae
tendineae and
the AV ring,
which is the
connective tissue
supporting the
AV valve leaflet

When audible, is
caused by
vibration of the
ventricular wall
during atrial
contraction
Usually
associated with
a stiffened
ventricle.

Murmur:
Abnormal
movement of
blood across
valves and
between
cardiac
chambers
Divided into:
-ventricular
contraction
(systole)
-ventricular
filling
(diastole)

9. Heart Failure

Pasien 59 thn
Sesak napas, riwayat hipertensi dengan BP 150/90
PF : distensi vena leher, krepitasi pada kedua basal
paru, dan edema pada extremitas

Symptoms of heart failure

http://www.aafp.org/afp/2006/0301/afp20060301p841-f1.gif

Diastole process by which

the heart returns to its
relaxed state
the cardiac muscle is
perfused.
Diastolic dysfunction
the heart is able to meet
the bodys metabolic
needs,at a higher filling
pressure
Transmission of higher
end-diastolic pressure to
the pulmonary circulation
pulmonary congestion
dyspnea right-sided
heart failure.

10. Anti Hipertensi

Nyeri kepala hilang timbul selama 1 minggu, mual

muntah, riwayat hipertensi selama 10 tahun
PF : TD 180/110, GDS 375 dan proteinuria +1

11. Syok Anafilaktik

, 25 thn
Luka robek di kaki akibat kecelakaan suntik
lidocaine 1% infiltrasi untuk anestesi luka robeknya
5menit kemudian tjd gatal2 pada ekstremitas,
muka flushing, kepala melayang dan sulit bernafas
PF : BP 80/40, HR 84x/menit, RR 32x/menit, suhu
37 c, auskultasi : stridor wheezing

Vasodilatation
mucosaoedema

Oedem
larynx

Stridor

Brochospasm

Wheezing

12. Acute coronary syndrome

Keluhan 1 jam yang lalu nyeri dada seperti ditindih

beban berat
EKG irama sinus , ST Elevasi V1-V4, denyut jantung
72x/menit, peningkatan enzim jantung serial

http://ceaccp.oxfordjournals.org/c
ontent/4/6/175.full

Left coronary artery

mensuplai area:

Anterior LV
The bulk of the
interventricular septum
(anterior two thirds)
The apex
Lateral and posterior LV
walls

Right coronary artery

mensuplai area:

Right ventricle (RV)

The posterior third of the
interventricular septum
The inferior wall
(diaphragmatic surface) of
the left ventricle (LV)
A portion of the posterior
wall of the LV (by means of
the posterior descending
branch)

EKG

http://acutemed.co.uk/diseases/ACS+%28Acute+Coronary+Syndrome%29

13. Spirometri pada PPOK

, 68 tahun
Sesak nafas + batuk sejak 3 minggu, dahak kental
kuning sampai kecoklatan. Riwayat batuk darah
disangkal. Perokok berat sejak usia 17th
PF : hemithorax cembung dan perkusi hipersonor di
kedua lapang paru

Obstructive lung disease reduced ventilation the ratio of the

duration of expiration to that of inspiration is increased obstructed
expiration distends the alveolar ductules (centrilobular emphysema), lung
recoil decreases (compliance increases) and the midposition of breathing
is shifted toward inspiration (barrel chest) raises the functional residual
capacity

14. Terapi Asma

Asma sudah 10 tahun

PF : RR 32x/ menit, FN 110x/ menit

GINA Report 2011

MANAGEMENT
IN STABLE
CONDITION

Pathophysiology of
Asthma

Algorithm
of
Asthma
Diagnosis

http://www.eguidelines.co.uk

Terapi Oksigen
Devices

Flow Rate
(L/min

Oxygen
Concentration

Description

Nasal Cannula

15

2844%

Rebreathing
Mask/Simple
Oxygen Mask

6-10

35-60%

-First third of exhaled gases mix with

reservoir
-Exhaled gases from upper airway
are oxygen rich

Non Rebreathing
Mask

10-12

95%

Two valves added to prevents:

-Entrainment of room air during
inspiration
-Retention of exhaled gases during
expiration

Venturi Mask

4-8

25-60%

Ventilator

can be set

21-100%

GINA report 2011

15.Hipoaktivitas Kelenjar Adrenal

, 40 th
Letih lemah sejak 2 bulan yll, saat ini terapi TB,
mengeluh bb turun, dibawah siku warna kulit
tampak menjadi hitam
PF : TD 80/50, nadi 72, tidak ada penyakit jantung

Adrenal Insufficiency

Adrenal tuberculosis is a manifestation of disseminated

disease presenting rarely as adrenal insufficiency
Addison's disease results from progressive destruction of
the adrenals, which must involve >90% of the glands
before adrenal insufficiency appears
The adrenal is a frequent site for chronic granulomatous
diseases, predominantly tuberculosis(70%-90% cases),
but also histoplasmosis, coccidioidomycosis, and
cryptococcosis

Effects and
Symptoms of
Adrenocortical
Hormone
Deficiency

16. Sindrom Cushing

, 25 tahun
Kenaikan BB 10 kg dalam dua bulan. asupan
makan tidak banyak bertambah meski cepat lapar.
Riwayat alergi makanan membeli sendiri obat
alergi atau jamu-jamuan.
PF:TB 158 cm, BB 65 kg (IMT = 26 Overweight),
TD 140/90 mmHg Hipertensi, FN 80x/menit, RR
18 x/menit dan suhu 36,5 C

16. Sindrom Cushing

Cushing's syndrome
(hyperadrenocorticalism/hypercortisolism)
The clinical condition resulting from chronic exposure
to excessive circulating levels of glucocorticoids
The most common cause: excess ACTH secretion from
the anterior pituitary gland (Cushing's disease).

Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5th
ed. McGraw-Hill; 2006.

