Professional Documents
Culture Documents
A. Respiratory Disorders
i. Pulmonary Embolism
a. Acute RF
b. Chronic RF
C. Renal Disorders
i. Renal Failure
a. Acute RF
b. Chronic RF
D. Cardiovascular Disorders
i. Angina Pectoris
a. Right-sided CF
b. Left-sided CF
v. Thromboembolism
viii. Dysrhythmias
a. Sinus Node
1. Sinus Bradycardia
2. Sinus Tachycardia
b. Atrial Dysrhythmias
2. Atrial Flutter
3. Atrial Fibrillation
c. Junctional Dysrhythmias
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d. Ventricular Dsyrhythmias
2. Ventricular Tachycardia
3. Ventricular Fibrillation
4. Ventricular Asystole
E. Burns
Part I.
A. Infections
i. STDs
a. Cndidiasis
b. Trichomoniasis
d. Chlamydia Trachomatis
e. Syphilis
f. Gonorrhea
g. HPV
h. Group B Streptococci
i. HIV
B. Hematologic Disorders
i. Anemias
a. Iron Deficiency
c. Sickle Cell
i. UTI
D. Respiratory Disorders
i. Acute Nasopharyngitis
ii. Influenza
iii. Pneumonia
iv. Asthma
v. Tuberculosis
E. Rheumatic Disorders
F. Gastrointestinal Disorders
i. Appendicitis
G. Neurologic Disorders
i. Siezure
H. Musculoskeletal Disorders
i. Scoliosis
I. Cardiovascular Disorders
J. Endocrine Disorders
i. Thyroid Dysfunction
a. Hypothyroidism
b. Hyperthyroidism
iv. Hyperglycemia
K. Mental Illness
L. Trauma
i. Trauma Care
a. Abortion
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1. Spontaneous
2. Threatened
3. Imminent
4. Complete
5. Incomplete
6. Missed
7. Recurrent
8. Complications of Abortion
b. Ectopic pregnancy
b. Incompetent Cervix
a. Placenta Previa
b. Abruptio Placenta
a. Mild Preeclampsia
b. Severe Preeclampsia
c. Eclampsia
d. HELLP Syndrome
ix. Polyhydramnios
xi. Psuedocyesis
A. Part I
i. Small-for-Gestational-Age Infant
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iv. Apnea
vii. Hyperbilirubinemia
a. RH incompatibility
b. ABO incompatibility
x. Twin-to-twin Transfusion
i. Maternal Infection
b. Congenital Rubella
c. Ophthalmia Neonatorum
d. Hepatitis B
a. Diabetic Mother
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Venous stasis
eg. atrial fibrillation, heart failure
immobility, polycythemia
pregnancy, varicose veins
embolus
Pulmonary embolism
decreased/nonperfusion of alveoli distal to occlusion
decreased C02
bronchoconstriction
hypoxia release of mediators at the injury site increased right ventricular workload
shock
death
Clinical Manifestations
Shortness of breath and/or tachypnea- a response to the hypoxia that develops from impaired gas exchange
Cough
Hemoptysis – occurs when an infaction at or near the periphery of the lung begins 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 exchange
Jugular vein distention – a result of pulmonary hypertension and the decreased effectiveness of the right ventricle
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Hypotension – observed with large pulmonary embolism and is related to the decrease in cardiac output after ventricular dysfunction
Diagnosis
Chest radiograph – excludes other reasons that may cause the same clinical manifestations. 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 risk for developing pulmonary embolism, prophylactic
measures should be instituted such as intravenous or subcutaneous heparin (Lovenox) or oral anticoagulants such as warfarin (Coumadin). The
goal of therapy is to prevent thrombi formation, limit thrombi growth, and encourage 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 infusion adjusted every 4-6 hours, depending on the
institution’s protocol. Activated partial thromboplastin time (apt) should be maintained 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 embolectomy 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 used 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 (DVT) that may lead to a thrombotic pulmonary embolism.
Interventions should include early ambulation, use of pneumatic stockings, support hose, and passive range-of-motion exercises. All of these
improve venous blood flow and increase circulation.
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 alveollocapillary membrane that occurs as a result of an injury to the lungs.
This inflammation causes noncardiogenic pulmonary edema with severely impaired gas exchange.
Pathophysiology
lung injury
alveolar collapse
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Clinical Manifestations:
1. Rapid onset of severe dyspnea
2. Anxiety
3. Labored breathing and tachypnea
In patients with ARDS, PaO2 will be low, despite oxygen administration, pCO2 will decrease as a result of hyperventilation.
Medical Management: The main goals in the treatment of ARDS include improving and maintaining oxygenation, maintaining fluid and electrolyte
imbalances, providing adequate nitrition, and preventing respiratory and metabolic complications.
1. Primary focus of management includes identification and treatment of the condition.
2. Supportive Therapy: Intubation and mechanical ventilation to maintain adequate gas exchange
3. Circulatory support, adequate fluid volume and nutritional support. Fluid restriction is generally observed to prevent further leakage of fluid into
the alveoli and to decrease pulmonary edema, but fluid restriction can also cause a decrease in cardiac output and blood pressure.
4. Supplemental oxygen is used as the patient begins the initial spiral of hypoxemia. 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 exchange 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 decreasing 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 position
3. The nurse should explain all procedures and deliver care in a calm, reassuring manner
4. Rest is essential to reduce oxygen consumption
Nursing Diagnosis: Impaired gas exchange r/t inadequate respiratory center activity, chest wall movement, airway obstruction, fluids in the lungs
RESPIRATORY FAILURE
Respiratory failure is a sudden and life-threatening deterioration of the gas exchange 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.
Pathophysiology:
Clinical Manifestations:
Early signs are those associated with impaired oxygenation
Restlessness, fatigue, headache, dyspnea, air hunger, tachycardia, tachypnea, central 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 adequate 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 blood gases, pulse oximetry and vital signs
Implement strategies to prevent complications: turning schedule, mouth care, skin care, ROM
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Mechanical ventilation is a form of artificial ventilation that takes over all or part of the work performed by the respiratory muscles and organs. It is
initiated when the patient’s ability to oxygenate and exchange carbon dioxide is impaired. 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 disease 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 tube, mimicking respiration.
Modes of Ventilation
There are various modes of ventilation that may be used to ventilate and oxygenate 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 rate. 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 used 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 volume at a preset rate and is synchronized with patient’s
effort. This mode allows for spontaneous breathing between ventilated breaths and prevents competition between the patient and the
ventilator. When a spontaneous breath occurs, it is at the patient’s own rate and tidal volume. SIMV is the most 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 compliance. 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 ventilation allows for a longer period for gas exchange to
improve oxygenation. This mode is generally used in patients with ARDS. This type of ventilatory mode creates an abnormal breathing
pattern for the patient; consequently the patient may become uncomfortable and anxious.
6. Constant positive airway pressure (CPAP) provided positive pressure during spontaneous 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. Greater than 10 cm water pressure may increase intrathoracic pressure to the point that 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 expiration 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.
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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
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 mediastinum 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 placed at some point. Endotracheal tubes (oral or nasal) are not
intended for long-term management and may lead to other problems such as mucosal breakdown, skin ulcerations (lips), sinusitis, and vocal cord
paralysis or damage (or both).
The following are practices performed for patients receiving mechanical ventilation.
• The respiratory status is assessed every 4 hours and more frequently when a change 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, increased 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 the tube and preventing inadvertent extubation by staff
or patient. Placement is maintained until extubation.
• The endotracheal tube is repositioned per institutional policy to prevent pressure sores.
• Secretions are suctioned to maintain an open airway. Amount, color, and consistency 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 occur.
• Continuous pulse oximetry and ABGs are monitored for assessing the oxygenation status; the physician is notified of any changes in
parameters.
• The patient is frequently positioned to allow for optimal ventilation, to prevent complications, to mobilize secretions, and to promote
comfort.
• Ventilator circuit is monitored for moisture or water trapping in tubing and emptied 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 oxygenation.
• Alternative methods of communication are provided for patients to decrease anxiety and maintain some control over their environment.
• Mouth and lip care is provided at least once very shift to keep mucous membranes moist.
