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1
ACUTE BIOLOGIC CRISES (24 HOURS)
COURSE OUTLINE
1. High Risk Adult (8 hours)
A. Respiratory Disorders
i. Pulmonary Embolism
ii. Acute Respiratory Distress Syndrome (ARDS)
iii. Respiratory Failure
a. Acute RF
b. Chronic RF
iv. Mechanical Ventilators
B. Endocrine/ Metabolic Disorders
i. Diabetic Ketoacidosis (DKA)
ii. Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)
iii. Thyrotoxic Crisis (Thyroid Storm)
iv. Adrenal Crisis (Peochromocytoma)
v. Hepatic Failure (Hepatic Coma)
C. Renal Disorders
i. Renal Failure
a. Acute RF
b. Chronic RF
D. Cardiovascular Disorders
i. Angina Pectoris
ii. Myocardial Infarction
iii. Congestive Heart Failure
a. Right-sided CF
b. Left-sided CF
iv. Cardiogenic Shock
v. Thromboembolism
vi. Pericardial Effusion & Cardiac Tamponade
vii. Cardiac Arrest
viii. Dysrhythmias
a. Sinus Node
1. Sinus Bradycardia
2. Sinus Tachycardia
b. Atrial Dysrhythmias
1. Premature Atrial Complex (PAC)
2. Atrial Flutter
3. Atrial Fibrillation
c. Junctional Dysrhythmias
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
2
d. Ventricular Dsyrhythmias
1. Premature ventricular Complex
2. Ventricular Tachycardia
3. Ventricular Fibrillation
4. Ventricular Asystole
E. Burns
2.High Risk Pregnancy (12 Hours)
Part I.
A. Infections
i. STDsa. Cndidiasis
b. Trichomoniasis
c. Bacterial Vaginosis (Gardnerella)
d. Chlamydia Trachomatis
e. Syphilis
f. Gonorrhea
g. HPV
h. Group B Streptococci
i.
HIV
ii. TORCH infections
B. Hematologic Disorders
i. Anemias
a. Iron Deficiency
b. Folic Acid Deficiency
c. Sickle Cell
ii. Coagulation Disorders
a. Idiopathic Thrombocytopenic Purpura
C. Renal and Urinary Disorders
i. UTI
ii. Chronic Renal Disease
D. Respiratory Disorders
i. Acute Nasopharyngitis
ii. Influenza
iii. Pneumonia
iv. Asthma
v. Tuberculosis
vi. Cystic Fibrosis
NCM 104 1st sem S.Y. 2007-2008
3
E. Rheumatic Disorders
i. Juvenile Rheumatoid Arthritis
ii.Systemic Lupus Erythematosus (SLE)
F. Gastrointestinal Disorders
i. Appendicitis
ii. Hiatal Hernia
iii. Cholecystitis & Cholelithiasis
iv. Viral Hepatitis
v. Inflammatory Bowel Disease
G. Neurologic Disorders
i. Siezure
ii. Myasthenia Gravis
iii. Multiple Sclerosis
H. Musculoskeletal Disorders
i. Scoliosis
I. Cardiovascular Disorders
i. Left Sided Heart Failure
ii. Right Sided heart Failure
iii. Peripartal Heart Disease
iv. Artificial valve Prosthesis
v. Chronic hypertensive Vascular Disease
vi. Venous Thromboembolic Disease
J. Endocrine Disorders
i. Thyroid Dysfunction
a. Hypothyroidism
b. Hyperthyroidism
ii. Diabetes Mellitus
iii. Gestational Diabetes
iv. Hyperglycemia
K. Mental Illness
L. Trauma
i. Trauma Care
ii. Open wounds
iii. Battered woman
PART II. COMPLICATIONS OF PREGNANCY
A. Bleeding During Pregnancy
i.
First Trimester Bleeding
a. Abortion
NCM 104 1st sem S.Y. 2007-2008
4
1. Spontaneous
2. Threatened
3. Imminent
4. Complete
5. Incomplete
6. Missed
7. Recurrent
8. Complications of Abortionb. Ectopic pregnancy
ii.
Second Trimester Bleeding
a. Gestational Trophoblastic Disease (H. Mole)
b. Incompetent Cervix
iii.
Third Trimester Bleeding
a. Placenta Previa
b. Abruptio Placenta
iv.
Preterm labor
v.
Disseminated Intravascular Coagulation (DIC)
vi.
Preterm Rupture of Membrane (PROM)
vii.
Pregnancy Induced Hypertension (PIH)
a. Mild Preeclampsia
b. Severe Preeclampsia
c. Eclampsia
d. HELLP Syndrome
viii.
Multiple Pregnancy
ix.
Polyhydramnios
x.
Post term pregnancy
xi.
Psuedocyesis
xii.
Isoimmunization (RH Incompatibility)
xiii.
Fetal Death
3. High Risk Newborn (4 hours)
A. Part I
i. Small-for-Gestational-Age Infant ii. Large-for-Gestational-Age Infant iii. Pr
eterm Infant
iv. Post Term Infant
B. Part II: Illness of the Newborn
i. Respiratory Distress Syndrome
NCM 104 1st sem S.Y. 2007-2008
5
ii. Transient Tachypnea
iii. Meconium Aspiration Syndrome
iv. Apnea
v. Sudden Infant Death Syndrome (SIDS)
vi. Preventricular Leukomalacia (PVL)
vii. Hyperbilirubinemia
viii. Erythroblastosis Fetalis
a. RH incompatibility
b. ABO incompatibility
ix. Hemorrhagic Disease
x. Twin-to-twin Transfusion
xi. Necrotizing Enterocolitis
C. The Newborn at risk due to:
i. Maternal Infection
a. Group B Hemolytic Streptococcal Infection
b. Congenital Rubella
c. Ophthalmia Neonatorum
d. Hepatitis B
e. Generalized Herpes Virus
ii. Maternal Illness
a. Diabetic Mother
b. Drug Dependent Mother
c. Fetal Alcohol Syndrome (FAS)
NCM 104 1st sem S.Y. 2007-2008
6
ACUTE BIOLOGIC CRISES
HIGH RISK ADULT
RESPIRATORY DISORDERS
PULMONARY EMBOLISM
Occurs when a pulmonary embolus [thrombotic (blood clot) or nonthrombotic (fat)
emboli] lodges in the pulmonary artery system. This
blockage obstructs blood flow to the lung tissue supplied by the affected vessel
. Thrombotic emboli mainly originate from the deep veins of the legs, right vent
ricle of the heart, or pelvis. Nonthrombotic emboli mainly originate from fat re
lease after skeletal injuries, amniotic fluid, air, and foreign bodies.
The Virchow’s Triad
-three conditions and risk factors that can predispose a patient
or that can precipitate the formation of venous thrombi
Venous stasis
eg. atrial fibrillation, heart failure
immobility, polycythemia
pregnancy, varicose veins
Vessel wall injury
Coagulation problems
eg. infection, trauma
Pathophysiologic Changes
embolus
lodge in the pulmonary vasculature
Pulmonary embolism
decreased/nonperfusion of alveoli distal to occlusion
infarction of pulmonary vessel
impaired gas exchange
decreased C02
bronchoconstriction
shunting of blood to ventilated areas of the lungs
increased pulmonary resistance
hypoxia
release of mediators at the injury site
increased right ventricular workload
pulmonary vasoconstriction
right ventricular failure
pulmonary hypertension
left ventricular failure
decreased cardiac output
decreased blood pressure
shock
death
Clinical Manifestations
Shortness of breath and/or tachypnea- a response to the hypoxia that develops fr
om impaired gas exchange
Cough
Hemoptysis – occurs when an infaction at or near the periphery of the lung begin
s to hemorrhage
Chest pain – generally comes from an infarction of the pulmonary vessel near the
area in which the pleural nerves innervate. Usually
worsen when the patient takes a deep breath.
Tachycardia – a response to the decrease in oxygenation and impaired gas exchang
e
Jugular vein distention – a result of pulmonary hypertension and the decreased e
ffectiveness of the right ventricle
NCM 104 1st sem S.Y. 2007-2008
7
Hypotension – observed with large pulmonary embolism and is related to the decre
ase in cardiac output after ventricular dysfunction
Diagnosis
Chest radiograph – excludes other reasons that may cause the same clinical manif
estations. May show pulmonary artery distention, an
elevation of the diaphragm, and small infiltrates or pleural effusions.
ABG analysis – can reveal respiratory alkalosis, low partial pressure of oxygen,
and low partial pressure of carbon dioxide
Electrocardiogram – involve transient nonspecific ST segment and T wave changes
Management
The best treatment for pulmonary embolism is PREVENTION. When patients are at ri
sk for developing pulmonary embolism, prophylactic
measures should be instituted such as intravenous or subcutaneous heparin (Loven
ox) or oral anticoagulants such as warfarin (Coumadin). The
goal of therapy is to prevent thrombi formation, limit thrombi growth, and encou
rage breakdown of existing thrombi.
Management of hypoxia may require supplemental oxygen, intubation and mechanical
ventilation.
Heparin Therapy
-
started with a bolus (usually based on patient’s weight) and a continuous infusi
on adjusted every 4-6 hours, depending on the
institution’s protocol. Activated partial thromboplastin time (apt) should be ma
intained at 1.5-2.0 times the normal value.
-
generally continued for 7-14 days while the patient is on bedrest
-
reversal agent (antidote) is protamine sulfate
The reversal agent for warfarin (Coumadin) is vitamin K or fresh frozen plasma.
Surgical intervention is rarely used and is considered a last resort.Pulmonary e
mbolectomy is the removal of a clot from the larger vessel of the
pulmonary vasculature. This surgery carries a high risk of death and is only use
d in those patients who do not respond or have contraindications to
other interventions.
Nursing Responsibilities
The main nursing goal is to prevent the development of deep venous thrombosis (D
VT) that may lead to a thrombotic pulmonary embolism.
Interventions should include early ambulation, use of pneumatic stockings, suppo
rt hose, and passive range-of-motion exercises. All of these
improve venous blood flow and increase circulation.
Other nursing interventions include the following:
Signs and symptoms of DVT are monitored in the lower extremities (calf pain or t
enderness, redness, swelling, warmth, pain on
dorsiflexion of foot [Homan’s sign]). If Homan’s sign is positive, DO NOT retest
it; doing so may dislodge the clot.
Prescribed oxygen therapy is maintained, and the patient is asked to cough and d
eep breath every 2 hours
Signs and symptoms of respiratory distress or a worsening of pulmonary status (h
eart failure, pulmonary edema) are monitored, and the
physician is notified of any developments.
ABG analysis is monitored and pulse oximetry is continuously taken
Patient is positioned for comfort and maximal oxygenation, as well as to promote
the expulsion of secretions.
Signs and symptoms of bleeding are monitored when anticoagulant or thrombolytic
therapy is in progress. (eg. blood in stool or urine,
pale mucous membranes, petechiae, echymosis, complaints of back or flank pain).
ACUTE RESPIRATORY DISTRESS SYNDROME
A clinical syndrome characterized by a sudden and progressive pulmonary edema,
increasing bilateral infiltrates, hypoxemia refractory to
oxygen supplementation and reduced lung compliance
A syndrome with inflammation and increased permeability of the alveollocapillar
y membrane that occurs as a result of an injury to the lungs.
This inflammation causes noncardiogenic pulmonary edema with severely impaired g
as exchange.
Etiologic Factors Related to ARDS :
1. Aspiration (gastric secretions, drowning, hydrocarbons)
2. Drug ingestion and overdose
3. Hematologic disorders
4. Prolonged inhalation of high concentrations of oxygen, smoke, or corrosive su
bstances
5. Localized infection (bacterial, fungal, viral pneumonia)
6. Metabolic disorders ( pancreatitis, uremia)
7. Shock (any cause)
8. Trauma ( pulmonary contusion, multiple fractures, head injury)
9. Fat or air embolism
10. Systemic sepsis
Pathophysiology
lung injury
immune system initiates an inflammatory response
activation of neutrophils, macrophages, and endotoxins into the lungs
and the release of mediators
increased alveolomembrane permeability
fluid enters into the lung tissue
Acute Respiratory Distress Syndrome
alveolar collapse
narrowing of airways
pulmonary vasoconstriction
hypoxia
pulmonary hypertension
hyperventilation
right ventricular dysfunction
NCM 104 1st sem S.Y. 2007-2008
8
respiratory failure
decreased cardiac output
Clinical Manifestations:
1. Rapid onset of severe dyspnea
2. Anxiety
3. Labored breathing and tachypnea
Assessment: Intercostal retractions and crackles
In patients with ARDS, PaO2 will be low, despite oxygen administration, pCO2 wil
l decrease as a result of hyperventilation.
Medical Management: The main goals in the treatment of ARDS include improving an
d maintaining oxygenation, maintaining fluid and electrolyte
imbalances, providing adequate nitrition, and preventing respiratory and metabol
ic complications.
1. Primary focus of management includes identification and treatment of the cond
ition.
2. Supportive Therapy: Intubation and mechanical ventilation to maintain adequat
e gas exchange
3. Circulatory support, adequate fluid volume and nutritional support. Fluid res
triction is generally observed to prevent further leakage of fluid into
the alveoli and to decrease pulmonary edema, but fluid restriction can also caus
e a decrease in cardiac output and blood pressure.
4. Supplemental oxygen is used as the patient begins the initial spiral of hypox
emia. Oxygen toxicity may develop if high concentrations of oxygen
are used for longer than 24-48 hours.
5. Positive end-expiratory pressure (PEEP)- generally leads to improved gas exch
ange and allows for lower concentrations of oxygen to be used
6. Hypovolemia must be carefully treated
7. Intravenous crystalloid solutions are administered
8. Pulmonary artery pressure catheters are used to monitor patients fluid status
Nursing Management:
1. Positioning is important. Nurse should turn the patient frequently to improve
ventilation and perfusion in the lungs and enhance secretion
drainage.Prone positioning is an intervention that may improve oxygenation by de
creasing edema and atelectasis, thereby providing an
improved distribution of oxygen throughout the lungs.
2. Nurse must closely monitor rapid changes in oxygenation with changes in posit
ion
3. The nurse should explain all procedures and deliver care in a calm, reassurin
g manner
4. Rest is essential to reduce oxygen consumption
Nursing Diagnosis: Impaired gas exchange r/t inadequate respiratory center activ
ity, chest wall movement, airway obstruction, fluids in the lungs
RESPIRATORY FAILURE
Respiratory failure is a sudden and life-threatening deterioration of the gas e
xchange function of the lung.
Exists when the exchange of oxygen for carbon dioxide in the lungs can not keep
up with the rate of oxygen consumption and carbon dioxide
production by the cells of the body.
ACUTE RESPIRATORY FAILURE (ARF)
Defined as a fall in arterial oxygen tension and a rise in arterial carbon diox
ide tension.
The ventilation and/or perfusion mechanisms in the lung are impaired.
Respiratory system mechanisms leading to ARF include:
1. Alveolar hypoventilation
2. Diffusion abnormalities
3. Ventilation-perfusion mismatching
4. Shunting
Pathophysiology:
Common Causes of Acute Respiratory Failure:
Decreased Respiratory Drive
May occur with severe brain injury, large lesions of the brain stem (multiple s
clerosis), use of sedative medications, and metabolic disorders
such as hyperthyroidism. This disorders impair the normal response of chemorecep
tors in the brain to normal respiratory stimulation
Dysfunction Of The Chest Wall
The impulses arising in the respiratory center travel through nerves that exten
d from the brain stem down the spinal cord to receptors in the
muscles of respiration. Thus, any disease of the nerves, spinal cord, muscles or
neuromuscular junction involved in respiration seriously
affects ventilation and may lead to ARF
Dysfunction Of Lung Parenchyma
Pleural effusion, hemothorax, pneumothorax, and upper airway obstruction are co
nditions that interfere with ventilation by preventing
expansion of the lung. These conditions, which may cause respiratory failure, us
ually are produced by an underlying lung disease, pleural
disease, trauma and injury.
Other diseases and conditions of the lung that lead to ARF include pneumonia, s
tatus asthmaticus, lobar atelectasis, pulmonary embolism and
pulmonary edema
Other Factors
In the postoperative period, esp. after major thoracic or abdominal surgery, in
adequate ventilation and respiratory failure may occur. Causes of
ARF during this period include the effects of anesthetic agents, analgesics, and
sedatives; they may depress respiration and lead to
hypoventilation
Early signs are those associated with impaired oxygenation
Restlessness, fatigue, headache, dyspnea, air hunger, tachycardia, tachypnea, c
entral cyanosis, diaphoresis and finally, respiratory arrest
Physical findings: use of accessory muscles, decreased breath sounds
Medical Management:
Objectives of treatment are to correct the underlying cause and to restore adeq
uate gas exchange in the lung
Intubation and mechanical ventilation
Nursing Management:
Assist with intubation
Assess respiratory status by monitoring patient’s level of response, arterial b
lood gases, pulse oximetry and vital signs
Implement strategies to prevent complications: turning schedule, mouth care, sk
in care, ROM
CHRONIC RESPIRATORY FAILURE
Defined as a deterioration in the gas exchange function of the lung that has de
veloped insidiously or has persisted for a long period after an
episode of ARF
NCM 104 1st sem S.Y. 2007-2008
9
Patients develop a tolerance to the worsening hypoxemia and hypercapnia
Patient with chronic respiratory failure may develop Acute respiratory failure
– seen in COPD patients who develops an exacerbation or
infection that causes additional deterioration of the gas exchange mechanism
2 Causes of Chronic Respiratory Failure:
1. COPD
2. Neuromuscular Diseases
What is Mechanical Ventilation?
Mechanical ventilation is a form of artificial ventilation that takes over all o
r part of the work performed by the respiratory muscles and organs. It is initia
ted when the patient’s ability to oxygenate and exchange carbon dioxide is impai
red. Mechanical ventilation may be indicated for the following reasons:•
Hypoxemia
•
Respiratory Distress
•
Atelectasis
•
To reduce intracranial pressure
•
Aspiration
•
Pulmonary Edema
•
Pulmonary Embolism
•
To stabilize the chest wall
•
Respiratory Muscle Fatigue
•
Acute Respiratory Distress
Syndrome
•
Over sedation
The main goal of mechanical ventilation is to support gas exchange until the dis
ease process or condition is resolved.
Positive –pressure ventilation is the most common form of mechanical ventilation
used in the acute care setting. This form of ventilation forces
oxygen into the lungs, either through an endotracheal tube or a tracheostomy tub
e, mimicking respiration.
Modes of Ventilation
There are various modes of ventilation that may be used to ventilate and oxygena
te the patient. Essentially, these modes are ways in which
ventilation is triggered; they allow the patient some or all control over his or
her breathing.
1.Controlled ventilation (CV) delivers a preset volume or pressure at a preset r
ate. This mode takes away all control of breathing from
the patient; it is primarily used for patients who have no respiratory effort at
all.
2.Assist-control ventilation (ACV) delivers a preset volume or pressure whenever
the patient initiates a breath. If the patient does not
initiate a breath by a preset time, the ventilator will give one. This mode is u
sed primarily for the patient with normal breathing but who
has weak respiratory muscles or who cannot achieve an adequate volume on his or
her own.
3.Synchronized intermittent mandatory ventilation (SIMV) delivers a preset volum
e at a preset rate and is synchronized with patient’s
effort. This mode allows for spontaneous breathing between ventilated breaths an
d prevents competition between the patient and the ventilator. When a spontaneou
s breath occurs, it is at the patient’s own rate and tidal volume. SIMV is the m
ost common mode used and allows for weaning from the ventilator.
4.Pressure-controlled ventiation (PCV) delivers a positive pressure breath until
a maximum amount of pressure is reached; then the
breath stops. The maximum pressure limit is preset and helps prevent barotraumas
(damage from the pressure) to the lungs. The
amount of volume that is delivered varies, based on airway resistance and lung c
ompliance. Usually the maximal pressure limit is set to
achieve a goal tidal volume that is designed by the physician.
5.Inverse-ratio ventilation (IRV) is used when the inspiratory time is increased
and the expiratory time is decreased. With IRV the
inspiration-expiration (I/E) ratios used most are 1:1 and 2:1. This mode of vent
ilation allows for a longer period for gas exchange to
improve oxygenation. This mode is generally used in patients with ARDS. This typ
e of ventilatory mode creates an abnormal breathing
pattern for the patient; consequently the patient may become uncomfortable and a
nxious.
6.Constant positive airway pressure (CPAP) provided positive pressure during spo
ntaneous breaths; the ventilator will not initiate any
breaths. This mode increases oxygenation by opening any closed alveoli that may
occur at end-expiration. CPAP generally ranges from 5-10 cm water pressure. Grea
ter than 10 cm water pressure may increase intrathoracic pressure to the point t
hat it affects the patient’s venous return, decreasing cardiac output and blood
pressure. CPAP at this level may also cause a pneumothorax to occur
7.Positive end-expiratory pressure (PEEP) adds positive pressure during expirati
on of each ventilated breath.
Ventilator settings must be individualized to each patient to allow for optimal
gas exchange. Settings are generally based on arterial blood gas
(ABG) measurements and arterial oxygen saturation level.
NCM 104 1st sem S.Y. 2007-2008
10
Ventilator Setting
Description
Ranges
VT (Tidal Volume)
Amount of oxygen delivered to patient
with each preset ventilated breath
5-15 ml/kg (average 10ml/kg)
Respiratory rate
Number of breaths per minute that
ventilator is set to deliver
4-20 breaths/min
FiO2 (Fraction of Inspired Oxygen)
Percentage of oxygen delivered by
ventilator with each breath
21%-100%
I/E Ratio ( inspiratory to expiratory)
Duration of I/E time
1:2 (unless IRV is used)
Sensitivity
Determines amount of effort patient
must generate before ventilator will
give a breath
Too low – patient will have to work
harder to obtain a breath
Too high – patient may fight ventilator
Flow rate
Determines how fast VT will be
delivered during inspiration
High – increase airway pressure
Low – decrease airway pressure
Pressure limits
Regulates maximum amount of
pressure the ventilator will generate to
deliver preset VT
Ventilated breath is stopped when
pressure limit is reached
Barotrauma occurs when high airway pressures cause overdistention of the alveoli
, rupture and leakage of air. Barotrauma can cause
pneumothorax, subcutaneous emphysema, or crepitus. Air can leak under the medias
tinum or into the pericardium or peritoneum, causing
problems with organs located in these areas.
A patient needing long-term ventilatory management will need a tracheostomy plac
ed at some point. Endotracheal tubes (oral or nasal) are not intended for long-t
erm management and may lead to other problems such as mucosal breakdown, skin ul
cerations (lips), sinusitis, and vocal cord paralysis or damage (or both).
The following are practices performed for patients receiving mechanical ventilat
ion.
•
The respiratory status is assessed every 4 hours and more frequently when a chan
ge in condition occurs. Close attention is paid to
breathing sounds and the amount of patient effort.
•
Signs of hypoxia are assessed. These signs include restlessness, anxiety, increa
sed heart rate and blood pressure, increased
respiratory rate, and oxygen saturation via pulse oximetry less than 90%.
•
Endotracheal or tracheostomy tube placement is maintained by properly securing t
he tube and preventing inadvertent extubation by staff
or patient. Placement is maintained until extubation.
•
The endotracheal tube is repositioned per institutional policy to prevent pressu
re sores.
•
Secretions are suctioned to maintain an open airway. Amount, color, and consiste
ncy of the secretions are noted, as well as how the
patient tolerated the procedure.
•
Ventilator settings and alarms are verified once a shift or when any changes occ
ur.
•
Continuous pulse oximetry and ABGs are monitored for assessing the oxygenation s
tatus; the physician is notified of any changes in
parameters.
•
The patient is frequently positioned to allow for optimal ventilation, to preven
t complications, to mobilize secretions, and to promote
comfort.
•
Ventilator circuit is monitored for moisture or water trapping in tubing and emp
tied when necessary. Moisture may impede the flow of
oxygen and may provide a medium for bacterial growth.
•
A functioning manual resuscitation bag is maintained at bedside at all times in
case of malfunctioning equipment.
•
The patient is medicated as needed to decrease anxiety and facilitate oxygenatio
n.
•
Alternative methods of communication are provided for patients to decrease anxie
ty and maintain some control over their environment.
•
Mouth and lip care is provided at least once very shift to keep mucous membranes
moist.
NCM 104 1st sem S.Y. 2007-2008
11
ENDOCRINE/METABOLIC DISORDERS
DIABETIC KETOACIDOSIS
DKA is caused by an absence or markedly inadequate amount of insulin. First, be
cause the beta cells in the pancreas have the inability to
produce insulin, the ensuing hyperglycemia causes a hyperosmolar state. This hyp
erosmolarity results in fluid shifting from inside the cell to the serum; eventu
ally this fluid is lost in the urine, causing electrolyte shifts and total body
dehydration. Other metabolic derangements occur because no insulin exists to all
ow glucose to enter the cells; therefore cells begin to break down fats and prot
eins to use for fuel. This process causes the formation of ketones. Ketones decr
ease the blood pH and the bicarbonate concentration causing a ketosis. DKA is on
e of the more serious metabolic crises that can result from hyperglycemia in pat
ients with uncontrolled diabetes mellitus.
Three Main Clinical Features of DKA:
1. Hyperglycemia
2. Dehydration and electrolyte loss
3. Acidosis
Three Main Causes of DKA:
1. Decreased or missed dose of insulin
2. Illness or infection
3. Undiagnosed and untreated diabetes
1. Acetone breath
2. Poor appetite or anorexia
3. Nausea and vomiting
4. Abdominal pain
5. Blurred vision
6. Weakness
7. Headache
8. Dehydration
9. Thirst or polydipsia
10. Orthostatic hypotension
11. Hyperventilation (Kussmaul respirations)
12. Mental status changes in DKA vary from patient to patient
Assessment and Diagnostic Findings :
1. Blood glucose levels may vary from300 to 800 mg/dl
2. The severity of DKA is not necessarily related to the blood glucose level
3. Evidence of DKA is reflected in low serum bicarbonate and low pH values
Prevention :
1. Patients must be taught “sick day “rules for maintaining their diabetes when
ill.
2. The most important issue is not to eliminate insulin doses when nausea and vo
miting occur and then attempt to consume frequent small portions
of carbohydrates
3. Drinking fluids every hour is important to prevent dehydration
4. Patients are taught to have available foods for use on sick days.
5. Supply of urine test strips and blood glucose test strips should be available
. Patients must know how to contact their physician
Medical Management :
1. Rehydration is important for maintaining tissue perfusion and enhancing the e
xcretion of excessive glucose by the kidneys
2. The major electrolyte of concern during treatment of DKA is potassium. Potass
ium replacement is vital to avoid dysrhythmias that may occur with
hypokalemia
3. Insulin is usually infused IV at a slow, continuous rate
4. Dextrose is added to IVF, such as normal saline solution when blood glucose l
evel reach 250 to 300 mg/dl to avoid too rapid drop in the blood
glucose level
Nursing Management :
1. Nursing care focuses on monitoring fluid and electrolyte status, blood glucos
e levels, administering fluids, insulin and other medications and
preventing complications such as fluid overload.
2. Urine output is monitored to ensure adequate renal function
3. ECG is monitored for dysrhythmias
4. VS, arterial blood gases and other clinical findings are recorded on a flow s
heet
HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC COMA
Background: Hyperosmolar hyperglycemic nonketotic coma (HHNC) is a metabolic der
angement that occurs principally in patients with adult-
onset diabetes. The condition is characterized by hyperglycemia, hyperosmolarity
, and an absence of significant ketosis.
Despite the name, coma is present in fewer than 10% of cases. Most patients pres
ent with severe dehydration and focal or global neurologic
deficits. In many cases, the clinical features of HHNC and diabetic ketoacidosis
(DKA) overlap and are observed simultaneously.
Pathophysiology: HHNC most commonly develops in patients with diabetes who have
some concomitant illness that leads to a reduced fluid
intake. Infection is the most common cause, but many other conditions can cause
altered mentation and/or dehydration. Frequently, this
concomitant illness is not identifiable.
Hyperglycemia and hyperosmolarity lead to osmotic diuresis and an osmotic shift
of fluid to the intravascular space, resulting in further intracellular
dehydration.
Unlike patients with DKA, patients with HHNC do not develop ketoacidosis, but th
e reason for this is not known. Contributing factors include the limitation on k
etogenesis by hyperosmolarity, the lower levels of free fatty acids available fo
r ketogenesis, the availability of insulin in amounts sufficient to inhibit keto
genesis but not sufficient to prevent hyperglycemia, and the hepatic resistance
to glucagon in these patients.
Management: refer to DKA
THYROTOXIC CRISIS (THYROID STORM)
A severe form of hyperthyroidism marked by sudden release of thyroid hormone in
to the blood stream
Precipitating Factors :
1. Stress such as injury, infection, thyroidal and non-thyroid surgery, tooth ex
traction, insulin reaction, diabetic acidosis, pregnancy, digitalis
NCM 104 1st sem S.Y. 2007-2008
12
intoxication, abrupt withdrawal of anti-thyroid medications, extreme emotional s
tress, or vigorous palpation of the thyroid.
Clinical Manifestations :
1. High fever
2. Diaphoresis
3. Cardiopulmonary symptoms : extreme tachycardia, HPN, arrhythmias, CHF, pulmon
ary edema
4. CNS symptoms : increasing feeling of tremulousness to severe agitation, psych
osis with developing apathy, irritability, coma , heat intolerance
5. GI disturbance : weight loss, diarrhea, abdominal pain
6. Increased T3T4 and elevated BUN
Medical Management:
1. Immediate objectives are to reduced body temperature and heart rate and to pr
event vascular collapse
2. Humidified oxygen is administered to improve tissue oxygenation and meet meta
bolic demands
3. Monitor respiratory status by arterial blood gas or pulse oximetry
4. PTU or methimazole is administered to impede formation of thyroid hormone and
block conversion of T4 to T3, the more active form of thyroid
hormone
5. Hydrocortisone is prescribed to treat shock or adrenal insufficiency.
6. Iodine is administered to decrease output of T4 from the thyroid gland
7. For cardiac problems, Sympatholytic agents may be administered. Propranolol i
n combination with digitalis, has been effective in reducing
severe cardiac problems
ADRENAL CRISIS
Pheochromocytoma
A tumor that originates from the chromaffin cells of the adrenal medulla
Peak incidence is between ages 20 and 50 years old
The cause of high BP in 0.9% to 2.2% of patients with HPN
One form of HPN that is usually cured by surgery
Typical triad of symptoms: Headache, Diaphoresis, Palpitations
HPN may be intermittent or persistent
Tremor, flushing and anxiety
Hyperglycemia may result from conversion of liver and muscle glycogen to glucos
e
Clinical picture is usually characterized by:
1. Acute, unpredictable attacks, lasting seconds or several hours
2. Patient is anxious, tremulous and weak
3. Headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea
4. Polyuria, nausea, vomiting, diarrhea, abdominal pain
5. Feeling of impending doom
6. Palpitations and tachycardia
7. BP as high as 350/200 mm Hg
Assessment/Diagnostic Findings:
Signs of sympathetic nervous system over activity: 5 H’s (HPN, headache, hyperh
idorsis (excessive sweating), hypermetabolism, and
hyperglycemia)
Medical Management:
Pharmacologic Therapy
Close monitoring of ECG changes and careful administration of alpha-adrenergic
blocking agents, muscle relaxants – to lower BP quickly
Long-acting alpha blocker to prepare patient for surgery
Beta-adrenergic blocking agents for patients with cardiac dysrhythmias
Surgical Management:
Adrenalectomy- surgical removal of the tumor
HEPATIC FAILURE (Hepatic Coma)
An end stage of liver disease, usually arises as a complication of conditions t
hat cause liver dysfunction although it can be idiopathic
Also called Hepatic coma because the patient’s neurologic status gradually dete
riorates
Represents the most advanced stage of hepatic encephalopathy
A life threatening crisis may occur if the serum ammonia level rises, causing c
erebral ammonia intoxication
Causes:
1. Cirrhosis
2. Hepatitis
3. Drug or toxin-induced damage
4. Fatty liver
5. Portal HPN
6. Surgically-created portal systemic shunts that bypass the liver and allow tox
ins into the blood
Pathophysiology:
Liver disease alters liver structure and compromises essential functions. This l
eads to impaired protein, fat and carbohydrate metabolism, fluid and
electrolyte imbalance, poor lymphatic drainage, reduced coagulation and impaired
detoxification of ammonia and of the metabolites. Ammonia
accumulation and intoxication is the primary pathogenesis of hepatic failure and
the ensuing encephalopathy. Ammonia accumulates because liver
cells cannot detoxify and convert to urea the ammonia that is in constant supply
in GI tract blood. Remaining liver functions may become impaired
and may be difficult to treat or control. Hepatic failure may progress insidious
ly to a comatose state from which the patient rarely recovers.