17. Komplikasi Akut DM

, 20 th
Gaduh gelisah sejak 2 jam yll. Riwayat DM (+)
obat suntikan sejak 3 bulan yll, 2 hari ini
menghentikan obat.
PF TB 155cm, BB 45kg, apatis, RR 32x/menit, tensi
90/60 mmHg, nadi 110x/menit, nafas kussmaul,
lidah kering, turgor kulit menurun

Acute Effect of Diabetes

Mellitus
(Diabetic Ketoacidosis)

Effect on Insufficiency of Insulin

18. Terapi Hipertiroid

, 30 tahun
Dada berdebar-debar sejak 1 minggu yll, gelisah,
sulit tidur, mudah lelah, dan diare
PF : TD 130/80 mmHg, HR 120x/mnt, RR 24x/mnt,
mata exopthalmus, pembesara kelenjar tiroid difus,
akral hangat
Laboratorium: peningkatan T3 dan T4, TSH rendah

Laboratorium Assesment for Thyroid Function

19. Disorder of Calcium Metabolism

, 35 tahun
Pasca tiroidektomi sering mengalami kaku dan
kejang

Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5th
ed. McGraw-Hill; 2006.

19. Disorder of
Calcium Metabolism

Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5th
ed. McGraw-Hill; 2006.

20. Arthritis

Wanita, 30 tahun
Nyeri dan bengkak pada sendi metakarpophalang
dan interfalang kedua tangan, dan bengkak pada
sendi lutut. Dirasakan saat bangun pagi
LED 184 mm(), kadar urat serum 6,2 mg/dl

Rheumatoid Arthritis
Definition:
Chronic inflammatory
Autoimmune disorder, that affect the joints and may cause systemic
manifestation

Reumatoid Arthritis
a score of 6 fulfilling the requirements for RA

RA Patophysiology

21. Malaria

, 25 tahun
Penurunan kesadaran 2 jam yll, riwayat demam
hilang timbul, demam tinggi, menggigil dan
keringat dingin
PF: TD 100/70 mmHg, S 38,5oC, kulit tampak
pucat, konjungtiva anemis.
Lab : ditemukan plasmodium sausage shape

Malaria Life Cycle

Pathogenesis of Cerebral Malaria

Possible cause:
Binding of
parasitized red cells
in cerebral
capillaries
permeability of the
blood brain barrier
Excessive induction
ofcytokines

http://www.microbiol.unimelb.edu.au

22. Dengue Infection

, 17 tahun
Demam sejak 4 hari yang lalu disertai nyeri kepala,
mual, nyeri otot dan sendi.
PF : TSS, TD 120/80 mmHg, Suhu 38,3C, Nadi
98x/menit. Konjungtiva pucat (-). Thoraks: BJ I-II
normal, vesikuler. Abdomen : nyeri tekan
epigastrium (+). Ext : petechiae pada lengan atas
kanan dan kiri.
Lab: Hb 12 g/dL, hematokrit 36%, Leukosit 4700,
Trombosit 98000

Pathophysiology of Dengue Fever

Dengue Infection: Classification

ILMU BEDAH, ANESTESI

DAN RADIOLOGI

23. Primary Survey

A.

B.

C.

D.

E.

Airway
Establish patent airway
Breathing
Assess and ensure adequate oxygenation
Circulation
Level of consciousness
Skin color and temperature
Pulse rate and character
Disability
Baseline neurologic evaluation
GCS scoring
Pupillary response
Environment
Completely undress the patient

and ventilation
Control hemorrhage
Restore volume
Reassess parameters

ATLS

optimized by optima

Secondary Survey
Componet:
A. History namponade
Allergic Medication Past illness
Last meals Event
B. Physical exam : head to toe
C. Every orrifice examination

D. Complete Neurological
examination

E. Special diagnostic tests

optimized by optima

F. Re-evaluation

24. Classification of Wounds

1.

2.

3.

An incised wound that is clean and sutured closed is said to

heal by primary intention.
Often, because of bacterial contamination or tissue loss, a
wound will be left open to heal by granulation tissue
formation and contraction; this constitutes healing by
secondary intention.
Delayed primary closure, or healing by tertiary intention,
represents a combination of the first two, consisting of the
placement of sutures, allowing the wound to stay open for a
few days, and the subsequent closure of the sutures

8th ed Schwartz's

Principles of Surgery

8th ed Schwartz's Principles

of Surgery

25. Shock
Definition
A physiologic state
characterized by
Inadequate tissue
perfusion
Clinically manifested by
Hemodynamic
disturbances
Organ dysfunction

optimized by optima

Hypovolemic Shock

Hemorrhagic Shock
Parameter

II

III

IV

Blood loss (ml)

<750

7501500

15002000

>2000

Blood loss (%)

<15%

1530%

3040%

>40%

Pulse rate
(beats/min)

<100

>100

>120

>140

Blood pressure

Normal

Normal

Decreased

Decreased

Respiratory rate
(bpm)

1420

2030

3040

>35

>30

2030

515

Negligible

Normal

Anxious

Confused

Lethargic

Urine output
(ml/hour)
CNS symptoms
Crit Care. 2004; 8(5): 373381.

optimized by optima

26. WHO Pain Management Stepladder

optimized by optima

Mekanisme kerja nsaid

optimized by optima

Mekanisme kerja opioid

optimized by optima

27. Hemothorax

Occurs when pleural space fills with blood

Usually occurs due to lacerated blood vessel in
thorax
As blood increases, it puts pressure on heart and
other vessels in chest cavity
Each Lung can hold 1.5 liters of blood

27-28 CHEST TRAUMA

Hemothorax

optimized by optima

Hemothorax

Hemothorax

May put pressure on the heart

Where does the blood come from.