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ENDOCRINE/METABOLIC DISORDERS
DIABETIC KETOACIDOSIS
DKA is caused by an absence or markedly inadequate amount of insulin. First, because the beta cells in the pancreas have the inability to
produce insulin, the ensuing hyperglycemia causes a hyperosmolar state. This hyperosmolarity results in fluid shifting from inside the cell to
the serum; eventually this fluid is lost in the urine, causing electrolyte shifts and total body dehydration. Other metabolic derangements occur
because no insulin exists to allow glucose to enter the cells; therefore cells begin to break down fats and proteins to use for fuel. This process
causes the formation of ketones. Ketones decrease the blood pH and the bicarbonate concentration causing a ketosis. DKA is one of the
more serious metabolic crises that can result from hyperglycemia in patients with uncontrolled diabetes mellitus.
Clinical Manifestations:
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
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 vomiting 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 excretion of excessive glucose by the kidneys
2. The major electrolyte of concern during treatment of DKA is potassium. Potassium 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 level 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 glucose 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 sheet
Background: Hyperosmolar hyperglycemic nonketotic coma (HHNC) is a metabolic derangement 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 present 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 the reason for this is not known. Contributing factors include the
limitation on ketogenesis by hyperosmolarity, the lower levels of free fatty acids available for ketogenesis, the availability of insulin in amounts
sufficient to inhibit ketogenesis but not sufficient to prevent hyperglycemia, and the hepatic resistance to glucagon in these patients.
Precipitating Factors :
1. Stress such as injury, infection, thyroidal and non-thyroid surgery, tooth extraction, insulin reaction, diabetic acidosis, pregnancy, digitalis
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intoxication, abrupt withdrawal of anti-thyroid medications, extreme emotional stress, or vigorous palpation of the thyroid.
Clinical Manifestations :
1. High fever
2. Diaphoresis
3. Cardiopulmonary symptoms : extreme tachycardia, HPN, arrhythmias, CHF, pulmonary edema
4. CNS symptoms : increasing feeling of tremulousness to severe agitation, psychosis 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 prevent vascular collapse
2. Humidified oxygen is administered to improve tissue oxygenation and meet metabolic 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 in 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
Clinical Manifestations:
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 glucose
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, hyperhidorsis (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
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 toxins into the blood
Pathophysiology:
Liver disease alters liver structure and compromises essential functions. This leads 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 insidiously to a comatose state from which the patient rarely recovers.
Clinical Findings:
Stage 1
Slight personality and mood changes, disorientation, forgetfulness, slurred speech, 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 behavior, 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
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The pupil is comatose and does not react to stimuli. Pupils are dilated and lack corneal and deep tendon reflexes. Extremities are flaccid and
may assume flexion or extension posturing, decebrate rigidity. The EEG is markedly abnormal.
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 different kidney and urinary tract diseases.
Results when the kidneys are unable to remove the body’s metabolic wastes or perform their regulatory functions
The substances normally eliminated in the urine accumulate in the body fluids as a result of impaired renal excretion and lead to a disruption
in endocrine and metabolic functions and fluid and electrolyte, an acid-base disturbances.
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 transfusion reaction may also cause intrarenal failure. Medications may also predispose a patient to intrarenal damage, esp. nonsteroidal
anti-inflammatory drugs and ACE inhibitors
3. Post renal conditions. Postrenal causes of acute renal failure are usually the result of an obstruction somewhere distal to the kidney.
2. Period of Oliguria – accompanied by a rise in the serum concentration of substances 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 output, which signals that glomerular filtration has started to recover.
Laboratory values start rising and eventually begin a downward trend.Uremic symptoms may still be present. The patient must be closely monitored
for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase.
4. Period of Recovery – signals the improvement of renal function. Laboratory values return to the patient’s normal level.
Clinical Manifestations:
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
Prevention:
1. Renal function must be monitored closely if patient has been taking nephrotoxic antibiotic agents or has been exposed to environmental toxins.
Blood should be drawn for determining baseline and monitoring serum BUN and creatinine 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 fluid excesses, or performing dialysis
4. The elevated potassium levels may be reduced by administering ion-exchange resins (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
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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 dialysis. 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 potassium 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 deep 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 prominences, 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 and support during this time.
Pathophysiology:
As renal function declines, the end products of protein metabolism (which are normally excreted in urine) accumulate in the blood. Uremia develops
and adversely affects every system in the body.
Stage 1
Reduced renal reserve. Characterized by a 40 to 75% loss of nephron function. The 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 report polyuria and nocturia.
Stage 3
Renal Disease. Edema, metabolic acidosis, and hypocalcemia occur. Patient may exhibit 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 impaired. 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.
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 analysis
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, low 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 antacids that bind dietary phophorus in the GIT
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Antihypertensive and Cardiovascular agents. HPN is managed by intravascular control and a variety of hypertensive medications. CHF and
pulmonary edema may require treatment with fluid restriction, low sodium diets, diuretics, inotropic agents 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. The side rails must be padded to protect the patient
Erythropoietin. Anemia associated with CRF is treated with recombinant human erythropoietin (Epogen)
2. Nutritional Therapy
> Includes careful regulation of protein intake, fluid intake to balance fluid losses, sodium intake to balance sodium losses and some restriction of
potassium
3. Dialysis
> Hyperkalemia is usually prevented by ensuring adequate dialysis treatments with 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 retention of sodium and water
2. Altered nutrition; less than body requirements r/t anorexia, nausea and vomiting, 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 dialysis 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 imbalance
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 independence
CARDIOVASCULAR DISORDERS
ANGINA PECTORIS
- literally translates as pain in the chest. This symptom occurs as a result of myocardial 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 atheorsclerosis, angina, cerebrovascular
accident, myocardial infarction (MI), and heart failure.
The coronary arteries, which arise from the ascending aorta immediately on exiting 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 when the myocardium requires more oxygen during times of
increased work, the coronary arteries cannot increase flow because they are already 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 factors can adversely affect this relationship. The demand for
oxygen is increased whenever anyone of the following is increased: heart rate, afterload (hypertension), wall ension (ventricular volume or
pressure), myocardial wall thickness (hypertrophy), or contractility. All of these factors make the heart work harder. Conversely, the oxygen supply
is decreased whenever any of the following occur: hypotension, anemia, respiratory insufficiency, or tachycardia, which allows minimal time for
diastolic filling.
In the absence of adequate oxygen and glucose, cellular metabolism shifts from the 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 acidic environment activates chemical nociceptors, which transmit pain impulses to 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 predictable 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 event is discontinued or when nitroglycerin is administered in the
prescribed fashion. If the pain is unrelieved by either rest or nitroglycerin, the patient may then be at risk for an MI. As previously discussed,
stable angina is a result of atherosclerotic plaque that has narrowed the arteries. 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, intensity 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 individual with CAD.
3. Prinzmetal’s angina (variant angina)
The least common type of angina. It is unpredictable in onset, duration, and intensity and occurs almost exclusively at rest. Vasospasm of
one or more of the coronary arteries is the underlying cause, which can occur with or without associated atherosclerosis.
Clinical Manifestations
The cardinal symptom of angina is chest pain or discomfort. However, many patients describe feeling vague sensations of discomfort, tightness,
pressure, heaviness, aching or squeezing. Others complain of heartburn or indigestion during an attack. The most common location is substernal;
however, the pain or discomfort may radiate to the neck, jaw, back, shoulders, left arm, or occasionally the right arm.
When asked to demostrate or point to the location of the pain, typically patients will clench one or two fists over the substernal region when
experiencing myocardial ischemia. This display is known as the Levine’s sign. Other associated sighs and symptoms include pallor, diaphoresis,
cold skin, shortness of breath, weakess, dizziness, anxiety, and feelings of impending doom.
When an individual complains of chest pain, the source of pain should be considered cardiac until proven otherwise. However, it is prudent
to consider both cardiac and noncardiac causes of chest pain as possible differentials.
Electrocardiogram (ECG) – remains the “gold-standard” for a first-line, noninvasive tool for diagnosis.
Percutaneous transluminal coronary angioplasty (PTCA) – involves the passage of an inflatable balloon catheter into the stenotic coronary
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vessel, which is then dilated, resulting in compression of the atherosclerotic plaque and widening of the vessel
Coronary artery bypass grafting (CABG) – done by harvesting either a saphenous vein 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. The 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 imparts practical tools with which the patient can effectively manage the
condition at home to achieve the highest level of wellness and independent functioning.
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 continuous cardiac monitoring are essential parts of the ongoing assessment. The most crucial part of the assessment focuses on the
current attack; emphasis must be placed on evaluating the pain itself and any precipitating events.