Clinical Findings:
Stage 1
Slight personality and mood changes, disorientation, forgetfulness, slurred spe
ech, slight tremors, periods of lethargy and euphoria, mild
confusion, inability to concentrate, hyperactive reflexes, sleep-wake patterns,
handwriting starts to decline and mild asterixis (flapping tremors
of the hand) may appear
Stage 2
The patient grows more disoriented and drowsy. He may display inappropriate beh
avior, mood swings, agitation, apraxia. His hand writing
becomes illegible and asterixes may become pronounced
Stage 3
The patient becomes severely confused and may become combative, incoherent and
hard to arouse. Sleeps most of the time. You may detect
hyperactive deep tendon reflexes and rigid extremities
Stage 4
NCM 104 1st sem S.Y. 2007-2008
13
The pupil is comatose and does not react to stimuli. Pupils are dilated and lac
k corneal and deep tendon reflexes. Extremities are flaccid and
may assume flexion or extension posturing, decebrate rigidity. The EEG is marked
ly abnormal.
Assessment and Diagnostic Findings:
1. Elevated arterial ammonia blood levels
2. The encephalogram shows generalized slowing and an increase in amplitude of b
rain waves and the appearance of characteristic triphasic
waves
3. Occasionally, fetor hepaticus, a characteristic breath odor like freshly mowe
d grass, acetone, or old wine, may be noticed.
4. In a more advanced stage, there are gross disturbances of consciousness and t
he patient is completely disoriented with respect to time and
place
5. With further progression of the disorder, the patient lapses into frank coma
and may have seizures.
Intervention:
1. Anti-infective agents – to decrease bacterial action in the colon.
2. Ammonia detoxicants – to reduce ammonia. Lactulose (Duphulac) is administered
3. Cleansing enemas with diluted acetic acid or neomycin
4. Discontinuation of any precipitating substance: Dietary proteins, sedatives,
diuretic therapy, analgesics
5. IV administration of glucose to minimize protein breakdown
6. Oxygen administration
7. Correction of any electrolyte imbalance
8. Promote rest, comfort and quiet environment
Nursing Diagnosis:
1. Altered thought process
2. Potential impaired skin integrity
3. Impaired skin integrity
RENAL DISORDER
RENAL FAILURE
Renal Failure is a systemic disease and is a final common pathway of many diffe
rent kidney and urinary tract diseases.
Results when the kidneys are unable to remove the body’s metabolic wastes or pe
rform their regulatory functions
The substances normally eliminated in the urine accumulate in the body fluids a
s a result of impaired renal excretion and lead to a disruption
in endocrine and metabolic functions and fluid and electrolyte, an acid-base dis
turbances.
ACUTE RENAL FAILURE
Acute renal failure is a sudden and almost complete loss of kidney function ove
r a period of hours to days.
Categories of Acute Renal Failure:
1. Prerenal Condition (hypoperfusion of kidney). Occurs as a result of impaired
blood flow that leads to hypoperfusion of the kidney and a drop
in the GFR. Common clinical situations are volume-depletion states (hemorrhage o
r gastrointestinal losses), impaired cardiac performance and
vasodilation (sepsis or anaphylaxis)
2. Intrarenal. Intrarenal causes of acute renal failure are the result of actual
parenchymal damage to the glomeruli or kidney tubules. Conditions
such as burns crush injuries, and infections, as well as nephrotoxic agents, may
lead to acute tubular necrosis and cessation of renal function. Severe transfus
ion reaction may also cause intrarenal failure. Medications may also predispose
a patient to intrarenal damage, esp. nonsteroidal anti-inflammatory drugs and AC
E inhibitors
3. Post renal conditions. Postrenal causes of acute renal failure are usually th
e result of an obstruction somewhere distal to the kidney.
PHASES OF ACUTE RENAL FAILURE:
1. Initiation period – begins with the initial insult and ends when oliguria dev
elops.
2. Period of Oliguria – accompanied by a rise in the serum concentration of subs
tances usually excreted by the kidney (urea, creatinine, uric acid,
organic acids and the intracellular cations – potassium and magnesium
3. Period of diuresis – The patient experiences a gradual increase in urinary ou
tput, which signals that glomerular filtration has started to recover.
Laboratory values start rising and eventually begin a downward trend.Uremic symp
toms may still be present. The patient must be closely monitored
for dehydration during this phase; if dehydration occurs, the uremic symptoms ar
e likely to increase.
4. Period of Recovery – signals the improvement of renal function. Laboratory va
lues return to the patient’s normal level.
1. May appear critically ill and lethargic
2. Persistent nausea, vomiting and diarrhea
3. The skin and mucous membranes are dry due to dehydration
4. Uremic fetor – breath have the odor of urine
5. CNS manifestations: drowsiness, headache, muscle twitching, and seizures
1. Changes in urine. The urinary output varies (from scanty to normal volume). H
ematuria may be present and urine has low-specific gravity.
Patients with prerenal azotemia have a decreased amount of sodium. Those patient
s with intrarenal azotemia usually have urinary sodium levels
greater than 40 mEq/L.
2. Increased blood urea nitrogen and creatinine levels (Azotemia)
3. Hyperkalemia
4. Metabolic acidosis
5. Calcium and Phosphorus Abnormalities
6. Anemia – due to reduced erythropoietin production, uremic gastrointestinal le
sions, reduced Rbc lifespan, and blood loss
Prevention:
1. Renal function must be monitored closely if patient has been taking nephrotox
ic antibiotic agents or has been exposed to environmental toxins.
Blood should be drawn for determining baseline and monitoring serum BUN and crea
tinine levels by 24 hours after initiation of medication therapy
Medical Management:
1. Prerenal azotemia is treated by optimizing renal perfusion.
2. Postrenal failure is treated by relieving the obstruction
3. Overall, medical management includes maintaining fluid balance, avoiding flui
d excesses, or performing dialysis
4. The elevated potassium levels may be reduced by administering ion-exchange re
sins (sodium polystyrene sulfonate “kayexalate”)
5. Diuretics are used for management of volume status
6. Low-dose dopamine is often used to dilate the renal arteries
NCM 104 1st sem S.Y. 2007-2008
14
7. Atrial natriuretic peptide – inhibits sodium and water absorption and dilates
the afferent arteriole, thus improving blood flow to the glomerulus
8. Correction of acidosis and elevated phosphate levels. When severe acidosis is
present, the arterial blood gases or serum bicarbonate levels
must be monitored because patient may require sodium bicarbonate therapy or dial
ysis. Patient’s elevated phosphate level may be controlled with
phophate-binding agents (aluminum hydroxide).
9. Nutritional Therapy. Dietary proteins are limited to about 1 g/kg during the
oliguric phase. High-carbohydrate meals to meet caloric requirements.
Foods and fluids containing potassium and phosphorus are restricted.
Nursing Management:
1. Monitoring fluid and electrolyte balance. Hyperkalemia is the most immediate
life-threatening imbalance seen in acute renal failure.
2. Reducing metabolic rate. To reduce catabolism and the subsequent release of p
otassium and accumulation of endogenous waste products. Bed
rest is indicated and fever and infection are prevented or treated promptly.
3. Promoting pulmonary function. Patient is assisted to turn, cough and take dee
p breaths frequently to prevent atelectasis and respiratory
infection.
4. Preventing Infection. Asepsis is essential with invasive lines and catheters
5. Providing skin care. Meticulous skin care is important. Massaging bony promin
ences, turning the patient frequently, and bathing the patient with
cool water are comforting and prevent skin breakdown
6. Providing support. The patient and family will need assistance, explanation a
nd support during this time.
CHRONIC RENAL FAILURE
CRF is a progressive, irreversible deterioration in renal function in which the
body’s ability to maintain metabolic and fluid and electrolyte
balance fails, resulting in uremia or azotemia (retention of urea and other nitr
ogenous wastes in the blood)
Pathophysiology:
As renal function declines, the end products of protein metabolism (which are no
rmally excreted in urine) accumulate in the blood. Uremia develops
and adversely affects every system in the body.
4 Stages of Chronic Renal Disease:
Stage 1
Reduced renal reserve. Characterized by a 40 to 75% loss of nephron function. Th
e patient usually does not have symptoms because the
remaining nephrons are able to carry out the normal functions of the kidney.
Stage 2
Renal Insufficiency. Occurs when 75 to 90% of nephron function is lost. At this
point, the serum creatinine and blood urea nitrogen rise, the kidney
loses its ability to concentrate urine and anemia develops. The patient may repo
rt polyuria and nocturia.
Stage 3
Renal Disease. Edema, metabolic acidosis, and hypocalcemia occur. Patient may ex
hibit overt uremia with cardiovascular, gastrointestinal, and
neurologic complications.
Stage 4
End-stage renal Disease (ESRD). The final stage of CRF occurs when there is less
than 10% nephron function remaining. All of the normal
regulatory, excretory, and hormonal functions of the kidney are severely impaire
d. ESRD is evidenced by elevated creatinine and blood urea
nitrogen levels as well as electrolyte imbalances. Once the patient reaches this
point, dialysis is usually indicated.
Signs And Symptoms Of CRF:
1. Neurologic
Weakness and fatigue; confusion; inability to concentrate; disorientation; trem
ors; seizures; asterixis; restlessness of legs; burning of soles of
feet; behavior changes.
2. Integumentary
Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis; purpura; thin, b
rittle nails; coarse, thinning hair
3. Cardiovascular
HPN; pitting edema (feet , hands, sacrum), periorbital edema; pericardial frict
ion rub; engorged neck veins; pericarditis; pericardial effusion;
pericardial tamponade; hyperkalemia; hyperlipidemia
4. Pulmonary
Crackles; thick, tenacious sputum; depressed cough reflex; pleuritic pain; shor
tness of breath; tachypnea; kussmaul-type respirations; uremic
pneumonitis; “ uremic lung
5. Gastrointestinal
Ammonia odor to breath (uremic fetor); metallic taste; mouth ulcerations and bl
eeding; anorexia; nausea and vomiting; hiccups; constipation
or diarrhea; bleeding from GIT
6. Hematologic
Anemia; thrombocytopenia
7. Reproductive
Amenorrhea; testicular atrophy; infertility; decreased libido
8. Musculoskeletal
Muscle cramps; loss of muscle strength; renal osteodystrophy; bone pain; bone f
ractures; foot drop
Assessment And Diagnostic Findings:
•
Glomerular Filtration Rate. Decreased GFR can be detected by obtaining a 24-hour
urine analysis for creatinine clearance. As GFR
decreases, the creatinine clearance value decreases, whereas the serum creatinin
e and BUN levels increase.
•
Sodium and Water Retention. The kidney is unable to concentrate or dilute the ur
ine normally in ESRD. Some patients retain sodium and
water, increasing the risk for edema, CHF, and HPN.
•
Acidosis. With advanced renal disease, metabolic acidosis occurs because the kid
ney is unable to excrete increased loads of acid.
•
Anemia. Anemia develops as a result of inadequate erythoropoietin production, th
e shortened life span of RBC’s, nutritional deficiencies, and
the patient’s tendency to bleed, particularly from GIT
•
Calcium and Phosphorus Imbalance. The body’s serum calcium and phosphate levels
have a reciprocal relationship in the body; as one rises,
the other decreases.
Complications:
1. Hyperkalemia. Due to decreased excretion, metabolic acidosis, catabolism, and
excessive intake (diet, medications, fluids)
2. Pericarditis. Due to retention of uremic waste products and inadequate analys
is
3. Hypertension. Due to sodium and water retention and malfunction of the rennin
-angiotensin-aldosterone system
4. Anemia. Due to decrease erythropoietin, decreased RBC life span, GIT bleeding
and blood loss during dialysis.
5. Bone disease and metastatic calcifications. Due to retention of phosphorus, l
ow serum calcium levels, abnormal vitamin D metabolism, and
elevated aluminum levels
Medical Management:
1. Pharmacologic Therapy
Antacids. Hyperphosphatemia and hypocalcemia are treated with aluminum based ant
acids that bind dietary phophorus in the GIT
NCM 104 1st sem S.Y. 2007-2008
15
Antihypertensive and Cardiovascular agents. HPN is managed by intravascular cont

rol and a variety of hypertensive medications. CHF and pulmonary edema may requi
re treatment with fluid restriction, low sodium diets, diuretics, inotropic agen
ts such as digitalis, or dobutamine, and dialysis.
Anticonvulsants. If seizures occurs. The onset of seizure is recorded along with
the type, duration and general effect on the patient.
Intravenous Diazepam or phenytoin is usually administered to control seizures. T
he side rails must be padded to protect the patient
Erythropoietin. Anemia associated with CRF is treated with recombinant human ery
thropoietin (Epogen)
2. Nutritional Therapy
> Includes careful regulation of protein intake, fluid intake to balance fluid l
osses, sodium intake to balance sodium losses and some restriction of
potassium
3. Dialysis
> Hyperkalemia is usually prevented by ensuring adequate dialysis treatments wit
h potassium removal and careful monitoring of all medications for
their potassium intake
Nursing Management
Nursing Diagnoses:
1. Fluid volume excess r/t decreased urine output, dietary excesses, and retenti
on of sodium and water
2. Altered nutrition; less than body requirements r/t anorexia, nausea and vomit
ing, dietary restrictions, and altered oral mucous membranes
3. Knowledge deficit regarding condition and treatment regimen
4. Activity intolerance r/t fatigue, anemia, retention of waste products, and di
alysis procedure
5. Self-esteem disturbance r/t dependency, role changes, changes in body image,
and sexual dysfunction
Nursing Care:
1. Directed toward assessing fluid status and identifying potential sources of i
mbalance
2. Implementing a dietary program to ensure proper nutritional intake within the
limits of the treatment regimen
3. Promoting positive feelings by encouraging increased self-care and greater in
dependence
CARDIOVASCULAR DISORDERS
ANGINA PECTORIS
-
literally translates as pain in the chest. This symptom occurs as a result of my
ocardial ischemia. Anginal chest
pain is transient, lasting only 3-5 minutes and is usually relieved whenever the
precipitating event is discontinued
or nitroglycerin is administered. The most common cause of angina is preexisting
cardiovascular disease, which
narrows or occludes the arteries that feed the heart muscle. Numerous disorders
occur along the
pathophysiologic continuum of cardiovascular disease; these include atheorsclero
sis, angina, cerebrovascular
accident, myocardial infarction (MI), and heart failure.
The coronary arteries, which arise from the ascending aorta immediately on exiti
ng the heart, normally supplies the myocardium with adequate
oxygen and nutrient-rich blood to meet metabolic demands. In the atherosclerotic
heart, arteries are chronically dilated beyond narrowed or
partially obstructed areas to meet the heart’s metabolic demands at rest. Thus w
hen the myocardium requires more oxygen during times of
increased work, the coronary arteries cannot increase flow because they are alre
ady maximally dilated. An oxygen deficit is created as a result of
the oxygen supply being less than the cellular demands.
The oxygen imbalance created with angina can be quite precarious, and many facto
rs can adversely affect this relationship. The demand for
oxygen is increased whenever anyone of the following is increased: heart rate, a
fterload (hypertension), wall ension (ventricular volume or
pressure), myocardial wall thickness (hypertrophy), or contractility. All of the
se factors make the heart work harder. Conversely, the oxygen supply
is decreased whenever any of the following occur: hypotension, anemia, respirato
ry insufficiency, or tachycardia, which allows minimal time for
diastolic filling.
In the absence of adequate oxygen and glucose, cellular metabolism shifts from t
he efficient oxidative phosphorylation, which yields a large amount of adenosine
triphosphate (ATP) to the inefficient glycolysis; this action not only yields a
very small amount of ATP but it also yields lactic acid as a by-product. This a
cidic environment activates chemical nociceptors, which transmit pain impulses t
o the brain, and the individual experiences chest pain. At this point the damage
is reversible; in other words, if the flow of oxygen and glucose-rich blood is
restored, no permanent damage results. However, if the oxygen deficit continues
and the lactic acid is allowed to build up, cellular metabolism and function can
be altered to the point of irreversible cell death or myocardial infarction (MI
).
Types of Angina
1.Stable angina (classic or exertional angina).
The primary differentiating factor about this type of angina is that it is predi
ctable and occurs intermittently over an extended period. It occurs
with the same pattern of onset, duration, and intensity each time. Further, the
same precipitating activity (most often physical in nature) usually
brings on stable angina. The pain is relieved either when the precipitating even
t is discontinued or when nitroglycerin is administered in the
prescribed fashion. If the pain is unrelieved by either rest or nitroglycerin, t
he patient may then be at risk for an MI. As previously discussed,
stable angina is a result of atherosclerotic plaque that has narrowed the arteri
es. The chronically dilated vessel is unable to dilate further to
meet metabolic demands.
2. Unstable angina (progressive, crescendo, preinfarction angina, acute coronary
insufficiency)
This type is potentially life-threatening because it signifies advanced ischemic
heart disease. This type of angina is most often unpredictable.
Moreover, unstable angina attacks tend to occur with increasing frequency, inten
sity and duration. No precipitating event is necessary. In fact,
these attacks are brought on at times of complete rest. An individual previously
diagnosed with stable angina can progress to unstable angina;
alternatively, unstable angina may be the first clinical manifestation in an ind
ividual with CAD.
3.Prinzmetal’s angina (variant angina)
The least common type of angina. It is unpredictable in onset, duration, and int
ensity and occurs almost exclusively at rest. Vasospasm of
one or more of the coronary arteries is the underlying cause, which can occur wi
th or without associated atherosclerosis.
The cardinal symptom of angina is chest pain or discomfort. However, many patien
ts describe feeling vague sensations of discomfort, tightness, pressure, heavine
ss, aching or squeezing. Others complain of heartburn or indigestion during an a
ttack. The most common location is substernal; however, the pain or discomfort m
ay radiate to the neck, jaw, back, shoulders, left arm, or occasionally the righ
t arm.
When asked to demostrate or point to the location of the pain, typically patient
s will clench one or two fists over the substernal region when
experiencing myocardial ischemia. This display is known as the Levine’s sign. Ot
her associated sighs and symptoms include pallor, diaphoresis,
cold skin, shortness of breath, weakess, dizziness, anxiety, and feelings of imp
ending doom.
When an individual complains of chest pain, the source of pain should be conside
red cardiac until proven otherwise. However, it is prudent
to consider both cardiac and noncardiac causes of chest pain as possible differe
ntials.
Electrocardiogram (ECG) – remains the “gold-standard” for a first-line, noninvas
ive tool for diagnosis.
Percutaneous transluminal coronary angioplasty (PTCA) – involves the passage of
an inflatable balloon catheter into the stenotic coronary
NCM 104 1st sem S.Y. 2007-2008
16
vessel, which is then dilated, resulting in compression of the atherosclerotic p
laque and widening of the vessel
Coronary artery bypass grafting (CABG) – done by harvesting either a saphenous v
ein from the leg or the left internal mammaryartery and then
used to bypass areas of obstruction in the heart
Nursing Responsibilities
In caring for patients with angina, the focus of the nurse’s role is two-fold. T
he first priority is appropriate treatment of the acute attack to alleviate
discomfort and, if possible, to avert untoward sequelae. The second priority is
geared toward extensive education that not only empowers the
patient to become an active participant in his or her well being but also impart
s practical tools with which the patient can effectively manage the
condition at home to achieve the highest level of wellness and independent funct
ioning.
During an acute anginal attack, it is imperative that the nurse performs a rapid
and focused physical assessment and health history. Frequent vital signs and co
ntinuous cardiac monitoring are essential parts of the ongoing assessment. The m
ost crucial part of the assessment focuses on the current attack; emphasis must
be placed on evaluating the pain itself and any precipitating events.
The nurse must ask the following questions:
How severe is the pain? (scale of 1-10)
What does the pain feel like?
Where is the pain? Does it move or radiate? Is it diffused or well localized?
Did the pain start suddenly or gradually?
How long does it last?
How frequently does it occur?
What makes the pain worse? What brings the pain on?
What makes the pain better? What resolves the pain?
Has the pain been increasingly worse with each attack?
Another critical nursing function is prompt institution of prescribed medical an
d pharmacologic therapies such as frequently used acronymMON A,
which stands for:
•
Morphine,
•
Oxygen,
•
Nitroglycerine, and
•
Aspirin.
Although nitrates are unable to dilate severely atherosclerotic vessels that are
already maximally dilated, its administration during an unstable
angina attack can prevent progression to an MI or death in 51% to 72% of patient
s.
Other nursing measures that are beneficial to the patient who is suffering an an
ginal attack include helping the patient into a comfortable position,
promoting rest and relaxation, and encouraging slow, deep breathing.
ACUTE MYOCARDIAL INFARCTION
As with angina, acute myocardial infarction occurs when the heart muscle is depr
ived of oxygen and nutrient-rich blood. However, in the case of MI, this depriva
tion occurs over a sustained period to the point at which irreversible cell deat
h and necrosis take place. This deprivation leads to structural and functional c
hanges within the affected area of myocardial tissue. As with angina, too, under
lying coronary artery disease (CAD) is the most common cause of MI. With these b
asic similarities in mind, many components of the MI disease process and treatme
nt either overlap to some degree or further develop along the continuum of cardi
ovascular diseases.
Infarction results from sustained ischemia and is irreversible causing cellular
death and necrosis.
Circumstances that can cause an imbalance in supply and demand of oxygen and nut
rient-rich blood:
Physical exertion
Emotional stress
Weather extremes
Digestion after a heavy meal
Valsalva maneuver
Hot baths or showers
Sexual excitation
Pathophysiologic chaaracteristics
The hallmark of MI is severe, unrelenting chest pain. As with angina, the pain i
s typically described as crushing, pressure-filled, vise-like, tight,
constricting, or squeezing. The most common location of the pain is substernal,
with radiation to the neck, jaw, or left arm. Leass frequently, pain
is reported in the shoulders, back, or right arm. In addition, a positive Levine
’s sign (one or two fists clenched over the chest area when the
patient is asked to localize the pain) can contribute to the diagnosis.
The major difference in the clinical presentation of MI compared with that of an
gina is the onset, severity, and duration. Chest pain aassociated with MI usuall
y has an abrupt onset and can occur during activity, rest, or even sleep. The pa
in described during MI is typically more severe than anginal pain, lasting at le
ast 20-30 minutes, and it is not relieved with either rest or nitroglycerin.
However, not all patients will experience the same clinical presentation.
During MI, associated clinical manifestations can range from vague sensations of
“just not feeling well” to the loss of consciousness or cardiac
arrest. Often the skin is diaphoretic with a pale or ashen appearance, which occ
urs because of peripheral vasoconstriction as the body shunts
blood to the vital core. The initial surge of catecholamines can contribute to a
variety of signs and symptoms such as tachycardia, hypertension,
anxiety, palpitations, apprehension, and feelings of impending doom. Stimulation
of the medulla is mediated via vasovagal reflexes and can result
in nausea and vomiting. Fever may be present secondary to the activation of the
inflammatory process. As the infarction progresses and the
heart’s pumping ability becomes impaired, cardiac output drops. Associated with
decreased cardiac output is hypotension, restlessness, dyspnea,
jugular vein distention, oliguria, and confusion.
Electrocardiogram – capable of diagnosing MI in 80% of patients, making it an in
dispensable, noninvasive, and cost-effective tool.
Evolving MI will show ST elevation which indicates acute myocardial necrosis. Th
e development of Q wave may be
observed which signifies further electrical abnormalities. It may be an indicati
on of worsening ischemia and necrosis.
Cardiac Enzymes
During the infarction process, cell membranes rupture, allowing intracellular en
zymes to spill out into the blood stream. Blood sample drawn at
certain times during or after MI can be sent to the laboratory where enzymes can
be measured and interpreted to determine the presence of an
NCM 104 1st sem S.Y. 2007-2008
17
infarction.
Cardiac Enzyme Laboratory Findings
Enzyme
Earliest Rise (in hours)
Peak (in hours)
Return to Baseline
Creatinine kinase (CK)
CK-MB
Myoglobin
Troponin 1
2-6
4-8
0.5-1.0
1-6
18-36
15-24
6-9
7-24
3-6 days
3-4 days
12 hours
10-14 days
Troponin 1 is the newest cardiac marker and is a protein found only in myocardia
l cells. It is a quick, rapid test that, if elevated, indicated MI.
First-Line and Initial Treatment for Myocardial Infarction
Provide oxygen
Obtain a 12-lead ECG
Monitor vital signs and pulse oximetry
Monitor continuous cardiac rhythm with ST segment monitoring
Conduct history and physical examinations
Administer medications (thrombolytic therapy and anticoagulant therapy
Nursing Interventions:
1.Bedrest must be enforced.
2. The nurse should assist with all position changes and personal hygiene to avo
id any exertional effort.
3. Monitor I&O particularly urine output because this is a reliable indictor of
cardiac output and systemic perfusion.
4. Administer stool softener as ordered to prevent straining and vasovagal stimu
lation which can cause precipitous bradycardia
CARDIAC FAILURE
CONGESTIVE HEART FAILURE (CHF)
Often referred to as cardiac failure, is the inability of the heart to pump suf
ficient blood to meet the needs of the tissues for oxygenation and
nutrients.
CHF is most commonly used when referring to left-sided and right-sided failure
The incidence of CHF increases with age
Pathophysiology:
Cardiac failure most commonly occurs with disorders of cardiac muscles that resu
lt in decreased contractile properties of the heart. Common underlying condition
s that lead to decreased myocardial contractility include myocardial dysfunction
, arterial hypertension, and valvular dysfunction. Myocardial dysfunction may be
due to coronary artery disease, dilated cardiomyopathy, or inflammatory and deg
enerative diseases of the myocardium. Atherosclerosis of the coronary arteries i
s the primary cause of heart failure. Ischemia causes myocardial dysfunction bec
ause of resulting hypoxia and acidosis (from accumulation of lactic acid). Myoca
rdial infarction causes focal myocellular necrosis, the death of myocardial cell
s, and a loss of contractility; the extent of the infarction is prognostic of th
e severity of CHF.
Dilated cardiomyopathy causes diffuse cellular necrosis, leading to decreased co
ntractility. Inflammatory and degenerative diseases of the
myocardium, such as myocarditis, may also damage myocardial fibers, with a resul
tant decrease in contractility.
Systemic or pulmonary HPN increases afterload which increases the workload of th
e heart and in turn leads to hypertrophy of myocardial muscle
fibers; this can be considered a compensatory mechanism because it increases con
tractility.
Valvular heart disease is also a cause of cardiac failure. The valves ensure tha
t blood flows in one direction. With valvular dysfunction, valve has increasing
difficulty moving forward. This decreases the amount of blood being ejected, inc
reases pressure within the heart, and eventually leads to pulmonary and venous c
ongestion.
Etiologic Factors :
1. Increased metabolic rate (eg. fever, thyrotoxicosis)
2. Hypoxia
3. Anemia
VENTRICULAR FAILURE
LEFT-SIDED CARDIAC FAILURE
Pulmonary congestion occurs when the left ventricle cannot pump the blood out o
f the chamber. This increases pressure in the left ventricle
and decreases the blood flow from the left atrium. The pressure in the left atri
um increases, which decreases the blood flow coming from the pulmonary vessels.
The resultant increase in pressure in the pulmonary circulation forces fluid int
o the pulmonary tissues and alveoli; which impairs gas exchange
1. Dyspnea on exertion
2. Cough
3. Adventitious breath sounds
4. Restless and anxious
5. Skin appears pale and ashen and feels cool and clammy
6. Tachycardia and palpitations
7. Weak, thready pulse
8. Easy fatigability and decreased activity tolerance
RIGHT-SIDED CARDIAC FAILURE
NCM 104 1st sem S.Y. 2007-2008
18
When the right ventricle fails, congestion of the viscera and the peripheral ti
ssues predominates. This occurs because the right side of the
heart cannot eject blood and thus cannot accommodate all the blood that normally
returns to it from the venous circulation.
1. Edema of the lower extremities (dependent edema)
2. Weight gain
3. Hepatomegaly (enlargement of the liver)
4. Distended neck veins
5. Ascites (accumulation of fluid in the peritoneal cavity)
6. Anorexia and nausea
7. Nocturia (need to urinate at night)
8. Weakness
Medical Management
The basic objectives in CHF management are the following:
1. Reducing the workload on the heart
2. Increasing the force and efficiency of myocardial contraction
3. Eliminating the excessive accumulation of body water by avoiding excess fluid
, controlling the diet, and monitoring diuretic and angiotensin-
converting enzyme (ACE) inhibitor therapy
Pharmacologic Therapy:
If the patient is in mild failure, usually an ACE inhibitor is prescribed. A diu
retic is added if there is no improvement or if there are signs of fluid
overload. Next, digitalis is added if the symptoms continue. If symptoms are sev
ere, all three medications are usually started immediately.
ACE Inhibitors. Promote vasodilation and diuresis by decreasing afterload and pr
eload eventually decreasing the workload of the heart.
Diuretic Therapy. A diuretic is one of the first medications prescribed to a pat
ient with CHF. Diuretics promote the excretion of sodium and water
through the kidneys.
Digitalis. This medication increases the force of myocardial contraction and slo
ws conduction through the AV node. It improves contractility thus,
increasing left ventricular output.
Dobutamine.(Dobutrex) is an intravenous medication given to patients with signif
icant left ventricular dysfunction. A catecholamine, it stimulates the
beta1-adrenergic receptors. Its major action is to increase cardiac contractilit
y.
Milrinone (Primacor). A phosphodiesterase inhibitor that prolongs the release an
d prevents the uptake of calcium. This in turn, promotes
vasodilation, causing a decrease in preload and afterload and decreasing the wor
kload of the heart.
Other medications. Anticoagulants may be prescribed. Beta-adrenergic blockers ma
ybe indicated in patients with mild or moderate failure.