Lots of blood vessels

S/S of Hemothorax

Anxiety/Restlessness
Tachypnea
Signs of Shock
Frothy, Bloody Sputum
Diminished Breath Sounds on Affected Side
Tachycardia
Flat Neck Veins

Treatment for Hemothorax

ABCs with c-spine control

as indicated
Secure Airway assist
ventilation if necessary
General Shock Care due to
Blood loss
Consider Left Lateral
Recumbent position if not
contraindicated
RAPID TRANSPORT
Contact Hospital and ALS
Unit as soon as possible

BLS Plus Care

Monitor Cardiac Rhythm

Establish Large Bore IV preferably 2 and draw
blood samples
Airway management to include Intubation
Rapid Transport
If Development of Hemo/Pneumothorax needle
decompression may be indicated

Simple/Closed Pneumothorax

Opening in lung tissue that

leaks air into chest cavity
Blunt trauma is main cause
May be spontaneous
Usually self correcting

Simple/Closed Pneumothorax
S/S :
Chest Pain
Dyspnea
Tachypnea
Decreased Breath
Sounds on Affected
Side

Th/
ABCs with C-spine control
Airway Assistance as
needed
If not contraindicated
transport in semi-sitting
position
Provide supportive care
Contact Hospital and/or
ALS unit as soon as possible

Open Pneumothorax

Opening in chest cavity

that allows air to enter
pleural cavity
Causes the lung to
collapse due to
increased pressure in
pleural cavity
Can be life threatening
and can deteriorate
rapidly

Open Pneumothorax

Inhale

Exhale

Open Pneumothorax
optimized by optima

Inhale

Exhale

Open Pneumothorax

Inhale
Exhale

Open Pneumothorax

Open Pneumothorax
S/S :
Dyspnea
Sudden sharp pain
Subcutaneous
Emphysema
Decreased lung sounds
on affected side
Red Bubbles on
Exhalation from wound
(Sucking chest wound)

Th/ :
ABCs with c-spine control
as indicated
High Flow oxygen
Listen for decreased
breath sounds on affected
side
Apply occlusive dressing
to wound
Notify Hospital and ALS
unit as soon as possible

Sucking Chest Wound

Occlusive Dressing

28. Tension Pneumothorax

Each time we inhale,

the lung collapses further.
There is no place for the air to
escape..

Air builds in pleural

space with no where
for the air to escape
Results in collapse of
lung on affected side
that results in pressure
on mediastium,the
other lung, and great
vessels
optimized by optima

Each time we inhale,

the lung collapses further. There
is no place for the air to
escape..
The trachea is
pushed to
the good side

Heart is being
compressed

S/S of Tension Pneumothorax

Anxiety/Restlessness
Severe Dyspnea
Absent Breath sounds
on affected side
Tachypnea
Tachycardia
Poor Color

Accessory Muscle Use

JVD
Narrowing Pulse
Pressures
Hypotension
Tracheal Deviation
(late if seen at all)

Treatment of Tension Pneumothorax

ABCs with c-spine as indicated

Needle Decompression of Affected Side
High Flow oxygen including BVM
Treat for S/S of Shock
Notify Hospital and ALS unit as soon as possible
If Open Pneumothorax and occlusive dressing
present BURP occlusive dressing

Needle Decompression

Locate 2-3 Intercostal space midclavicular line

Cleanse area using aseptic technique
Insert catheter ( 14g or larger) at least 3 in length
over the top of the 3rd rib( nerve, artery, vein lie
along bottom of rib)
Remove Stylette and listen for rush of air
Place Flutter valve over catheter
Reassess for Improvement

Needle Decompression

29. Ureterolithiasis

Urinary tract stone disease

Signs:

Flank pain
Irritative voiding symptom
Nausea
microscopic hematuria

Urinary crystals of calcium

oxalate, uric acid, or cystine
may occasionally be found
upon urinalysis
Diagnosis: IVP

optimized by optima

30. Hirschsprung disease

Definitions

Congenital megacolon
the absence of myenteric
and submucosal ganglion
cells in the distal
alimentary tract
decreased motility in the
affected bowel segment

Pathophysiology

Results from the absence of

parasympathetic ganglion
cells in the myenteric and
submucosal plexus of the
rectum and/or colon.
These ganglion cells arrive in
the proximal colon by 8
weeks of gestational age
and in the rectum by 12
weeks of gestational age.
Arrest in migration leads to
an aganglionic segment.

Hirschsprung disease
Predilection

Frequency

approximately 1 per 5000 live

births.
Sex: 4 times more common in
males than females.
Age:
Nearly all children with
Hirschsprung disease are
diagnosed during the first 2
years of life.
one half are diagnosed before
they are aged 1 year.
Minority not recognized until
later in childhood or adulthood.
Mortality/Morbidity:
The overall mortality of
Hirschsprung enterocolitis is 2530%,.

Classical HD (75% of cases):

Rectosegmoid
Long segment HD (20% of
cases)
Total colonic aganglionosis (312% of cases)
rare variants include the
following:
Total intestinal aganglionosis
Ultra-short-segment HD
(involving the distal rectum
below the pelvic floor and the
anus)

Clinical presentation

Rontgen :
Newborns :
Failure to pass meconium within
Plain abdominal radiography
the first 48 hours of life
Dilated bowel
Abdominal distension that is
Air-fluid levels.
relieved by rectal stimulation or
Empty rectum
enemas
Contrast enema
Vomiting
Transition zone
Neonatal enterocolitis
Abnormal, irregular contractions of
Symptoms in older children and
aganglionic segment
adults include the following:
Delayed evacuation of barium
Severe constipation
Biopsy :
Abdominal distension
absence of ganglion cells
hypertrophy and hyperplasia of
Bilious vomiting
nerve fibers,
Failure to thrive

HD-Assosciated enterocolitis

Abdominal distension, explosive diarrhea, vomiting,

fever, lethargy, rectal bleeding, or shock
The risk is greatest:
before

HD is diagnosed
after the definitive pull-through operation.
children with Down syndrome

Treatment
Hirschsprung disease

Surgical removal or
bypass of the
aganglionic bowel,

HD-Associated enterocolitis

Rehydration,
intravenous antibiotics
and colonic irrigations.

31. Peritonitis
Peritonitis
Infection, or rarely some other type of
inflammation, of the peritoneum.
Peritoneum is a membrane that covers
the surface of both the organs that lie in
the abdominal cavity and the inner
surface of the abdominal cavity itself.

Intra-abdominal infections result in 2 major

clinical manifestations

Early or diffuse infection results in localized or

generalized peritonitis.
Late and localized infections produces an intraabdominal abscess.