Another critical nursing function is prompt institution of prescribed medical and pharmacologic therapies such as frequently used acronym MONA,
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 patients.
Other nursing measures that are beneficial to the patient who is suffering an anginal attack include helping the patient into a comfortable position,
promoting rest and relaxation, and encouraging slow, deep breathing.
As with angina, acute myocardial infarction occurs when the heart muscle is deprived of oxygen and nutrient-rich blood. However, in the case of
MI, this deprivation occurs over a sustained period to the point at which irreversible cell death and necrosis take place. This deprivation leads to
structural and functional changes within the affected area of myocardial tissue. As with angina, too, underlying coronary artery disease (CAD) is
the most common cause of MI. With these basic similarities in mind, many components of the MI disease process and treatment either overlap to
some degree or further develop along the continuum of cardiovascular 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 nutrient-rich blood:
Physical exertion
Emotional stress
Weather extremes
Digestion after a heavy meal
Valsalva maneuver
Hot baths or showers
Sexual excitation
Pathophysiologic chaaracteristics
Clinical Manifestations
The hallmark of MI is severe, unrelenting chest pain. As with angina, the pain is 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 angina is the onset, severity, and duration. Chest pain aassociated
with MI usually has an abrupt onset and can occur during activity, rest, or even sleep. The pain described during MI is typically more severe than
anginal pain, lasting at least 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 occurs 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 indispensable, noninvasive, and cost-effective tool.
Evolving MI will show ST elevation which indicates acute myocardial necrosis. The development of Q wave may be
observed which signifies further electrical abnormalities. It may be an indication of worsening ischemia and necrosis.
Cardiac Enzymes
During the infarction process, cell membranes rupture, allowing intracellular enzymes 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
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infarction.
Troponin 1 is the newest cardiac marker and is a protein found only in myocardial cells. It is a quick, rapid test that, if elevated, indicated MI.
Nursing Interventions:
1. Bedrest must be enforced.
2. The nurse should assist with all position changes and personal hygiene to avoid 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 stimulation 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 sufficient 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 result in decreased contractile properties of the heart. Common
underlying conditions 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 degenerative diseases of the
myocardium. Atherosclerosis of the coronary arteries is the primary cause of heart failure. Ischemia causes myocardial dysfunction because of
resulting hypoxia and acidosis (from accumulation of lactic acid). Myocardial infarction causes focal myocellular necrosis, the death of myocardial
cells, and a loss of contractility; the extent of the infarction is prognostic of the severity of CHF.
Dilated cardiomyopathy causes diffuse cellular necrosis, leading to decreased contractility. Inflammatory and degenerative diseases of the
myocardium, such as myocarditis, may also damage myocardial fibers, with a resultant decrease in contractility.
Systemic or pulmonary HPN increases afterload which increases the workload of the heart and in turn leads to hypertrophy of myocardial muscle
fibers; this can be considered a compensatory mechanism because it increases contractility.
Valvular heart disease is also a cause of cardiac failure. The valves ensure that blood flows in one direction. With valvular dysfunction, valve has
increasing difficulty moving forward. This decreases the amount of blood being ejected, increases pressure within the heart, and eventually leads to
pulmonary and venous congestion.
Etiologic Factors :
1. Increased metabolic rate (eg. fever, thyrotoxicosis)
2. Hypoxia
3. Anemia
VENTRICULAR FAILURE
Clinical Manifestations :
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
When the right ventricle fails, congestion of the viscera and the peripheral tissues 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.
Clinical Manifestations:
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
Pharmacologic Therapy:
If the patient is in mild failure, usually an ACE inhibitor is prescribed. A diuretic 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 severe, all three medications are usually started immediately.
ACE Inhibitors. Promote vasodilation and diuresis by decreasing afterload and preload eventually decreasing the workload of the heart.
Diuretic Therapy. A diuretic is one of the first medications prescribed to a patient with CHF. Diuretics promote the excretion of sodium and water
through the kidneys.
Digitalis. This medication increases the force of myocardial contraction and slows conduction through the AV node. It improves contractility thus,
increasing left ventricular output.
Dobutamine.(Dobutrex) is an intravenous medication given to patients with significant left ventricular dysfunction. A catecholamine, it stimulates the
beta1-adrenergic receptors. Its major action is to increase cardiac contractility.
Milrinone (Primacor). A phosphodiesterase inhibitor that prolongs the release and prevents the uptake of calcium. This in turn, promotes
vasodilation, causing a decrease in preload and afterload and decreasing the workload of the heart.
Other medications. Anticoagulants may be prescribed. Beta-adrenergic blockers maybe 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 input)
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 hypotensive from dehydration
7. Examine skin turgor and mucous membranes for signs of dehydration
8. Assess for symptoms of fluid overload (orthopnea, paroxysmal nocturnal dyspnea, and dyspnea on exertion)
Assessment
The focus of the nursing assessment for the patient with cardiac failure is directed 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 shortness 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 beginning 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 the 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 the 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 oxygenation
4. Non-compliance r/t to lack of knowledge
5. Powerlessness r/t inability to perform role responsibilities secondary to chronic illness and hospitalization.
Potential Complications:
1. Cardiogenic shock
2. Dysrhythmias
3. Thromboembolism
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Nursing Interventions:
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 pacing and prioritization of activities. The schedule should
alternate activities with periods of rest and avoid having two significant energy-consuming activities occur on the same day or in immediate
succession.
4. Controlling Anxiety
The nurse should take steps to promote physical comfort and psychological support. A family member’s presence provides reassurance.
Speaking in a slow, calm, and confident manner is helpful. Stating specific, brief 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 influence their direction, their lives, and their outcomes.
The nurse needs to assess for factors contributing to a perception of powerlessness 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 needed 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 pressure 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 ventricle also leads to increased pulmonary pressures, pulmonary
congestion, and pulmonary edema, exacerbating the hypoxia and resulting ischemia of vital organs.
Clinical Manifestations:
1. Tissue hypoperfusion – classic signs of cardiogenic shock manifested as cerebral hypoxia (restlessness, confusion, agitation), low blood
pressure, rapid and weak pulse, cold and clammy skin, increased respiratory crackles, hypoactive bowel sounds, and decreased urinary output.
2. Initially, arterial blood gas analysis may show respiratory alkalosis.
3. Dysrhythmias are common
2. The systemic vascular resistance is elevated due to the sympathetic nervous system 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 causes fluid retention and further vasoconstriction.
4. The increases in HR, circulating volume, and vasoconstriction occur to maintain 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 patient becomes unresponsive, severe hypotension occurs, and the
patient develops shallow respirations, cold, cyanotic or mottled skin, and absent bowel sounds.
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
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Pharmacologic Therapy:
Most medication are administered IV because of the decreased perfusion to the gastrointestinal 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 pumping action of the heart. The device inflates during diastole, increasing
the pressure in the aorta and therefore increasing perfusion. It deflates just before systole, lessening the pressure within the aorta before
ventricular contraction, decreasing the amount of resistance the heart has to overcome 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 interventions and for the development of complications
3. The patient is always treated in intensive care environment because of the frequency of nursing interventions and the technology required for
effective medical management.
THROMBOEMBOLISM
The decreased mobility of the patient with cardiac diseases and the impaired circulation 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, kidneys, intestines, or lungs
The most common problem is pulmonary embolism. The symptoms of pulmonary embolism 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, producing 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
Clinical Manifestations:
1. The patient may complain of a feeling of fullness within the chest. The feeling 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
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 circulation. 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.
Clinical Manifestations:
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 compression
4. Defibrillation – restoring the heart beat
Restoring Circulation
After performing ventilation, the carotid pulse is assessed and external cardiac 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 lower half of the sternum, two fingerwidths from the tip of the
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xiphoid and positions the other hand on top of the first hand. The fingers should 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 care unit for close monitoring. Continuous electrocardiographic monitoring
and frequent BP assessment are essential until hemodynamic stability is reestablished.
DYSRHYTHMIAS
Disorders of the formation and/or conduction of the electrical impulse within the heart. This can cause disturbances of the heart rate, the heart
rhythm, or both.
Types of 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
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
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, hyperthyroidism, pulmonary disease, moderate to heavy
ingestion of alcohol and the aftermath of open heart surgery
Treatment:
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Treatment depends on its cause and duration and the patient’s symptoms and instability
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 and unstable atrial flutter
To prevent recurrence and to promote heart rate control over a long period, quinidine, 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 to medications
3. Junctional Dysrhythmias
B. Junctional Rhythm
Occurs when the AV node, instead of the SA node, becomes the pacemaker of the heart.