Nutritional Therapy:
1. A low-sodium diet
2. Avoidance of excessive amount of fluids
Nursing Management:
1. Record intake and output to identify a negative balance (more output than inp
ut)
2. Weigh patient daily at the same time
3. Auscultate lung sounds daily to detect a decrease or an absence of pulmonary
crackles
4. Determine the degree of jugular distention
5. Identify and evaluate severity of dependent edema
6. Monitor pulse rate and BP, and make sure the patient does not become hypotens
ive from dehydration
7. Examine skin turgor and mucous membranes for signs of dehydration
8. Assess for symptoms of fluid overload (orthopnea, paroxysmal nocturnal dyspne
a, and dyspnea on exertion)
Nursing Process: The Patient With Cardiac Failure
Assessment
The focus of the nursing assessment for the patient with cardiac failure is dir
ected toward observing for signs and symptoms of pulmonary and
systemic fluid overload.
Health History
The nurse explores sleep disturbances, particularly sleep suddenly interrupted
by shortness of breath.
The nurse finds out about the number of pillows needed for sleep (indication of
dyspnea)
Find out also the activities of daily living and the activities that causes sho
rtness of breath
Physical Examination
The lungs are auscultated at frequent intervals to detect crackles and wheezes
or their absence. The rate and depth of respiration are also
noted.
The heart is auscultated for an S3 heart sound, a sign that the heart pump is b
eginning to fail and that increased blood volume remains in the
ventricle with each beat. HR and rhythm are also noted.
Jugular vein distention is also assessed. Distention greater than 3 cm above th
e sternal angle is considered abnormal.
Sensorium and level of consciousness must be evaluated
Dependent parts of the patient’s body are assessed for perfusion and edema.
The liver is examined for hepatojugular reflux.
Output is measured carefully to establish a baseline against which to measure t
he effectiveness of diuretic therapy. Intake and output record
are maintained
Nursing Diagnoses:
1. Activity intolerance r/t imbalance between oxygen supply and demand secondary
to decreased CO
2. Excess fluid volume r/t excess fluid/sodium intake or retention secondary to
CHF and its medical therapy
3. Anxiety r/t breathlessness and restlessness secondary to inadequate oxygenati
on
4. Non-compliance r/t to lack of knowledge
5. Powerlessness r/t inability to perform role responsibilities secondary to chr
onic illness and hospitalization.
Potential Complications:
1. Cardiogenic shock
2. Dysrhythmias
3. Thromboembolism
NCM 104 1st sem S.Y. 2007-2008
19
4. Pericardial effusion and pericardial tamponade
Planning And Goals:
1. Promoting activity while maintaining vital signs within identified range
2. Reducing fatigue
3. Relieving fluid overload symptoms
4. Decreasing the incidence of anxiety or increasing patient’s ability to manage
anxiety
5. Teaching the patient about the self-care program.
6. Encouraging the patient to verbalize his ability to make decisions and influe
nce outcomes.
1. Promoting Activity Tolerance
The patient is encouraged to perform an activity more slowly than usual, for a
shorter duration, or with assistance initially.
Barriers that could limit abilities to perform an activity are identified
Pacing and prioritizing activities will maintain the patient’s energy to allow
participation in regular exercise.
Vital signs should be taken before, during and immediately after an activity to
identify whether they are within the predetermined range.
2. Reducing Fatigue
The nurse and patient can collaborate to develop a schedule that promotes pacin
g and prioritization of activities. The schedule should
alternate activities with periods of rest and avoid having two significant energ
y-consuming activities occur on the same day or in immediate
succession.
3. Managing Fluid Volume
The nurse monitors the patient’s fluid status closely. Auscultating the lungs,
comparing daily body weights, monitoring intake and output and
assisting the patient to adhere to a low-sodium diet.
The nurse needs to position the patient or teach the patient how to assume a po
sition that shifts fluid away from the heart.
The nurse needs to assess for skin breakdown and institute preventive measures
4. Controlling Anxiety
The nurse should take steps to promote physical comfort and psychological suppo
rt. A family member’s presence provides reassurance.
Speaking in a slow, calm, and confident manner is helpful. Stating specific, bri
ef directions for an activity is helpful in decreasing anxiety.
5. Minimizing Powerlessness
Patients need to recognize that they are not helpless and that they can influen
ce their direction, their lives, and their outcomes.
The nurse needs to assess for factors contributing to a perception of powerless
ness and intervene accordingly. Contributing factors may
include lack of knowledge, hospital policies, and lack of opportunities to make
decisions.
Taking time to listen to patient encourages them to express their concerns and
questions
Provide the patient with decision-making opportunities
Provide encouragement and praise
Expected Outcomes:
1. Demonstrates tolerance for increased activity
2. Has less fatigue and dyspnea
3. Maintains fluid balance
4. Is less anxious
5. Adheres to self-care regimen
6. Makes decisions regarding care and treatment
7. Absence of complications
CARDIOGENIC SHOCK
Occurs when the heart cannot pump enough blood to supply the amount of oxygen n
eeded by the tissues.
Pathophysiology:
The heart muscle loses its contractile power, resulting in a marked reduction in
SV and CO, sometimes called “forward failure”. The damage to
myocardium results in a decrease in CO, which in turn reduces arterial blood pre
ssure and tissue perfusion in the vital organs (heart, brain,
kidneys). Flow to the coronary artery is reduced, resulting in decreased oxygen
supply to the myocardium, which in turn increases ischemia and
further reduces the heart’s ability to pump. The inadequate emptying of the vent
ricle also leads to increased pulmonary pressures, pulmonary
congestion, and pulmonary edema, exacerbating the hypoxia and resulting ischemia
of vital organs.
1. Tissue hypoperfusion – classic signs of cardiogenic shock manifested as cereb
ral hypoxia (restlessness, confusion, agitation), low blood
pressure, rapid and weak pulse, cold and clammy skin, increased respiratory crac
kles, hypoactive bowel sounds, and decreased urinary output.
2. Initially, arterial blood gas analysis may show respiratory alkalosis.
3. Dysrhythmias are common
1. The use of a Pulmonary Artery catheter to measure left ventricular pressures
and CO is important in assessing the severity of the problem and
planning management. The PA wedge pressure is elevated and the CO is decreased a
s the left ventricle loses its ability to pump.
2. The systemic vascular resistance is elevated due to the sympathetic nervous s
ystem stimulation that occurs as a compensatory response to the
decrease in blood pressure.
3. The decreased blood flow to the kidneys causes a hormonal response that cause
s fluid retention and further vasoconstriction.
4. The increases in HR, circulating volume, and vasoconstriction occur to mainta
in circulation to the brain, heart and lungs, however, the workload
of the heart is increased.
5. Continued cellular hypoperfusion eventually results in organ failure. The pat
ient becomes unresponsive, severe hypotension occurs, and the
patient develops shallow respirations, cold, cyanotic or mottled skin, and absen
t bowel sounds.
6. Arterial blood gas analysis shows metabolic acidosis
7. All laboratory results indicate organ dysfunction.
Medical Management:
1. Reduce any further demand on the heart
2. Improve oxygenation and restore tissue perfusion
3. Diuretics, vasodilators, and mechanical devices (filtration and dialysis)
4. Intravenous volume expanders (normal saline, lactated Ringer’s solution, and
albumin) are given for hypovolemia or low intravascular volume.
5. Strict bed rest to conserve energy
NCM 104 1st sem S.Y. 2007-2008
20
6. Oxygen administration is increased for hypoxemia
7. Intubation and sedation may be necessary to maintain oxygenation balance.
Pharmacologic Therapy:
Most medication are administered IV because of the decreased perfusion to the g
astrointestinal system
1. Pressor agents are medications used to raise BP and increase CO. Many pressor
medications are catecholamines ( norepinephrine and high-
dose dopamine) to promote perfusion to the heart and brain.
2. Diuretics and vasodilators may be administered to reduce the workload of the
heart.
3. Positive inotropic medications are given to increase myocardial contractility
4. Circulatory assist devices: Intra-aortic balloon pump – to augment the pumpin
g action of the heart. The device inflates during diastole, increasing
the pressure in the aorta and therefore increasing perfusion. It deflates just b
efore systole, lessening the pressure within the aorta before
ventricular contraction, decreasing the amount of resistance the heart has to ov
ercome to eject blood and therefore decreasing the amount of work
the heart must complete to eject blood.
Nursing Management:
1. Nurse must carefully assess the patient, observe the cardiac rhythm, measure
hemodynamic parameters, and record fluid intake and urinary
output.
2. The patient must be closely monitored for responses to the medical interventi
ons and for the development of complications
3. The patient is always treated in intensive care environment because of the fr
equency of nursing interventions and the technology required for
effective medical management.
THROMBOEMBOLISM
The decreased mobility of the patient with cardiac diseases and the impaired ci
rculation that accompany these disorders contribute to the
development of intracardiac and intravascular thrombosis.
Intracardiac Thrombus
Detected by an echocardiogram and treated with anticoagulants, such as warfarin
.
A part of the thrombus may become detached and may be carried to the brain, kid
neys, intestines, or lungs
The most common problem is pulmonary embolism. The symptoms of pulmonary emboli
sm include chest pain, cyanosis, and shortness of
breath, rapid respirations and hemoptysis. (see discussion on pulmonary embolism
)
The pulmonary embolus may block the circulation to a part of the lung, producin
g an area of pulmonary infarction
Systemic embolism may present as cerebral, mesenteric, or renal infarction
An embolism can also compromise the blood supply to an extremity
PERICARDIAL EFFUSION AND CARDIAC TAMPONADE
Pathophysiology:
Pericardial effusion refers to the escape of fluid into the pericardial sac. Nor
mally, the pericardial sac contains less than 50 ml of fluid, which the
heart needs to decrease friction for the beating heart. An increase in pericardi
al fluid raises the pressure within the pericardial sac and compresses
the heart. This results in :
Increased right and left ventricular-end diastolic pressures
Decreased venous return
Inability of the ventricles to distend adequately
Pericardial fluid may accumulate slowly without causing noticeable symptoms. A r
apidly developing effusion, however, can stretch the pericardium
to its maximum size and, because of increased pericardial pressure, and reduce v
enous return to the heart, and decrease cardiac output. The
result is cardiac tamponade.
1. The patient may complain of a feeling of fullness within the chest. The feeli
ng of pressure may result from stretching of the pericardial sac
2. Engorged neck veins
3. Shortness of breath
4. A drop and fluctuation in BP
1. Pericardial effusion is detected by percussing the chest and noting an extens
ion of flatness across the anterior aspect of the chest
2. Echocardiogram to confirm diagnosis
Medical Management:
1. Pericardial Fluid Aspiration (pericardiocentesis) – performed to remove fluid
from the pericardial sac
2. Pericardiotomy. A portion of pericardium is sliced to permit the pericardial
fluid to drain into the lymphatic system.
CARDIAC ARREST
Occurs when the heart ceases to produce an effective pulse and blood circulatio
n. It may be due to a cardiac electrical event, as when the HR
is too fast or too slow or when there is no heart rate at all.
1. Loss of consciousness, pulse and BP
2. Ineffective respiratory gasping
3. The pupils of the eyes dilate within 45 seconds.
4. Seizures may or may not occur
Emergency Management:
Cardiopulmonary Resuscitation
1. Airway – maintain open airway
2. Breathing – provide artificial circulation by rescue breathing
3. Circulation – promoting artificial circulation by external cardiac compressio
n
4. Defibrillation – restoring the heart beat
Maintaining Airway and Breathing
The first step in CPR is to obtain an open airway. Any obvious material in the
mouth and throat should be removed. The chin is directed up
and back or the jaw (mandible) is lifted forward. The rescuer “looks, listen. an
d feels” for air movement. An oropharyngeal airway is inserted if available. Two
rescue ventilations over 3 to 4 seconds are provided using a bag or mouth-mask
device. If the first rescue ventilation entered easily, then the patient is vent
ilated with 12 breaths per minute and the open airway is maintained. Endotrachea
l intubation is performed to ensure an adequate airway and ventilation.
Restoring Circulation
After performing ventilation, the carotid pulse is assessed and external cardia
c compressions are provided when no pulse is detected.
1. Compressions are performed with the patient on a firm surface (Cardiac board
, floor)
2. The rescuer (facing the patient’s head) places the heel of one hand on the l
ower half of the sternum, two fingerwidths from the tip of the
NCM 104 1st sem S.Y. 2007-2008
21
xiphoid and positions the other hand on top of the first hand. The fingers shoul
d not touch the chest wall.
3. Using the body weight while keeping the elbows straight, the rescuer presses
quickly downward from the shoulder area to deliver a forceful
compression to the victim’s lower sternum toward the spine.
4. The chest compression rate is 80 to 100 times/minute
Follow-up Monitoring
1. After successful resuscitation, the patient is transferred to an intensive ca
re unit for close monitoring. Continuous electrocardiographic monitoring
and frequent BP assessment are essential until hemodynamic stability is reestabl
ished.
DYSRHYTHMIAS
Disorders of the formation and/or conduction of the electrical impulse within t
he heart. This can cause disturbances of the heart rate, the heart
rhythm, or both.
Normal Electrical Conduction
The electrical impulse that stimulates and paces the cardiac muscle normally ori
ginates in the sinus node, located near the vena cava in the right
atrium. Normally, the impulse occurs at a rate between 60 and 100 times a minute
in the adult. The impulse quickly travels from the sinus node
through the atria to the atrioventricular (AV) node causing the atria to contrac
t. The structure of the AV node slows the impulse, which allows time
for the atria to contract and the ventricles to fill with blood. From the AV nod
e, the impulse travels quickly along the right and left bundle branches
and the Purkinje fibers, located in the ventricular muscle. The electrical stimu
lation of the ventricles, in turn, causes the ventricles to contract
(systole). Then the electromechanical impulse completes the circuit and the cycl
e begins again. In this way, sinus rhythm promotes cardiovascular
circulation. The electrical stimulus causes the mechanical event of the heart.
Depolarization. The electrical stimulation: the mechanicalcontraction is called
systole.
Repolarization. The electrical relaxation and mechanicalrelax ation is called d
iastole.
Influences on Heart Rate and Contractility
Heart rate is influenced by the autonomic nervous system, which consists of sym
pathetic and parasympathetic fibers.
Stimulation of the sympathetic system increases heart rate.
Sympathetic stimulation also causes the constriction of peripheral blood vessel
s and, therefore, an increase in BP
Parasympathetic stimulation slows the heart rate
Manipulation of the autonomic nervous system may increase or decrease the incid
ence of dysrhythmias
Types of Dysrhythmias
1. Sinus Node Dysrhythmias
A. Sinus Bradycardia
Occurs when the sinus node creates an impulse at a slower –than-normal rate.
Etiology:
1. Slower metabolic needs (sleep, athletic training, hypothyroidism)
2. Vagal stimulation (vomiting, suctioning, severe pain, extreme emotions)
3. Medications
4. Increased intracranial pressure and MI
Treatment:
1. Atropine 0.5 to 1.0 mg given quickly and IV as bolus – medication of choice
2. Catecholamines and emergency transcutaneous pacing
B. Sinus Tachycardia
Occurs when the sinus node creates an impulse at a faster-than-normal rate.
It may be caused by acute blood loss, anemia shock, hypovolemia, hypervolemia,
CHF, pain, hypermetabolic state, fever, exercise, anxiety or
sympathomimetic medications.
Treatment:
1. Calcium channel blockers (ex. Diltiazem)
2. Beta-blockers (ex. Propranolol)
C. Sinus Arrhythmia
Occurs when the sinus node creates an impulse at an irregular rhythm; the rate
increases with inspiration and decreases with expiration
2. Atrial Dysrhythmias
A. Premature Atrial Complex (PAC)
This is a single ECG complex that occurs when an electrical impulse starts in t
he atrium before the next normal impulse of the SA node.
The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardi
um
PAC’s are common in normal hearts. The patient may say “My heart skipped a beat
.” A pulse deficit may exist.
If PAC’s are infrequent, no treatment is necessary.
B. Paroxysmal Atrial Tachycardia
A term used to indicate a tachycardia characterized by abrupt onset and abrupt
cessation and a QRS of normal duration.
Now called AV nodal reentry tachycardia
C. Atrial Flutter
Occurs in the atrium and creates impulses at an atrial rate between 250 and 400
times per minute
May cause serious signs and symptoms: chest pain, shortness of breath, and low
blood pressure.
Treatment:
1. If patient is unstable, electrical cardioversion is indicated
2. If patient is stable, diltiazem, verapamil, beta-blockers or digitalis may be
administered IV to slow the ventricular rate.
D. Atrial Fibrillation
Causes a rapid, disorganized, and uncoordinated twitching of atrial musculature
.
The most common dysrhythmias
Usually associated with advanced age, valvular heart disease, cardiomyopathy, h
yperthyroidism, pulmonary disease, moderate to heavy
ingestion of alcohol and the aftermath of open heart surgery
Treatment:
NCM 104 1st sem S.Y. 2007-2008
22
Treatment depends on its cause and duration and the patient’s symptoms and inst
ability
In some cases, AF converts to sinus rhythm within 24 hours without treatment
Both stable and unstable AF of short duration are treated the same as stable an
d unstable atrial flutter
To prevent recurrence and to promote heart rate control over a long period, qui
nidine, procainnamide, flecainide, sotalol, or amiodatone may
be prescribed
Anti-coagulation therapy is indicated if patient is elderly or has hypertension
, heart failure or a history of stroke.
Pacemaker or surgery is sometimes indicated for patients who are unresponsive t
o medications
3. Junctional Dysrhythmias
A. Premature Junctional Complex
An impulse that starts in the AV nodal area before the next normal sinus impuls
e.
Causes include: digitalis toxicity, congestive heart failure, and coronary arte
ry disease
Rarely produce any significant symptoms
Treatment is the same as for frequent PAC’s
B. Junctional Rhythm
Occurs when the AV node, instead of the SA node, becomes the pacemaker of the h
eart.
Junctional rhythm may produce signs and symptoms of reduced cardiac output. If
so, the treatment is the same as for sinus bradycardia.
C. AV Nodal Reentry Tachycardia
Occurs when an impulse is conducted to an area in the AV node that causes the i
mpulse to be rerouted back into the same area over and
over again at a very fast rate.
Factors associated with the development of AV nodal reentry tachycardia include
caffeine, nicotine, hypoxemia, and stress
Signs and symptoms vary with the rate and duration of the tachycardia and the p
atient’s underlying condition. Usually of short duration,
resulting only in palpitations. A fast rate may reduce cardiac output, resulting
in significant signs and symptoms such as restlessness, chest
pain, shortness of breath, pallor, hypotension and loss of consciousness
Treatment:
Treatment is aimed at breaking the reentry of the impulse.
1. Vagal maneuvers, such as carotid sinus massage, gag reflex, breath holding, a
nd immersing the face in ice water – increase parasympathetic
stimulation, causing slower conduction through the AV node and blocking the reen
try of the rerouted impulse.
Because of the risk of a cerebral embolic event, carotid sinus massage is contr
aindicated in patients with carotid bruits.
2. If vagal maneuvers are ineffective, the patient may then receive a bolus of a
denosine, verapamil, or diltiazem.
3. Cardioversion is the treatment of choice if the patient is unstable or does n
ot respond to the medications.
4. Intravenous adenosine may be prescribed to cause a conversion to sinus rhythm
.
4. Ventricular Dysrhythmias
A. Premature Ventricular Complex (PVC)
PVC is an impulse that starts in a ventricle before the next normal sinus impul
se.
PVC’s can occur in healthy people, esp. with the use of caffeine, nicotine, and
alcohol.
Also caused by cardiac ischemia or infarction, increased workload on the heart
(ex. Exercise, fever. Hypervolemia, CHF, and tachycardia),
digitalis toxicity, hypoxia, acidosis, and electrolyte imbalances, esp. hypokale
mia
In the absence of disease, PVC’s are not serious. In the patient with acute MI,
PVC’s may indicate the need for more aggressive therapy.
The following are warning or complex PVC’s (precursors of ventricular tachycard
ia) : (1) more than 6/minute (2) multifocal (having different
shapes), (3) two in a row (pair), and (4) occurring on the T wave (the vulnerabl
e period of ventricular depolarization)
Treatment:
1. Lidocaine is the medication most commonly used for immediate short-term thera
py
B. Ventricular Tachycardia
Defined as three or more PVC’s in a row, occurring at a rate exceeding 100 beat
s/minute.
Ventricular tachycardia is usually associated with coronary artery disease and
may precede ventricular fibrillation.
Ventricular tachycardia is an emergency because the patient is usually unrespon
sive and pulseless.
Treatment:
1. Lidocaine is the initial choice
2. Cardioversion maybe indicated if the medications are ineffective or if the pa
tient becomes unstable
3. Immediate defibrillation
Ventricular tachycardia in a patient who is unconscious and without pulse is tr
eated in the same manner as ventricular fibrillation.
C. Ventricular Fibrillation
A rapid but disorganized ventricular rhythm that causes ineffective quivering o
f the ventricles.
This dysrhythmias is always characterized by the absence of an audible heartbea
t, a palpable pulse, and respirations.
Cardiac arrest and death are imminent if VF is uncorrected
Treatment:
1. Immediate defibrillation and activation of emergency services. Placing a call
for emergency assistance takes precedence over initiating CPR
2. After a successful defibrillation, eradicating causes and administering anti
dysrhythmics medication are treatments to prevent the recurrence of
V F.
D. Idioventricular Rhythm
Also called ventricular rhythm, occurs when the impulse starts in the conductio
n system below the AV node
Commonly causes the patient to lose consciousness and experience other signs an
d symptoms of reduced cardiac output. In such cases,
treatment is the same as for any bradycardia, including identifying the underlyi
ng etiology, administering IV atropine, and initiating emergency
transcutaneous pacing.
Bed rest is prescribed so as not to increase cardiac workload
E. Ventricular Asystole
Commonly called flatline, ventricular asystole is characterized by absent QRS c
omplexes, although P waves may be apparent for a short
duration.
There is no heartbeat, no palpable pulse, and no respiration.
Without treatment, ventricular asystole is fatal.
NCM 104 1st sem S.Y. 2007-2008
23
Treatment:
1. CPR
2. Rapid assessment to identify possible causes
3. Intubation and establishment of IV access are the first recommended actions
4. Bolus of IV epinephrine and to be repeated at 3-5 minutes intervals
5. Sodium bicarbonate maybe administered IV
Nursing Process: The Patient With A Dysrhythmia
Assessment
Major areas of assessment include possible causes of the dysrhythmias and the d
ysrhythmia’s effect on the heart’s ability to pump an
adequate blood volume
When cardiac output is reduced, the amount of oxygen reaching the tissues and v
ital organs is diminished. This diminished oxygen produces
the signs and symptoms associated with dysrhythmias.
A health history is obtained to identify possible causes and past incidences of
syncope (fainting), lightheadedness, dizziness, fatigue, chest
discomfort, and palpitations.
Psychosocial assessment is also performed to identify the possible effects of d
ysrhythmia
Physical assessment is conducted to confirm the data obtained from the history
and to observe for signs of diminished cardiac output during
the dysrhythmic event, esp. changes in level of consciousness. Skin may be pale
and cool. Signs of fluid retention, such as neck vein
distention, crackles and wheezes in the lungs may be detected during auscultatio
n.
The rate and rhythm of apical and peripheral pulses are assessed and any pulse
deficit is noted.
The chest is auscultated for extra heart sounds, esp. S3 and S4, measures BP an
d determines pulse pressures. A declining pulse pressure
indicates reduced cardiac output.
Diagnosis:
1. Potential/actual decrease in cardiac output
2. Anxiety related to fear of the unknown
3. Lack of knowledge about the dysrhythmias and its treatment.
Potential Complications: Ischemic Heart Disease
1. Monitoring and Managing the Dysrhythmias
Controlling the incidence or effect of dysrhythmias is often achieved by the us
e of ant-idysrhythmic medications
A constant serum blood level of the medication is maintained to maximize benefi
cial effects and minimize adverse effects
If the patient is hospitalized, an ECG is initiated and rhythm strips are analy
zed to track dysrhythmias
BP, rate and depth of respirations, pulse rate and rhythm are evaluated regular
ly to determine the hemodynamic effect of the dysrhythmias
2. Minimizing Anxiety
Nurse must maintain a calm and reassuring attitude
Maximize the patient’s control and to make the unknown less threatening
Evaluation
Expected Outcomes:
1. Cardiac output is maintained
2. Anxiety is minimized
3. The patient knows about dysrhythmias and its treatment
Adjunctive Modalities and Management
1. Cardioversion and Defibrillation
Treatment for tachydysrhythmias.
Used to deliver an electrical current to stimulate a critical mass of myocardial
cells. This allows the sinus node to recapture its role as the
heart’s pacemaker.
One major difference between cardioversion and defibrillation has to do with th
e timing of the delivery of electrical current.
Defibrillation is usually performed as an emergency treatment, whereas cardiove
rsion is usually a planned procedure
Cardioversion involves the delivery of a “timed” electrical current to terminat
e a tachydysrhythmia.
Defibrillation is the treatment of choice for ventricular fibrillation and puls
eless ventricular tachycardia.
2. Pacemaker Therapy
An electronic device that provides electrical stimuli to the heart muscle.
Usually used when a patient has a slower-than-normal impulse formation
May also be used to control tachydysrhythmias that do not respond to medication
therapy
Complications of Pacemakers:
1. Local infection at the entry site of the leads or at the subcutaneous site
2. Bleeding and hematoma at the lead-entry sites or at the subcutaneous sites fo
r permanent generator placement
3. Hemothorax from puncture of the subclavian vein or internal mammary artery
4. Ventricular ectopy and tachycardia from irritation of the ventricular wall by
the endocardial electrode
5. Movement or dislocation of the lead placed transvenously (perforation of the
myocardium)
6. Phrenic nerve, diaphragmatic (hiccupping) or skeletal muscle stimulation may
occur if the lead is dislocated or if the delivered energy is set high
7. Rarely, cardiac tamponade occurs after removal of epicardial wires
8. Dislodgement of the pacing electrode – most common complication. Minimizing p
atient activities can help to prevent this complication.
BURNS
There are 4 major goals relating to burns:
1. Prevention
2. Institution of lifesaving measures for the severely burned person
3. Prevention of disability and disfigurement through early, specialized, indivi
dual treatment
4. Rehabilitation through reconstructive surgery and rehabilitative programs
Pathophysiology:
Burns are caused by a transfer of energy from a heat source to the body. Heat ma
ybe transferred through conduction or electromagnetic radiation.
Burns are categorized as thermal (including electrical burns), radiation or chem
ical. Tissue destruction results from coagulation, protein
denaturation, or ionization of cellular contents. The skin and the mucosa of the
upper airways are the sires of tissue destruction. Deep tissues,
including the viscera, can be damaged by electrical burns or through prolonged c
ontact.
The depth of the injury depends on the temperature of the burning agent and the
duration of contact with the agent.
NCM 104 1st sem S.Y. 2007-2008
24
Classification of Burns
Burn injuries are described according to the depth of the injury and the extent
of body surface area (BSA) injured.
Characteristics of Burns according to Depth
Factors to consider in the determination of depth :
1. History of how the injury occurred
2. Causative agent, such as flame or scalding liquid
3. Temperature of the burning agent
4. Duration of contact with the agent
5. Thickness of the skin
Extent of Body Surface Area Injured
Rule of Nines
An estimation of the total BSA involved in a burn is simplified using the rule
of nines
Lund and Browder Method
A more precise method of estimating the extent of a burn
Recognizes that the percentage of BSA of various anatomic parts, especially the
head and legs, changes with growth.
By dividing the body into very small areas and providing an estimate of the pro
portion of BSA accounted for by such body parts, one can
obtain a reliable estimate of the total BSA burned.
The initial evaluation is made on the patient’s arrival at the hospital.
Palm Method
A method to estimate the percentage of scattered burns.
The size of the patient’s palm is approximately 1% of BSA. The size of the palm
can be used to assess the extent of burn injury.
Local and Systemic Responses to Burns
Burns that do not exceed 25% of the total BSA produce a primarily local respons
e
Burns that exceed 25% BSA may produce both a local and a systemic response, whi
ch is considered a major burn injury.
Overview of physiologic changes after a major burn injury
Cardiovascular Response
Cardiac output decreases before any significant change in blood volume is evide
nt. As fluid loss continuous and vascular volume decreases,
cardiac output continuous to fall and blood pressure drops. This is the onset of
burn shock. In response, the sympathetic nervous system
releases catecholamines, resulting in an increase in peripheral resistance (vaso
constriction) and an increase in pulse rate. Peripheral
vasoconstriction further decreases cardiac output.
Prompt fluid resuscitation maintains the blood pressure in the low-normal range
and improves cardiac output. Despite adequate fluid
resuscitation, cardiac filling pressures remain low during the burn-shock period
. If inadequate fluid resuscitation occurs, distributive shock will
occur.
Generally, the greatest volume of fluid leak occurs in the first 24 to 36 hours
after the burn, peaking by 6 to 8 hours.
As the capillaries begin to regain their integrity, burn shock resolves and flu
id returns to the vascular compartment.
As fluid is reabsorbed from the interstitial tissue into the vascular compartme
nt, blood volume increases.
If renal and cardiac function is adequate, urinary output increases.
Patients with severe burns develop massive systemic edema. As edema increases i
n circumferential burns, pressure on small blood vessels
and nerves in distal extremities causes an obstruction of blood flow and consequ
ent ischemia. This complication is known as compartment syndrome. The physician
may need to perform an esharotomy, a surgical incision into the eschar (devitali
zed tissue resulting from a burn), to relieve the constricting effect of the bur
ned tissue.
Effects on Fluids, Electrolytes, and Blood Volume
Circulating blood volume decreases dramatically during burn shock. Evaporative
fluid loss through the burn may reach 3 to 5 L or more over a
period of 24 hours until the burn surfaces are covered.
During the shock, serum sodium levels vary in response to fluid resuscitation.
Usually hyponatremia (sodium depletion) is present, as water
shifts from the interstitial to the vascular space.
Immediately after burn injury, hyperkalemia (excessive K) results from massive
cell destruction. Hypokalemia may occur later with fluid shifts
and inadequate potassium intake.
At the time of burn injury, some red blood cells may be destroyed and/or damage
d resulting in anemia. Despite this, patient’s hematocrit may
be elevated due to plasma loss
Blood transfusions are required periodically to maintain adequate hemoglobin le
vels for oxygen delivery.
Abnormalities in coagulation, including a decrease in platelets (thrombocytopen
ia) and prolonged clotting and prothrombin time, also occur
with burn injury.
Pulmonary Response
Inhalation injury is the leading cause of death in fire victims.
One third of all burn injuries have a pulmonary problem related to the burn inj
ury.
Even without pulmonary injury, hypoxemia may be present. Early in the post burn
period, catecholamine release in response to the stress of
the burn injury alters peripheral blood flow, thereby reducing oxygen delivery t
o the periphery. Later, hypermetabolism and continued
catecholamine release lead to increased tissue oxygen consumption, which can lea
d to hypoxemia.
Categories of Pulmonary Injury:
1. Upper Airway Injury
Results from direct heat or edema.
Manifested by mechanical obstruction of the upper airway, including the pharynx
and larynx
Because of the cooling effect of rapid vaporization in the pulmonary tract, dir
ect heat injury does not normally occur below the level of the
bronchus.
Treated by early nasotracheal or endotracheal intubation.
2. Inhalation below the glottis
Results from inhaling the products of incomplete combustion or noxious gases. T
hese products include carbon monoside, sulfur oxides,
nitrogen oxides, aldehydes, cyanide, ammonia, chlorine, phosgene, benzene, and h
alogens.
The injury results directly from chemical irritation of the pulmonary tissues a
t the alveolar level.
Inhalation injuries below the glottis cause loss of ciliary action, hypersecret
ion, severe mucosal edema, and possibly bronchospasm.