2 Major Types

Primary: Caused by the

spread of an infection from
the blood & lymph nodes to
the peritoneum. Very rare <
1%

Usually occurs in people who

have an accumulation of fluid
in their abdomens (ascites).
The fluid that accumulates
creates a good environment
for the growth of bacteria.

Secondary: Caused by the

entry of bacteria or enzymes
into the peritoneum from the
gastrointestinal or biliary tract.
This can be caused due to an
ulcer eating its way through
stomach wall or intestine
when there is a rupture of the
appendix or a ruptured
diverticulum.
Also, it can occur due to an
intestine to burst or injury to
an internal organ which bleeds
into the internal cavity.

Signs & Symptoms

Swelling & tenderness in

the abdomen
Fever & Chills
Loss of Appetite
Nausea & Vomiting
Increased breathing &
Heart Rates
Shallow Breaths
Low BP
Limited Urine Production
Inability to pass gas or
feces

Exam :
The usual sounds made by
the active intestine and
heard during examination
with a stethoscope will be
absent, because the
intestine usually stops
functioning.
The abdom may be rigid
and boardlike
Accumulations of fluid will
be notable in primary due
to ascites.

Evaluation
Lab :
Blood Test
Samples of fluid from
the abdomen
CT Scan
Chest X-rays
Peritoneal lavage.

th/
Hospitalization is
common.
Surgery is often
necessary to remove the
source of infection.
Antibiotics are
prescribed to control the
infection & intravenous
therapy (IV) is used to
restore hydration.

Stomach/duodenum Perforation
Presentation :
abdominal

pain

Pain

on palpation
Release pain
rigidity
peritonism,

shock
Air under diaphragm on
X-ray
Treatment
antibiotics,
repair

resuscitate

Mekanisme Sekresi Asam lambung

optimized by optima

Blunt Abdominal Trauma

The most commonly injured organs

Spleen
Liver
Retroperitoneum

small

bowel
kidneys
Bladder
Colorectum
Diaphragm
pancreas

32. Shock

Cardiogenic shock - a major component of the the

mortality associated with cardiovascular disease (the
#1 cause of U.S. deaths)
Hypovolemic shock - the major contributor to early
mortality from trauma (the #1 cause of death in those
< 45 years of age)
Septic shock - the most common cause of death in
American ICUs (the 13th leading cause of death overall
in US)

Shock: Definitions

Kumar and Parrillo (1995) - The state in which

profound and widespread reduction of effective tissue
perfusion leads first to reversible, and then if
prolonged, to irreversible cellular injury.

Shock: Classification

Hypovolemic shock - due to decreased circulating blood volume in

relation to the total vascular capacity and characterized by a reduction
of diastolic filling pressures
Cardiogenic shock - due to cardiac pump failure related to loss of
myocardial contractility/functional myocardium or structural/ mechanical
failure of the cardiac anatomy an characterized by elevations of
diastolic filling pressures and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of diastolic
filling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid resuscitation)
by increased cardiac output and decreased SVR

Hypovolemic

Hemorrhagic
Trauma
Gastrointestinal
Retroperitoneal

Fluid depletion
(nonhemorrhagic)

External fluid loss

Dehydration
Vomiting
Diarrhea
Polyuria

Interstitial fluid redistribution

Thermal injury
Trauma
Anaphylaxis
Increased vascular
capacitance (venodilatation)
Sepsis
Anaphylaxis
Toxins/drugs

CARDIOGENIC

Myopathic

Blunt Cardiac Injury (trauma)

Myocarditis

Cardiomyopathy

Post-ischemic myocardial
stunning

Septic myocardial depression

Pharmacologic : Calcium
channel blockers
Mechanical

Valvular failure (stenotic or

regurgitant)

Hypertropic cardiomyopathy

Ventricular septal defect

Arrhythmic

Bradycardia

Tachycardia

EXTRACARDIAC OBSTRUCTIVE

Impaired diastolic filling

(decreased ventricular preload)
Direct venous obstruction (vena
cava)
intrathoracic obstructive
tumors
Increased intrathoracic pressure
Tension pneumothorax
Mechanical ventilation (with
excessive pressure or volume
depletion)
Asthma
Decreased cardiac compliance
Constrictive pericarditis
Cardiac tamponade

Impaired systolic contraction

(increased ventricular afterload)
Right ventricle
Pulmonary embolus (massive)
Acute pulmonary
hypertension
Left ventricle
embolus
Aortic dissection

DISTRIBUTIVE

Septic (bacterial, fungal, viral, rickettsial)

Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
Adrenal

crisis
Thyroid storm

Toxic (e.g., nitroprusside, bretylium)

CLINICAL MARKERS OF SHOCK

Brachial systolic blood pressure: <110mmHg

Sinus tachycardia: >90 beats/min

Respiratory rate: <7 or >29 breaths/min
Urine Output: <0.5cc/kg/hr
Metabolic acidemia: [HCO3]<31mEq/L or base
deficit>3mEq/L
Hypoxemia: 0-50yr: <90mmHg; 51-70yr: <80mmHg;
>71yo<70mmHg;
K
Cutaneous vasoconstriction vs.

l
vasodilation.
k
j

Mental Changes: anxiousness, agitation, indifference,

lethargy, obtundation

Etiology & Hemodynamic Changes in Shock

Etiology of shock

example

CVP

CO

SVR

VO2 sat

preload

hypovolemic

low

low

high

low

contractility

cardiogenic

high

low

high

low

afterload

distributive

Etiology & Hemodynamic Changes in Shock

(Afterload)
ETIOLOGY OF
SHOCK

EXAMPLE

AFTERLOAD

DISTRIBUTIVE

CVP

CO

SVR

VO2 SAT

Hyperdynamic Septic

Low/High

High

Low

High

Hypodynamic Septic

Low/High

Low

High

Low/High

Neurogenic

Low

Low

Low

Low

Anaphylactic

Low

Low

Low

Low

HYPOVOLEMIC SHOCK
Decreased preload->small ventricular end-diastolic
volumes -> inadequate cardiac generation of pressure and
flow
Causes:

bleeding: trauma, GI bleeding, ruptured aneurysms,

hemorrhagic pancreatitis
protracted vomiting or diarrhea
adrenal insufficiency; diabetes insipidus
Dehydration

third spacing: intestinal obstruction, pancreatitis,

cirrhosis

Hypovolemic Shock

Signs & Symptoms: Hypotension, Tachycardia, MS

change, Oliguria, Deminished Pulses.
Markers: monitor UOP,CVP, BP, HR, Hct, MS, CO, lactic
acid and PCWP
Treatment: ABCs, IVF (crystalloid), Trasfusion Stem
ongoing Blood Loss