Junctional rhythm may produce signs and symptoms of reduced cardiac output. If so, the treatment is the same as for sinus bradycardia.
Treatment:
Treatment is aimed at breaking the reentry of the impulse.
1. Vagal maneuvers, such as carotid sinus massage, gag reflex, breath holding, and immersing the face in ice water – increase parasympathetic
stimulation, causing slower conduction through the AV node and blocking the reentry of the rerouted impulse.
Because of the risk of a cerebral embolic event, carotid sinus massage is contraindicated in patients with carotid bruits.
2. If vagal maneuvers are ineffective, the patient may then receive a bolus of adenosine, verapamil, or diltiazem.
3. Cardioversion is the treatment of choice if the patient is unstable or does not respond to the medications.
4. Intravenous adenosine may be prescribed to cause a conversion to sinus rhythm.
4. Ventricular Dysrhythmias
Treatment:
1. Lidocaine is the medication most commonly used for immediate short-term therapy
B. Ventricular Tachycardia
Defined as three or more PVC’s in a row, occurring at a rate exceeding 100 beats/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 unresponsive and pulseless.
Treatment:
1. Lidocaine is the initial choice
2. Cardioversion maybe indicated if the medications are ineffective or if the patient becomes unstable
3. Immediate defibrillation
Ventricular tachycardia in a patient who is unconscious and without pulse is treated in the same manner as ventricular fibrillation.
C. Ventricular Fibrillation
A rapid but disorganized ventricular rhythm that causes ineffective quivering of the ventricles.
This dysrhythmias is always characterized by the absence of an audible heartbeat, 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
VF.
D. Idioventricular Rhythm
Also called ventricular rhythm, occurs when the impulse starts in the conduction system below the AV node
Commonly causes the patient to lose consciousness and experience other signs and symptoms of reduced cardiac output. In such cases,
treatment is the same as for any bradycardia, including identifying the underlying 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 complexes, 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.
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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
Assessment
Major areas of assessment include possible causes of the dysrhythmias and the dysrhythmia’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 vital 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 dysrhythmia
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 auscultation.
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 and 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.
Nursing Interventions:
1. Monitoring and Managing the Dysrhythmias
Controlling the incidence or effect of dysrhythmias is often achieved by the use of ant-idysrhythmic medications
A constant serum blood level of the medication is maintained to maximize beneficial effects and minimize adverse effects
If the patient is hospitalized, an ECG is initiated and rhythm strips are analyzed to track dysrhythmias
BP, rate and depth of respirations, pulse rate and rhythm are evaluated regularly 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
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 for 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 patient 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, individual 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 maybe transferred through conduction or electromagnetic radiation.
Burns are categorized as thermal (including electrical burns), radiation or chemical. 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 contact.
The depth of the injury depends on the temperature of the burning agent and the duration of contact with the agent.
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Classification of Burns
Burn injuries are described according to the depth of the injury and the extent of body surface area (BSA) injured.
Rule of Nines
An estimation of the total BSA involved in a burn is simplified using the rule of nines
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.
Cardiovascular Response
Cardiac output decreases before any significant change in blood volume is evident. 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 (vasoconstriction) 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 fluid returns to the vascular compartment.
As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases.
If renal and cardiac function is adequate, urinary output increases.
Patients with severe burns develop massive systemic edema. As edema increases in circumferential burns, pressure on small blood vessels
and nerves in distal extremities causes an obstruction of blood flow and consequent ischemia. This complication is known as compartment
syndrome. The physician may need to perform an esharotomy, a surgical incision into the eschar (devitalized tissue resulting from a burn), to
relieve the constricting effect of the burned tissue.
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 injury.
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 to the periphery. Later, hypermetabolism and continued
catecholamine release lead to increased tissue oxygen consumption, which can lead to hypoxemia.
1. Airway
2. Breathing
3. Circulation; Cervical spine immobilization for all high voltage electrical injury; 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 the 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 pressure are monitored frequently
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 percentage 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 established that salt and water are required in burn
patients, but that colloid may or may not be useful during the first 24 to 48 postburn 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 initially 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 pump at the cellular level. Thus, patients with very large burns
may need proportionately more milliliters of fluid per percent of burn than those with smaller burns
Most fluid replacement formulas use isotonic electrolyte solutions.
Another fluid replacement method requires hypertonic electrolyte solutions. This 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 edema results from administering hypertonic solutions.
Goals of Fluid Replacement Therapy: A systolic blood pressure exceeding 100 mm Hg, 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 include hematocrit and hemoglobin and serum sodium levels.
Infection Prevention
Burn wound is an excellent medium for bacterial growth and proliferation.
Bacteria such as Staphylococcus, Proteus, Pseudomonas, Escherichia coli, and Klebsiella find optimal conditions for growth within the burn
wound. The burn eschar is a non-viable crust, no blood supply; therefore, neither polymorphonuclear leucocytes or antibodies nor systemic
antibiotics can reach the area.
Phenominal numbers of bacteria- 1 billion per gram of tissue- may appear and spread 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 intestinal tract.
Major secondary source is the environment.
Cap, gown, mask and gloves are worn while caring for patient with open burn wounds. 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 and 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 and syringe
Wound cleaning is usually performed daily.
When the eschar begins to separate from the viable tissue beneath, more frequent cleaning and debridement may be necessary
After burn wounds are cleaned, they are gently patted with towel and the prescribed method of wound care is performed.
Whatever is the method of wound care, the goal is to protect the wound from overwhelming proliferation of pathogenic organisms. Patient
comfort and ability to participate are also important considerations.
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 free 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 prevent excessive evaporative fluid losses.
A cradle may be placed over the patient to prevent sheets from coming in contact 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 are applied under sterile conditions in the operating room.
Their purpose is to protect the graft, promoting an optimal condition for its adherence 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 fingers 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 administered.
> A mask, hair cover, disposable plastic apron or cover gown, and gloves are worn by health care personnel.
Dressings that adhere to the wound can be removed more easily if they are moistened 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
Natural Debridement
The dead tissue separates from the underlying viable tissue spontaneously. After partial and full- thickness burns occur, bacteria that are
present at the interface of the burned tissue and the viable tissue underneath gradually 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 eschar 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 tissue) 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 performed 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 occlusive dressing.
The use of surgical excision carries with it risks and complications, especially 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).
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 topical antibacterial such as silver nitrate is also available.
One new biologic dressing that has shown promise for permanent burn wound coverage is Alloderm.
Alloderm is processed dermis from human cadaver skin. When a donor site is taken for an autologous skin graft, both the epidermal and
dermal layers of skin are removed from the donor site. However, Alloderm provides a permanent dermal layer replacement.
Use of alloderm allows the surgeon to take a thinner skin graft consisting of the 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 grafts; donor sites heal much more quickly than conventional donor
sites because only the epidermal layer has been taken.
Autografts
The ideal means of covering burn wounds because they come from the patient’s own skin and thus are not rejected by the patient’s immune
system.
They can be split-thickness, full-thickness, pedicle flaps, or cultured epithelium. 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 pieces, 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 under the graft.
Using expanded grafts may be necessary in large wounds but should be viewed as a compromise in terms of cosmetics.
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 and 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 excruciating pain with exposure to air currents.
Although, nerve endings are destroyed in full-thickness burns, there is deep pain and pain in adjacent structures.
The primary pain is intense in the initial acute post burn phase. This pain gradually 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 itching, 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 anesthesia administered IV are also used.
Sedation with anti-anxiety agents such as lorazepam (Ativan) or midazolam(Versed) may be indicated in addition to analgesia.
Patient-controlled analgesia, using both continuous and bolus morphine infusions, and sustained release oral morphine, given every 12 hours
have helped burn patients.
Self-administered nitrous oxide also helps to make dressing changes tolerable to 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 reduce the overall pain experience for burn patients.
Nutritional Support
Hypermetabolism persist after burn injury until wounds are closed, thereby increasing the basal metabolic need by as much as 100%.
The goal of nutritional support is to promote a state of positive nitrogen balance.
The nutritional support required is based on the patient’s preburn status and the extent of total BSA burned.
Several formulas exist for estimating the daily metabolic expenditure and caloric 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 per day
Adequate vitamins and minerals are also needed.