The pulmonary surfactant is reduced, resulting in atelectasis (collapse of alve
oli). Expectoration of carbon particles in the sputum is the
cardinal sign of this injury.
Carbon monoxide is the most common cause of inhalation injury because it is a b
yproduct of the combustion of organic materials and is
NCM 104 1st sem S.Y. 2007-2008
25
therefore present in smoke.
Treatment usually consists of early intubation and mechanical ventilation with
100% oxygen. Using 100% oxygen is essential to accelerate the
removal of carbon monoxide from the hemoglobin molecule.
Indicators of possible pulmonary damage:
1. History indicating hat the burn occurred in an enclosed area
2. Burns of the face or neck
3. Singed nasal hair
4. Hoarseness, voice change, dry cough, stridor, sooty sputum
5. Bloody sputum
6. Labored breathing or tachypnea (rapid breathing) and other signs of reduced o
xygen levels (hypoxemia).
7. Erythema and blistering of the oral or pharyngeal mucosa
Pulmonary Complications secondary to Inhalation Injury:
1. Acute respiratory failure
Occurs when impairment of ventilation and gas exchange is life-threatening.
The immediate intervention is intubation and mechanical ventilation.
If ventilation is impaired by restricted chest excursion, immediate escharotomy
is needed.
2. Acute respiratory distress syndrome
> May develop in the first few days after injury secondary to systemic and pulmo
nary responses to the burn and inhalation injury.
Other Systemic Responses
Renal function may be altered as a result of decreased blood volume. If there i
s inadequate blood flow through the kidney, the hemoglobin and
myoglobin occlude the renal tubules, resulting in acute tubular necrosis and ren
al failure.
The immunologic defenses of the body are greatly altered by burn injury. The lo
ss of skin integrity is compounded by the release of abnormal
inflammatory factors. Immunosuppression places the patient at high risk for seps
is.
Loss of skin also results in an inability to regulate body temperature. Burn pa
tients may therefore exhibit low body temperature in the early
hours after burn injury, but as hypermetabolism resets core temperatures, burn p
atients becomes hyperthermic for most of the postburn
period, even in the absence of infection.
Two potential gastrointestinal complications may occur: paralytic ileus (absenc
e of intestinal peristalsis) and Curling’s ulcer. Decreased
peristalsis and bowel sounds are manifestations of paralytic ileus resulting fro
m burn trauma. Gastric distention and nausea may lead to
vomiting unless gastric decompression is initiated.
Management Of The Patient With A Burn Injury
A. Emergent/Resuscitative Phase of Burn Care
The first priority in on-the-scene care for a burn victim is to prevent injury
to the rescuer.
Airway, Breathing, Circulation
It is important to remember the ABC’s of all trauma care because the systemic e
ffects pose a greater threat to life.
1. Airway
2. Breathing
3. Circulation; Cervical spine immobilization for all high voltage electrical in
jury; Cardiac monitoring for all electrical injuries for at least 24 hours
after cessation of dysrhythmias.
Breathing must be assessed and a patent airway established immediately during t
he initial minutes of emergency care. Immediate therapy is
directed toward establishing an airway and administering humidified 100% oxygen.
The circulatory system must also be assessed quickly. Apical pulse and blood pr
essure are monitored frequently
Management of Fluid Loss and Shock
Next to respiratory difficulties, the most important is preventing irreversible
shock by replacing lost fluids and electrolytes. Survival of burn
victims depends on adequate fluid resuscitation.
1. Fluid Replacement
Some combination of fluid categories may be used: Colloids (whole blood, plasma
, and plasma expanders) and crystalloids/electrolytes
(physiologic sodium chloride or lactated Ringer’s solution)
Formulas have been developed for estimating fluid loss based on the estimated p
ercentage of burns BSA and the weight of the patient.
Length of time is also very important in calculating estimated fluid needs.
The formulas are individualized to meet the requirements of each patient
The NIH Consensus Development Conference on Supportive Therapy in Burn Care est
ablished that salt and water are required in burn
patients, but that colloid may or may not be useful during the first 24 to 48 po
stburn hours
The consensus formula provides for the volume of balanced saline solution to be
administered in the first 24 hours in a range of 2 to 4 mL/kg
per percent burn.
Generally, 2mL/kg/ percent burn of lactated Ringer’s solution may be used initi
ally for adults. This is the most common fluid replacement in
use today.
Studies show that with large burn, there is a failure of the sodium-potassium p
ump at the cellular level. Thus, patients with very large burns
may need proportionately more milliliters of fluid per percent of burn than thos
e with smaller burns
Most fluid replacement formulas use isotonic electrolyte solutions.
Another fluid replacement method requires hypertonic electrolyte solutions. Thi
s method uses concentrated solutions of sodium chloride and
lactate (a balanced salt solution). The rationale for this replacement method is
that by increasing serum osmolality, fluid will be pulled back into
the vascular space from the interstitial space. Reduced systemic and pulmonary e
dema results from administering hypertonic solutions.
Goals of Fluid Replacement Therapy: A systolic blood pressure exceeding 100 mm H
g, pulse rate less than 110/minute, and urine output of 30 to
50 ml/hour.
Another gauge for fluid requirements and response to fluid resuscitation includ
e hematocrit and hemoglobin and serum sodium levels.
Nursing Process: Care during the Emergent/Resuscitative Phase
Nursing assessment in the emergent phase of burn injury focuses on the major pr
iorities for any trauma patient; the burn wound is a
secondary consideration.
Aseptic management of the burn wounds and invasive line continues.
The nurse checks vital signs frequently. Respiratory status is monitored closel
y. Apical, carotid, and femoral pulses are evaluated
Cardiac monitoring for patients with cardiac problems, electrical injury or res
piratory problems or if the pulse is dysrhythmic or the rate is
abnormally slow or rapid.
Determining BP is a problem if all extremities are burned. A sterile dressing u
nder the BP cuff will protect the wound from contamination. A
NCM 104 1st sem S.Y. 2007-2008
26
Doppler UTZ or a non-invasive electronic BP may be helpful.
In severe burns, an arterial catheter is used for BP measurement and for collec
ting blood specimen
Peripheral pulses of burned extremities are checked hourly. Doppler is used.
Elevation of burned extremities is crucial to decrease edema.
Elevation of the lower extremities on pillows and of the upper extremities on p
illows or by suspension using intravenous poles may be helpful.
Large-bore IV lines and Indwelling urinary catheter are inserted.
Assessment includes monitoring of fluid intake and output.
Urine output, an excellent indicator of circulatory status, is monitored carefu
lly.
The amount of urine first recorded may assist in determining the extent of preb
urn renal function and fluid status.
Burgundy-colored urine suggests the presence of hemochromogen and myoglobin res
ulting from muscle damage. This is associated with
deep burns caused by electrical injury.
Glucosuria results from the release of stored glucose from the liver in respons
e to stress.
Infusion pumps and rate controllers are used to deliver a prescribed IV fluids
Monitoring IV therapy is a major nursing responsibility.
Body temperature, body weight, preburn weight, and history of allergies, tetanu
s immunization, past medical and surgical problems, current
illnesses, and use of medication are assessed.
A head-to-toe assessment is performed, focusing on signs/symptoms of concomitan
t illness, injury, or developing complications.
Patients with facial burns should have eye examination for potential injuries t
o the cornea
Assessment should include the time of injury, mechanism of burn, whether the bu
rn occurred in closed space.
The neurologic assessment focuses on the client’s level of consciousness, psych
ological status, pain and anxiety levels, and behavior
Acute or Intermediate Phase of Burn Care
Begins 48 to 72 hours after the burn injury.
Attention is directed toward continued assessment and maintenance of respirator
y and circulatory status, fluid and electrolyte balance, and
gastrointestinal function.
Airway obstruction caused by upper airway edema can take as long as 48 hours to
develop. Changes may occur as the effects of resuscitative
fluid and the chemical reaction of smoke ingredients with lung tissues become ap
parent. The patient’s arterial blood gas values and other
parameters determine the need for intubation and mechanical ventilation.
If cardiac or renal function is inadequate, fluid overload occurs and symptoms
of congestive heart failure may result. Vasoactive medications,
diuretics, and fluid restriction may be used to support circulatory function and
prevent congestive heart failure and pulmonary edema
Cautious administration of fluids and electrolytes continuous because of the sh
ifts in fluid from the interstitial to intravascular compartments.
Blood components are administered as needed to treat blood loss and anemia
A resetting of the core body temperature in severely burned patients results in
a body temperature slightly higher than normal for several
weeks after the burn injury. Bacteremia and septicemia also causes fever in many
patients.. Acetaminophen and hypothermia blankets may be
required to maintain body temperature to reduce metabolic stress and tissue oxyg
en demand.
Central venous, peripheral arterial or pulmonary artery thermodilution catheter
s may be required for monitoring venous and arterial pressures.
However, invasive vascular lines are avoided because they provide an additional
port for infection.
Infection progressing to septic shock is the major cause of death in patients w
ho have survived the first few days after a major burn injury. The
immunosuppression places the patient at high risk for sepsis. The infection that
begins within the burn site may spread to the bloodstream.
Infection Prevention
Burn wound is an excellent medium for bacterial growth and proliferation.
Bacteria such as Staphylococcus, Proteus, Pseudomonas, Escherichia coli, and Kl
ebsiella find optimal conditions for growth within the burn
wound. The burn eschar is a non-viable crust, no blood supply; therefore, neithe
r polymorphonuclear leucocytes or antibodies nor systemic
antibiotics can reach the area.
Phenominal numbers of bacteria- 1 billion per gram of tissue- may appear and sp
read to the blood stream or release their toxins, which reach
distant sites.
Fungi such as Candida albicans also grow easily in burn wounds
The primary source of bacterial infection appears to be the patient’s intestina
l tract.
Major secondary source is the environment.
Cap, gown, mask and gloves are worn while caring for patient with open burn wou
nds. Clean technique is used when caring directly for burn
wounds.
Antibiotics are seldom given prophylactically because of the risk of promoting
resistant strains of bacteria.
Tissue specimens are taken for culture regularly to monitor colonization of the
wound by microbial organisms.
Systemic antibiotics are administered when there is documentation of burn wound
sepsis or other positive cultures such as urine, sputum, or
blood.
Wound Cleaning
Hydrotherapy in the form of shower carts, individual showers and bed baths.
Because of the high risk of infection and sepsis, the use of plastic liners and
thorough decontamination of hydrotherapy equipment and wound
care areas are necessary to prevent cross-contamination.
Tap water alone can be used for burn wound cleansing.
Hydrotherapy in any form should be limited to 20 to 30 minute period to prevent
chilling and additional metabolic stress.
Hydrotherapy provides an excellent opportunity for exercising the extremities a
nd cleaning the entire body.
At the time of wound cleaning, all skin is inspected for any hints of redness,
breakdown, or local infection.
Hair in and around burn area, except the eyebrows, should be clipped short.
Intact blisters may be left, but the fluid should be aspirated with a needle an
d syringe
Wound cleaning is usually performed daily.
When the eschar begins to separate from the viable tissue beneath, more frequen
t cleaning and debridement may be necessary
After burn wounds are cleaned, they are gently patted with towel and the prescr
ibed method of wound care is performed.
Whatever is the method of wound care, the goal is to protect the wound from ove
rwhelming proliferation of pathogenic organisms. Patient
comfort and ability to participate are also important considerations.
Topical Antibacterial Therapy
Topical antibacterial therapy does not sterilize the burn wound; it simply redu
ces the number of bacteria so that the overall microbial
population can be controlled by the body’s host defense mechanisms
The three most commonly used topical agents are Silver sulfadiazine (Silvadene)
, silver nitrate, and Mafenide acetate (Sulfamylon)
No single agent is universally effective. Using different agents at different t
imes in the postburn period may be necessary. Prudent use and
alternation of antimicrobial agents results in less-resistant strains of bacteri
a, greater effectiveness of the agents.
Before a topical agent is applied, the previously applied topical agent must be
thoroughly removed.
Wound Dressing
After the wound is cleaned, patted dry and applied topical agent; the wound is
then covered with several layers of dressings.
A light dressing is used over joints to allow for motion, light dressing is als
o applied over areas for which a splint has been designed to
conform to the body contour for proper positioning
Circumferential dressings should be applied distally to proximal.
If the hand or foot is burned, the fingers and toes should be individually wrap
ped to promote adequate healing.
Exposure Method
NCM 104 1st sem S.Y. 2007-2008
27
Occasionally, a wound is treated by exposing it to air. Wound care proceeds in
the same manner and a topical agent is applied, but no
dressings are applied.
The success of exposure method depends on keeping the immediate environment fre
e of organisms. Everything coming in contact with the
patient must be sterile. Those who come in direct contact must wear masks, caps,
sterile gowns and gloves; visitors are instructed to wear
protective garb and not to touch the bed or hand anything to the patient.
The room must be maintained at warm temperature with 40 to 50% humidity to prev
ent excessive evaporative fluid losses.
A cradle may be placed over the patient to prevent sheets from coming in contac
t with the burn area, to minimize the effects of air currents (to
which burn patient is sensitive)
Occlusive Method
An occlusive dressing is a thin gauze that is either impregnated with a topical
antimicrobial or that is applied after topical antimicrobial
application
Occlusive dressing are most often used over areas with new skin grafts. These a
re applied under sterile conditions in the operating room.
Their purpose is to protect the graft, promoting an optimal condition for its a
dherence to the recipient site.
Ideally, these dressings remain in place for 3 to 5 days.
Precautions are taken to prevent two body surfaces from touching, such as finge
rs or toes, ear and scalp, areas under the breasts, any point
of flexion, or between the genital folds.
Dressing Changes
> Dressings are changed approximately 20 minutes after an analgesic is administe
red.
> A mask, hair cover, disposable plastic apron or cover gown, and gloves are wor
n by health care personnel.
Dressings that adhere to the wound can be removed more easily if they are moist
ened with saline solution or if the patient is allowed to soak
for a few moments in the tub.
The patient may participate, providing some degree of control over this painful
procedure.
Wound Debridement
Debridement has two goals:
1. To remove contaminated tissue, thereby protecting the patient from invasion o
f bacteria
2. To remove devitalized tissue or burn eschar in preparation for grafting and w
ound healing.
Natural Debridement
The dead tissue separates from the underlying viable tissue spontaneously. Afte
r partial and full- thickness burns occur, bacteria that are
present at the interface of the burned tissue and the viable tissue underneath g
radually liquefy the fibrils of collagen that hold the eschar in
place for the first or second postburn week.
Using antibacterial topical agents tends to slow down this natural process of e
schar separation
Mechanical Debridement
Involves using surgical scissors and forceps to separate and remove the eschar.
This is carried out to the point of pain and bleeding
Dressings are also helpful debriding agents. Coarse-mesh dressings applied dry
or wet-to-dry (applied wet and allowed to dry) will slowly
debride the wound of exudates and eschar when they are removed.
Surgical Debridement
An operative procedure involving either primary excision (surgical removal of t
issue) of the full thickness of the skin or shaving the burned skin
layers gradually down to freely bleeding, viable tissue.
Surgical excision is initiated early in burn wound management. This may be perf
ormed a few days after or as soon as the patient is
hemodynamically stable and edema has decreased.
Ideally, the wound is then covered immediately with a skin graft and an occlusi
ve dressing.
The use of surgical excision carries with it risks and complications, especiall
y with large burns. The procedure creates a high risk for extensive
bleeding (as much as 100 to 125 ml of blood per percent BSA excised).
Grafting the Burn Wound
If wounds are deep (full thickness) reepitheliazation is not possible. Therefor
e coverage of the burn wound is necessary until coverage with a
graft of the patient’s own skin (autograft) is possible.
The purpose of wound coverage is to decrease the risk for infection; prevent lo
ss of protein, fluid, and electrolytes through the wound; and
minimize heat loss through evaporation.
The main areas for skin grafting include the face, for cosmetic and psychologic
al reasons; the hands and other functional areas such as the
feet; and areas that involve joints.
Grafting permits earlier functional ability and reduces contractures (shrinkage
of burn scar through collagen maturation).
When burns are extensive, the chest and abdomen maybe grafted first to reduce t
he burn surface.
During wound healing, granulation tissue develops. It fills the space created b
y the wound, creates a barrier to bacteria, and serves as a bed
for epithelial cell growth.
Richly vascular tissue is pink, firm, shiny, and free of exudates and debris. I
t should have a bacterial count of less than 100,000 per gram of
tissue to optimize graft take.
A preoperative culture is mandatory before grafting, because enzymes of bacteri
a can dissolve a graft and lead to its failure. Beta hemolytic
streptococci are a major factor in graft failure.
Biologic Dressings (Homografts And Heterografts)
In extensive burns, biologic dressings can be lifesaving by providing temporary
wound closure and protecting the granulation tissue until
autografting is possible.
Biologic dressing may also be used to debride untidy wounds after eschar separa
tion.
With each biologic dressing change, debridement occurs.
Once the biologic dressing appears to be taking or adhering to the granulating
surface with minimal underlying exudation, the patient is ready
for an autograft.
Biologic dressing also provides immediate coverage for clean, superficial burns
and decreases the wound’s evaporative water and protein
loss.
Biologic dressing decrease pain by protecting nerve endings and are an effectiv
e barrier against water loss and entry of bacteria.
When applied to superficial partial-thickness wounds, they seem to speed healin
g.
Biologic dressings consist of homografts (or allografts) and heterografts(or xe
nografts).
Homografts are skin obtained from living or recently deceased humans. The amnio
tic membrane (amnion) from the human placenta may also
be used as a biologic dressing.
Heterografts consist of skin taken from animals (usually pigs).
Most biologic dressings are used as temporary coverings of burn wounds and are
eventually rejected because of the body’s immune reaction
to them as foreign.
Homografts tend to be the most expensive biologic dressings. They are available
from skin banks in fresh and cryopreserved (frozen) forms.
Homografts are thought to provide the best infection control. Of all the biolog
ic and bio synthetic dressings available. Revascularization occurs
within 48 hours, and the graft may be left place for several weeks.
NCM 104 1st sem S.Y. 2007-2008
28
Amnion is low in cost, however, amnion grafts do not become vascularized by the
patient’s vessels and can be left in place only briefly.
Pigskin is available from commercial suppliers. Pigskin impregnated with a topi
cal antibacterial such as silver nitrate is also available.
One new biologic dressing that has shown promise for permanent burn wound cover
age is Alloderm.
Alloderm is processed dermis from human cadaver skin. When a donor site is take
n for an autologous skin graft, both the epidermal and
dermal layers of skin are removed from the donor site. However, Alloderm provide
s a permanent dermal layer replacement.
Use of alloderm allows the surgeon to take a thinner skin graft consisting of t
he epidermal layer only. The patient’s epidermal layer is placed
directly over the dermal base (Alloderm).
Use of Alloderm has resulted in less scarring and contractures with healed graf
ts; donor sites heal much more quickly than conventional donor
sites because only the epidermal layer has been taken.
Biosynthetic And Synthetic Dressings
Currently, the most widely used synthetic dressing is Biobrane, which is compos
ed of nylon. Silastic membrane combined with a collagen
derivative.
Less costly than homograft or pigskin.
Biobrane dressings adhere to donor sites and meticulously clean debrided partia
l-thickness wounds; they will remain until spontaneous
epitheliazation and wound healing occur.
Like biologic dressing, Biobrane protects the wound from fluid loss and bacteri
al invasion.
Biobrane is also useful for intermediate or long-term closure of a surgically e
xcised wound until an autograft becomes available.
Like Biologic dressing, Biobrane should not be used over grossly contaminated o
r necrotic wounds.
Several other synthetic dressings are available: Op-site, a thin, transparent,
polyurethane elastic film, can be used to cover clean partial-
thickness wounds and donor sites. This dressing is occlusive and waterproof but
permeable to water vapor and air; this permeability provides
protection from microbial contamination and allows for the exchange of gases. Ot
her synthetic dressings are Tegaderm, N-Terface, and
Duoderm.
Artificial skin (Integra) is the newest type of synthetic dressing. A dermal an
alogue, Integra is composed of two main layers. The epidermal
layer, consisting of Silastic, acts as a bacterial barrier and prevents water lo
ss from the dermis. The dermal layer is composed of animal
collagen. It interfaces with the open wound surface and allows migration of fibr
oblasts and capillaries into the material.
Autografts
The ideal means of covering burn wounds because they come from the patient’s ow
n skin and thus are not rejected by the patient’s immune
system.
They can be split-thickness, full-thickness, pedicle flaps, or cultured epithel
ium. Full-thickness and pedicle flaps are commonly used for
reconstructive surgery, months or years after the initial injury.
Split-thickness autografts can be applied in sheets or in postage stamp-like pi
eces, or they can be expanded by meshing so that they can
cover 1.5 to 9 times more than a given donor site area. Skin meshers enable the
surgeon to cut tiny slits into a sheet of donor skin, making it
possible to cover large areas with smaller amounts of donor skin. These expanded
grafts cling to the recipient site more easily than sheet
grafts and prevent the accumulation of blood, serum, air, or purulent material u
nder the graft.
Using expanded grafts may be necessary in large wounds but should be viewed as
a compromise in terms of cosmetics.
Care of the Patient with an Autograft
Occlusive dressings are commonly used initially after grafting to immobilize th
e graft.
Occupational therapists may be helpful in constructing splints to immobilize ne
wly grafted areas to prevent dislodging the graft
If the graft is dislodged, sterile saline compresses will help prevent drying o
f the graft until the physician reapplies it.
The patient is positioned and turned carefully to avoid disturbing the graft or
putting pressure on the graft site.
If an extremity has been grafted, it is elevated to minimize edema.
The patient begins exercising the area 5 to 7 days after grafting.
Care of Donor site
Moist gauze is applied at the time of surgery to maintain pressure and to stop
any oozing.
A thrombostatic agent such as thrombin or epinephrine may be applied directly t
o the site.
The donor site may be applied with a single-layer gauze impregnated with petrol
atum, scarlet red, or bismuth to new biosynthetic dressings
such as Biobrane.
Donor site must remain clean, dry, and free from pressure.
Because a donor site is usually a partial-thickness wound, it will heal spontan
eously within 7 to 14 days with proper care
Pain Management
Pain management is the most difficult challenges facing the burn team.
Many factors contribute to the patient’s burn pain experience: severity of the
pain, health provider’s pain assessment, the appropriateness and
adequacy of pharmacologic treatment of pain, the multiple procedures involved an
d assessment of the effectiveness of pain relief measures.
The outstanding features of burn pain are its intensity and long duration.
Wound care carries with it anticipation of pain and anxiety.
In partial-thickness burn, the nerve endings are exposed, resulting to excrucia
ting pain with exposure to air currents.
Although, nerve endings are destroyed in full-thickness burns, there is deep pa
in and pain in adjacent structures.
The primary pain is intense in the initial acute post burn phase. This pain gra
dually subsides. However, until the skin heals or graft are applied
and taken, the pain level remains high because of treatment-induced pain. Wound
cleaning, dressing changes, debridement, and physical
therapy inflict intense pain. Discomforts related to tissue healing, such as itc
hing, tingling, and tightness of contracting skin and joints adds to
the duration and intensity of pain.
Because pain can not be eliminated short of anesthesia, the goal is to minimize
the pain with analgesics before the patien faces wound care
procedures.
Bolus doses of opioids, usually morphine, are often provided. Ketamine anesthes
ia administered IV are also used.
Sedation with anti-anxiety agents such as lorazepam (Ativan) or midazolam(Verse
d) may be indicated in addition to analgesia.
Patient-controlled analgesia, using both continuous and bolus morphine infusion
s, and sustained release oral morphine, given every 12 hours
have helped burn patients.
Self-administered nitrous oxide also helps to make dressing changes tolerable t
o those patients who have sufficient hand function to hold a
mask to their faces intermittently during dressing changes.
Early surgical excision with grafting under anesthesia may be the best way to r
educe the overall pain experience for burn patients.
Nutritional Support
Hypermetabolism persist after burn injury until wounds are closed, thereby incr
easing the basal metabolic need by as much as 100%.
The goal of nutritional support is to promote a state of positive nitrogen bala
nce.
The nutritional support required is based on the patient’s preburn status and t
he extent of total BSA burned.
Several formulas exist for estimating the daily metabolic expenditure and calor
ic requirements of burn patients.
Protein requirements may range from 1.5 to 4 g of protein per kg of body weight
every 24 hours
Lipids are included in the nutritional support because of their importance for
wound healing, cellular integrity, and absorption of fat-soluble
vitamins.
Carbohydrates are included to meet caloric requirements as high as 5,000 cal pe
r day
Adequate vitamins and minerals are also needed.
The proportions of fat, protein, and carbohydrate are planned for maximal use.
NCM 104 1st sem S.Y. 2007-2008
29
Overfeeding can be detrimental. Therefore, a dietitian familiar with current co
ncepts in nutrition for burn patients is necessary.
As soon as GIT function resumes, nutritional support begins. The enteral route
is preferred. In patients with extensive burns, tube feedings
may be indicated to ensure daily calories needed.
Indications for Total parenteral nutrition (TPN) include weight loss greater th
an 10% of normal body weight, inadequate intake of enteral
nutrition prolonged wound exposure, and malnutrition or debilitated condition be
fore injury.
DISORDERS OF WOUND HEALING
SCARS
Results from excessive abnormal healing or inadequate new tissue formation.
Hypertrophic scars and wound contractures are more likely to occur if the initi
al burn injury extends below the level of the deep dermis.
Healing of such deep wounds result in the replacement of normal integument
Compression measures are instituted early in the burn wound treatment to preven
t scar formation. Ace wraps are used to promote adequate
circulation, used as the first form of compression.
Scar management occurs mainly in the rehabilitative phase, after the wounds are
closed.
KELOIDS
A large, heaped-up mass of scar tissue.
Keloids tend to be found in darkly pigmented people, grow outside of wound marg
ins, and recur after surgical excision.
FAILURE TO HEAL
Failure to heal may be due to many factors, including infection and inadequate
nutrition
A serum albumin level of less than 2g/dL is a usual factor
CONTRACTURES
The burn wound tissue shortens because of the force exerted by the fibroblasts
and the flexion in natural wound healing.
An opposing force provided by splints, traction, and purposeful movement and po
sitioning must be used to counteract deformity in burns
affecting joints.
Nursing Process: Burn Care During The Acute Phase
Assessment
Continued assessment focuses on hemodynamic alterations, wound healing, pain an
d psychosocial responses, and early detection of
complications.
Nurse assess VS frequently
Continued assessment of peripheral pulses is essential for the first few post b
urn days while edema continuous to increase, potentially
damaging peripheral nerves and restricting blood flow.
Observation of the electrocardiogram may give clues to cardiac dysrhythmias res
ulting from potassium imbalance, preexisting cardiac
disease, or the effects of electrical injury or burn shock
Assessment focuses on hemodynamic alterations, wound healing, pain and psychoso
cial responses, and early detection of complications.
Assessment of respiratory and fluid status is the highest priority for detectio
n of complications.
Assess VS
Assessment of peripheral pulses while edema continuous to increase, damaging pe
ripheral nerves and restricting blood flow
ECG may give clues to cardiac dysrhythmias resulting from potassium imbalance,
preexisting cardiac disease, or the effects of electrical injury
or burn shock
Assessment of residual gastric volumes and pH in the patient with a NGT- gives
clues to early sepsis or the need for antacid therapy. Blood in
the gastric fluid or stools must also be reported
Important wound assessment include size, color, odor, eschar, exudates, abscess
formation under the eschar, epithelial buds (small pearl-like
clusters of cells on the wound surface), bleeding, granulation tissue appearance
, progress of grafts and donor sites, and quality of surrounding
skin
Assessment on pain and psychosocial responses, daily body weights, caloric inta
ke, general hydration, and serum electrolyte and hemoglobin
levels and hematocrit
Assessment for excessive bleeding from blood vessels adjacent to areas of surgi
cal site and debridement
Potential Complications:
1. Congestive heart failure and pulmonary edema
2. Sepsis
3. Acute Respiratory Failure
4. Visceral Damage
Planning and Goals:
The major goals:
restoration of normal fluid balance,
absence of infection,
attainment of anabolic state and normal weight,
improved skin integrity,
reduction of pain and discomfort
optimal physical mobility
adequate patient and family coping
adequate patient and family knowledge of burn treatment
absence of complications
Restoring Normal Fluid Balance
Monitor IV and oral intake to reduce risk for fluid overload and consequent CHF
1. Use IV infusion pumps
2. Daily weights are obtained
Low-dose dopamine to increase renal perfusion
Diuretics to increase urine output
Preventing Infection
A clean and safe environment
Detect early signs of infection – culture results and WBC counts are monitored
Aseptic technique for wound care procedures. Hand washing before and after each
patient contact
Fresh flowers, plants or fresh fruit baskets should not be allowed inside the r
oom because of the risk of microorganism growth
Visitors are screened to avoid exposing the immunocompromised patient to pathog
ens
NCM 104 1st sem S.Y. 2007-2008
30
Maintaining Adequate Nutrition
Oral fluids should be initiated slowly when bowel sounds resumes. If vomiting a
nd abdominal distention do not occur, fluids may be gradually
increased
The nurse collaborates with the dietitian to plan a protein-and calorie-rich di
et
If caloric goals can not be met by oral feeding, a feeding tube is inserted
Promoting Skin Integrity
Assess and record changes or progress in wound healing
Wound care
Topical antibacterial agents
Relieving Pain and Discomfort
Pain is more severe in partial-thickness burns than in full-thickness burns bec
ause the nerve endings are not destroyed. Cover exposed nerve
endings to help reduce pain
Analgesics and anti-anxiety medications
Teach relaxation techniques
Give patient control over wound care
Pain-relieving distractions: video programs/games, hypnosis
Complete treatments and dressings quickly. Analgesics before any painful proced
ures
Oral anti-pruritic agents, cool environment, frequent lubrication of skin with
water or silica-based lotion – to reduce discomfort in itching
Exercise and splinting to prevent skin contracture
Promoting Physical Mobility
Early priority is to prevent complications resulting from immobility
Deep breathing, turning, and proper positioning to prevent atelectasis and pneu
monia, control edema and to prevent pressure ulcers and
contractures.
Early sitting and ambulation
When lower extremities are burned elastic bandage are applied before the patien
t is placed in an upright position. This bandages promote
venous return and minimize swelling
Passive and active ROM to prevent contracture
Splints or other functional devices are used for contracture control. Monitor s
plinted areas for signs of vascular insufficiency and nerve
compression
Strengthening Coping Strategies
The patient is facing the reality of burn trauma and is grieving over obvious l
oss. Depression, regression and manipulative disorders are
common problems
Develop effective coping strategies by:
1. Setting specific expectations for behavior
2. Promoting truthful communications to build trust
Patient always ventilates feelings of anger – enlist someone to whom patient ca
n vent feelings without fear of retaliation
Monitoring and Managing Potential Complications:
Congestive Heart Failure and Pulmonary Edema
Patient is assessed for pulmonary overload – may occur as fluid is mobilized fr
om the interstitial compartment back into the intravascular
compartment. If the cardiac and renal system cannot compensate for the excess va
scular volume, CHF and pulmonary edema may result.
Crackles in the lungs and increased difficulty with respiration may indicate a
fluid buildup in the lungs.