SEPTIC/INFLAMMATORY SHOCK
Mechanism: release of inflammatory mediators leading to

1. Disruption of the microvascular endothelium

2. Cutaneous arteriolar dilation and sequestration of blood in
cutaneous venules and small veins
Causes:

1. Anaphylaxis, drug, toxin reactions

2. Trauma: crush injuries, major fractures, major burns.
3. infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis,
meningitis, cholangitis, pyelonephritis, necrotic tissue,
pancreatitis, wet gangrene, toxic shock syndrome, etc.

Septic/Inflammatory Shock
Signs: Early warm w/ vasodilation, often adequate urine
output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.

Monitor/findings: Earlyhyperglycemia, respiratory

alkylosis, hemoconcentration,
WBC typically normal or low.
Late Leukocytosis, lactic acidosis
Very Late Disseminated Intravascular
Coagulation & Multi-Organ
System Failure.
Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess)
pressors.

CARDIOGENIC SHOCK
Mechanism: Intrinsic abnormality of heart -> inability to
deliver blood into the vasculature with adequate power
Causes:
1. Cardiomyopathies: myocardial ischemia, myocardial infarction,
cardiomyopathy, myocardiditis, myocardial contusion

2. Mechanical: cardiac valvular insufficiency, papillary muscle rupture,

septal defects, aortic stenosis
3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrial
fibrillation, atrial flutter, ventricular fibrillation)
4. Obstructive disorders: PE, tension peneumothorax, pericardial
tamponade, constrictive pericaditis, severe pulmonary hypertension

Cardiogenic Shock

Characterized by high preload (CVP) with low CO

Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP, oliguria
Monitor/findings: CXR pulm venous congestion, elevated CVP,
Low CO.
Tx: CHF diuretics & vasodilators +/- pressors.
LV failure pressors, decrease afterload,
intraaortic ballon pump &
ventricular assist device.

NEUROGENIC SHOCK
Mechanism: Loss of autonomic
innervation of the cardiovascular system
(arterioles, venules, small veins, including
the heart)
Causes:
1. Spinal cord injury
2. Regional anesthesia
3. Drugs
4. Neurological disorders

Neurogenic Shock

Characterized by loss of vascular tone & reflexes.

Signs: Hypotension, Bradycardia, Accompanying
Neurological deficits.
Monitor/findings: hemodynamic instability, test
bulbo-carvernous reflex
Tx: IVF, vasoactive medications if refractory

33. FOREHAND FRACTURE

Montegia Fracture Dislocation

It is a fracture of the proximal

1/3rd of the Ulna with
dislocation of head of radius
anteriorly. Posteriorly or
laterally
Head of Radius dislocates
same direction as fracture
It requires ORIF or it will
redisplace

Montegia : Lateral displacement

optimized by optima

Galliazi Fracture

It is a fracture of distal
Radius and dislocation of
inferior Radio- Ulnar joint
Like Montegia fracture if
treated conservatively it
will redisplace
This fracture appeared in
acceptable position after
reduction and POP

Greenstick Fractures

Colles Fracture

Most common fracture in Osteoporotic

bones
Extra-Articular : 1 inch of distal Radius
Results from a fall on dorsi flexed wrist
Typical deformity : Dinner Fork
Deformity is : Impaction, dorsal displacement
and angulation, radial displacement and
angulation and avulsion of ulnar styloid
process

Colles Fracture

optimized by optima

# distal 1 Impaction ,Dorsal displacement

and dorsal tilt

Colles Fracture

optimized by optima

Smith Fracture

Smith Fracture

Almost the opposite of Colles fracture

Much less common compared to colles
Results from a fall on palmer flexed wrist
Typical deformity : Garden Spade
Management is conservative : MUA and Above
Elbow POP

34. LOW BACK PAIN

Herniated Nucleus Pulposus

The progressive
degeneration of a disc, or
traumatic event, can lead
to a failure of the annulus
to adequately contain the
nucleus pulposus
This is known as herniated
nucleus pulposus (HNP) or
a herniated disc

Herniated Nucleus Pulposus

Symptoms
Back

pain
Leg pain
Dysthesias
Anesthesias

Herniated Nucleus Pulposus

Varying degrees
Disc bulge

Mild symptoms

Usually go away with

nonoperative treatment

Rarely an indication
for surgery

Extrusion (herniation)

Moderate/severe symptoms

Nonoperative treatment

Herniated Nucleus Pulposus

Diagnosis

Magnetic resonance imaging

(MRI)/patient exam

Nonoperative Care

Initial bed rest

Nonsteroidal antiinflammatory (NSAID)
medication
Physical therapy

Exercise/walking

Steroid injections

Herniated Nucleus Pulposus

Surgical care
Failure of nonoperative
treatment
Minimum

of 6 weeks in

duration
Can be months
Discectomy

Removal

of the
herniated
portion of the disc
Usually through a small
incision
High success rate

Herniated Nucleus Pulposus

Cauda Equina Syndrome

Caused by a central disc

herniation
Symptoms include bilateral
leg pain, loss of perianal
sensation, paralysis of the
bladder, and weakness of
the anal sphincter
Surgical intervention in
these cases is urgent

Spondylolisthesis

Gradation of
spondylolisthesis

Meyerdings Scale
Grade 1 = up to 25%
Grade 2 = up to 50%
Grade 3 = up to 75%
Grade 4 = up to 100%
Grade 5 >100%
(complete dislocation,
spondyloloptosis)