The proportions of fat, protein, and carbohydrate are planned for maximal use.
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Overfeeding can be detrimental. Therefore, a dietitian familiar with current concepts 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 than 10% of normal body weight, inadequate intake of enteral
nutrition prolonged wound exposure, and malnutrition or debilitated condition before injury.
SCARS
Results from excessive abnormal healing or inadequate new tissue formation.
Hypertrophic scars and wound contractures are more likely to occur if the initial 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 prevent 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 margins, 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 positioning must be used to counteract deformity in burns
affecting joints.
Potential Complications:
1. Congestive heart failure and pulmonary edema
2. Sepsis
3. Acute Respiratory Failure
4. Visceral Damage
Nursing Interventions:
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 room because of the risk of microorganism growth
Visitors are screened to avoid exposing the immunocompromised patient to pathogens
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Sepsis
Early signs are increased in temperature, increased pulse rate, flushed dry skin, increased pulse rate, widened pulse pressure, and flushed
dry skin in unburned areas
Wound and blood cultures
Antibiotics
Visceral Damage
Assess for signs of necrosis of visceral organs due to electrical injury. Tissues affected are usually between the entrance and exit wounds of
the electrical burn
All patients with electrical burns should undergo electrocardiographic monitoring
Assess for pain relate to deep muscle ischemia
Fasciotomies are performed to relieve the swelling and ischemia in the muscles
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D. Past Medical History – important because a past condition may become active during or immediately following pregnancy.
1. Any abdominal surgery, kidney, heart, etc.
E. Gynecologic History – her past experience with her reproductive system may have some influence on how well she accepts a pregnancy.
1. When was her menarche
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F. Obstetric History :
1. Review pregnancy briefly.
2. Determine woman’s status with respect to the number of times she has been pregnant (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 down 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
B. System Assessment
1. General Appearance and Mental Status
Physical examination always begins with inspection of general appearance to form 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 themselves by the manner in which they dress, speak and
body posture they assume
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 congestion.
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
8. Neck
Slight thyroid hypertrophy may occur with pregnancy because the overall metabolic rate is increased.
Encourage a woman to continue to use iodized salt during pregnancy and to eat seafood at least once weekly to supply enough iodine
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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 the natural one; blue streaking of veins becomes
prominent; colostrums may be expelled as early as the 16th week of pregnancy; any 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 pregnancy, 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 cannot 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 commonly occurs from pelvic pressure preventing venous
return.
b. INTERNAL GENITALIA
1. Cervix should be in the center and color should be almost purple when pregnant.
Retroverted Uterus – cervix positioned anteriorly
Anteverted Uterus – cervix positioned posteriorly.
1. Nulligravida – woman who is not or never has been pregnant, the cervical os is round and small.
2. A woman who has had a previous pregnancy, the cervical os has a slitlike appearance.
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 infection, the epithelium of the cervical canal often enlarges and
spreads onto the area surrounding the os. Giving the cervix a reddened appearance called erosion. This area bleeds easily if touched.
Trichomoniasis – a protozoal infection, generally gives signs of redness; a profuse, 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 extreme 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 occasionally 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 (DES) in utero, who have multiple sexual partners, who have
a history of human papillomavirus (HPV), cigarette smokers, who were sexually active before age 21
d. VAGINAL INSPECTION
A culture for gonorrhea, chlamydia or group B streptococcus may be taken. All these 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 pregnancy. Female children of mothers who took DES are
prone to develop adenosis or overgrowth of cervical endothelium (which is possibly associated with vaginal cancer).
f. RECTOVAGINAL EXAMINATION
To assess the strength and irregularity of the posterior vaginal wall
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 sacral 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.
3. The Ischial Tuberosity – The distance between the ischial tuberosities, or the 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
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 level present during pregnancy.
2. Occurs frequently to women being treated with an antibiotic for another infection.
3. Occurs frequently in women with gestational diabetes
4. Mostly seen in women with HIV infection
Treatment : Local application of an antifungal cream such as miconazole cream (Monistat) or oral fluconazole (Diflucan)
Complications :
1. If untreated during pregnancy, it may cause a candidal infection, or thrush, in the NB.
Assessment :
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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 teratogenic effects if used during the first trimester of pregnancy.
Etiology :
Probably associated with preterm labor, premature rupture of membranes and post cesarean section infection
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 are 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 because of possible long bone deformities; Erythromycin and
Amoxicillin are used instead.
It is important that chlamydia infections be treated because they are associated 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 on 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 antibody reaction test.
Treatment :
1. One injection of Benzathine penicillin G is the drug of choice during pregnancy
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 endometritis 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 urethra
Treatment :
1. Traditionally treated with amoxicillin and probenecid but the incidence of penicillinase-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 lead to blindness in the NB (Ophthalmia neonatorum).
2. Major cause of pelvic infectious disease and infertility
Etiology :
1. Women who have multiple sexual partners
Assessments :
1. Discrete papillary structures at first which spreads, enlarges and coalesce to form large, cauliflower-like lesions
2. Tend to increase in size during pregnancy because of the high vascular flow in the pelvic area.
3. They may become secondarily ulcerated and infected; when this occurs, a foul vulvar odor may develop
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Treatment :
1. Aimed at dissolving the lesions and also ending any secondary infection present.
2. Trichloroacetic acid (TCA) or Bichloroacetic acid (BCA) applied to the lesions 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.
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 infected 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
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
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 symptoms
2. Seroconversion in which the woman converts from having no HIV antibodies in blood 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 infections.
3. Tuberculosis occurs at a higher rate with HIV people and may grow worse during pregnancy
Dx: ELISA antibody reaction. For confirmation a Western blot analysis is required.
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 trimethoprim 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 administered by aerosol.
3. Kaposi’s sarcoma, malignancy that tends to occur with AIDS, is normally treated with chemotherapy. Chemotherapy is contraindicated during
early pregnancy because of the potential for fetal injury but is used later in pregnancy to halt malignant growths.
4. Thrombocytopenia (lowered platelet count) may be present which may make the woman a poor candidate for an epidural injection for anesthesia
during labor or for episiotomy. She may need a platelet transfusion to restore coagulation ability
5. Newborns of HIV-positive mothers are treated with zidovudine for the 1 st 6 weeks of life to try to prevent seroconversion and trimethroprim-
sulfamethoxazole to prevent P. carinii pneumonia
TORCH infections
The term TORCH 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 just 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 suffers from chorioretinitis and
microcephaly. Approximately 10% to 15% of these babies 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, serious 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 include bone lesions, anemia, low birth weight,
hepatomegaly, splenomegaly, jaundice, petechiae, heart disease, pneumonia, cataracts, 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 the NB
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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.
Etiology :
1. Occurs most often in multiple pregnancies because of the increased fetal demand.
2. In women with a secondary hemolytic illness in which there is rapid destruction and production of red blood cells
3. In women who are taking hydantoin, a drug that interferes with folate absorption.
4. Alcohol abuse – suppresses the metabolic effects of folic acid
Assessment:
The main symptom of folic acid deficiency anemia is a history of severe, progressive fatigue. Associated findings include shortness of breath,
palpitations, diarrhea, nausea, anorexia, headaches, forgetfulness, and irritability. The impaired oxygen-carrying capacity of the blood from
lowered hemoglobin levels may produce complaints of weakness and light-headedness.
Therapeutic Management :
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
Complications:
1. Increased incidence of asymptomatic bacteriuria, resulting in an increased incidence 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 those 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 hemoglobin 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.
Therapeutic Management :
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1. Replace sickle cells with normal cells by exchange transfusion periodically throughout 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 administered 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.
Signs/Symptoms :
1. Menorrhagia
2. Frequent episodes of epistaxis
3. Prolonged bleeding time
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
Therapeutic Management :
1. Platelet transfusion to temporarily increase platelet count
2. Oral prednisone is effective
Causes :
1. In pregnant woman, because of the dilated ureters from the effect of progesterone, stasis of urine occurs.
2. .Minimal glucosuria that occurs with pregnancy contributes to the growth of organisms.
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 with 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
Therapeutic Management :
1. Urine for culture and sensitivity test to detect infection and to determine which antibiotic to be used.
2. Amoxicillin, ampicillin and cephalosporins are effective against most organisms causing UTI.
3. Sulfonamides can be used early in pregnancy but not near term because they interfere with protein binding of bilirubin.