1. Patient is positioned comfortably with the head of the bed raised to promote
lung expansion and gas exchange
2. Provide supplemental oxygen
3. Administer IV diuretics
Sepsis
Early signs are increased in temperature, increased pulse rate, flushed dry ski
n, increased pulse rate, widened pulse pressure, and flushed
dry skin in unburned areas
Wound and blood cultures
Antibiotics
Acute Respiratory Failure and Acute Respiratory Distress Syndrome
Patient is assessed for increased difficulty in breathing, change in respirator
y pattern, onset of adventitious (abnormal) sounds
Signs of hypoxia (decreased O2 to the tissues), decreased breath sounds, wheezi
ng, tachypnea, stridor
Patients receiving mechanical ventilation must be assessed for a decrease in ti
dal volume and lung compliance
Key sign of ARDS is hypoxemia while receiving 100% oxygen, decreased lung compl
iance and significant shunting
Management includes intubation and mechanical ventilation
Visceral Damage
Assess for signs of necrosis of visceral organs due to electrical injury. Tissu
es affected are usually between the entrance and exit wounds of
the electrical burn
All patients with electrical burns should undergo electrocardiographic monitori
ng
Assess for pain relate to deep muscle ischemia
Fasciotomies are performed to relieve the swelling and ischemia in the muscles
Rehabilitation Phase Of Burn Care
Rehabilitation begins immediately after the burn has occurred
Wound healing, psychosocial support, and restoring maximal functional activity
remain priorities
Continued focus on maintaining fluid and electrolyte balance and improving nutr
itional status
Reconstructive surgery to improve body appearance and function
Psychological and vocational counseling and referral to support groups
NCM 104 1st sem S.Y. 2007-2008
31
HIGH RISK PREGNANCY
Definition: One in which a concurrent disorder, pregnancy-related complication,
or external factor jeopardizes the health of the mother and/or fetus.
Many factors enter into the categorization of high risk.
No tool is perfect because the concept of high risk is a very individualized on
e
The woman identified this way needs close observation during pregnancy to see t
hat pregnancy is progressing well
The infant born of a woman identified this way needs close observation in the n
eonatal period until it is confirmed that no anomalies exist
The failure to identify risk potential in pregnancy leads to increased perinata
l mortality
ASSESSMENT FOR A FIRST PREGNANCY VISIT :
1. HEALTH HISTORY
Purpose :
a. To establish rapport
b. To gain information about the woman’s physical and psychosocial health
c.
To obtain a basis for anticipatory guidance for the pregnancy
A. Demographic Data : Name, age, address, telephone number, health insurance
B. Chief Concern – Reason why the woman has come to the health care setting.
1. Was the pregnancy planned?
2. Inquire date of last menstruation
3. Ask if she has had a pregnancy test
4. Elicit information about signs of early pregnancy
5. Observe for discomforts of pregnancy
6. Has she been exposed to contagious diseases
7. Has she taken any medicine that might be harmful to fetal growth
C. Family Profile – helps to know the woman earlier
1.Identify support persons, Family composition
2.What is her occupation, source of income, Nutrition, sleep pattern, hobbies, l
iving conditions
D. Past Medical History – important because a past condition may become active d
uring or immediately following pregnancy.
1. Any abdominal surgery, kidney, heart, etc.
E. Gynecologic History – her past experience with her reproductive system may ha
ve some influence on how well she accepts a pregnancy.
1. When was her menarche
NCM 104 1st sem S.Y. 2007-2008
32
2. What is the length and duration of menstrual cycle
F. Obstetric History:
1. Review pregnancy briefly.
2. Determine woman’s status with respect to the number of times she has been pre
gnant (gravida) and the number of children above the
age of viability she has previously delivered (para).
3. A more comprehensive system for classifying pregnancy status (GTPAL or GTPALM
) provides greater detail on the pregnancy history. By
this system, the gravida classification remains the same, but para is broken dow
n into :
T : The # of full-term infants born (37 weeks or after)
P : The # of preterm infants born (infants born before 37 weeks)
A : The # of spontaneous or induced abortions
L : The # of living children
M : Multiple pregnancies
G. Typical Day History
Information about a woman’s current nutrition, elimination, sleep, recreation a
nd interpersonal interactions can be elicited best by asking
the woman to describe a typical day of her life.
H. Review of Systems – Brief review of all body systems
a. Head – Ask about headache, head injury, seizures, dizziness
b. Eyes – Inquire about vision, eyeglasses, eye diseases
c.
Ears – Infection, discharges, pain
d. Nose – Bleeding, discharges, colds, allergy, sinuses
e. Mouth and pharynx –Dentures, teeth, toothache, bleeding, pain, surgery
f.
Neck – stiffness, masses
g. Breast – lumps, secretion, pain, tenderness
h. Respiratory – cough, wheezing, asthma, SOB
i.
Cardiovascular – heart murmur, history of heart disease, HPN
j.
G.I.T – pre-pregnant weight, diarrhea, constipation, hemorrhoids, ulcer
k.
Genito-urinary – infection, STD’s
l.
Extremities – varicose veins, pain or stiffness of joints, fractures
m. Skin – rashes, acne, psoriasis
I. Support Persons Role
Questions asked to the support person : Current health status, feelings and con
cern about the pregnancy, knowledge of pregnancy
and childbirth
2. PHYSICAL EXAMINATION
A. Baseline Data : to establish a baseline for future comparison
-
Weight, Height, BP, PR, RR
-
FHR : 120-160 beats/min
-
10-12 weeks (Doppler)
-
18-20 weeks (Stethoscope)
-
Fundic height:
12-14 weeks – Symphysis pubis
20-22 weeks – Umbilicus
36 weeks - Xiphoid process
40 weeks - Xiphoid process
B. System Assessment
1. General Appearance and Mental Status
Physical examination always begins with inspection of general appearance to for
m a general impression of the woman’s health and
well-being.
A physical examination at a first prenatal visit typically includes inspection
of body systems, with emphasis on changes that occur with
pregnancy.
General appearance is important because it reveals how people feel about themse
lves by the manner in which they dress, speak and
body posture they assume
2. Head and Scalp
Examine head for symmetry, normal contour and tenderness
Examine hair for distribution, thickness, excessive dryness or oiliness, cleanl
iness, or the use of hair dye.
Look for chloasma (extra pigment on the skin)
3. Eyes
Edema in the eyelids
Spots before the eyes
Diplopia (double vision)
-
may indicate PIH
4. Nose
Increased level of estrogen associated with pregnancy may cause nasal congestio
n.
5. Ears
The nasal stuffiness that accompanies pregnancy may lead to blocked Eustachian
tubes and therefore a feeling of fullness or
dampening of sound during early pregnancy.
6. Sinuses
Sinuses should feel nontender
7. Mouth, Teeth and Throat
Pregnant woman is prone to vitamin deficiency because of the rapid growth of th
e fetus.
Assess carefully for cracked corners of the mouth that would reveal vitamin A d
eficiency.
Assess carefully for pinpoint lesions with an erythematous base on the lips; th
ese suggest a herpes infection
Gingival hypertrophy may result from estrogen stimulation during pregnancy.
Teach all women not to neglect good dental hygiene while pregnant
8. Neck
Slight thyroid hypertrophy may occur with pregnancy because the overall metabol
ic rate is increased.
Encourage a woman to continue to use iodized salt during pregnancy and to eat s
eafood at least once weekly to supply enough iodine
NCM 104 1st sem S.Y. 2007-2008
33
for thyroxine production with this increased rate.
9. Lymph Nodes
No palpable lymph nodes should be present.
10. Breasts
As pregnancy begins, the breast undergo the following : Breast areola darkens;
Montgomery’s tubercles become prominent; Breast
size increases; breast tone affirms; secondary areola may develop surrounding th
e natural one; blue streaking of veins becomes
prominent; colostrums may be expelled as early as the 16th week of pregnancy; an
y supernumerary nipple also may become darker.
All women should be instructed on monthly breast self examination.
11. Heart
Heart rate should range from 70 to 80 beats/minute.
No accessory sounds or murmurs should be present.
Because of the breast size , it may be difficult to hear the woman’s heart beat
during pregnancy
Many women notice occasional palpitations (heart skipping a beat) during pregna
ncy, especially when lying supine. Teach pregnant
woman to rest or sleep on their side (left side is best) to avoid this problem.
12. Lungs
Late in pregnancy, diaphragmatic excursion is lessened because the diaphragm ca
nnot descend as fully as usual because of the
distended uterus.
13. Back
Assess the spine for any abnormal curve that would suggest scoliosis.
14. Rectum
Assess the pregnant woman’s rectum closely for hemorrhoidal tissue, which commo
nly occurs from pelvic pressure preventing venous
return.
15. Extremities and Skin
Assess the upper extremities. Many women develop palmar erythema and itching ea
rly in pregnancy from a high estrogen level and
perhaps subclinical jaundice.
Assess the lower extremities carefully for varicosities, filling time of the to
enails (should be under 5 seconds) and edema.
Assess the gait of pregnant women to see that they are keeping their pelvis tuc
ked under the weight of their abdomen.
MEASUREMENT OF FUNDAL HEIGHT AND FETAL HEART SOUNDS
12-14 weeks of pregnancy – uterus is palpable over the symphysis pubis as a fir
m globular sphere
20-22 weeks – reaches umbilicus
36 weeks – xiphoid process
40 weeks – often return to 4 about 4 cm below the xiphoid due to lightening
Auscultate for fetal heart sounds (120 to 160 beats/minute. These can be heard
at 10 to 12 weeks if Doppler is used. 18 to 20
weeks if regular stethoscope is used.
Palpate for fetal outline and position after the 28th week.
PELVIC EXAMINATION
> Reveals information on the health of both internal and external reproductive o
rgans
a. EXTERNAL GENITALIA – note for :
1.Signs of inflammation
2.Irritation
3.Infection
4.Herpes simplex II virus infection
5.Rectocele
6.Cystocele
b. INTERNAL GENITALIA
1. Cervix should be in the center and color should be almost purple when pregnan
t.
Retroverted Uterus – cervix positioned anteriorly
Anteverted Uterus – cervix positioned posteriorly.
1. Nulligravida – woman who is not or never has been pregnant, the cervical os i
s round and small.
2. A woman who has had a previous pregnancy, the cervical os has a slitlike appe
arance.
3. If the woman had a cervical tear during a previous birth, the cervical os may
appear as a transverse crease.
4. If a cervical infection is present, a mucus discharge maybe present. With inf
ection, the epithelium of the cervical canal often enlarges and
spreads onto the area surrounding the os. Giving the cervix a reddened appearanc
e called erosion. This area bleeds easily if touched.
Trichomoniasis – a protozoal infection, generally gives signs of redness; a pro
fuse, whitish, bubbly discharge; and petechial spots on the
vaginal walls.
Candidal (Monilial) infection – presents with thick, white vaginal patches that
may bleed if scraped away.
A gonorrheal infection – presents with a thick, greenish-yellow discharge and e
xtreme inflammation.
Chlamydia infection – shows few symptoms.
Carcinoma of the cervix appears as an irregular, granular growth at the os.
Cervical polyps (red, soft, pedunculated protrusions) also may be seen occasion
ally at the os.
c. PAPANICOLAOU SMEAR
Weapon for detecting cervical cancer
American Cancer Society recommends a pap smear every 3 years in women who have
had 2 consecutive negative tests.
Recommended more frequently to women who were exposed to diethylstilbestrol (DE
S) in utero, who have multiple sexual partners, who have
a history of human papillomavirus (HPV), cigarette smokers, who were sexually ac
tive before age 21
d. VAGINAL INSPECTION
A culture for gonorrhea, chlamydia or group B streptococcus may be taken. All t
hese organism can cause disease in the NB so it is best if they
can be eradicated during pregnancy
Any areas of inflammation, ulceration, lesions or discharge should be noted
Vaginal examination is critical for a woman whose mother took DES during her pr
egnancy. Female children of mothers who took DES are
prone to develop adenosis or overgrowth of cervical endothelium (which is possib
ly associated with vaginal cancer).
e. EXAMINATION OF PELVIC ORGANS
A bimanual (two-handed) examination is performed to assess the position, contou
r, consistency, and tenderness of pelvic organs
Abnormalities that can be noted by bimanual examination include ovarian cysts,
enlarged fallopian tubes (perhaps from pelvic Inflammatory
Disease) and an enlarged uterus.
NCM 104 1st sem S.Y. 2007-2008
34
An early sign of pregnancy (Hegar’s sign) is elicited on bimanual examination.
f. RECTOVAGINAL EXAMINATION
To assess the strength and irregularity of the posterior vaginal wall
e. ESTIMATING PELVIC SIZE
It is hard to see from the outward appearance of a woman whether her pelvis is
adequate for the passage of a fetus.
Pelvic measurements should be taken if the woman is pregnant and if she has nev
er given birth vaginally
In sonogram, estimations may be made by a combination of pelvic pelvimetry and
fetal sonogram
Estimation of pelvic adequacy must be done at least by the 24th week of pregnan
cy, because by this time, there is danger that the fetal head
will reach a size that will interfere with safe passage and birth if the pelvic
measurements are small
Once a woman has given birth vaginally, her pelvis has been approved adequate,
and it is not necessary to take pelvic measurements.
Types of Pelvis
> Categorized into 4 groups :
•
Gynecoid : normal female pelvis
•
Anthropoid : Ape-like pelvis
•
Platypelloid : Flattened pelvis
•
Android : Male pelvis
PELVIC MEASUREMENTS
Internal pelvic measurements give the actual diameters of the inlet and outlet
through which the fetus must pass. The following measurements
are made most commonly :
1. The Diagonal Conjugate – The distance between the anterior surface of the sac
ral prominence and the anterior surface of the inferior margin of
the symphysis pubis. The most useful measurement for estimation of pelvic size,
because it suggests the anteroposterior diameter of the pelvic
inlet.
2. The True Conjugate – Conjugate Vera.
The measurement between the anterior surface of the sacral prominence and the po
sterior surface of the inferior margin of the symphysis pubis.
3. The Ischial Tuberosity – The distance between the ischial tuberosities, or th
e transverse diameter of the outlet. A diameter of 11 cm is
considered adequate because it will allow the widest diameter of the fetal head.
3. LABORATORY ASSESSMENT
•
Blood Studies
•
Urinalysis
•
Tuberculosis Testing
•
Ultrasound
IDENTIFYING THE HIGH-RISK PREGNANCY
Some women enter pregnancy with a chronic illness that, when superimposed on th
e pregnancy, makes it high risk.
Other women enter pregnancy in good health but then develop a complication of p
regnancy that causes it to become high risk.
A combination of particular instances – poverty, lack of support people, poor c
oping mechanisms, genetic inheritance, or past history of
pregnancy complications can cause a pregnancy to be categorized as high risk.
FACTORS THAT CATEGORIZE A PREGNANCY AS HIGH RISK
A. Infections During Pregnancy
•
Maternal infections during pregnancy may contribute significantly to fetal morbi
dity and mortality.
•
Infections in this category may be caused by various viruses. Other organisms li
ke bacteria, spirochetes, protozoa, or yeast may also cause maternal infections,
which are harmful to the developing fetus. Even though the infection in the mot
her may be very mild, the effects on the fetus may be catastrophic.
•
Most organisms cross the placenta and infect the fetus, causing birth anomalies.
The fetus may also acquire the organism as it
travels the birth canal during labor, causing illness after birth.
SEXUALLY TRANSMITTED DISEASES AND PREGNANCY
Spread through sexual contact with an infected partner.
All STD’s can be prevented to some extent by the use of safer sex practices.
Treatment begins with determining the causative organism so the appropriate ant
ibiotic or antifungal medication can be prescribed.
Nursing Diagnosis : Pain related to vulvar irritation secondary to existence of
STD
1. THE WOMAN WITH CANDIDIASIS
Candidiasis causes a vaginal infection spread by the fungus Candida.
Assessment :
1. Thick, cream cheeselike vaginal discharge and extreme pruritus.
2. Vagina appears red and irritated
Etiology :
1. Occurs more frequently during pregnancy because of the increased estrogen lev
el present during pregnancy.
2. Occurs frequently to women being treated with an antibiotic for another infec
tion.
3. Occurs frequently in women with gestational diabetes
4. Mostly seen in women with HIV infection
Dx : Diagnosed by microscopic analysis
Treatment : Local application of an antifungal cream such as miconazole cream (M
onistat) or oral fluconazole (Diflucan)
Complications :
1. If untreated during pregnancy, it may cause a candidal infection, or thrush,
in the NB.
2. THE WOMAN WITH TRICHOMONIASIS
A single-cell protozoan spread by coitus.
Assessment :
NCM 104 1st sem S.Y. 2007-2008
35
1. A yellow-gray, frothy, odorous vaginal discharge.
2. Vulvar itching, edema, and redness
Dx: Diagnosed by examination of vaginal secretions on a wet slide that has been
treated with Potassium Hydoxide (KOH).
Treatment :
Topical clotrimazole instead of metronidazole because of its possible teratogeni
c effects if used during the first trimester of pregnancy.
Etiology :
Probably associated with preterm labor, premature rupture of membranes and post
cesarean section infection
3. THE WOMAN WITH BACTERIAL VAGINOSIS (GARDNERELLA INFECTION)
Local infection of the vagina by the invasion, most commonly, of Gardnerella or
ganisms.
Assessments :
1. Discharge is gray and has a fishlike odor
2. Intense pruritus
Treatment :
1. Metronidazole for non pregnant women.
2. Because Metronidazole is contraindicated during the first trimester, women ar
e usually treated with a topical cream
Complications :
1. Untreated bacterial infections are associated with amniotic fluid infections,
perhaps, preterm labor and premature rupture of membranes.
4. CHLAMYDIA TRACHOMATIS
One of the most common types of vaginal infections seen during pregnancy.
> Infection is caused by a gram-negative intracellular parasite
Assessment :
1. Heavy gray-white vaginal discharge
Dx: Diagnosis is made by culture of the organism from vaginal secretions using a
specific chlamydia culture kit.
Treatment :
1. Therapy is usually with tetracyclines but contraindicated during pregnancy be
cause of possible long bone deformities; Erythromycin and
Amoxicillin are used instead.
It is important that chlamydia infections be treated because they are associate
d with PROM, preterm labor and endometritis in the postpartal
period.
An infant who is born while a chlamydia infection is present in the vagina can
suffer from conjunctivitis or pneumonia after birth.
5.SYPHILIS
A systemic disease caused by the spirochete Treponema pallidum.
Assessment :
1.The 1st stage results in a painless ulcer (chancre) on the vulva or vagina.
2. Hepatic and splenic enlargement, headache, anorexia, and maculopapular rash o
n the palms of the hand and the soles of the feet
( secondary syphilis; occurring about two months after initial infection
Complications :
1. Spontaneous Abortion
2. Preterm Labor
3. Stillbirth
4. Congenital anomalies in the NB
Dx: All pregnant women are screened for syphilis by VDRL, RPR or FTA-ABS antibod
y reaction test.
Treatment :
1. One injection of Benzathine penicillin G is the drug of choice during pregnan
cy
6.THE WOMAN WITH GONORRHEA
A sexually transmitted disease caused by the gram-negative coccus Neisseria gon
orrhea.
Assessments :
1. May not produce symptoms in some women
2. A yellow-green vaginal discharge may be present
Gonorrhea is associated with spontaneous abortion, preterm birth, and endometri
tis in the postpartal period.
Also a cause of pelvic infectious disease and infertility.
Dx : Diagnosis is made by culture of the organism from the vagina, rectum or ure
thra
Treatment :
1. Traditionally treated with amoxicillin and probenecid but the incidence of pe
nicillinase-producing strains has made this therapy ineffective.
2. Oral Cefixime and Ceftriaxone sodium IM are now the drug of choice.
3. Sexual partner should also be treated to prevent infection.
Complications :
1. If untreated at time of birth, it can cause severe eye infection that can lea
d to blindness in the NB (Ophthalmia neonatorum).
2. Major cause of pelvic infectious disease and infertility
7.THE WOMAN WITH HUMAN PAPILLOMA VIRUS INFECTION
The Human papilloma virus (HPV) causes fibrous tissue overgrowth on the externa
l vulva (condyloma acuminatum)
Etiology :
1. Women who have multiple sexual partners
Assessments :
1. Discrete papillary structures at first which spreads, enlarges and coalesce t
o form large, cauliflower-like lesions
2. Tend to increase in size during pregnancy because of the high vascular flow i
n the pelvic area.
3. They may become secondarily ulcerated and infected; when this occurs, a foul
vulvar odor may develop
NCM 104 1st sem S.Y. 2007-2008
36
Treatment :
1. Aimed at dissolving the lesions and also ending any secondary infection prese
nt.
2. Trichloroacetic acid (TCA) or Bichloroacetic acid (BCA) applied to the lesion
s weekly
3. Large lesions may be removed by laser therapy, cryocautery or knife excision.
4. If present at time of birth and obstruct birth canal, a CS maybe performed
Complications :
1. Associated with the development of cervical cancer later in life.
8.THE WOMAN WITH A GROUP B STREPTOCOCCI INFECTION
Etiology :
1. Occurs at a higher incidence during pregnancy
Assessment :
1. Patient usually experiences no symptoms.
Complications :
1. Urinary Tract Infection (UTI)
2. Intra-amniotic Infection leading to preterm birth
3. Postpartal endometritis
4. 40 % to 70% of neonates whose mothers have an active infection will become in
fected from placental transferal or from direct contact with the
organisms at birth.
5. Infected neonates may develop severe pneumonia, sepsis, respiratory distress
syndrome or meningitis
Dx: Women are screened at 35 to 38 weeks of pregnancy by a vaginal culture.
Treatment :
1. Broad spectrum penicillin such as ampicillin
2. Women who experience rupture of membranes at less than 37 weeks of pregnancy
are treated with Ampicillin IV
9.THE WOMAN WITH HUMAN IMMUNODEFICIENCY VIRUS (HIV) INFECTION
The HIV virus, which leads to AIDS, is the most serious of the STD’s because it
may be fatal to both mother and child.
Etiology :
1. Multiple sexual partners of the individual or sexual partner
2. Bisexual partners
3. IV drug use by the individual or sexual partner
4. Blood transfusions
Assessment :
1. Initial invasion of the virus, which may be accompanied by mild, flu-like sym
ptoms
2. Seroconversion in which the woman converts from having no HIV antibodies in b
lood serum to having antibodies positive for HIV.
3. Weight loss and fatigue (wasting syndrome)
4. Opportunistic infections and possible malignancies
Complications :
1. It may invade cerebral spinal fluid and cause extreme neurologic involvement
2. Higher risk for the development of toxoplasmosis and cytomegalovirus infectio
ns.
3. Tuberculosis occurs at a higher rate with HIV people and may grow worse durin
g pregnancy
Dx: ELISA antibody reaction. For confirmation a Western blot analysis is require
d.
Complications :
1. HIV is associated with low birth weight and preterm birth.
2. If the mother is untreated, 20% to 50% of infants born to HIV-positive women
will develop AIDS in the first year of life.
Therapeutic Management :
1. If Pneumocystis carinii pneumonia develops, the woman is treated with trimeth
oprim with sulfamethoxazole. Trimethoprim may be teratogenic in
early pregnancy; sulfamethoxazole may lead to increased bilirubin in the newborn
if administered late in pregnancy..
2. Pentamidine, the drug of choice for PCP in nonpregnant women, maybe administe
red by aerosol.
3. Kaposi’s sarcoma, malignancy that tends to occur with AIDS, is normally treat
ed with chemotherapy. Chemotherapy is contraindicated during
early pregnancy because of the potential for fetal injury but is used later in p
regnancy to halt malignant growths.
4. Thrombocytopenia (lowered platelet count) may be present which may make the w
oman a poor candidate for an epidural injection for anesthesia
during labor or for episiotomy. She may need a platelet transfusion to restore c
oagulation ability
5. Newborns of HIV-positive mothers are treated with zidovudine for the 1st 6 we
eks of life to try to prevent seroconversion and trimethroprim-
sulfamethoxazole to prevent P. carinii pneumonia
Nursing Diagnosis: Risk for opportunistic infections
TORCH infections
The termTO R C H was applied to perinatal infections (T, toxoplasmosis; O, other
; R, rubella; C, cytomagalovirus; H, herpes).
•
Toxoplasmosis – caused by the protozoan organism Toxoplasmosis gondii, which is
contracted from oocytes in cat feces or by eating
uncooked meat. When primary infection, which is generally asymptomatic, occurs j
ust before or during early pregnancy, congenital infection may result. This can
lead to the birth of a child who is mentally and physically retarded, and who su
ffers from chorioretinitis and microcephaly. Approximately 10% to 15% of these b
abies die, and most of the survivors are severely compromised. Sulfamethoxazole
may reduce the fetal impact.
•
Other – includes the STDs, hepatitis
•
Rubella – although most concerns are for infection in the first trimester, serio
us problem are known to occur when the infection develops
as late as the fifth month of gestation, and later infections may be responsible
for more subtle problems. Infections in the first trimester
may result in abortion in more than 33% of cases.
•
Cytomegalovirus – most common of perinatal infections. Congenital defects includ
e bone lesions, anemia, low birth weight,
hepatomegaly, splenomegaly, jaundice, petechiae, heart disease, pneumonia, catar
acts, chorioretinitis, microcephaly, obstructive
hydrocephaly, intracranial calcifications, and encephalitis.
•
Herpes (HERPES SIMPLEX VIRUS TYPE 2)
Genital herpes infection is a sexually transmitted disease caused by the herpes
simplex virus (HSV) type 2.
Herpes can be transmitted across the placenta to cause congenital infection in t
he NB
NCM 104 1st sem S.Y. 2007-2008
37
Herpes can be transmitted at birth if active lesions are present at that time in
the vagina or vulva.
When infection in the NB occurs, Congenital Herpes can result.
To avoid transmission, CS may be scheduled. If no lesions are present, a vaginal
birth is preferable.
Dx : Appearance of lesions, PAP smear, enzyme Immunosorbent Assay (ELISA)
Treatment :
1. Drug of choice is acyclovir (Zovirax) in an ointment or oral form
2. Women can reduce the pain of infection by sitz baths or applying warm. Moist
tea bags to the lesions.
Assessment :
Painful, small, pinpoint vesicles surrounded by erythema on the vulva or in the
vagina 3-7 days after exposure.
B. HEMATOLOGIC DISORDERS AND PREGNANCY
Hematologic disorders during pregnancy involve either blood formation or coagul
ation disorders.
Anemia And Pregnancy
Because the blood volume expands during pregnancy, most women have a pseudoanem
ia of early pregnancy. This is normal and should not
be confused with the true anemia that can occur as a complication of pregnancy.
Nursing Diagnosis: Risk for altered tissue perfusion
1. THE WOMAN WITH IRON DEFICIENCY ANEMIA
Most common anemia of pregnancy
Iron deficiency anemia is characteristically a microcytic (small-sized red bloo
d cell), hypochromic (less Hgb than the average red blood cell)
anemia, because when an adequate supply of iron is not ingested, iron is unavail
able for incorporation into red blood cells and so cells are not
as large or as rich in hemoglobin as normally. Both Hgb and Hct will be reduced.
1. All women should take prenatal vitamins that contain an iron supplement of 60
mg of elemental iron as prophylactic therapy.
2. Advise women to take iron supplements with orange juice or a Vitamin C supple
ment.
3. They need to eat diet high in iron and vitamins
3. For severe iron deficiency anemia, and patient is noncompliant with oral iron
therapy, Iron Dextran IM or IV can be administered.
Etiology :
1. Diet low in iron
2. Heavy menstrual periods
3. unwise weight-reducing programs
4. Low socio-economic status
Complications :
1. Low fetal birth weight
2. Preterm birth
Assessment :
1. Extreme fatigue and poor exercise tolerance.
2. THE WOMAN WITH FOLIC ACID DEFICIENCY ANEMIA
Folic acid or Folacin is necessary for both the normal formation of red blood c
ells in the mother.
Associated with a decrease in neural tube defects in the fetus.
Etiology :
1. Occurs most often in multiple pregnancies because of the increased fetal dema
nd.
2. In women with a secondary hemolytic illness in which there is rapid destructi
on and production of red blood cells
3. In women who are taking hydantoin, a drug that interferes with folate absorpt
ion.
4. Alcohol abuse – suppresses the metabolic effects of folic acid
Assessment:
The main symptom of folic acid deficiency anemia is a history of severe, progres
sive fatigue. Associated findings include shortness of breath, palpitations, dia
rrhea, nausea, anorexia, headaches, forgetfulness, and irritability. The impaire
d oxygen-carrying capacity of the blood from lowered hemoglobin levels may produ
ce complaints of weakness and light-headedness.
Megaloblastic anemia (enlarged red blood cells) – anemia that develops.
The mean corpuscular volume will be elevated.
May be a factor in early abortion or abruptio placenta
1. Vitamin supplement of 400 ug of folic acid daily
2. assist with planning a well balanced diet that includes meals and snacks that
are high in folic acid (eg. Asparagus, beef liver, brocolli,
green and leafy vegetables, mushrooms, oatmeal, peanut butter, red beans, whole
wheat bread)
3. Encourage to eat and drink a rich source of vitamin C at each meal to enhance
absorption of folic acid
3. THE WOMAN WITH SICKLE CELL ANEMIA
Sickle cell anemia is a recessively inherited hemolytic anemia caused by an abn
ormal amino acid in the beta chain of hemoglobin. (The amino
acid valine is substituted for glutamic acid in the sixth position of the beta c
hain causing the hemoglobin structure to change.) It is a congenital hematologic
disease that causes impaired circulation, chronic ill health, and premature dea
th. Patients who suffer from this disease inherit the sickling gene from both pa
rents, although some parents may only be carriers and don’t experience the sympt
oms. If both parents are carriers, chances are that one in four of their childre
n will be affected.
Infection, exposure to cold, high altitudes, overexertion or other situations t
hat cause cellular oxygen deprivation may trigger a sickle cell crisis.
The deoxygenated, sickle-shaped red blood cells stick to the capillary wall and
each other, blocking blood flow and causing cellular hypoxia.
The crisis worsens as tissue hypoxia and acidic waste products cause more sickli
ng and cell damage.
Complications:
1. Increased incidence of asymptomatic bacteriuria, resulting in an increased in
cidence of pyelonephritis.
2. In pregnancy, blockage to the placental circulation can lead to direct fetal
compromise with low birth weight and possibly death.
3. The anemia can threaten the pregnant woman’s life if vital blood vessels as t
hose to the liver, kidneys, heart, lungs, or brain become blocked.
Assessment :
1. Hemolysis in a sickle cell crisis may occur so rapidly that a woman’s hemoglo
bin level can fall to 5 or 6 mg/100 ml in a few hours.
2. Rise in indirect bilirubin level
3. Susceptible to bacteriuria, preeclampsia and UTI’s
4. Assess for pooling of blood in the lower extremities
5. Severe abdominal pain, muscle spasms, leg pains, painful and swollen joints,
fever, vomiting, hematuria, seizures, stiff neck, coma and
paralysis.
NCM 104 1st sem S.Y. 2007-2008
38
1. Replace sickle cells with normal cells by exchange transfusion periodically t
hroughout the pregnancy.
2. If a crisis occurs, control pain, administer oxygen as needed
3. Increase fluid volume of the circulatory system to lower viscosity. Fluid adm
inistered is often hypotonic(0,45 saline) to keep plasma tension low
4. As a rule, women with sickle cell anemia should not be given iron supplement
because the woman’s cells can’t absorb iron in the usual manner;
taking supplements can lead to iron overload.
5. Keep woman well hydrated during labor.
COAGULATION DISORDERS AND PREGNANCY
Most coagulation disorders are sex linked, or only occurs in males, so have lit
tle effect on pregnancies.