Spondylolisthesis

Symptoms
Low back pain
With or without buttock or
thigh pain
Pain aggravated by standing
or walking
Pain relieved by lying down
Concomitant spinal stenosis,
with or without leg pain, may
be present
Other possible symptoms
Tired legs, dysthesias,
anesthesias
Partial pain relief by leaning
forward or sitting

Spondylolisthesis

Diagnosis

Plain radiographs
CT, in some cases with
leg symptoms

Nonoperative Care

Rest
NSAID medication
Physical therapy
Steroid injections

Spondylolisthesis

Surgical care

Failure of nonoperative
treatment
Decompression and fusion

Instrumented
Posterior approach
With interbody fusion

Spondylolysis

Spondylolysis

Also known as pars defect

Also known as pars fracture
With or without
spondylolisthesis
A fracture or defect in the
vertebra, usually in the
posterior elementsmost
frequently in the pars
interarticularis

Spondylolysis

Symptoms

Low back pain/stiffness

Forward bending
increases pain
Symptoms get worse
with activity
May include a stenotic
component resulting in
leg symptoms
Seen most often in athletes

Gymnasts at risk
Caused by repeated strain

Spondylolysis

Diagnosis

Plain oblique radiographs

CT, in some cases

Nonoperative care

Limit athletic activities

Physical therapy

Most fractures heal without

other medical intervention

Spondylolysis

Surgical care
Failure

of nonoperative treatment
Posterior fusion
Instrumented
May

require decompression

Ankylosing spondilitis

optimized by optima

35. ABDOMINAL INJURIES

Causes

injuries to the
abdomen, pelvis
and genitalia are
generally caused by
accidents involving
high kinetic energy
and acceleration or
deceleration forces

Open vs. Closed Injuries

Abdominal injuries can be

either open or closed
Open injuries are caused by
sharp or high velocity
objects that create an
opening between the
peritoneal cavity and the
outside of the body

Closed injuries are caused

by compression trauma
associated with
deceleration forces and
include:
contusions
ruptures
lacerations
shear

injuries

Hollow and Solid Organs

The type of injury will depend on whether the organ injured is
solid or hollow.

hollow organs include:

stomach
intestines
gallbladder
bladder

solid organs
include:
liver
spleen
kidneys

Abdominal Injuries
Hollow Organ Injuries

when hollow organs

rupture, their highly
irritating and
infectious contents
spill into the
peritoneal cavity,
producing a painful
inflammatory reaction
called peritonitis

Solid Organ Injuries

damage to solid organs

such as the liver can cause
severe internal bleeding
blood in the peritoneal
cavity causes peritonitis
when patients injure solid
organs, the symptoms of
shock may overshadow
those from peritonitis

Abdominal Injuries

Abdominal injuries can

be obvious, such as an
open wound, or subtle,
such as a blow to the
flank that initially
causes little pain, but
damages the liver or
spleen

Suspect abdominal
internal injury in any
patient who has a
penetrating abdominal
wound or has suffered
compression trauma to
the abdomen

Liver

Largest organ in abdominal

cavity
Right upper quadrant
Injured from trauma to:

Eighth through twelfth

ribs on right side of
body
Upper central part of
abdomen

Suspect liver injury when:

Steering wheel injury

Lap belt injury
Epigastric trauma

After injury, blood and bile

leak into peritoneal cavity

Shock
Peritoneal irritation

Management:

Resuscitation
Laparotomy and repair
or resection.
Avulsion of pedicle is
fatal

Spleen

Upper left quadrant

Rich blood supply
Slightly protected by organs
surrounding it and by lower rib
cage
Most commonly injured organ
from blunt trauma
Associated intraabdominal
injuries common
Suspect splenic injury in:
Motor vehicle crashes
Falls or sports injuries
involving was an impact to the
lower left chest, flank, or
upper left abdomen

Kehrs sign
Left

upper quadrant pain

radiates to left shoulder
Common complaint with
splenic injury

Management :
Resuscitation.
Laparotomy (repair, partial
excision or splenectomy)
Observation in hospital for
patients with sub-capsular
haematoma

Stomach/duodenum

Not commonly injured by blunt trauma

Protected location in abdomen
Penetrating trauma may cause gastric transection or
laceration

Signs of peritonitis from leakage of gastric contents

Diagnosis confirmed during surgery

Unless nasogastric drainage returns blood

Stomach/duodenum
Perforation

Presentation :

Bleeding

abdominal pain
rigidity
peritonism, shock
Air under diaphragm on
X-ray

Haematemesis +/ Melaena
Severity

Treatment
Antibiotics
resuscitate
repair

Presentation :

Increased PR>90
Fall BP<100

Treatment :
transfusion
inject DU

36. ILEUS

Introduction and Definitions

Accounts for 5% of all acute surgical admissions
Patients are often extremely ill requiring prompt
assessment, resuscitation and intensive monitoring
Obstructive ileus
A mechanical blockage arising from a structural abnormality
that presents a physical barrier to the progression of gut
contents.
Paralytic Ileus
is a paralytic or functional variety of obstruction
Obstruction is: Partial or complete
Simple or strangulated

Pathophysiology I

8L of isotonic fluid received by the small intestines (saliva,

stomach, duodenum, pancreas and hepatobiliary )
7L absorbed
2L enter the large intestine and 200 ml excreted in the faeces
Air in the bowel results from swallowed air ( O2 & N2) and bacterial
fermentation in the colon ( H2, Methane & CO2),
600 ml of flatus is released
Enteric bacteria consist of coliforms, anaerobes and strep.faecalis.
Normal intestinal mucosa has a significant immune role
Distension results from gas and/ or fluid and can exert hydrostatic
pressure.
In case of BO Bacterial overgrowth can be rapid
If mucosal barrier is breached it may result in translocation of bacteria and
toxins resulting in bactaeremia, septaecemia and toxaemia.

Pathophysiology II
Obstruction results in:
1.
2.
3.
4.
5.
6.
7.
8.

Initial overcoming of the obstruction by increased paristalsis

Increased intraluminal pressure by fluid and gas
Vomiting
sequestration of fluid into the lumen from the surrounding
circulation
Lymphatic and venous congestion resulting in oedematous tissues
Factors 3,4,5 result in hypovolaemia and electrolyte imbalance
Further: localised anoxia, mucosal depletion necrosis and perforation
and peritonitis.
Bacterial over growth with translocation of bacteria and its toxins
causing bacteraemia and septicaemia.