Acute nasopharyngitis (common colds) tends to be more severe during pregnancy because during this period estrogen stimulation normally
causes some degree of nasal congestion.
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.
Treatment :
1. Appropriate antibiotic
2. Oxygen administration
3. Ventilation support maybe necessary in severe cases.
Symptoms :
1. Difficulty with air exchange; on exhalation, she makes a high pitched whistling sound (bronchial wheezing)
Asthma has the potential of reducing oxygen supply to the fetus if a major attack 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 choice. If ineffective, theophylline, a corticosteroid or cromolyn
sodium may be added to the regimen.
Assessment:
1. Chronic cough
2. weight loss
3. Hemoptysis
4. Night sweats
5. Low-grade fever
6. Chronic fatigue
Therapeutic Management :
1. Isoniazid (INH) and ethambutol Hcl are drugs of choice. INH may result in a peripheral neuritis if the woman does not take supplemental
pyridoxine (vitamin B6). Ethambutol may cause optic nerve involvement in the mother.
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.
Complications :
1. Increased risk for preterm labor
2. Risk for perinatal death
3. High possibility of developing DM due to pancreas involvement
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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 breastfeed because their breast milk contains more fatty acid.
Pathology :
The disease pathology is synovial membrane destruction. Inflammation with effusion, 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 salicylates is prolonged pregnancy (salicylates interferes with
prostaglandin synthesis, so labor contractions are not initiated). The woman is asked to decrease salicylate intake 2 weeks before term to avoid the
problem.
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 urine output. Proteinuria and edema may begin.
Women will be monitored by frequent serum creatinine levels to assess kidney function. Dialysis or plasmapheresis may be necessary.
Women are asked to reduce salicylate close to birth to reduce possibility of bleeding in the NB
Hydrocortisone IV is administered during labor to help the woman to adjust to the 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.
Nursing Diagnosis: Risk for altered nutrition, less than body requirements
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 abdomen 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 peristalsis tends to cause an inflamed appendix to rupture.
Therapeutic Management :
1. CS if fetus is near term, then remove appendix.
2. Laparoscopy – if condition occurs in early pregnancy
Symptoms :
1. Heartburn
2. Gastric regurgitation
3. Indigestion
4. Dysphagia
5. Possible weight loss due to inability to eat
6. Hematemesis in extreme cases
Therapeutic Management :
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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
Therapeutic Management :
1. Lower fat intake. Low fat but fat free diet because of the importance of linoleic 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
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
Therapeutic Management :
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 administered to the NB
Infants should be observed for infection
Mother should not breastfeed because HB Ag antigens can be recovered from breast milk.
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 conditions
> 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 because it may interfere with bilirubin binding sited and can cause
neonatal jaundice.
Etiology :
1. Head trauma
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2. Meningitis
3. Cause of recurrent seizures are unknown (idiopathic)
Therapeutic Management :
1. “Do not take medication during pregnancy” rule does not apply to seizure control medications. The risk of adverse maternal or fetal outcome
from seizures during pregnancy is greater than the risk of teratogenicity from taking anticonvulsant drugs.
Complications :
1. Infants may have an increased danger of neural tube disorders and childhood malignancies as a result of folic acid displacement from maternal
medication.
2. Infants are also prone to hemorrhagic disease because of decreased Vit K coagulation factors at birth.
Tonic-clonic seizures (sustained full-body involvement) could affect the fetus because of anoxia that can occur form spasms of chest muscles.
Administer oxygen by mask is good prophylaxis to ensure adequate fetal oxygenation
Woman is advised to inform health personnel that she has recurrent seizures and the medications she is taking
A woman who has recurrent convulsions may worry that her child will have seizures as the child grows older.
If seizures are result of acquired disorder, assure the woman that her child will have no tendency toward seizures.
Treatment :
1. Administration of anti-cholinesterase drugs such as neostigmine and pyridostigmine counteract fatigue and muscle weakness and enable about
80% of normal muscle function
2. Plasmapheresis (withdrawal and replacement of plasma) to remove immune complexes 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 anticholinesterase drugs (headaches, sweating, abdominal cramps,
nausea, vomiting, diarrhea, excessive salivation, bronchospasm). Warn her to avoid strenuous exercise, stress, infection, and unnecessary
exposure to the sun or cold weather. Caution 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.
Etiology :
1. exact cause is unclear; however, current theories suggest that it may be caused 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 independence by finding new ways to perform daily activities.
⇒ Explain the value of a well balanced nutritious diet that contains sufficient fiber.
⇒ 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
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
Therapeutic Management :
1. Stainless steel rods (Harrington rods) implanted on both sides of spinal vertebrae to strengthen and straighten the spine.
2. CS, if pelvis is distorted.
I. CARDIOVASCULAR DISORDERS AND PREGNANCY
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Clinical Manifestations :
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
Therapeutic Management :
1. Anti-hypertensives
2. Beta-blockers to decrease the force of myocardial contractions
Peripartal cardiomyopathy – extremely rare condition that originate late in pregnancy. 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)
Therapeutic Management :
1. Reduced activity
2. Diuretic and digitalis therapy
3. Low dose heparin to decrease the risk of thromboembolism.
4. Immunosuppressive therapy
Fetal Assessment :
1. Low birth weights
2. Severe fetal distress
Nursing Diagnosis : Knowledge deficit regarding the effects of maternal cardiovascular disease
Nursing Interventions :
1. Promote rest
2. Promote healthy nutrition
3. Educate regarding medication
4. Educate regarding avoidance of Infection
Signs/symptoms :
1. Chest pain
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Therapeutic Management :
1. Avoid use of constrictive knee-high stockings,
2. Do not cross legs
3. Bed rest
4. Heparin IV administration
Signs/symptoms :
1. Easy fatigability
2. Obese
3. dry skin
4. Little tolerance for cold
5. Extreme nausea and vomiting
Therapeutic Management :
1. Thyroxine – to supplement lack of thyroid hormone. As a rule, her dose of thyroxine will be increased for the duration of pregnancy to simulate
the effect that would normally occur in pregnancy
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 rapid heart rate cannot adjust to the increasing serum
volume occurring with pregnancy.
Complications :
1. PIH
2. Fetal growth restriction
3. preterm labor
Therapeutic Management :
1. Thiomides to reduce thyroid activity. Unfortunately, these drugs are teratogens 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 drugs are excreted in breast milk.
Pathophysiology :
The pancreas has both endocrine and exocrine types of tissue. The Islets of Langerhans 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 metabolism 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 lowered, production decreases. Both the ability to secrete additional insulin and the action to decrease production are
immediate responses.
The primary problem of any woman with DM is control of the balance between insulin and blood glucose to prevent hyperglycemia or hypoglycemia
Glomerular filtration of glucose is increased causing slight glycosuria. The rate of insulin secretion is increased, and the fasting blood sugar is
lowered.
All women appear to develop insulin resistance as pregnancy progresses, a phenomenon that is probably caused by the presence of the
hormone human placental lactogen and high levels of cortisol, estrogen, progesterone 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 infants.
At birth, infants are more prone to hypoglycemia, respiratory distress syndrome, hypocalcemia, and hyperbilirubinemia.
Pathophysiology
• In gestational diabetes mellitus, insulin antagonism by placental hormones, human placental lactogen, progesterone, cortisol, and
prolactin leads to increased blood glucose levels. The effect of these hormones peaks at about 26 weeks gestation. This is called the
diabetogenic effect of pregnancy.
• The pancreatic beta cell functions are impaired in response to the increased pancreatic stimulation and induced insulin resistance.
• Pregnancy complicated by diabetes pits the mother at high risk for the development 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 ketoacidosis. 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 signs of hyper and hypoglycemia
• Teach client how to control diabetes in pregnancy, advise changes that need to be 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 measures
Nursing Interventions :
1. Education regarding nutrition
2. Education regarding exercise
Therapeutic Management :
1. Insulin
2. monitor fetal well-being
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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 information given to them.
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
5. Risk for infection
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.
Therapeutic Management :
1. Immediate Care
Interventions in emergency situations must be quick yet always remember that the 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.
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 toxoid is administered.
> If the woman did not have tetanus immunization within 10 years, tetanus toxoid plus immune tetanus globulin is administered.
Knife wounds cause deep penetration and are often directed into the abdomen. Most 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 strain 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 globulin 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 vessels may ooze and form ecchymosis or hematoma at the
site.