Von Willebrand’s disease is a coagulation disorder inherited as an autosomal do
minant trait that does occur in women.
Signs/Symptoms :
1. Menorrhagia
2. Frequent episodes of epistaxis
3. Prolonged bleeding time
IDIOPATHIC THROMBOCYTOPENIC PURPURA :
A decrease in number of platelets
Etiology:
- unknown but assumed to be autoimmune illness
Signs/Symptoms :
1. Miniature petechiae or large ecchymoses appear on the woman’s body.
2. Frequent nose bleeds may occur
3. Marked thrombocytopenia
1. Platelet transfusion to temporarily increase platelet count
2. Oral prednisone is effective
C. RENAL AND URINARY DISORDERS AND PREGNANCY
Adequate kidney function is important to successful pregnancy outcome; any cond
ition that interferes with kidney or urinary function is
therefore potentially serious.
1. THE WOMAN WITH A URINARY TRACT INFECTION
The organism most commonly responsible for UTI is Escherichia coli
Causes :
1. In pregnant woman, because of the dilated ureters from the effect of progeste
rone, stasis of urine occurs.
2. .Minimal glucosuria that occurs with pregnancy contributes to the growth of o
rganisms.
3. Women with known vesicoureteral reflux often develop UTI or pyelonephritis.
Complications :
1. Asymptomatic infections can flame into pyelonephritis.
2. Increased incidence of preterm labor, PROM and fetal loss may be associated w
ith pyelonephritis
Assessments :
1. Pain on urination
2. Frequency of urination
3. Hematuria
4. Bacterial count of more than 100,000 colonies per milliliter in a clean-catch
specimen
1. Urine for culture and sensitivity test to detect infection and to determine w
hich antibiotic to be used.
2. Amoxicillin, ampicillin and cephalosporins are effective against most organis
ms causing UTI.
3. Sulfonamides can be used early in pregnancy but not near term because they in
terfere with protein binding of bilirubin.
Nursing Diagnosis: Risk for infection
Common Measure to prevent UTI :
1. Voiding frequently (at least every two hours)
2. Wiping front to back after bowel movements
3. Wearing cotton, not synthetic fiber underwear
4. Voiding immediately after sexual intercourse
2. THE WOMAN WITH CHRONIC RENAL DISEASE
Pregnancy increases the work load of the kidneys because the woman’s kidneys mu
st excrete waste products not only for herself but for the
fetus for 40 weeks.
Many women with renal disease take a corticosteroid at a maintenance level. An
effect that may occur is that the infant may be hyperglycemic
at birth because of the suppression of insulin activity by corticosteroid.
Infants of women with renal disease tend to have intrauterine growth restrictio
n from lessened placental perfusion.
Women may develop severe anemia because their diseased kidneys do not produce e
rythropoietin
Many women with renal disease have elevated blood pressure.
Women with kidney disease who normally have an elevated serum creatinine level
more than 2.0 mg/dl may be advised not to undertake a
pregnancy or the increased strain on already damaged kidneys could lead to kidne
y failure
Women with kidney transplants should be considered individually to determine wh
ether they will be able to carry a pregnancy to term before a
pregnancy is initiated.
Women with severe renal disease may require dialysis to aid kidney function dur
ing pregnancy. This is associated with a risk of preterm labor
because progesterone is removed with the dialysis. To prevent this complication
Progesterone IM may be administered before dialysis
D. RESPIRATORY DISORDERS AND PREGNANCY
Chronic respiratory conditions may worsen in pregnancy because the rising uteru
s compresses lung space.
Any respiratory disorder can pose serious hazards to the fetus if allowed to pr
ogress to the point where the mother’s oxygen-carbon dioxide
exchange is altered.
Nursing Diagnosis: Risk for ineffective breathing pattern
1. THE WOMAN WITH ACUTE NASOPHARYNGITIS
NCM 104 1st sem S.Y. 2007-2008
39
Acute nasopharyngitis (common colds) tends to be more severe during pregnancy b
ecause during this period estrogen stimulation normally
causes some degree of nasal congestion.
2. THE WOMAN WITH INFLUENZA
Influenza is caused by a virus that is identified as Type A, B or C.
Type A causes most infections.
Assessment :
1. Disease spreads in epidemic form
2. High fever
3. Extreme prostration
4. Aching pains in the back and extremities
5. A sore, raw throat.
Correlate with preterm labor and abortion
Treated with antipyretic to control fever and perhaps a prophylactic antibiotic
to prevent a secondary infection such as pneumonia.
Exposure to influenza while in utero was associated with the development of sch
izophrenia in later life. Later studies do not show this
association.
3. THE WOMAN WITH PNEUMONIA
Pneumonia is the bacterial or viral invasion of lung tissue.
Pneumonia poses a serious complication of pregnancy because fluid collects in a
lveolar spaces causing limited oxygen-carbon dioxide
exchange in the lungs.
After the invasion, an acute inflammatory response occurs with exudates of red
blood cells, fibrin, and polymorphonuclear leukocytes into the
alveoli. This process confines the bacteria or virus within segments of the lobe
s of the lungs.
Treatment :
1. Appropriate antibiotic
2. Oxygen administration
3. Ventilation support maybe necessary in severe cases.
There is tendency of preterm labor late in pregnancy
4. THE WOMAN WITH ASTHMA
Asthma is paroxysmal wheezing and dyspnea in response to an inhaled allergen.
With inhalation of allergen, there is an immediate histamine release from IgE i
mmunoglobulin interaction. This results in constriction of the
bronchial smooth muscle, marked mucosal swelling, and the production of thick br
onchial secretions. These 3 processes reduce the lumen of
air passages markedly.
Symptoms :
1. Difficulty with air exchange; on exhalation, she makes a high pitched whistli
ng sound (bronchial wheezing)
Asthma has the potential of reducing oxygen supply to the fetus if a major atta
ck should occur.
Many women find their asthma improved during pregnancy by the high circulating
levels of corticosteroid.
Women with asthma have a higher rate of preterm birth
Treatment :
1. Beta-adrenergic agonists such as terbutaline and albuterol are the drugs of c
hoice. If ineffective, theophylline, a corticosteroid or cromolyn
sodium may be added to the regimen.
5. THE WOMAN WITH TUBERCULOSIS
With TB, lung tissue is invaded by mycobacterium tuberculosis, an acid-fast bac
illus
Assessment:
1. Chronic cough
2. weight loss
3. Hemoptysis
4. Night sweats
5. Low-grade fever
6. Chronic fatigue
1. Isoniazid (INH) and ethambutol Hcl are drugs of choice. INH may result in a p
eripheral neuritis if the woman does not take supplemental
pyridoxine (vitamin B6). Ethambutol may cause optic nerve involvement in the mot
her.
2. Maintain an adequate level of calcium
3. A woman is advised to wait 1 to 2 years after the infection becomes inactive
before attempting to conceive.
TB lesions never really disappear but are only “closed off” and made inactive.
Recent inactive TB can become active during pregnancy, because pressure on the
diaphragm from below changes the shape of the lungs,
and a sealed pocket may be broken in this process.
Recent inactive TB may also become active during the post-partal period, as the
lung suddenly returns to its more vertical pre-pregnant
position and breaks open calcium deposits.
Although TB can be spread by the placenta to the fetus, it is usually spread to
the infant after birth
A woman should have at least 3 negative sputum cultures before she holds/cares
for her infant. If negative, there is no need to isolate infant
from mother; she can even breastfeed.
6. THE WOMAN WITH CYSTIC FIBROSIS
Cystic Fibrosis is a recessively inherited disease in which there is generalize
d dysfunction of the exocrine glands. This dysfunction leads to
mucus secretions, particularly in the pancreas and lungs, so thick that normal s
ecretion is blocked.
Women may have lessened fertility from inability of sperm to migrate through vi
scid cervical mucus.
Symptoms :
1. Chronic respiratory
2. Over inflation of lungs from the thickened mucus
3. Inability to digest fat and protein because the pancreas cannot release amyla
se.
Complications :
1. Increased risk for preterm labor
2. Risk for perinatal death
3. High possibility of developing DM due to pancreas involvement
NCM 104 1st sem S.Y. 2007-2008
40
Treatment :
1. Pancrelipase – to supplement pancreatic enzymes
2. Bronchodilator
3. Antibiotic
4. Postural drainage daily – to reduce a buildup of lung secretions
5. Iron supplement – because panrelipase interferes with iron absorption
6. Monitor for serum glucose to detect development of gestational diabetes
It is not usually recommended for postpartum women with cystic fibrosis to brea
stfeed because their breast milk contains more fatty acid.
E. RHEUMATIC DISORDERS AND PREGNANCY
Nursing Diagnosis : Pain related to rheumatic disorder during pregnancy
1. THE WOMAN WITH JUVENILE RHEUMATOID ARTHRITIS
Juvenile Rheumatoid Arthritis is a disease of connective tissue with joint infl
ammation and contracture, probably the result of an autoimmune
response.
Pathology :
The disease pathology is synovial membrane destruction. Inflammation with effusi
on, swelling, erythema, and painful motionof the joints occurs.
Overtime, formation of granulation tissue can fill the joint space, resulting in
permanent disfigurement and loss of joint motion.
Treatment :
1. Corticosteroids and salicylate therapy – a danger of large amounts of salicyl
ates is prolonged pregnancy (salicylates interferes with prostaglandin synthesis
, so labor contractions are not initiated). The woman is asked to decrease salic
ylate intake 2 weeks before term to avoid the problem.
2. THE WOMAN WITH SYSTEMIC LUPUS ERYTHEMATOSUS
SLE is a multisystem chronic disease of connective tissue that can occur in wom
en of childbearing age.
Highest incidence is in women ages 20 to 40 years
Widespread degeneration of connective tissue occurs with the onset of illness
Assessment :
1. Marked skin change is erythematous “butterfly-shaped” rash on the face.
Most serious of the kidney changes are fibrin deposits that plug and block the
glomeruli, leading to necrosis and scarring.
The thickening of collagen tissue in the blood vessels causes vessel obstructio
n, blood flow to the vital organs become compromised and to
the fetus if blood flow to the placenta is obstructed
Treatment :
1. Corticosteroid, NSAID’s and salicylate therapy to reduce symptoms of joint pa
in and inflammation.
Complication :
1. Acute nephritis with glomeruli destruction
2. Higher incidence of abortion and preterm births.
3. Infants may be born with lupuslike rash, anemia and thrombocytopenia.
4. Congenital heart block can occur in the NB.
With nephritis, BP will rise. Patient will develop hematuria and decreased urin
e output. Proteinuria and edema may begin.
Women will be monitored by frequent serum creatinine levels to assess kidney fu
nction. Dialysis or plasmapheresis may be necessary.
Women are asked to reduce salicylate close to birth to reduce possibility of bl
eeding in the NB
Hydrocortisone IV is administered during labor to help the woman to adjust to t
he stress at this time.
Infant of a woman who has SLE tends to be small for gestational age due to the
decreased blood flow to placenta.
F. GASTROINTESTINAL DISORDERS AND PREGNANCY
Minor gastrointestinal disorders are common in pregnancy (nausea, heartburn, co
nstipation). Acute abdominal pain or vomiting are causes for
concern
Women who have colostomies can complete pregnancy without difficulties.
Nursing Diagnosis: Risk for altered nutrition, less than body requirements
1. THE WOMAN WITH APPENDICITIS
Appendicitis is inflammation of the appendix.
Assessment :
1. Nausea
2. Generalized abdominal discomfort
3. Vomiting
4.Sharp, peristaltic, lower right quadrant pain
5. Leukocytosis
6. Elevated temperature
7. Ketones in the urine
In the pregnant woman, the appendix is often displaced so far upward in the abd
omen that the localized pain may be so high it resembles pain
of gallbladder disease.
Advise woman not to take food, liquid, or laxatives because increasing peristal
sis tends to cause an inflamed appendix to rupture.
1. CS if fetus is near term, then remove appendix.
2. Laparoscopy – if condition occurs in early pregnancy
2. THE WOMAN WITH A HIATAL HERNIA
Hiatal Hernia is a condition in which a portion of the stomach extends and prot
rudes up through the diaphragm into the chest cavity.
Symptoms :
1. Heartburn
2. Gastric regurgitation
3. Indigestion
4. Dysphagia
5. Possible weight loss due to inability to eat
6. Hematemesis in extreme cases
Dx : Diagnosed by direct endoscopy or sonogram
NCM 104 1st sem S.Y. 2007-2008
41
1. Antacids to relieve pain
2. Elevate head when sleeping
3. THE WOMAN WITH CHOLECYSTITIS AND CHOLELITHIASIS
Etiology :
1. Associated with women older than 40 years
2. Obesity
3. Multiparity
4. High fat diet
5. Gallstones are formed from cholesterol
Symptoms :
1. Aching and pressure in the right epigastrium
2. Jaundice
1. Lower fat intake. Low fat but fat free diet because of the importance of lino
leic acid for fetal growth.
2. IVF for acute episodes to provide fluid and nutrients
3. Analgesics
4. Laparoscopy if cannot be controlled by conservative management
Dx : Sonogram
4. THE WOMAN WITH VIRAL HEPATITIS
Hepatitis is liver disease that may occur from invasion of the A, B, C, or D vi
rus.
Hepatitis A is spread mainly by contact with another person or by ingestion of
fecally contaminated water or shellfish
Incubation period 2 to 6 weeks.
Prophylactic gamma globulin to prevent the disease after exposure.
Hepatitis B (serum hepatitis) is spread by transfusion of contaminated blood or
blood products; it can be spread by semen or vaginal
secretions and thus considered STD.
Incubation period 6 weeks to 6 months
Hepatitis B vaccine may be administered to those who are at high risk
Assessment :
1.Nausea, vomiting
2. Liver is tender to palpation
3. Dark yellow urine
4. Light colored stools
5. Jaundice
6. On physical examination, liver is enlarged
7. Elevated bilirubin
8. Increased liver enzymes
Dx : Liver Biopsy
1. Bed rest
2. High calorie diet
3. Contact precautions when giving care
Complications :
1. Abortion and preterm labor
2. Infants with mothers who have HB Ag-positive will develop chronic hepatitis
After birth, infant should be washed well to remove any maternal blood.
Hepatitis B immune globulin (HBIG) and Hepa B immunization should be administer
ed to the NB
Infants should be observed for infection
Mother should not breastfeed because HB Ag antigens can be recovered from breas
t milk.
5. THE WOMAN WITH INFLAMMATORY BOWEL DISEASE
Crohn’s Disease (inflammation of the terminal ileus) and ulcerative colitis (in
flammation of the distal colon)
Etiology :
1. Occurs most often in young adults Between ages 12 and 30 years
2. Cause is unknown but an autoimmune process may be responsible
Symptoms :
1. Shallow ulcers
2. Chronic diarrhea
3. weight loss
4. Occult blood in stool
5.Nausea and vomiting
6. Obstruction and fistula formation with peritonitis can occur in extreme condi
tions
> Malabsorption particularly of Vit B12 occurs
Complications :
1. Interferes with fetal growth
Therapy :
1. Total rest for GI tract by total parenteral nutrition
2. Sulfasalazine, an anti inflammatory. Close to birth, dosage is reduced becaus
e it may interfere with bilirubin binding sited and can cause
neonatal jaundice.
G. NEUROLOGIC DISORDERS AND PREGNANCY
Any neurologic disease with symptoms of seizures must be carefully managed duri
ng pregnancy because anoxia caused by severe seizures
could deprive the fetus with oxygen, with serious outcomes.
Nursing Diagnosis : Risk for Injury (maternal)
1. THE WOMAN WITH A SEIZURE DISORDER
Etiology :
1. Head trauma
NCM 104 1st sem S.Y. 2007-2008
42
2. Meningitis
3. Cause of recurrent seizures are unknown (idiopathic)
1. “Do not take medication during pregnancy” rule does not apply to seizure cont
rol medications. The risk of adverse maternal or fetal outcome
from seizures during pregnancy is greater than the risk of teratogenicity from t
aking anticonvulsant drugs.
Complications :
1. Infants may have an increased danger of neural tube disorders and childhood m
alignancies as a result of folic acid displacement from maternal
medication.
2. Infants are also prone to hemorrhagic disease because of decreased Vit K coag
ulation factors at birth.
Nursing Diagnosis : Risk for altered placental perfusion
Tonic-clonic seizures (sustained full-body involvement) could affect the fetus b
ecause of anoxia that can occur form spasms of chest muscles.
Administer oxygen by mask is good prophylaxis to ensure adequate fetal oxygenat
ion
Woman is advised to inform health personnel that she has recurrent seizures and
the medications she is taking
Nursing Diagnosis: Risk for altered parenting
A woman who has recurrent convulsions may worry that her child will have seizur
es as the child grows older.
If seizures are result of acquired disorder, assure the woman that her child wi
ll have no tendency toward seizures.
2. THE WOMAN WITH MYASTHENIA GRAVIS
Myasthenia Gravis is an autoimmune disorder characterized by the presence of an
IgG antibody against acetylcholine receptors in striated
muscle.
It produces sporadic but progressive weakness and abnormal fatigue in striated
(skeletal) muscles. This weakness and fatigue are
exacerbated by exercise and repeated movement but improved by anticholinesterase
drugs. Usually, myasthenia gravis affects muscles
innervated by the cranial nerves (face, lips, tongue, neck, and throat), but it
can affect any muscle group.
Other common signs of myasthenia gravis include weak eye closure, ptosis and di
plopia, blank masklike facial expression, difficulty chewing
and swallowing, a hanging jaw, bobbing motion of the head, and symptoms of respi
ratory failure if respiratory muscles are involved
Treatment :
1. Administration of anti-cholinesterase drugs such as neostigmine and pyridosti
gmine counteract fatigue and muscle weakness and enable about
80% of normal muscle function
2. Plasmapheresis (withdrawal and replacement of plasma) to remove immune comple
xes from the bloodstream
Interventions:
1. Help the woman plan daily activities to coincide with energy peaks.
2. Teach the client how to recognize adverse effects and signs of toxicity of an
ticholinesterase drugs (headaches, sweating, abdominal cramps, nausea, vomiting,
diarrhea, excessive salivation, bronchospasm). Warn her to avoid strenuous exer
cise, stress, infection, and unnecessary exposure to the sun or cold weather. Ca
ution her to avoid taking other medications without consulting her primary care
giver.
3. Magnesium sulfate should be avoided because it can diminish the acetylcholine
effect and therefore increase disease symptoms.
3. THE WOMAN WITH MULTIPLE SCLEROSIS
Nerve fibers become demyelinated and lose function. Pregnant women with this di
sorder grow increasingly fatigued as pregnancy
progresses.
Other signs and symptoms include visual disturbances such as optic neuritis, di
plopia and blurred vision, sensory impairment such as
paresthesia, urinary disturbances such as incontinence, frequency, urgency, and
infections, emotional lability such as mood swings, irritability
and euphoria and other associated signs like poorly articulated speech and dysph
agia
Etiology :
1. exact cause is unclear; however, current theories suggest that it may be caus
ed by an autoimmune response to a slow-acting or latent viral
infection or by environmental or genetic factors
2. Predominant in women between 20-40 years old (childbearing age)
Treatment :
1. ACTH or a corticosteroid to strengthen nerve conduction
2. Plasmapheresis (withdrawal and replacement of plasma)
Interventions:
⇒
Emphasize the need to avoid stress, infections, and fatigue and to maintain inde
pendence by finding new ways to perform daily activities.
⇒
Explain the value of a well balanced nutritious diet that contains sufficient fi
ber.
⇒
Evaluate the need for bowel and bladder training
Complications :
1. UTI
2. Painless precipitous birth if quadriplegia is present
3. Dysreflexia from the pain of labor which leads to HPN, headache, diaphoresis
and bradycardia
H. MUSCULOSKELETAL DISORDERS AND PREGNANCY
1. THE WOMAN WITH SCOLIOSIS
Scoliosis is lateral curvature of the spine
Etiology :
1. Often in women approximately 12 years of age
Complications :
1. Cosmetic deformity
2. Because of chest compression, interferes with respiration and heart action
3. Pelvic distortion
1. Stainless steel rods (Harrington rods) implanted on both sides of spinal vert
ebrae to strengthen and straighten the spine.
2. CS, if pelvis is distorted.
I. CARDIOVASCULAR DISORDERS AND PREGNANCY
NCM 104 1st sem S.Y. 2007-2008
43
1. THE WOMAN WITH LEFT-SIDED HEART FAILURE
Occurs with conditions such as mitral stenosis, mitral insufficiency and aortic
coarctation.
Occurs when the left ventricle is unable to move forward the volume of blood re
ceived by the left atrium from the pulmonary circulation
1. Productive cough of blood-speckled sputum
2. Fatigue, weakness, dizziness
3. Orthopnea
4. Paroxysmal nocturnal dyspnea - suddenly waking at night short of breath
Complications :
1. High risk for Abortion
2. preterm labor
3. Maternal death
1. Anti-hypertensives
2. Beta-blockers to decrease the force of myocardial contractions
2. THE WOMAN WITH RIGHT-SIDED FAILURE
Congenital heart defects such as pulmonary valve stenosis and atrial and ventri
cular septal defects may result in right-sided heart failure.
Occurs when the output of the right ventricle is less than the blood volume the
heart receives at the right atrium from the vena cava or venous
circulation. Back pressure from this results in congestion of the systemic venou
s circulation and decreases cardiac output to the lungs.
Blood pressure falls in the aorta because less blood is reaching it ;
Pressure is high in the vena cava
Both jugular venous distention and increased portal circulation occur.
Both the liver and spleen become distended
Distention of abdominal vessels can lead to exudates of fluid from the vessels
into the peritoneal cavity (ascites). Fluid moves from the
systemic circulation into interstitial spaces (peripheral edema).
Liver enlargement can cause extreme dyspnea and pain because it will put extrem
e pressure on the diaphragm.
Eisenmenger’s syndrome – congenital anomaly most apt to cause right-sided failu
re (A right-to-left atrial or ventricular septal defect with
accompanying pulmonary stenosis). They need oxygen administration and frequent a
rterial gases to ensure fetal growth.
3. THE WOMAN WITH PERIPARTAL HEART DISEASE
Peripartal cardiomyopathy – extremely rare condition that originate late in preg
nancy. Due to the effect of pregnancy on the circulatory system.
Cause is unknown. May occur from previously undetected heart disease
Signs/symptoms :
1. Late in pregnancy, woman develops signs of myocardial failure : Shortness of
breath, chest pain, and edema
2. Cardiomegaly (enlargement of the heart)
1. Reduced activity
2. Diuretic and digitalis therapy
3. Low dose heparin to decrease the risk of thromboembolism.
4. Immunosuppressive therapy
Assessment Of The Woman With Cardiac Disease:
1.Fatigue
2. Cough
3. Increased respiratory rate
4. tachycardia
5. Poor fetal heart tone variability from poor tissue perfusion
6. Decreased amniotic fluid from intrauterine growth retardation
7. Edema from poor venous return
8. Irregular pulse
9. Chest pain on exertion
Diagnostic Assessment : Chest x-ray, ECG
Fetal Assessment :
1. Low birth weights
2. Severe fetal distress
Nursing Diagnosis : Knowledge deficit regarding the effects of maternal cardiova
scular disease
Nursing Interventions :
1. Promote rest
2. Promote healthy nutrition
3. Educate regarding medication
4. Educate regarding avoidance of Infection
4. THE WOMAN WITH AN ARTIFICIAL VALVE PROSTHESIS
Many women with valve prosthesis take oral anticoagulants to prevent formation
of blood clots at valve site. However, these medications
increase the risk of congenital anomalies in infants
Women are placed on heparin therapy before becoming pregnant
Observe for signs of premature separation of the placenta during pregnancy and
labor because anticoagulant in the mother may cause
placental dislodgement.
5. THE WOMAN WITH CHRONIC HYPERTENSIVE VASCULAR DISEASE
Women with chronic hypertensive vascular disease come into pregnancy with eleva
ted BP. This kind of HPN is usually associated with
arteriosclerosis or renal disease
Fetal well-being is compromised by poor placental perfusion during pregnancy
Management is similar with PIH
6. THE WOMAN WITH VENOUS THROMBOEMBOLIC DISEASE
Incidence increases during pregnancy due to acombination of stasis of blood in
the lower extremities from uterine pressure and
hypercoagulability (effect of increased estrogen)
Signs/symptoms :
1. Chest pain
NCM 104 1st sem S.Y. 2007-2008
44
2. Sudden onset of dyspnea
3. Cough with hemoptysis
4. Tachycardia or missed beats
5. Severe dizziness or fainting from lowered blood pressure
1. Avoid use of constrictive knee-high stockings,
2. Do not cross legs
3. Bed rest
4. Heparin IV administration
J. ENDOCRINE DISORDERS AND PREGNANCY
1. THE WOMAN WITH A THYROID DYSFUNCTION
Thyroid gland enlarges slightly due to increased vascularity, as a normal effec
t of pregnancy
Nursing Diagnosis: Risk for maternal and fetal injury
A. THE WOMAN WITH HYPOTHYROIDISM
A rare condition in pregnancy because women with symptoms of untreated hypothyr
oidism are anovulatory and often unable to conceive
Signs/symptoms :
1. Easy fatigability
2. Obese
3. dry skin
4. Little tolerance for cold
5. Extreme nausea and vomiting
1. Thyroxine – to supplement lack of thyroid hormone. As a rule, her dose of thy
roxine will be increased for the duration of pregnancy to simulate
the effect that would normally occur in pregnancy
C.
THE WOMAN WITH HYPERTHYROIDISM
Symptoms :
1. Rapid heart rate
2. Exophthalmos
3. Heat Intolerance
4. Nervousness
5. Heart palpitation
6. Weight loss
If undiagnosed, woman may develop heart failure during pregnancy because her ra
pid heart rate cannot adjust to the increasing serum
volume occurring with pregnancy.
Complications :
1. PIH
2. Fetal growth restriction
3. preterm labor
1. Thiomides to reduce thyroid activity. Unfortunately, these drugs are teratoge
ns and possibly enlarges thyroid gland of the fetus. Woman should
be regulated on the lowest dose possible
Women on anti-thyroid drugs may be advised not to breastfeed because these drug
s are excreted in breast milk.
2. THE WOMAN WITH DIABETES MELLITUS
DM is an endocrine disorder in which the pancreas is unable to produce adequate
insulin to regulate body glucose
Pathophysiology :
The pancreas has both endocrine and exocrine types of tissue. The Islets of Lan
gerhans form the endocrine portion. Alpha islet cells secrete
glucagons; beta islet cells secrete insulin.
Insulin is essential for carbohydrate metabolism and is important to the metabo
lism of fats and protein. The actual amount of insulin produced
is regulated by serum glucose levels. When serum glucose exceeds 100 mg/dl, beta
cells immediately increase insulin production. When blood serum levels are lowe
red, production decreases. Both the ability to secrete additional insulin and th
e action to decrease production are immediate responses.
The primary problem of any woman with DM is control of the balance between insul
in and blood glucose to prevent hyperglycemia or hypoglycemia
Glomerular filtration of glucose is increased causing slight glycosuria. The ra
te of insulin secretion is increased, and the fasting blood sugar is
lowered.
All women appear to develop insulin resistance as pregnancy progresses, a pheno
menon that is probably caused by the presence of the
hormone human placental lactogen and high levels of cortisol, estrogen, progeste
rone and catecholamines.
If the pancreas cannot respond by producing additional insulin, excess glucose
moves across placenta to fetus where fetal insulin metabolizes
it, and acts as growth hormone, promoting macrosomia
The continued use of glucose by the fetus may lead to hypoglycemia.
There is a high incidence of congenital anomaly, abortion, and stillbirth in in
fants.
At birth, infants are more prone to hypoglycemia, respiratory distress syndrome
, hypocalcemia, and hyperbilirubinemia.
3. THE WOMAN WITH GESTATIONAL DIABETES
Pregnant woman becomes diabetic usually at the midpoint of pregnancy when insul
in resistance become noticeable – Gestational Diabetes
Mellitus
Risk Factors for gestational diabetes :
1. Obesity
2. Age over 30 years
3. History of large babies
4. History of unexplained fetal loss
5. History of congenital anomalies in previous pregnancies
6. History of unexplained perinatal loss
7. Family history of diabetes
NCM 104 1st sem S.Y. 2007-2008
45
Pathophysiology
•
In gestational diabetes mellitus, insulin antagonism by placental hormones, huma
n placental lactogen, progesterone, cortisol, and prolactin leads to increased b
lood glucose levels. The effect of these hormones peaks at about 26 weeks gestat
ion. This is called the diabetogenic effect of pregnancy.
•
The pancreatic beta cell functions are impaired in response to the increased pan
creatic stimulation and induced insulin resistance.
•
Pregnancy complicated by diabetes pits the mother at high risk for the developme
nt of complications such as spontaneous abortion,
hypertensive disorders, preterm labor, infection, and birth complications.
•
The effects of diabetes on the fetus include hypoglycemia, hyperglycemia, and ke
toacidosis. Hyperglycemic effects can include
a. congenital defects
b. macrosomia
c.
intrauterine growth restriction
d. intrauterine fetal death
e. delayed lung maturity
f.
neonatal hypoglycemia
g. neonatal hyperbilirubinemia
Assessment :
1. Dizziness
2. Confusion if hyperglycemic
3. Thirst
4. Increased risk of PIH
5. Congenital anomalies
6. Macrosomia
7. Poor fetal heart tone variability and rate from poor tissue perfusion
8. Hydramnios
9. Glycosuria, polyuria
10. Possibility of increased monilial infection
Nursing Interventions
•
Teach the client the effects and interactions of diabetes and pregnancy and sign
s of hyper and hypoglycemia
•
Teach client how to control diabetes in pregnancy, advise changes that need to b
e made in nutrition and activity patterns to promote
normal glucose levels and prevent complications.
•
Advise client of increased risk of infection and how to avoid it.
•
Observe and report any signs of pre-eclampsia.
•
Monitor fetal status throughout pregnancy
•
Assess status of mother and baby frequently
-
carefully monitor fluid, calories, glucose and insulin during labor and delivery
-
continue careful observation in postdelivery period
4. HYPERGLYCEMIA
Nursing Diagnoses :
1. Risk for altered tissue perfusion
2. Altered nutrition less than body requirements r/t inability to use glucose
3. Risk for ineffective individual coping
4. Risk for infection
5. Fluid volume deficit r/t polyuria accompanying disorder
6. Knowledge deficit r/t difficult and complex health problem
7. Health-seeking behaviors r/t to voiced need to learn home glucose monitoring
8. Noncompliance r/t discouragement, misunderstanding or fear of therapeutic mea
sures
Nursing Interventions :
1. Education regarding nutrition
2. Education regarding exercise
1. Insulin
2. monitor fetal well-being
K. MENTAL ILLNESS AND PREGNANCY
Mental illness may precede or occur with pregnancy. Depression is the most comm
on mental illness seen.
Lithium, a mainstay of therapy for bipolar disorders is a known teratogen.
L. TRAUMA AND PREGNANCY
Trauma occurs at high incidence in childbearing years because for this age grou
p, automobile accidents, homicide, and suicide are among the
three leading causes of death.
High incidence occurs during the last trimester due to clumsiness, fainting and
hyperventilation.
Orthopedic injuries occur because the pregnant woman’s sense of balance is alte
red
PHYSIOLOGIC CHANGES IN PREGNANCY THAT AFFECT TRAUMA CARE
After a traumatic injury, a woman’s body will maintain her own homeostasis at t
he expense of the fetus.