Decompress with NGT

Replace lost fluid
Correct electrolyte abnormalities
Recognise strangulation and perforation
Systemic antibiotics.

1. History
The Universal Features
Colicky abdominal pain, vomiting, constipation (absolute), abdominal
distension.
Complete HX ( PMH, PSH, ROS, Medication, FH, SH)

High
Pain is rapid
Vomiting copious and
contains bile jejunal content
Abdominal distension is
limited or localized
Rapid dehydration

Distal small bowel

Pain: central and colicky
Vomitus is feculunt
Distension is severe
Visible peristalsis
May continue to pass
flatus and feacus before
absolute constipation

Colonic

Preexisting change in
bowel habit
Colicky in the lower
abdomin
Vomiting is late
Distension prominent
Cecum ? distended

Persistent pain may be a sign of strangulation

Relative and absolute constipation

Causes- Small Bowel

Luminal

Mural

Extraluminal

F. Body
Bezoars
Gall stone
Food Particles
A. lumbricoides

Neoplasms
lipoma
polyps
leiyomayoma
hematoma
lymphoma
carcinoid
carinoma
secondary Tumors
Crohns
TB
Stricture
Intussusception
Congenital

Postoperative
adhesions

Congenital
adhesions
Hernia
Volvulus

2. Examination
General
Vital signs:
P, BP, RR, T, Sat
dehydration
Anaemia, jaundice, LN
Assessment of vomitus if
possible
Full lung and heart
examination

Abdominal
Abdominal distension
and its pattern
Hernial orifices
Visible peristalsis
Cecal distension
Tenderness, guarding
and rebound
Organomegaly
Bowel sounds
High pitched
Absent

Rectal examination

Others
Systemic examination
If deemed necessary.
CNS
Vascular
Gynaecological
muscuoloskeltal

Initial Management in the ER

Resuscitate:

Air way (O2 60-100%)

Insert 2 lines if necessary
IVF : Crytloids at least 120 ml/h. (determined by estimated fluid loss and
cardiac function). Add K+ at 1mmmol/kg

Draw blood for lab investigations

Inform a senior member in the team.
NPO.
Decompress with Naso-gastric tube and secure in position
Insert a urinary catheter (hourly urinary measurements) and start a fluid
input / output chart
Intravenous antibiotics (no clear evidence)
If concerns exist about fluid overloading a central line should be inserted
Follow-up lab results and correction of electrolyte imbalance
The patient should be nursed in intermediate care
Rectal tubes should only be used in Sigmoid volvulus.

Indications for Surgery

Immediate intervention:
Evidence of strangulation (hernia.etc)
Signs of peritonitis resulting from perforation or
ischemia

Paralytic Ileus

Associated with the following conditions:

Postoperative and bowel resection

Intraperitoneal infection or inflammation

Ischemia

Extra-abdominal: Chest infection, Myocardia infarction

Endocrine: hypothyroidism, diabetes

Spinal and pelvic fractures

Retro-peritoneal haematoma

Metabolic abnormalities:

Hypokalaemia

Hyponatremia

Uraemia

Hypomagnesemia

Bed ridden

Drug induced: morphine, tricyclic antidepressants

Clinical Findings
Clinical features

Is there an under lying cause?

Is the abdomen distended but tenderness is not marked.

Is the bowel sounds diffusely hypoactive.

Radiological features:

Is the bowel diffusely distended

Is there gas in the rectum

Are further investigasions (CT or Gastrografin studies) helpful

in showing an obstruction.

Does the patient improve on conservative measures

37. BURN INJURY

Burn Injuries

Potential complications
Fluid and Electrolyte loss Hypovolemia
Hypothermia, Infection, Acidosis
catecholamine release, vasoconstriction
Renal or hepatic failure
Formation of eschar
Complications of circumferential burn

Burn Injuries

An important step in
management is to
determine depth and
extent of damage to
determine where and how
the patient should be
treated
Depth Classification
Superficial
Partial thickness
Full thickness

Thermal burn
Skin injury
Inhalation injury

Chemical burn
Skin injury
Inhalation injury
Mucous membrane
injury

Electrical burn

Lightning

Radiation burn

Burn Classifications

1st degree (Superficial burn)

Involves the epidermis
Characterized by reddening
Tenderness and Pain
Increased warmth
Edema may occur, but no
blistering
Burn blanches under pressure
Example - sunburn
Usually heal in ~ 7 days

Burn Classifications

2nd degree
Damage extends through the
epidermis and involves the dermis.
Not enough to interfere with
regeneration of the epithelium
Moist, shiny appearance
Salmon pink to red color
Painful
Does not have to blister to be 2nd
degree
Usually heal in ~7-21 days

Burn Classifications

3rd degree
Both epidermis and dermis are
destroyed with burning into SC fat
Thick, dry appearance
Pearly gray or charred black color
Painless - nerve endings are destroyed
Pain is due to intermixing of 2nd
degree
May be minor bleeding
Cannot heal and require grafting

Burn Injuries

Often it is not possible to predict the exact depth of

a burn in the acute phase. Some 2nd degree burns
will convert to 3rd when infection sets in. When in
doubt call it 3rd degree.

Body Surface Area Estimation

Rule of Nines
Adult

Palm Rule

Body Surface Area Estimation

Rule of Nines
Peds
For

each yr over 1 yoa,

subtract 1% from head
and add equally to legs

Palm Rule

38. ARTERIAL DISEASE

Arterial Disease

Raynaud phenomenon is a
vasospastic disease of the digital
arteries; occurs in susceptible
people when exposed to cool
temperatures or during emotional
stress.
Symptoms:
numbness,
paresthesias, or
Pain
Raynaud's syndrome is used to
encompass both the primary &
secondary conditions causing
Raynaud phenomenon.