To assess for abdominal bleeding, a diagnostic peritoneal lavage may be done, UTZ may also be done.
Traumatic blow to the abdomen could cause dislodgement of the placenta (abruptio placentae) or preterm labor.
Palpate the uterus for any bleeding and count fetal heart tones using Doppler instrument.
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 uterine 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 point 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 from 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 the 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 usual
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 can have adequate calcium for new bone growth
9. BURNS
Burns are dangerous to the pregnant woman because of the thermal injury that occurs and the inhalation of carbon monoxide gases which
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can lead to extreme fetal hypoxia as carbon monoxide crosses the placenta in place 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 from hypovolemia or an electrolyte imbalance can occur.
A body response to a harsh trauma such as burn is the production of prostaglandins, which may cause preterm labor.
Maternal and fetal prognosis are poor if burns cover more than 50% of body surface area.
Interestingly, burn tissue heals more quickly than normal during pregnancy. This is probably related to the increased metabolism and to the
increased corticosteroid serum level that keeps inflammation and damage to tissue from the pressure of edema from occurring.
Assessment :
A battered woman may come for care late in pregnancy because her partner may control her transportation or money; she may fear that a
health care provider will report the abuse; pretending that the pregnancy does not 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 strangulation.
Battered woman may be anxious to hear baby’s heartbeat because her partner recently 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 abusing 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.
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
3. Risk for infection
4. Altered tissue perfusion r/t hypertension of pregnancy
5. Knowledge deficit r/t signs and symptoms of possible complications
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
1. ABORTION
A. SPONTANEOUS ABORTION
Abortion-any interruption of a pregnancy before the fetus is viable. A non-viable 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 chromosomal aberration.
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2. Immunologic factors
3. Implantation abnormalities – placental circulation will not be well established and fetal formation will be inadequate.
4. Corpus luteum fails to produce enough progesterone to maintain the deciduas basalis
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 further bleeding.
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 abnormalities such as gestational trophoblastic disease (H mole).
D. COMPLETE ABORTION
> Entire products of conception (fetus, membrane, and placenta) are expelled spontaneously 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 retained 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 cervix followed by oxytocin stimulation.
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
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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 filling 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 spontaneous 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 against 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 induction drugs
f. IUD
Therapeutic Management:
1. Laboratories: Hgb, Blood typing and Xmatching, HCG level for immediate pregnancy 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 damaged 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 ectopic pregnancy.
Abdominal Pregnancy
> Very rarely after ectopic pregnancy, the product of conception is expelled into 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
Etiology:
1. Occur most often in women from low socioeconomic groups who have a low protein 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 pregnancy
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 fresh flow, accompanied by discharge of the clear fluid-filled vesicles.
Therapeutic Management:
1. Suction curettage – to evacuate the mole
2. Every woman who had history of GTD should have a blood test for HCG every 2 to 4 weeks along with pelvic examination
3. Thereafter, HCG levels and possibly chest xray are done once a month for a full 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 and 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 to strengthen it and prevent from dilating.
3. Emergent cerclage – sutures placed in the cervix as prophylaxis against pretem birth.
Occurs in 4 Degrees:
(1) Implantation in the lower rather than in the upper portion of the uterus (Low-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 previa)
(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
Therapeutic Management:
Complications:
1. Postpartal Hemorrhage – because the placental site is in the lower uterine segment 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.
Predisposing Factors:
1. High parity
2. Chronic hypertensive disease
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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 uterine musculature
5. Signs of shock
6. Uterus becomes tense and rigid to the touch
Therapeutic Management:
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 baselines
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
Therapeutic Management:
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 depressant action that slows and halts uterine contractions.
Fetal Assessment:
To evaluate fetal movement the woman lies down on her left side and times the number 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, she monitors again for second hour. If at the end of this second
hour fetal activity has not increased, she should report it immediately
Management:
1. If the fetus is very immature, a CS maybe planned to reduce pressure on the fetal head and reduce the possibility of subdural or intraventricular
hemorrhage
2. As a rule, artificial rupture of membranes should not be done due to possibility 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, although 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 excreting 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 circulatory system.
Pathophysiology
- precoagulant substances released in the blood trigger microthrombosis in peripheral vessels and paradoxical consumption of circulating
clotting factors
- fibrin-split products accumulate, further interfering with the clotting process
- platelet and fibrinogen levels drop
-
injury to vessel endothelium or blood cell injury to tissue with tissue factor
or thromboplastin release
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intrinsic extrinsic
production of microthrombi
hemorrhage
DIC
Symptoms:
1. Easy bruising or bleeding from an IV site. Bleeding may range from massive, unanticipated blood loss to localized bleeding.
2. Presence of special maternity problems
3. Prolonged prothrombin and partial thromboplastin time
Therapeutic Management:
1. Prompt recognition and adequate management of the underlying problem ( eg. delivery 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 necessary to replace blood loss
4. Anti-thrombin III factor, fibrinogen, or cryoprecipitate can be used to restore blood clotting
5. Fresh frozen plasma can also aid in restoring clotting function
Etiology:
1. Although cause is unknown, malpresentation and a contracted pelvis commonly accompany 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 pulmonary 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 of 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.
Therapeutic Management:
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 ampicillin 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, uterine tenderness, or odorous vaginal discharge.
2. Refrain from tub bathing, coitus, and douching because of the danger of introducing infection.
3. White cell count needs to be assessed daily. A count of more than 18,000/mm3 to 20,000/mm3 is suggestive of infection.
PREGNANCY-INDUCED HYPERTENSION (PIH)
A condition in which vasospasm occurs during pregnancy. The vasospasm may be caused by the action of prostaglandins (notably decreased
prostacyclin and increased thromboxane). Increased cardiac output may injure endothelial cells of the arteries, leading to spasm. Normally,
blood vessels during pregnancy are resistant to the effects of pressor substances such as angiotensin 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 rising 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 fetal 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 develop in kidney glomeruli because of the back pressure.
This leads to increased permeability of the glomerular membrane allowing the serum proteins, albumin and globulin to escape into the urine
(proteinuria). The degenerative changes also result in decreased glomerular filtration so there is lowered urine output and clearance of
creatinine. Increased tubular reabsorption of sodium occurs. Because sodium retains fluid, edema results.
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Vasospasm
Effects on the vascular system Effects on the renal system Effects on the interstitial
Tissues
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 prepregnancy 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 retention and lowered glomerular filtration rate.
Interventions:
- Promote bed rest as long as signs of edema or proteinuria are minimal, preferably left-side lying to promote uterine and placental
perfusion
- Provide well balanced diet with adequate protein and roughage, no sodium restriction
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 edema 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
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
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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 functions. It is an acronym that help identify the underlying signs
associated with the syndrome:
1. Hemolysis
2. Elevated Liver enzymes
3. Low Platelets
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 die 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, impaired blood vessels. Elevated liver enzymes are believed to
result from obstruction in liver flow by fibrin deposits. Low platelets are believed 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 abdomen 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 pressure and possibly prostaglandin release
3. Preterm rupture of membranes adds additional risks of both infection and prolapsed cord
Assessment:
1. Unusual rapid enlargement of uterus
2. Small parts of the fetus are difficult to palpate because the uterus is unusually tense
3. Extreme shortness of breath because of the overly distended uterus that pushes up against her diaphragm.
4. Lower extremity varicosities and hemorrhoids because of poor venous return from the extensive uterine pressure
5. Increased weight gain
Therapeutic Management:
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 effective in reducing the amount of fluid formed
6. If contractions begins, tocolysis with magnesium sulfate may be begun to prevent 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 prostaglandins
4. Myometrial quiescence or a uterus that does not respond to normal labor stimulation
Complications:
1. Macrosomia will create a delivery problem
2. Lack of growth
3. Oligohydramnios leading to variable decelerations may occur
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Therapeutic Management:
1. A nonstress test and/ or biophysical profile may be done to document the state 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
Therapeutic Management:
1. RHIG – administered to women at 28 weeks of pregnancy
2. Intrauterine transfusion – to restore fetal red blood cells. Done by injecting 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
Therapeutic Management:
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 contractions
3. Blood for coagulation studies to detect DIC
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 newborn
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
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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 preparation
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 pressure monitoring.
Nursing Diagnosis:
1. Ineffective airway clearance r/t presence of mucus or amniotic fluid in airway.
2. Risk for fluid volume deficit 3. Ineffective thermoregulation r/t newborn status and stress from birth weight variation.