The woman’s total plasma volume increases during pregnancy at term. This increa
se serves as a safeguard tot the woman if trauma with
bleeding should occur.
Fluid replacement volume would be high in case of injury because pregnant woman
needs more fluid to restore fully her circulatory volume.
Peripheral venous pressure in pregnant woman is unchanged, it tends to be highe
r in the lower extremities because of the compression of the
vena cava and back pressure. This causes lacerations of the legs or perineum to
bleed much more profusely than usual.
During pregnancy, leucocyte count rises so it is difficult to use this determin
ation as a sign of infection after an open wound.
Serum albumin level decreases during pregnancy, making the large loss that norm
ally occurs with burns a more serious than usual response.
Serum liver enzyme levels remain the same during pregnancy, so if these are ele
vated during trauma, liver trauma can be detected.
Bleeding into the abdominal cavity with an abdominal injury is apt to be forcef
ul and extreme because of the increased pressure in the pelvic
vessels.
Paracentesis is dangerous because the bowel, dislocated from its usual position
, can be easily punctured.
Culdocentesis may be done
Peritoneal lavage may reveal bleeding or bladder rupture best.
Bladder of pregnant woman is susceptible to rupture because it is the most ante
rior organ and is elevated abnormally.
After abdominal trauma, an indwelling bladder catheter is inserted to assess fo
r blood in the urine.
NCM 104 1st sem S.Y. 2007-2008
46
Emotional Considerations :
A feeling of guilt lowers self-esteem and increases the level of stress.
People under stress do not process well and so may not perceive correctly the i
nformation given to them.
Initial Assessments After Trauma During Pregnancy
> With multiple trauma, a nasogastric tube is usually passed to empty the stomac
h. A foley catheter is inserted to assess for urine output and to
rule out ruptured bladder.
To prevent supine hypotension syndrome, be sure the woman does not lie supine f
or an examination. If it is necessary for her to lie supine,
manually displace the uterus from the vena cava by placing rolled towels or a bl
anket under her right side to tip her body approximately 15o to
the side
Nursing Diagnosis :
1. Fear related to threat of injury to the fetus
2. Risk for fetal injury
3. Altered tissue perfusion r/t to severed artery
4. Ineffective breathing pattern related to lung lacerated by gunshot wound
6. Situational low self-esteem r/t occurrence of accident
7. Powerlessness r/t seriousness of the injury sustained or inability to prevent
accident from occurring.
1. Immediate Care
Interventions in emergency situations must be quick yet always remember that th
e woman’s primary health condition is that she is pregnant.
Cardiopulmonary resuscitation (CPR)
If there is blood loss, a central venous pressure line may be inserted.
If hypotension is present, it must be corrected quickly to maintain a pressure
gradient across the placenta. Epedrine is the drug of choice for a
pregnant woman because it has a minimal peripheral vasoconstriction effect.
Nursing Diagnosis : Risk for altered tissue perfusion
OPEN WOUNDS:
1. LACERATIONS
Bleeding should be halted by pressure on the edge of the laceration
2. PUNCTURE WOUNDS
If the woman has had tetanus immunization within the past 10 years, tetanus tox
oid is administered.
> If the woman did not have tetanus immunization within 10 years, tetanus toxoi
d plus immune tetanus globulin is administered.
Knife wounds cause deep penetration and are often directed into the abdomen. Mo
st stab wounds of the abdomen, however, occur in the
upper quadrants of the abdomen above the height of the uterus.
To determine the depth and extent of the wound, a fistulogram may be done.
If there is suspicion that there is bleeding in the abdomen, a celiotomy or an
exploratory surgical procedure into the abdominal cavity may be
performed
After surgical repair of an injured diaphragm, CS may be planned to avoid strai
n on a newly repaired diaphragm during labor
3. ANIMAL BITES
If the rabies immunization status of the dog is known, the wound is washed and
treated as a puncture wound.
If the dog is questionable, the woman must be administered rabies immune globul
in vaccine.
Pregnancy is not contraindicated to rabies immunization because contracting the
disease would be so much more serious
4. BLUNT ABDOMINAL TRAUMA
No visible break is present on the skin.
After injury, underlying tissues becomes edematous; broken underlying blood ves
sels may ooze and form ecchymosis or hematoma at the
site.
To assess for abdominal bleeding, a diagnostic peritoneal lavage may be done, U
TZ may also be done.
Traumatic blow to the abdomen could cause dislodgement of the placenta (abrupti
o placentae) or preterm labor.
Palpate the uterus for any bleeding and count fetal heart tones using Doppler i
nstrument.
Sonogram may be used to show that the placenta and uterus are intact
A pelvic examination is performed to assess for vaginal bleeding or seepage of
clear water that would suggest the amniotic membranes were
ruptured from the force of an abdominal blow.
If there is a uterine contraction, a uterine and fetal monitor should be placed
to estimate the strength and effect on the fetal heart rate and the
possibility that preterm labor has begun.
Magnesium sulfate is usually selected to halt preterm labor after trauma.
The possibility that placental blood will enter the maternal circulation with u
terine trauma is a threat to the Rh negative woman. Rh (-) woman
are therefore, administered Rh immune globulin (RHIG) after trauma.
5. GUNSHOT WOUNDS
Assessment of the wound includes inspection of the entry and exit point of the
bullet.
Uterine wall is so thick that it may trap a bullet; thus there may be no exit p
oint if the uterus is punctured.
Gunshot wounds are surgically cleaned and debrided, and is treated with a high
concentration of antibiotics
6. POISONING
Syrup of Ipecac is the best emetic to cause vomiting and discharge the poison f
rom the body and is safe during pregnancy.
Remember, some poisons can be more harmful if vomited than if allowed to remain
in the body.
7. CHOKING
It is difficult to use a Heimlich maneuver because of a lack of space between t
he uterus and the sternum and because the person can not
reach from the rear around the woman’s enlarged abdomen.
Late in pregnancy, a rescuer must use successive chest thrusts. P. 362 Nursing
procedure 14.2
8. ORTHOPEDIC INJURIES
A woman has poor balance late in pregnancy, she may trip more readily than usua
l
The extra weight pregnant woman carries puts a high proportion of weight on the
wrist, a serious wrist injury can occur
Applying ice to the area decreases swelling
X-ray may be done to determine a fracture.
Encourage high calcium intake if woman has fracture so both she and the fetus c
an have adequate calcium for new bone growth
9. BURNS
Burns are dangerous to the pregnant woman because of the thermal injury that oc
curs and the inhalation of carbon monoxide gases which
NCM 104 1st sem S.Y. 2007-2008
47
can lead to extreme fetal hypoxia as carbon monoxide crosses the placenta in pla
ce of the oxygen.
Smoke is irritating to the lung tissue and can result in extensive lung edema;
this can cause additional fetal hypoxia due to the lack of oxygen-
carbon dioxide exchange space.
Because the fluid and electrolyte loss can be great with burns, hypotension fro
m hypovolemia or an electrolyte imbalance can occur.
A body response to a harsh trauma such as burn is the production of prostagland
ins, which may cause preterm labor.
Maternal and fetal prognosis are poor if burns cover more than 50% of body surf
ace area.
Interestingly, burn tissue heals more quickly than normal during pregnancy. Thi
s is probably related to the increased metabolism and to the
increased corticosteroid serum level that keeps inflammation and damage to tissu
e from the pressure of edema from occurring.
THE BATTERED WOMAN
Abused women may be pregnant because they were unable to resist sexual advances
from their abusive partner.
Beatings may increase during pregnancy because stress is often a “trigger” to b
eatings, and pregnancy can increase the stress.
Assessment :
A battered woman may come for care late in pregnancy because her partner may co
ntrol her transportation or money; she may fear that a
health care provider will report the abuse; pretending that the pregnancy does n
ot exist to reduce stress in her home.
She may be noticeable that she purchases no maternity clothes.
She may decline laboratory tests if it involves transportation or money
Battered woman may have difficulty following recommended pregnancy nutrition.
She may leave before health personnel sees her at prenatal setting
She may grow anxious if her prenatal appointment is running late
She may call and cancel appointments frequently.
She may dress inappropriately.
Obvious bruises or lacerations, neck may reveal linear bruises from strangulati
on.
Battered woman may be anxious to hear baby’s heartbeat because her partner rece
ntly punched or kicked her abdomen and she is worried
that fetus might have been hurt. Minimal placental infarcts from blunt abdominal
trauma may lead to poor placental perfusion and low birth
weight.
A sonogram may be done for suspected abdominal trauma.
Fetal heart tones and fundal height should be recorded.
Nursing Diagnoses:
1. Powerlessness r/t perception that she is impossible to break away from abusin
g partner
2. Fear r/t constant threats of beatings
3. Social isolation r/t client’s need to hide evidence of abuse
3. Ineffective denial r/t inability to face the fact that spouse is abusive
4. Ineffective family coping; compromised r/t dysfunctional relationship between
client and abusive spouse.
Tasks the woman could accomplish to meet goals of care :
1. Client carries phone number for home for abused women with her.
2. Client and abusive partner continue to attend counseling sessions.
3. Client states she has filed restraining order against abusive partner
4. Client states she feels secure living at safe house
COMPLICATIONS OF PREGNANCY
Most women enter pregnancy in apparent good health and achieve normal pregnancy
and birth without complications. In a few women,
however, for reasons are usually unclear, unexpected deviations or complications
from the course of pregnancy occurs.
Nursing Diagnosis :
1. Anxiety r/t guarded pregnancy outcome
2. Fluid volume deficit r/t third-trimester bleeding
4. Altered tissue perfusion r/t hypertension of pregnancy
5. Knowledge deficit r/t signs and symptoms of possible complications
BLEEDING DURING PREGNANCY
Vaginal bleeding is a deviation from the normal that may occur at anytime durin
g the pregnancy
Primary causes of bleeding during pregnancy
1. BLEEDING AND THE DEVELOPMENT OF SHOCK
A woman with any degree of bleeding needs to be evaluated for hypovolemic shock
.
Process of shock due to blood loss
Therapeutic Management
Assessment :
1. Confusion
2. Pallor
3. Increased Pulse
4. Tachypnea
5. Decreased BP
6. Decreased cardiac output
7. Fetal bradycardia
8. Peripheral vasoconstriction
9. Decreased urinary output
10. Cold extremities
Nursing Diagnosis : Risk for fluid volume deficit
CONDITIONS ASSOCIATED WITH FIRST TRIMESTER BLEEDING
1. ABORTION
A. SPONTANEOUS ABORTION
Abortion-any interruption of a pregnancy before the fetus is viable. A non-viab
le fetus is usually defined as a fetus of 20 to 24 weeks’ gestation
or weighing 500 gms. A fetus born at this point would be considered a premature
or immature birth
1. Early abortion - occurs before week 16 of pregnancy
2. Late abortion - occurs between weeks 16-24.
Causes:
1. Abnormal fetal formation due either to a teratogenic factor or to a chromosom
al aberration.
NCM 104 1st sem S.Y. 2007-2008
48
2. Immunologic factors
3. Implantation abnormalities – placental circulation will not be well establish
ed and fetal formation will be inadequate.
4. Corpus luteum fails to produce enough progesterone to maintain the deciduas b
asalis
5. Infection
Assessment:
1. Vaginal spotting
2. History taking
B. THREATENED ABORTION
S/Sx:
-
Vaginal bleeding starts as scant bleeding usually bright red.
-
Slight cramping but no cervical dilatation
Intervention:
-
Limit activity to no strenuous activity for 24-48 hours is the key intervention.
-
Coitus is restricted for 2 weeks to prevent infection and to avoid inducing furt
her bleeding.
C. IMMINENT (INEVITABLE) ABORTION
A threatened abortion becomes an imminent or inevitable abortion if uterine con
tractions and cervical dilatation occur.
Symptoms:
1. Cramping or uterine contractions
Dx: UTZ
Tx:
1. D & C – to ensure all products of conception are removed.
2. Suction Curettage
3. Any tissue fragments should be saved to be examined for possible abnormalitie
s such as gestational trophoblastic disease (H mole).
D. COMPLETE ABORTION
> Entire products of conception (fetus, membrane, and placenta) are expelled spo
ntaneously without any assistance.
E. INCOMPLETE ABORTION
Part of the conception is expelled but the membranes or placenta is retained in
the uterus.
There is a danger of maternal hemorrhage as long as part of the conceptus is re
tained in the uterus.
Treatment:
1. Dilatation and Curettage
2. Suction Curettage
F. MISSED ABORTION
Fetus dies in uterus but is not expelled.
S/Sx:
1. no increase in fundic height
2. no fetal heart sounds heard
3. painless vaginal bleeding
Dx: UTZ
Treatment:
1. D & C
2 .If beyond 14 weeks maybe induced by prostaglandin suppository to dilate the c
ervix followed by oxytocin stimulation.
Cx: DIC (Disseminated Intravascular Coagulation)
G. RECURRENT ABORTION
3 spontaneous abortions that occurred in same gestational age.
Possible Causes:
1. defective spermatozoa or ova
2.endocrine factors
3.deviations of uterus
4.infection
5.autoimmune disorders
COMPLICATION OF ABORTION
1. HEMORRHAGE
With complete spontaneous abortion, serious or fatal hemorrhage is rare.
With an incomplete abortion or DIC, major hemorrhage is a possibility.
Therapeutic Management:
Immediately position the woman flat on bed & massage the uterine fundus to aid
contraction
D&C
Monitor VS to detect hypovolemic shock
Start blood transfusion
Direct replacement of fibrinogen
2. INFECTION
Observe for fever, abdominal pain, tenderness, foul vaginal discharges
Usually caused by E. Coli
Endometritis (Infection of the uterine lining) – is the infection that usually
occurs after abortion
3. SEPTIC ABORTION
> An abortion complicated by infection due to use of nonsterile instruments
S/S : Fever, crampy abdominal pain, uterine tenderness
Complications:
1. Toxic Shock Syndrome
NCM 104 1st sem S.Y. 2007-2008
49
2. Septicemia
3. Kidney Failure
4. Infertility
Laboratories:
1. CBC, Serum Electrolytes,
2. BT, Xmatching
3. Cultures of vaginal, cervical & urine specimen
Treatment:
1. Hydration
2. Antibiotic
3. D&C
4. TT or HTIG for Tetanus
A CVP or pulmonary artery catheter may be inserted to monitor left atrial filli
ng pressure and hemodynamic status.
Dopamine and digitalis may be necessary to maintain sufficient cardiac output.
Oxygen and perhaps ventilatory support may be necessary to maintain respiratory
functions.
4. ISOIMMNUNIZATION
Some blood from placental villi may enter maternal circulation, either by spont
aneous birth or by D&C. If the woman is Rh (-), enough Rh (+)
fetal blood may enter her circulation to cause Isoimmunization.
Isoimmunization – the production by her immunologic system of antibodies agains
t Rh(+) blood.
Treatment:
1. Women with Rh(-) blood should receive Rho (D antigen) immune globulin (RHIG)
to prevent the build up of antibodies in the event the conceptus
was Rh (+)
5. POWERLESSNESS
> A feeling of grief and sadness over the loss or that they have lost control of
their lives is to expected.
2. ECTOPIC PREGNANCY
Second most frequent cause of bleeding early in pregnancy.
Implantation occurs outside the uterine cavity.
Fertilization occurs normally in the distal third of the fallopian tube.
Causes:
a. Obstructions
b. Congenital malformations
c. Scars from tubal surgery
d. Tumors
e. Progestin-only Oral contraceptives, post conceptual estrogen, ovarian inducti
on drugs
f. IUD
Signs & Symptoms:
a. Bleeding – growing zygote ruptures the site of implantation which results to
tearing & destruction of blood vessels which results to bleeding
b. Sharp, stabbing pain
c. Vaginal spotting – placental detachment, uterine deciduas sloughs thus bleedi
ng occurs
d. Severe shock – evidenced by rapid pulse, rapid respirations and falling blood
pressure
e. Leucocytosis due to trauma
f. Rigid abdomen due to peritoneal irritation
g. positive Cullen’s Sign
h. Pain in the shoulders from blood in the peritoneal cavity causing irritation
to the phrenic nerve.
i. On vaginal examination, a tender mass is usually palpable in Douglas’ cul-de-
sac
j. Extensive or dull vaginal and abdominal pain
k. Excruciating pain on the cervix during pelvic examination
1. Laboratories: Hgb, Blood typing and Xmatching, HCG level for immediate pregna
ncy testing
2. IVF using a large gauge catheter to restore intravascular volume
3. Blood Transfusion if necessary
4. Laparotomy – to ligate the bleeding vessels and to remove or repair the damag
ed fallopian tube.
5. Women with Rh (-) blood should receive Rho (D) immune globulin (RHIG)
6. Methotrexate – if tube is not yet ruptured
7. Leucovorin
Nursing Diagnosis: Powerlessness r/t early loss of pregnancy secondary to ectopi
c pregnancy.
Abdominal Pregnancy
> Very rarely after ectopic pregnancy, the product of conception is expelled int
o the pelvic cavity. The placenta continues to grow in the fallopian
tube, spreading perhaps into the uterus or it may escape into the pelvic cavity
and successfully implant on an organ such as an intestine. The fetus
will grow in the pelvic cavity (an abdominal pregnancy).
History:
1. Previous uterine surgery
2. Sudden pain of ectopic pregnancy earlier in the pregnancy
Complications:
1. Hemorrhage
2. Bowel perforation and Peritonitis
CONDITIONS ASSOCIATED WITH SECOND TRIMESTER BLEEDING
1. GESTATIONAL TROPHOBLASTIC DISEASE (HYDATIDIFORM MOLE)
> Proliferation and degeneration of the trophoblastic villi. As the cells degene
rate, they become filled with fluid, appearing as fluid-filled, grape-sized
vesicles. Embryo dies.
NCM 104 1st sem S.Y. 2007-2008
50
Etiology:
1. Occur most often in women from low socioeconomic groups who have a low protei
n intake.
2. In young women (under age 18 years). In women older than 35 years
3. Women of Asian heritage
- cause essentially unknown
Assessment:
1. Uterus expands faster than normal; disproportionate to the length of pregnanc
y
2. No fetal heart sounds nor palpable fetal parts
3. A blood or urine test of HCG for pregnancy will be strongly positive
4. Excessive nausea and vomiting
5. A sonogram will show dense growth (a snowflake pattern)
6. Vaginal bleeding starting with spotting of dark brown blood or as a profuse f
resh flow, accompanied by discharge of the clear fluid-filled vesicles.
1. Suction curettage – to evacuate the mole
2. Every woman who had history of GTD should have a blood test for HCG every 2 t
o 4 weeks along with pelvic examination
3. Thereafter, HCG levels and possibly chest xray are done once a month for a fu
ll year.
4. Instruct woman to use a reliable contraceptive method during the year so that
a positive pregnancy test will not be confused with increasing
levels and developing malignancy.
5. Prophylactic course of Methotrexate, the drug of choice for choriocarcinoma.
Malignancy can be treated effectively with methotrexate.
2. INCOMPETENT CERVIX
> A cervix that dilates prematurely and therefore cannot hold a fetus until term
.
Signs/Symptoms:
1. A pink-stained vaginal discharged
2. Increased pelvic pressure which maybe followed by rupture of the membranes an
d discharge of the amniotic fluid
3. Uterine contractions
Etiology:
1. Associated with increased maternal age
2. Trauma to the cervix
3. Repeated D&C’s
Therapeutic Management
1. Cervical Cerclage – after one pregnancy loss due to an incompetent cervix to
prevent from happening again
2. McDonald or Shirodkar procedure – purse string sutures placed in the cervix t
o strengthen it and prevent from dilating.
3. Emergent cerclage – sutures placed in the cervix as prophylaxis against prete
m birth.
CONDITIONS ASSOCIATED WITH THIRD-TRIMESTER BLEEDING
1. PLACENTA PREVIA: Low implantation of the placenta.
Occurs in 4 Degrees:
(1) Implantation in the lower rather than in the upper portion of the uterus (Lo
w-lying placenta)
(2) Marginal implantation (the placenta edge approaches that of the cervical os)
(3) Implantation that occludes a portion of the cervical os (partial placenta pr
evia)
(4) Implantation that totally obstructs the cervical os (total placenta previa)
Assessment:
1. Vaginal bleeding – abrupt, painless, bright red
Etiology:
1. Increased parity
2. Advanced maternal age
3. Past cesarean births
4. Past uterine curettage
5. Multiple gestation
Immediate Care Measures:
1. Place woman immediately on bed rest in a side-lying position to ensure an ade
quate blood supply to the woman and fetus.
2. Determine vaginal blood loss
3. Never attempt a pelvic or rectal examination with painless bleeding late in p
regnancy because any agitation of the cervix may initiate a massive
hemorrhage.
3. Obtain baseline vital signs to determine whether symptoms of shock are presen
t
4. Monitor BP every 5 to 15 minutes
5. IVF therapy using a large gauge catheter
6. Monitor urine output frequently as an indicator of blood volume adequacy
7. Monitor fetal heart sounds and uterine contraction
8. Hgb, Hct. PT, PTT, fibrinogen, platelet count, type and xmatch or antibody sc
reen should be assessed to establish baselines, detect a possible
clotting disorder
9. Prepare BT if necessary
10. Prepare oxygen equipment in case of fetal distress.
Complications:
1. Postpartal Hemorrhage – because the placental site is in the lower uterine se
gment which does not contract as efficiently as the upper segment
2. Endometritis – because the placental site is close to the cervix, the portal
of entry for pathogens.
2. PREMATURE SEPARATION OF THE PLACENTA (ABRUPTIO PLACENTAE)
Predisposing Factors:
1. High parity
2. Chronic hypertensive disease
NCM 104 1st sem S.Y. 2007-2008
51
3. Hypertension of pregnancy
4. Direct trauma
5. Vasoconstriction from cocaine use
6. Cigarette smoking
Assessment:
1. Sharp, stabbing pain high in the uterine fundus
2. Tenderness on uterine palpation
3. Heavy bleeding
4. Hard, board-like uterus in cases of couvelaire uterus (Blood infiltrates uter
ine musculature
5. Signs of shock
6. Uterus becomes tense and rigid to the touch
1. Initial blood works – Hgb, typing and crossmatching
2. Start IVF with a large-gauge catheter
3. Administer oxygen by mask to limit fetal anoxia.
4. Monitor fetal heart sounds
5. Monitor and record maternal vital signs every 5 to 15 minutes to establish ba
selines
6. Keep in lateral position to prevent pressure on the vena cava and additional
compromising of fetal circulation.
7. Do not perform any vaginal or pelvic examination or give an enema
PRETERM LABOR
> Labor that occurs before the end of week 37 of gestation
Etiology:
1. HPN, UTI
2. Occurs more frequently in adolescent
3. Dehydration
4. Urinary Tract Infection
5. Chorioamnionitis
6. Continuous strenuous jobs during pregnancy that leads to fatigue
Signs/Symptoms:
1.Persistent, dull, low backache
2. Vaginal spotting
3. Feeling of pelvic pressure or abdominal tightening
4. Menstrual-like cramping
1. Bed rest – to relieve pressure of the fetus on the cervix
2. IVF therapy – hydration may have an influence on stopping contractions
Drug Administration:
1.Corticosteroid to the fetus – to accelerate the formation of lung surfactant
2. Tocolytic agent – drug used to halt labor
3. Magnesium sulfate – first drug used to halt contractions. Also has CNS depres
sant action that slows and halts uterine contractions.
Fetal Assessment:
To evaluate fetal movement the woman lies down on her left side and times the nu
mber of minutes it takes for her to feel 10 fetal movements
(about an hour) or counts the number of fetal movements she feels in 1 hour (10
to 12). If the time it takes to feel 10 fetal movements is twice what
it was the day before or she feels fewer than 5 movements during half an hour, s
he monitors again for second hour. If at the end of this second
hour fetal activity has not increased, she should report it immediately
Labor That Cannot Be Halted
> Labor is too far advanced that it cannot be halted.
1. The rupturing of membranes is a point of no return in stopping or delaying la
bor because of the increased risk of infection.
2. If the cervix is more than 50% effaced and 3-4 cm dilated
Management:
1. If the fetus is very immature, a CS maybe planned to reduce pressure on the f
etal head and reduce the possibility of subdural or intraventricular
hemorrhage
2. As a rule, artificial rupture of membranes should not be done due to possibil
ity of prolapse of the cord around a small head until the fetal head is
firmly engaged.
3. Administer analgesic agents with caution during preterm labor.
4. Monitor uterine contractions and fetal heart sounds during labor
5. Explain to the patient that an episiotomy may be made larger than usual, alth
ough the head of preterm maybe smaller it is more fragile and
excessive pressure might result in subdural or intraventricular hemorrhage that
could be fatal.
6. Forceps may be used at delivery to reduce pressure on the fetal head.
7. Clamp cord immediately after birth, an immature infant has a difficulty excre
ting large amount of bilirubin that will be formed if this extra blood is
added to the circulation. The extra amount of blood may also burden the circulat
ory system.
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
Acquired disorder of blood clotting.
Also known as consumptive coagulopathy
A diffuse, pathologic form of clotting, secondary to underlying disease/patholo
gy
Occurs in critical maternity problems such as abruptio placenta, intrauterine f
etal death, amniotic fluid embolism, pre-eclampsia/eclampsia,
hydatidiform mole and hemorrhagic shock
Pathophysiology
-
precoagulant substances released in the blood trigger microthrombosis in periphe
ral vessels and paradoxical consumption of circulating
clotting factors
-
fibrin-split products accumulate, further interfering with the clotting process
-
platelet and fibrinogen levels drop
-
causative or precipitating mechanism
injury to vessel endothelium or blood cell
injury to tissue with tissue factor
or thromboplastin release
NCM 104 1st sem S.Y. 2007-2008
52
intrinsic
extrinsic
production of microthrombi
consumption of clotting factors
thrombosis continues
activation of fibrinolytic system
(lysis of clots)
thrombocytopenia
vascular occlusion
digestion of fibrin clots
tissue or organ ischemia
release fibrin split or
or infarction
degradation products
hemorrhage
DIC
shock and circulatory collapse
Symptoms:
1. Easy bruising or bleeding from an IV site. Bleeding may range from massive, u
nanticipated blood loss to localized bleeding.
2. Presence of special maternity problems
3. Prolonged prothrombin and partial thromboplastin time
1. Prompt recognition and adequate management of the underlying problem ( eg. de
livery of the dead fetus and the placenta)
2. IV administration of heparin to halt the clotting
3. Institute nursing measures for severe bleeding/shock if needed. BT maybe nece
ssary to replace blood loss
4. Anti-thrombin III factor, fibrinogen, or cryoprecipitate can be used to resto
re blood clotting
5. Fresh frozen plasma can also aid in restoring clotting function
PRETERM RUPTURE OF MEMBRANES (PROM)
A spontaneous rupture of fetal membranes with loss of amniotic fluid before ons
et of regular contractions that results in progressive cervical
dilation.
Etiology:
1. Although cause is unknown, malpresentation and a contracted pelvis commonly a
ccompany the rupture
2. Associated with infection of the membranes (chorioamnionitis).
Complications:
1. Uterine and fetal infection
2. Increased pressure on the umbilical cord inhibiting the fetal nutrient supply
, or cord prolapse
3. Development of Potter – like syndrome of distorted facial features and pulmon
ary hypoplasia
4. Preterm labor
Assessment:
1. A sudden gush of clear fluid from the vagina with continued minimal leak
2. Sterile vaginal speculum examination is done to observe for vaginal pooling o
f fluid. The fluid is tested with nitrazine paper (appears blue). The
fluid can also be tested for ferning.
3. A sonogram may be done to assess amniotic fluid index.
4. Cultures for Neisseria gonorrhea and Chlamydia are usually taken.
5. Blood is drawn for white blood count and C – reactive protein.
1. Bed rest
2. Prophylactic administration of broad-spectrum antibiotics may delay onset of
labor and reduce infection in the newborn.
3. Women positive for streptococcus B need IV administration of penicillin or am
picillin to reduce the possibility of this infection in the newborn.
Health Education:
1. If at home, instruct to take temperature twice a day and to report a fever, u
terine tenderness, or odorous vaginal discharge.
2. Refrain from tub bathing, coitus, and douching because of the danger of intro
ducing infection.
3.White cell count needs to be assessed daily. A count of more than 18,000/mm3 t
o 20,000/mm3 is suggestive of infection.
PREGNANCY-INDUCED HYPERTENSION (PIH)
A condition in which vasospasm occurs during pregnancy. The vasospasm may be ca
used by the action of prostaglandins (notably decreased
prostacyclin and increased thromboxane). Increased cardiac output may injure end
othelial cells of the arteries, leading to spasm. Normally, blood vessels during
pregnancy are resistant to the effects of pressor substances such as angiotensi
n and norepinephrine so blood pressure remains normal during pregnancy. With PIH
, this reduced responsiveness to BP changes appears to be lost. Vasoconstriction
occurs, and BP increases dramatically.
The cardiac system is overwhelmed because the heart is forced to pump against r
ising peripheral resistance. This reduces the blood supply to
organs esp. the kidney, pancreas, liver, brain and placenta. Tissue hypoxia may
follow in the maternal vital organs; poor placental perfusion may reduce the fet
al nutrient and oxygen supply. Ischemia in the pancreas may result to epigastric
pain and an elevated amylase-creatinine ratio.
Spasm of the arteries in the retina leads to vision changes.
Vasospasm in the kidney increases blood flow resistance. Degenerative changes d
evelop in kidney glomeruli because of the back pressure.
This leads to increased permeability of the glomerular membrane allowing the ser
um proteins, albumin and globulin to escape into the urine
(proteinuria). The degenerative changes also result in decreased glomerular filt
ration so there is lowered urine output and clearance of
creatinine. Increased tubular reabsorption of sodium occurs. Because sodium reta
ins fluid, edema results.
NCM 104 1st sem S.Y. 2007-2008
53
Changes associated with PIH:
Vasospasm
Effects on the vascular system
Effects on the renal system
Effects on the interstitial
Tissues
Reduced glomerular filtration rate;
Increased glomerular membrane permeability
Vasoconstriction
Fluid diffusion from vascular space
Into interstitial space
Impaired organ perfusion
Increased serum blood urea nitrogen
And creatinine levels
Hypertension
Oliguria and proteinuria
Edema
Etiology:
1. Occurs more frequently in primiparas younger than age 20 years or older than
40 years
2. Low socio-economic background
3. Five or more pregnancies
4. Women of color
5. Multiple pregnancies
6. Hx of hydramnios
7. Heart disease, DM with renal involvement
8. Essential hypertension
9. Associated with poor calcium or magnesium intake
Pathophysiologic Events
Assessment:
1. HPN, proteinuria and edema are classic signs of PIH
Symptoms of PIH:
GESTATIONAL HYPERTENSION
An elevated blood pressure but has no proteinuria or edema.
MILD PREECLAMPSIA
BP rises 30 mm Hg or more systolic or 15 mm Hg or more diastolic above her prep
regnancy level, taken on two occasions at least 6 hours
apart
With proteinuria (1+ or 2+ on a reagent strip on a random sample).
Edema maybe present. This develops because of the protein loss, sodium retentio
n and lowered glomerular filtration rate.
Interventions:
-
Promote bed rest as long as signs of edema or proteinuria are minimal, preferabl
y left-side lying to promote uterine and placental
perfusion
-
Provide well balanced diet with adequate protein and roughage, no sodium restric
tion
SEVERE PREECLAMPSIA
Blood pressure has risen to 160 mm Hg systolic and 110 mm Hg diastolic or above
on at least two occasions 6 hours apart at bed rest or her
diastolic pressure is 30 mm Hg above prepregnancy level.