Vasospasm of digital arteries

obliterates the lumen
Inhibited blood flow triphasic color
response
fingers blanch to a distinct white as blood
flow is interrupted
cyanosis, related to local accumulation of
desaturated hemoglobin

ruddy color as blood flow resumes

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.
Brunicardi FC. Schwartz principles of surgery. 8th ed. McGraw-Hill; 2004.

Arterial Disease
Raynaud disease:

Raynaud phenomenon:

may appear as a component of other

conditions.
Mechanism:
Causes:
connective tissue diseases
sympathetic discharge in
(scleroderma & SLE)
response to cold,
arterial occlusive disorders.
vascular sensitivity to adrenergic
carpal tunnel syndrome,
stimuli, or
thermal or vibration injury.
In patients with connective tissue
vasoconstrictor stimuli
diseases/arterial occlusive disease: the
(serotonin, thromboxane, &
digital vascular lumen is largely
endothelin)
obliterated by sclerosis or
inflammation lower intraluminal
Treatment:
avoiding cold environments, dressing in warm pressure & greater susceptibility to
sympathetically mediated
clothes, & wearing insulated gloves or
vasoconstriction.
footwear.
Preventing vasospasm with CCB or alpha
blocker.
Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

Predominantly woman ages 20-40

39. Urine Incontinence

40. Urethral Trauma

Anterior Urethral Trauma

Position : Distal from

urogenital diagphram
Etiology :

Clinical Signs :

Straddle Injury
Instrumentation
Blood from urethral meatus
Hematom, perineal pain
Urinary retenstion

Radiology : urethrogram
Therapy :
Sistostomy

immediate repair
Tanagho EA, et al. Smiths general urology. 17th ed. McGraw-Hill; 2008.

Urethral Trauma
Posterior Urethral Trauma

Etiology

Clinical Symptoms

Radiology

Therapy

Pelvic bone fracture

Blood from meatus
Urinary retention
Pain, hematom on pubic region
Pelvic Photo
Urethrogram
Sistostomy
Repair 3-4 days later.

Tanagho EA, et al. Smiths general urology. 17th ed. McGraw-Hill; 2008.

41. Pericardial Disease

Etiology of cardiac tamponade:
neoplastic, postviral, & uremic
pericarditis.

Acute hemorrhage into

pericardium:
blunt/penetrating chest
trauma,
rupture of the left
ventricular free wall
following MI,
dissecting aortic aneurysm

Pulsus Paradoxus
decreased of SBP 10 mmHg during inspiration
Thorax expansion during
inspiration

Intrathoracic pressure become

more negative

Facilitates venous return &

right ventricle filling

Increase in RV size
diminishes LV filling

In cardiac tamponade, the normal

situation (left diagram) is
exaggerated because both ventricles
share a reduced, fixed volume as a
result of external compression by the
tense pericardial fluid.
Pulsus paradoxus may also be
manifested by other conditions in
which inspiration is exaggerated,
including severe asthma & COPD.

LV stroke volume & systolic

blood pressure decline slightly
McPhee SJ, et al. Pathophysiology of disease. 5th ed. McGraw-Hill; 2006.
Silbernagl S. Color atlas of pathophysiology. 1st ed. Thieme; 2000.
Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

Cardiac Tamponade
Management:
ABCs with c-spine control
as indicated
High Flow oxygen
Cardiac Monitor
Large Bore IV access
Rapid Transport
What patient needs is
pericardiocentesis

Pericardiosentesis
Using aseptic technique, Insert at
least 3 needle at the angle of the
Xiphoid Cartilage at the 7th rib

Advance needle at 45 degree

towards the clavicle while
aspirating syringe till blood return
is seen

Continue to Aspirate till syringe is

full then discard blood and
attempt again till signs of no more
blood

Closely monitor patient due to

small about of blood aspirated
can cause a rapid change in blood
pressure

42. COMPARTMENT SYNDROME

Compartment Syndrome
A condition in which
increased pressure within
a limited space
compromises the
circulation and function
of the tissues within that
space.

Elevated tissue pressure

within a closed fascial
space
Reduces tissue perfusion
- ischemia
Results in cell death necrosis

True Orthopaedic Emergency

Compartment Syndrome
Etiology
Compartment Size
tight

dressing; Bandage/Cast
localised external pressure; lying on limb
Closure of fascial defects

Compartment Content
Bleeding;

Fx, vas inj, bleeding disorders

Capillary Permeability;

Ischemia / Trauma / Burns / Exercise / Snake Bite /

Drug Injection / IVF

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Compartment Syndrome
Etiology

Fractures-closed and
open
Blunt trauma
Temp vascular
occlusion
Cast/dressing
Closure of fascial
defects
Burns/electrical

Exertional states
IV/A-lines
Intraosseous IV(infant)
Snake bite
Arterial injury

Compartment Syndrome
Diagnosis

Pain out of proportion

Palpably tense compartment
Pain with passive stretch
Paresthesia/hypoesthesia
Paralysis
Pulselessness/pallor

Clinical Evaluation
Pain and the aggravation of pain by passive
stretching of the muscles in the compartment in
question are the most sensitive (and generally the
only) clinical finding before the onset of ischemic
dysfunction in the nerves and muscles.

Clinical Evaluation

Pain most important. Especially pain out of

proportion to the injury (child becoming more and
more restless /needing more analgesia)
Most reliable signs are pain on passive stretching
and pain on palpation of the involved compartment
Other features like pallor, pulselessness, paralysis,
paraesthesia etc. appear very late and we should
not wait for these things.

Willis &Rorabeck OCNA 1990

Compartment Syndrome
Pressure Measurements

Infusion

manometer

16

- 18 ga.
Needle
(5-19 mm Hg higher)
transducer
monitor

saline

3-way

stopcock
(Whitesides, CORR
1975)

Catheter
wick
slit

wick

Arterial line

Stryker device
Side

port needle

Compartment Syndrome
Emergent Treatment

Remove cast or dressing

Place at level of heart
(DO NOT ELEVATE to optimize perfusion)
Alert OR and Anesthesia
Bedside procedure
Medical treatment

Surgical Treatment

Fasciotomy

Casts and tight

bandages

remove

or
loosen any
constricting
bandages

All compartments !!!

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