Assessment:
1. Extreme edema is noticeable in the woman’s face and hands as puffiness.
Nonpitting edema – If there is swelling or puffiness but the swelling cannot be
indented with finger pressure.
Slight indentation – 1+ pitting edema
Moderate indentation – 2+ pitting edema
Deep indentation – 3+ pitting edema
4+ pitting edema – indentation is so deep it remains after removal of fingers
2. Severe epigastric pain and nausea and vomiting possibly due to abdominal edem
a or ischemia to the pancreas and liver.
3. Pulmonary edema may cause them to feel short of breath
4. Cerebral edema will result in visual disturbances. May also produce symptoms
of severe headache and marked hyperflexia and perhaps muscle
clonus
Medical Management: Magnesium Sulfate
-
Magnesium sulfate acts upon the myoneural junction, diminishing neuromuscular tr
ansmission
-
It promotes maternal vasodilation, better tissue perfusion, and has anticonvulsa
nt effect. Keep in mind that for magnesium to be effective
as an anticonvulsant, serum magnesium levels should be between 5 and 8 mg/dl. Le
vels above 8 mg/dl indicate toxicity and place the
patient at risk for respiratory depression, cardiac arrhythmias, and cardiac arr
est.
-
Monitor client’s respirations, blood pressure, and reflexes, as well as urinary
output frequently.
-
Assess the client’s patellar reflex. If the client has received epidural anesthe
sia, test the biceps or triceps reflex. Diminished or hypoactive
reflexes suggest magnesium toxicity.
-
Assess for ankle clonus (alternating contractions and relaxations of the muscles
) by rapidly dorsiflexing the client’s ankle three times, then removing your han
d and observing the foot’s movement. If no further motion is noted, ankle clonus
is absent; if the foot continues to move involuntarily, clonus is present. Mode
rate (3-5 movements) or severe (6 or more movements) suggests possible magnesium
toxicity.
-
Antidote for excess levels of magnesium sulfate is calcium gluconate or calcium
chloride
Interventions
-
promote complete bedrest, left side lying
-
carefully monitor maternal/fetal vital signs
-
monitor intake and output
-
take daily weights
-
institute seizure precautions ( restrict visitors, minimize all stimuli, monitor
for hyperreflexia, administer sedatives as ordered)
-
instruct client about appropriate diet
-
continue monitoring for up to 48 hours post delivery
NCM 104 1st sem S.Y. 2007-2008
54
-
administer medications as ordered, vasodilator of choice is usually hydralazine
(apresoline)
ECLAMPSIA
The most severe classification of hypertension of pregnancy
Assessment:
-
increased hypertension precedes convulsion followed by hypotension, seizure may
recur
-
coma may ensue
-
labor may begin, putting fetus in great jeopardy
Complications:
1. Cerebral hemorrhage
2. Circulatory collapse
3. Renal failure
Interventions
-
minimize all stimuli
-
monitor vital signs
-
have airway, oxygen, and suction equipment available
-
administer medications as ordered
-
prepare for caesarian section when seizures stabilize
-
continue observations 48 hours post delivery
HELLP SYNDROME
is a category of PIH that involves changes in blood components and liver functi
ons. It is an acronym that help identify the underlying signs
associated with the syndrome:
1.Hemolysis
2.ElevatedLiver enzymes
3.LowPlatelets
HELLP syndrome develops in 12% of women with PIH. It can occur in primigravidas
and multigravidas. When it occurs, maternal and fetal
mortality is high; approximately one-fourth of women and one-third of infants di
e from this disorder. However, after birth, laboratory results return to
normal usually within 1 week and the mother experiences no further problems.
Etiology
Although the exact cause of HELLP is unknown, theories have been proposed about
the development of its signs and symptoms. Hemolysis
is believed to result because RBCs are damaged by their travel through small, im
paired blood vessels. Elevated liver enzymes are believed to
result from obstruction in liver flow by fibrin deposits. Low platelets are beli
eved to be the result of vascular damage secondary to vasospasm.
Intervention
-
monitor maternal and fetal vital signs
-
maintain a quiet, calm, dimly lit environment to reduce the risk of seizures
-
institute bleeding precautions
-
prepare patient for delivery
MULTIPLE PREGNANCY
Considered a complication of pregnancy because the woman’s body must adjust to
the effects of more than one fetus.
Incidence has increased dramatically due to use of fertility drugs
Assessment:
1. Uterus begins to increase in size faster than usual
2. Alpha-fetoprotein levels will be elevated
3. A sonogram will reveal multiple gestation sacs
4. At the time of quickening, flurries of action at different portions of her ab
domen are noted
5. On auscultation, multiple sets of fetal heart sounds may be heard
POLYHYDRAMNIOS
An excessive amniotic fluid formation.
Usually, amniotic fluid is between 500 and 1000 ml in amount at term. An amount
of more than 2000 ml or an amniotic fluid index above 24 cm
is considered hydramnios.
Complications:
1. Fetal malpresentation because of the extra uterine space
2. Premature rupture of membranes followed by preterm labor from the increased p
ressure and possibly prostaglandin release
3. Preterm rupture of membranes adds additional risks of both infection and prol
apsed cord
Assessment:
1. Unusual rapid enlargement of uterus
2. Small parts of the fetus are difficult to palpate because the uterus is unusu
ally tense
3. Extreme shortness of breath because of the overly distended uterus that pushe
s up against her diaphragm.
4. Lower extremity varicosities and hemorrhoids because of poor venous return fr
om the extensive uterine pressure
5. Increased weight gain
1. Bed rest
2. Encourage to eat a high fiber diet to avoid constipation
3. Assess vital signs and lower extremity edema
4. Amniocentesis – to give relief from the increasing pressure
5. A non steroidal anti inflammatory agent such as Indomethacin therapy may be e
ffective in reducing the amount of fluid formed
6. If contractions begins, tocolysis with magnesium sulfate may be begun to prev
ent or halt preterm labor
POST-TERM PREGNANCY
A pregnancy that exceeds 42 weeks
Etiology:
1. Occurs in approximately 10% of all pregnancies
2. Women who have long menstrual cycles (40 to 45 days)
3. Women on high dose of salicylates interferes with the synthesis of prostaglan
dins
4. Myometrial quiescence or a uterus that does not respond to normal labor stimu
lation
Complications:
1. Macrosomia will create a delivery problem
2. Lack of growth
3. Oligohydramnios leading to variable decelerations may occur
NCM 104 1st sem S.Y. 2007-2008
55
4. Fetus may suffer from lack of oxygen, fluid and nutrients
1. A nonstress test and/ or biophysical profile may be done to document the stat
e of placental perfusion
2. Prostaglandin gel applied to the cervix to initiate ripening or stripping of
membranes
3. Oxytocin infusion is a common method to induce labor.
4. CS if oxytocin is ineffective
PSEUDOCYESIS
False pregnancy
Assessment:
1. Nausea and vomiting
2. Amenorrhea
3. Enlargement of the abdomen
Etiology:
1. Woman’s desire to be pregnant actually causes physiologic changes
ISOIMMUNIZATION (RH INCOMPATIBILITY)
Occurs when an Rh (-) mother is carrying a fetus with an Rh (+) blood
1. RHIG – administered to women at 28 weeks of pregnancy
2. Intrauterine transfusion – to restore fetal red blood cells. Done by injectin
g red blood cells directly into a vessel in the fetal cord or depositing
them in the fetal abdomen using amniocentesis technique
FETAL DEATH
Obviously, one of the most severe complications of pregnancy.
Causes:
1. Chromosomal Abnormalities
2. Congenital malformations
3. Infections such as hepatitis B
4. Immunologic causes
5.Complications of maternal disease
Symptoms:
1. No fetal movements
2. No fetal heart tones
3. Painless spotting
4. Uterine contractions with cervical effacement and dilatation
1. Sonogram to confirm death of fetus
2. If labor does not begin spontaneously, it will be induced through combination
of prostaglandin gel application to the cervix to effect cervical
ripening and oxytocin or prostaglandin administration to begin uterine contracti
ons
3. Blood for coagulation studies to detect DIC
Nursing Diagnosis: Powerlessness related to fetal death
Nursing Intervention:
A. Healthy process of grieving
1. Give woman opportunities to express feelings
2. Encourage support person to stay with the woman during labor
3. Present the baby if parents wished to in a manner like she were a well newbor
n
4. Encourage parents to give name to the child to make him/her more normal
5. Explain how the anomaly affected the child
6. Explain hospital procedures regarding discharged
7. Ask about their desire for clergy or religious rites
HIGH RISK NEWBORN
NCM 104 1st sem S.Y. 2007-2008
56
A neonate is considered to be high risk if he has an increased chance of dying
during or shortly after birth or has a congenital or perinatal
problem that requires prompt intervention
Being able to predict that an infant is high risk allows for advanced preparati
on
Assessment:
All infants should be assessed for obvious congenital anomalies and gestational
age. Assessments are made under prewarmed radiant heat
warmer to safeguard against heat loss.
Assessment involves use of instrumentation such as cardiac, apnea and blood pre
ssure monitoring.
Nursing Diagnosis:
1. Ineffective airway clearance r/t presence of mucus or amniotic fluid in airwa
y.
2. Risk for fluid volume deficit 3. Ineffective thermoregulation r/t newborn sta
tus and stress from birth weight variation.
4. Risk for altered nutrition; less than body requirements
6. Risk for altered parenting
7. Diversional activity deficit (lack of stimulation) r/t illness at birth
Implementation:
1. Care should focus on conserving baby’s energy and providing a thermoneutral e
nvironment to prevent exhaustion and chilling.
2. Painful procedures should be kept to a minimum
3. Parent teaching and participation with care such as bathing or feeding
Outcome Evaluation:
1. Infant maintains patent airway
2. Infant tolerates all procedures without accompanying apnea
3. Infant demonstrates growth and development appropriate for gestational age, b
irth weight, and condition
4. Infant maintains body temperature at 37oC in open crib with one added blanket
.
5. Parents visits at least once a week and make three telephone calls to neonata
l nursery weekly
6. Parents demonstrate positive coping skills and behaviors in response to NB’s
condition
Neonatal Assessment
APGAR SCORE
During the initial examination of a neonate, expect to calculate an Apgar score
and make general observations about the neonate’s appearance
and behavior. Developed by anesthesiologist Dr. Virginia Apgar in 1952, Apgar sc
oring evaluates neonatal heart rate, respiratory effort, muscle
tone, reflex irritability, and color. Evaluation of each category is performed 1
minute after birth and again at 5 minutes after birth. Each item has a
maximum score of 2 and a minimum score of 0. The final Apgar score is the sum to
tal of the five items; a maximum score is ten.
Evaluation at 1 minute quickly indicates the neonate’s initial adaptation to ext
rauterine life and whether resuscitation is necessary. The 5-minute
score gives a more accurate picture of his over-all status.
Heart Rate. If the umbilical cord still pulsates, you can palpate the neonate’s
heart by placing your fingertips at the junction of the umbilical cord and the s
kin. The neonate’s cord stump continues to pulsate for several hours and is a go
od, easy place to check heart rate. You can also place to fingers or a stethosco
pe over the neonate’s chest at the fifth intercostal space to obtain an apical p
ulse. For accuracy, the heart rate should be counted for 1 full minute.
Respiratory Effort. Assess the neonate’s cry, noting its volume and vigor. Then
auscultate his lungs, using a stethoscope. Assess his respirations for depth and
regularity. If the neonate exhibits abnormal respiratory responses, begin neona
tal resuscitation then use the Apgar score to judge the progress and success of
resuscitation efforts.
Muscle Tone. Determine by evaluating the degree of flexion in the neonate’s arms
and legs and their resistance to straightening. This can be done
by extending the limbs and observing their rapid return to flexion – the neonate
’s normal state.
Reflex Irritability. Evaluate neonate’s cry. Initially, he may not cry but you s
hould be able to elicit a cry by flicking his soles. The usual response is a lou
d, angry cry. A high-pitched or shrill cry is abnormal. A newborn whose mother w
as heavily sedated tend to have a low score on this aspect.
Color. Observe skin color for cyanosis. A neonate usually has a pink body and bl
ue extremities. This condition calledacrocyanosis appears in
about 85% of normal neonates 1 minute after birth. Acrocyanosis results from dec
reased peripheral oxygenation caused by the
transition from fetal to independent circulation.
NCM 104 1st sem S.Y. 2007-2008
57
Sign
Apgar Score
012
Heart Rate
Absent
Less than 100 beats/min
More than 100 beats/min
Respiratory Effort
Absent
Slow, irregular
Good crying
Muscle tone
Flaccid/Limp
Some flexion and
resistance to extension of
extremities
Active motion
Reflex Irritability
No response
Grimace or weak cry
Vigorous cry
Color
Pallor, Cyanosis
Pink body, blue extremities
Completely pink
A total score of 7-10 indicates that the neonate is in good condition; 4-6, fair
condition (the neonate may have moderate central nervous system
depression, muscle flaccidity, cyanosis, and poor respirations); 0-3, danger (th
e neonate needs immediate resuscitation, as ordered).
HEAD TO TOE ASSESSMENT
The neonate should receive a thorough physical examination of each body part. Ho
wever, before each body part is examined, assess the general appearance and post
ure of the neonate. Neonates usually lie in a symmetrical, flexed position – the
characteristic “fetal position” – as a result of their position while in utero.
Skin.
Common findings in a neonatal assessment may include:
Acrocyanosis – caused by vasomotor instability, capillary stasis, and high hemog
lobin level for the first 24 hours after birth.
Milia- clogged sebaceous glands on the nose or chin
Lanugo- fine, downy hair appearing after 20 weeks of gestation on the entire bod
y, except the palms and soles
vernix caseosa – a white cheesy protective coating composed of desquamated epith
elial cells and sebum
erythema toxicum neonatorum – a transient maculopapular rash
telangiectasia – flat reddened vascular areas appearing on the neck, upper eyeli
d or upper lip
port-wine stain (nevus flammeus) – a capillary angioma located below the dermis
and commonly found on the face
strawberry hemangioma (nevus vasculosus) – a capillary angioma located in the de
rmal and subdermal skin layers indicated by a rough,
raised, sharply demarcated birthmark
sudamina or miliaria (distended sweat glands)- cause minute vesicles on the skin
surface, especially on the face
Mongolian spots – bluish black areas of pigmentation more commonly noted on the
back and buttocks of dark-skinned neonates
(regardless of race)
Make general observations about the appearance of the neonate’s skin in relation
ship to his activity, position, and temperature. Usually, the
neonate is redder when crying or hot. He may have transient episodes of cyanosis
when crying. Cutis marmorata is transient mottling when the
neonate is exposed to cooler temperatures.
Palpate the skin to assess skin turgor. To do this, roll a fold of skin on the n
eonate’s abdomen between your thumb and forefinger. Assess
consistency, amount of subcutaneous tissue, and degree of hydration. A well-hydr
ated infant’s skin returns to normal immediately upon release.
Head.
The neonate’s head is about ¼ of its body size. Six bones make up the cranium:
•
the frontal bone
•
the occipital bone
•
two parietal bones
•
two temporal bones
Bands of connective tissue, calledsutur es, lie between the junctures of these b
ones. At the juncture of the sutures are wider spaces of
membranous tissues, calledfontanels.
Fontanels.
The neonatal skull has two fontanels. The anterior fontanel is diamond-shaped an
d located at the juncture of the frontal and parietal bones. It
measures 1 1/8 to 1 5/8” (3-4cm) long and ¾” (2cm) to 1 1/8” wide. The anterior
fontanel closes in about 18 months. The posterior fontanel is
triangle-shaped. It is located at the juncture of the occipital and parietal bon
es and measures about ¾” across. The posterior fontanel closes in 8-
12 weeks.
The fontanels should feel soft to touch but shouldn’t be depressed. A depressed
fontanel indicates dehydration. In addition, fontanels shouldn’t
bulge. Bulging fontanels require immediate attention because they may indicate i
ncreased intracranial pressure. Pulsations in the fontanels reflect
the peripheral pulse.
NCM 104 1st sem S.Y. 2007-2008
58
Molding refers to asymmetry of the cranial sutures due to difficulties during va
ginal delivery; it isn’t seen in neonates born by cesarean delivery.
There are two types of cranial abnormalities:
•
Cephalhematoma occurs when blood collects between a skull bone and the periosteu
m. It is caused by pressure during delivery and
tends to spontaneously resolve in 3-6 weeks. A cephalhematoma doesn’t cross cran
ial suture lines.
•
Caput succedaneum is a localized edematous area of the presenting scalp. It is a
lso caused by pressure during delivery, but
disappears spontaneously in 3-4 days and can cross cranial suture lines
Craniotabes is localized softening of the cranial bones. It can be so soft it ca
n be indented by the pressure of the examining finger. The bone
returns to its normal contour when he pressure is removed. The pressure of the f
etal skull against the mother’s pelvic bone in utero probably
causes this. The condition corrects itself without treatment after a matter of m
onths
The degree of head control the neonate has should also be evaluated during this
part of the examination. If neonates are placed down on a firm
surface, they’ll turn their heads to the side to maintain an open airway. They a
lso attempt to keep their heads in line with their body when raised
by their arms. Although head lag is normal in the neonate, marked head lag is se
en in neonates with Down syndrome or brain damage and
hypoxic infants.
Eyes.
Neonates tend to keep their eyes tightly shut. Observe the lids for edema, which
is normally present for the first few days of life. The eyes should
also be assessed for symmetry in size and shape. Here are some common findings o
f neonatal eye examination:
The neonate’s eyes are usually blue or gray because of scleral thinness. Permane
nt eye color is established within 3-12 months.
Lacrimal glands are immature at birth, resulting in tearless crying for up to 2
months.
Neonate may demonstrate transient strabismus.
The Doll’s eye reflex (when the head is rotated laterally, the eyes deviate in t
he opposite direction or remain stationary) may persist for
up to 10 days.
Subconjunctival hemorrhages may appear from vascular tension changes during birt
h.
The corneal reflex is present but generally isn’t elicited unless a problem is s
uspected.
Nose.
Observe the neonate’s nose for shape, placement, patency and bridge configuratio
n.
Because neonates are obligatory nose breathers for the first few months of life,
nasal passages must be kept clear to ensure adequate respiration.
Neonates instinctively sneeze to remove obstruction. Test the patency of the nas
al passages by occluding each nares alternately while holding the
neonate’s mouth closed.
Mouth and Pharynx.
The neonate’s mouth usually has scant saliva and pink lips. Inspect the mouth fo
r its existing structures. The palate is usually narrow and highly
arched. Inspect the hard and soft palates for clefts.
Epstein pearls (pin-head sized, white or yellow, rounded elevations) may be foun
d on the gums or hard palate. These are caused by retained
secretions and disappear within a few weeks or months. The frenulum of the upper
lip may be quite thick. Precocious teeth may also be apparent.
The pharynx can be best assessed when the neonate is crying. Tonsillar tissue ge
nerally isn’t visible.
Ears.
Assess the neonate’s ears for placement on the head, amount of cartilage, open a
uditory canal, and hearing.
The neonate’s ears are characterized by incurving of the pinna and cartilage dep
osition. The pinna is usually flattened against the side of the head
from pressure in utero. The top of the ear should be above or parallel to an ima
ginary line from the inner to the outer canthus of the eye. Low-set
ears are associated with several syndromes, including chromosomal abnormalities.
Neck.
The neonate’s neck is typically short and weak with deep folds of skin. Observe
for range of motion, shape, and abnormal masses. Also, palpate
each clavicle and sternocleidomastoid muscle. Note the position of the trachea.
The thyroid gland generally isn’t palpable.
Chest.
Inspect and palpate the chest, noting shape, clavicles, ribs, nipples, breast ti
ssue, respiratory movement, and amount of cartilage in rib cage. The
neonatal chest is characterized by a cylindrical thorax (because the anteroposte
rior and lateral diameters are equal) and flexible ribs. Slight
intercostals retractions are usually seen on inspiration. The sternum is raised
and slightly rounded, and the xiphoid process is usually visible as a
small protrusion at the end of the sternum.
Breast engorgement from maternal hormones may be apparent, and the secretion of
“witch’s milk” may occur. Supernumerary nipples may be
located below and medial to the true nipples.
Lungs.
Normal respirations of the neonate are abdominal with a rate between 30 and 50 b
reaths/minute. After the first breaths to initiate respiration,
subsequent breaths should be easy and fairly regular. Occasional irregularities
may occur with crying, sleeping, and feeding.
It’s easiest to auscultate the lung fields when the neonate is quiet. Bilateral
bronchial breath sounds should be heard. Crackles soon after birth
represent the transition of the lungs to extrauterine life.
Heart.
The neonate’s heart rate is normally between 110 and 160 beats/minute. Because n
eonates have a fast heart rate, it’s difficult to auscultate the
specific components of the cardiac cycle. Heart sounds during the neonatal perio
d are generally of higher pitch, shorter duration, and greater
intensity than in later life. The first sound is usually louder and duller than
the second, which is sharp in quality. Murmurs are commonly heard,
especially over the base of the heart or at the third or fourth intercostals spa
ce at the left sternal border, due to incomplete functional closure of the
fetal shunts.
The apical impulse (point of maximal impulse) is at the fourth intercostals spac
e and to the left of the midclavicular line.
Abdomen.
The neonatal abdominal assessment should include:
Inspection and palpation of the umbilical cord
Evaluation of the size and contour of the abdomen
Auscultation of bowel sounds
Assessment of skin color
Observation of movement with respirations
Palpation of internal organs

The neonatal abdomen is usually cylindrical with some protrusion. Bowel sounds a
re heard a few hours after birth. A scaphoid (sunken anterior
wall) appearance indicates a diaphragmatic hernia. The umbilical cord is white a
nd gelatinous with two arteries and one vein and begins to dry
within 1-2 hours after delivery.
The liver is normally palpable 1” (2.5 cm) below the right costal margin. Someti
mes the tip of the spleen can be felt, but a spleen that’s palpable
more than 1/3” (1cm) below the left costal margin warrants further investigation
. Both kidneys should be palpable; this is easiest done soon after
delivery, when muscle tone is lowest. The suprapubic area is palpated for a dist
ended urinary bladder. The neonate should void within the first 24
hours of birth.
NCM 104 1st sem S.Y. 2007-2008
59
Femoral pulses should also be palpated at this point in the examination. Inabili
ty to palpate femoral pulses should signify coarctation of the aorta.
Anogenital Area.
The anus of the newborn must be inspected to be certain that it is present, pate
nt and is not covered by a membrane (imperforate anus). The time after birth tha
t the infant first passes meconium should be noted. If the newborn does not do s
o in the first 24 hours, the suspicion of imperforate anus or meconium ileus is
aroused.
Characteristics of a male neonate’s genitalia include rugae on the scrotum and t
estes descended into the scrotum. Scrotal edema may be present
for several days after birth due to the effects of maternal hormones. It may be
deeply pigmented in dark-skinned newborns.
Both testes should be present in the scrotum. Males with one or both undescended
testicles (cryptorchidism) need further referral to establish the
extent of the problem. It could be due to agenesis (absence of an organ), ectopi
c testes (the testes cannot enter the scrotum because the opening
of the scrotal sac is closed), or undescended testes (the vas deferens or artery
is too short to allow the testes to descend).
The urinary meatus is located in one of three places:
At the penile tip (normal)
On the dorsal surface (epispadias)
On the ventral surface (hypospadias)

In the female neonate, the labia majora cover the labia minora and clitoris. The
se structures may be prominent due to maternal hormones. Mucoid
vaginal discharge which may be blood-tinged (pseudomenstruation) may also occur
and the hymenal tag is present.
Extremities.
The extremities should be assessed for range-of-motion, symmetry, and signs of t
rauma. All neonates are bowlegged and have flat feet. The hips
should be assessed for dislocation. With the newborn in a supine position, both
legs can be flexed and abducted to such an extent (180 degrees)
that they touch or nearly touch the surface of the bed. If the hip joints seem t
o lock short of this distance, hip subluxation (a shallow and poorly
formed acetabulum) is suggested. If subluxation is present, when the infant’s le
g is held with the fingers on the greater and lesser trochanters and
the hip then abducted, a “clunk” of the femur head striking the shallow acetabul
um can be heard (Ortolani’s sign). If the hip can be felt to actually
slip in the socket, this is Barlow’s sign.
A neonate who was born in a frank breech position will tend to straighten the le
gs at the knee and bring them up to the face.
The fingertips, when arms are held down by the sides, should cover the proximal
thigh. Unusually short arms may signify achondroplastic
dwarfism.
Hyperflexibility of joints is characteristic of Down syndrome.
Some neonates may have abnormal extremities. They may bepolydactyl (more than 5
digits on an extremity) orsyndactyl (two or more digits
fused together).
The nailbeds should be pink, although they may appear slightly blue due to acroc
yanosis. Persistent cyanosis indicates hypoxia or
vasoconstriction.
The palms should have the usual creases. A single, tranverse palmar crease in co
ntrast to the three creases normally seen in a palm, called a
Simian crease, suggests Down syndrome.
Spine.
The neonatal spine should be straight and flat. The base of the spine should be
inspected carefully to e certain there is no pinpoint opening or
dimpling which may suggest spina bifida occulta.
The position of a baby presenting with a face presentation sometimes simulatesop
isthoto nos (back arched acutely with a deep concave
appearance, and the head is bent back on the neck.
NEUROLOGIC ASSESSMENT
An examination of the reflexes provides useful information about the neonate’s n
ervous system and his state of neurologic maturation. Some
reflexive behaviors in the neonate are necessary for survival whereas other refl
exive behaviors act as safety mechanisms.
Normal neonates display several types of reflexes. Abnormalities are indicated b
y absence, asymmetry, persistence, or weakness in these
reflexes:
Sucking – begins when a nipple is placed in the neonate’s mouth
Moro reflex – when the neonate is lifted above the crib and suddenly lowered; t
he arms and legs symmetrically extend and then abduct
while the fingers spread to form a “C”.
Rooting – when the neonate’s cheek is stroked, the neonate turns the head in th
e direction of the stroke
Tonic neck (fencing position) – when the neonate’s head is turned while he is l
ying in a supine position, the extremities on the same side
straighten and those on the opposite side flex
Babinski reflex – the sole on the side of the neonate’s small toe is stroked an
d the toes fan upward
Grasping - when a finger is placed in each of the neonate’s hands, the neonates
fingers grasp tightly enough to be pulled to a sitting
position
Stepping – when the neonate is held upright with the feet touching a flat surfa
ce, he responds with dancing or stepping movements
Startle – a loud noise such as a hand clap elicits neonatal arm abduction and e
lbow flexion and the neonate’s hands stay clenched
Trunk incurvature – when a finger is run laterally down the neonate’s spine, th
e trunk flexes and the pelvis swings toward the stimulated
side
Blinking – the neonate’s eyelids close in response to bright light
Acoustic Blinking – both eyes of the neonate blink in response to a loud noise
Perez reflex – when the neonate is suspended prone in one of the examiner’s han
ds and the thumb of the other hand is moved firmly up
he neonate’s spine from the sacrum, the neonate’s head and spine extend, the kne
es flex, the neonate cries, and he may empty his
bladder
Eight (8) Priorities In First Days Of Life :
1. Initiating and maintaining respirations
Resuscitation
Establishing an airway
Expanding the lungs
Drug Therapy
Maintaining effective ventilation
2. Establishing intrauterine circulation
3. Fluid and Electrolyte Balance
4. Thermometer Regulation
Radiant heat sources
Isolettes
Kangaroo Care
5. Preventing Infection
6. Establishing Parent-Infant Bonding
Following High-Risk Infants At Home
High-Risk Infants and Child Abuse
NCM 104 1st sem S.Y. 2007-2008
60
Providing for Growth and Development
7. Intake of adequate nourishment
8. Developmental care or care that balances physiologic needs and stimulation fo
r mental development
Whether they are preterm, term, or postterm, neonates are classified by weight i
n three ways
Large for gestational age (LGA) neonates
Appropriate for gestational age (AGA) neonates
Small for gestational age (SGA) neonates
THE SMALL-FOR-GESTATIONAL-AGE INFANT
Birth weight is below the 10th percentile on an intrauterine growth curve for t
hat age (based on a postnatal growth chart).
Infant may be born preterm, post term or term.
They are small for their age because they have experienced intrauterine growth
restriction (IUGR) or failed to grow at the expected rate in
utero
Causes:
1. Lack of adequate nutrition
2. Pregnant adolescents
3. Placental anomaly
Placenta is unable to obtain sufficient nutrients from the uterine arteries or
it is inefficient at transporting nutrients to the fetus
4. Placental damage
5. Women with systemic diseases that decrease blood flow to the placenta
6. Smoking or use of narcotics
7. Infants with intrauterine infections such as rubella or toxoplasmosis
8. Infants with chromosomal abnormalities
Assessment:
A. Prenatal Assessment
1. Fundal height during pregnancy is less than what is expected.
Dx Procedures:
1. Sonogram
2. Biophysical profile including nonstress test, placental grading , UTZ add inf
ormation on placental function
Appearance:
1. Below average in weight, length, and head circumference
2. May have a small liver
3. Poor skin turgor
4. Appears to have a large head because the rest of the body is small
5. Skull sutures widely separated
6. Hair is dull and lusterless
7. Sunken abdomen
8. Cord appears dry and may be stained yellow
- SGA neonates are prone to meconium aspiration because fetal hypoxia allows mec
onium to pass through a relaxed anal sphincter, thus causing
the neonate to experience reflexive gasping
In contrast, the child may have:
1. Better developed neurologic responses, sole creases, and ear cartilage
2. Skull may be firmer
3. Unusually active and alert for that weight that could be attributed to prolon
ged prenatal hypoxia
SGA infant needs careful assessment for possible congenital anomalies
Laboratory Findings:
1. High hematocrit level at birth
2. Increase in total number of red blood cells
3. Decrease serum glucose
Nursing Diagnosis: Ineffective breathing pattern related to underdeveloped body
system
Birth asphyxia is a common problem for SGA because they have underdeveloped che
st muscles and because they are at risk for developing
meconium aspiration syndrome due to anoxia during labor
Nursing Diagnosis:
Risk for ineffective thermoregulation
Risk for altered parenting
Mental development may have been impaired because of lack of oxygen and nourishm
ent in utero
SGA infants may always be below normal on standard growths chart and this inabi
lity to reach normal levels of growth and development may
interfere with bonding because the child does not meet the parents expectations
and eventually affects the child’s self-esteem
Nursing Intervention:
1. Discuss ways parents can promote the infants development once they are at hom
e
2. Adequate stimulation during the infant period to reach normal growth and deve
lopment
3. Encourage parents to provide toys that are suitable for their child’s chronol
ogic age
4. Play periods must be spaced with rest periods or hypoglycemia or apnea may oc
cur
THE LARGE-FOR-GESTATIONAL-AGE INFANT
An infant is large for gestational age (Macrosomia) if the birth weight is abov
e the 90% percentile on an intrauterine growth chart for that
gestational age
Causes:
1. Mothers with diabetes mellitus
2. Multiparous women
3. Transposition of the great vessels
4. Beckwith’s Syndrome, a rare condition characterized by overgrowth
5. Congenital anomalies such as omphalocele
Assessment:
NCM 104 1st sem S.Y. 2007-2008
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Antihypertensive and Cardiovascular agents. HPN is managed by intravascular cont

Palpation of internal organs

On the ventral surface (hypospadias)

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