4. Risk for altered nutrition; less than body requirements
5. Risk for infection
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 environment 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, birth 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 neonatal 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 scoring 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 total of the five items; a maximum score is ten.
Evaluation at 1 minute quickly indicates the neonate’s initial adaptation to extrauterine 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 skin. The neonate’s cord stump continues to pulsate for several hours and is a good, easy place to check heart rate. You can
also place to fingers or a stethoscope over the neonate’s chest at the fifth intercostal space to obtain an apical pulse. 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 neonatal 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 should be able to elicit a cry by flicking his soles. The usual response is a
loud, angry cry. A high-pitched or shrill cry is abnormal. A newborn whose mother was 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 blue extremities. This condition called acrocyanosis appears in
about 85% of normal neonates 1 minute after birth. Acrocyanosis results from decreased peripheral oxygenation caused by the
transition from fetal to independent circulation.
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Sign
Apgar Score
0
1
2
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 (the neonate needs immediate resuscitation, as ordered).
The neonate should receive a thorough physical examination of each body part. However, before each body part is examined, assess the general
appearance and posture 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 hemoglobin 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 body, except the palms and soles
vernix caseosa – a white cheesy protective coating composed of desquamated epithelial cells and sebum
erythema toxicum neonatorum – a transient maculopapular rash
telangiectasia – flat reddened vascular areas appearing on the neck, upper eyelid 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 dermal 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 relationship 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 neonate’s abdomen between your thumb and forefinger. Assess
consistency, amount of subcutaneous tissue, and degree of hydration. A well-hydrated 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, called sutures, lie between the junctures of these bones. At the juncture of the sutures are wider spaces of
membranous tissues, called fontanels.
Fontanels.
The neonatal skull has two fontanels. The anterior fontanel is diamond-shaped and 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 bones 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 increased intracranial pressure. Pulsations in the fontanels reflect
the peripheral pulse.
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Molding refers to asymmetry of the cranial sutures due to difficulties during vaginal 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 periosteum. It is caused by pressure during delivery and
tends to spontaneously resolve in 3-6 weeks. A cephalhematoma doesn’t cross cranial suture lines.
• Caput succedaneum is a localized edematous area of the presenting scalp. It is also 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 can 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 fetal skull against the mother’s pelvic bone in utero probably
causes this. The condition corrects itself without treatment after a matter of months
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 also 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 seen 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 of neonatal eye examination:
The neonate’s eyes are usually blue or gray because of scleral thinness. Permanent 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 the opposite direction or remain stationary) may persist for
up to 10 days.
Subconjunctival hemorrhages may appear from vascular tension changes during birth.
The corneal reflex is present but generally isn’t elicited unless a problem is suspected.
Nose.
Observe the neonate’s nose for shape, placement, patency and bridge configuration.
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 nasal passages by occluding each nares alternately while holding the
neonate’s mouth closed.
Epstein pearls (pin-head sized, white or yellow, rounded elevations) may be found 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 generally isn’t visible.
Ears.
Assess the neonate’s ears for placement on the head, amount of cartilage, open auditory canal, and hearing.
The neonate’s ears are characterized by incurving of the pinna and cartilage deposition. 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 imaginary 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 tissue, respiratory movement, and amount of cartilage in rib cage. The
neonatal chest is characterized by a cylindrical thorax (because the anteroposterior 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 breaths/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 neonates have a fast heart rate, it’s difficult to auscultate the
specific components of the cardiac cycle. Heart sounds during the neonatal period 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 space 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 space 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 are heard a few hours after birth. A scaphoid (sunken anterior
wall) appearance indicates a diaphragmatic hernia. The umbilical cord is white and 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. Sometimes 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 distended urinary bladder. The neonate should void within the first 24
hours of birth.
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Femoral pulses should also be palpated at this point in the examination. Inability 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, patent and is not covered by a membrane (imperforate anus). The time
after birth that the infant first passes meconium should be noted. If the newborn does not do so 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 testes 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), ectopic 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. These 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 trauma. 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 to lock short of this distance, hip subluxation (a shallow and poorly
formed acetabulum) is suggested. If subluxation is present, when the infant’s leg 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 acetabulum 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 legs 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 be polydactyl (more than 5 digits on an extremity) or syndactyl (two or more digits
fused together).
The nailbeds should be pink, although they may appear slightly blue due to acrocyanosis. Persistent cyanosis indicates hypoxia or
vasoconstriction.
The palms should have the usual creases. A single, tranverse palmar crease in contrast 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 simulates opisthotonos (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 nervous system and his state of neurologic maturation. Some
reflexive behaviors in the neonate are necessary for survival whereas other reflexive behaviors act as safety mechanisms.
Normal neonates display several types of reflexes. Abnormalities are indicated by 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; the 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 the direction of the stroke
Tonic neck (fencing position) – when the neonate’s head is turned while he is lying 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 and 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 surface, he responds with dancing or stepping movements
Startle – a loud noise such as a hand clap elicits neonatal arm abduction and elbow flexion and the neonate’s hands stay clenched
Trunk incurvature – when a finger is run laterally down the neonate’s spine, the 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 hands 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 knees flex, the neonate cries, and he may empty his
bladder
5. Preventing Infection
6. Establishing Parent-Infant Bonding
Following High-Risk Infants At Home
High-Risk Infants and Child Abuse
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Whether they are preterm, term, or postterm, neonates are classified by weight in three ways
Large for gestational age (LGA) neonates
Appropriate for gestational age (AGA) neonates
Small for gestational age (SGA) neonates
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 information 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 meconium to pass through a relaxed anal sphincter, thus causing
the neonate to experience reflexive gasping
Laboratory Findings:
1. High hematocrit level at birth
2. Increase in total number of red blood cells
3. Decrease serum glucose
Birth asphyxia is a common problem for SGA because they have underdeveloped chest 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 nourishment in utero
SGA infants may always be below normal on standard growths chart and this inability 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 home
2. Adequate stimulation during the infant period to reach normal growth and development
3. Encourage parents to provide toys that are suitable for their child’s chronologic age
4. Play periods must be spaced with rest periods or hypoglycemia or apnea may occur
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:
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Size of the uterus measures unusually large for the date of pregnancy. A sonogram can confirm suspicion.
A nonstress test to assess the placenta’s ability to sustain the large fetus during labor
Infant’s lung maturity may be assessed by amniocentesis
Baby is unable to descend through the pelvic rim during labor
CS may be necessary because of cephalopelvic disproportion or shoulder dystocia.
Appearance:
1. At birth, LGA infants may show immature reflexes and low scores on gestational age examinations in relation to their size.
2. Infant may have extensive bruising or a birth injury such as broken clavicle
3. Erb-Duchenne paralysis from trauma to the cervical nerves if the infant was delivered vaginally
4. Prominent caput succedaneum, cephalohematoma, or molding
CARDIOVASCULAR DYSFUNCTION
Heart rate should be carefully observed.
Cyanosis may be a sign of transposition of the great vessels, a serious heart anomaly
Polycythemia is caused by the infant’s system attempting to fully oxygenate all body tissues
Observe for signs of hyperbilirubinemia which may result from bruising and polycythemia
HYPOGLYCEMIA
Infants should be carefully assessed for hypoglycemia in the early hours of life because the infants use up nutritional stores readily to sustain
weight.
If mother has poor glucose control, the infant will have an increased blood glucose level in utero, which causes the infant to produce elevated
levels of insulin.
After birth, increased insulin levels will continue up to 24 hours of life, possibly causing rebound hypoglycemia
Outcome Evaluation: NB initiates breathing at birth; maintains normal NB respiratory rate at 30 to 60 breaths per minute
Nursing Diagnosis: Risk for altered nutrition; less than body requirements r/t additional nutrients needed to maintain weight and prevent
hypoglycemia
Outcome Identification: Infant will ingest adequate fluid and nutrients for growth during neonatal period
Outcome Evaluation: Infant’s weight loss follows percentile growth curve; skin turgor is good; specific gravity of urine 1.003 to 1.030; serum glucose
is above 45 mg/dl
Outcome Identification: Parents demonstrate adequate bonding behavior during neonatal period
Outcome Evaluation: Parents hold infant; speak of the child in positive terms; state accurately why the infant needs to be closely observed in
postnatal period
A preterm infant is usually defined as a live-born infant born before the end of week 37 of gestation
Weighs less than 2500 g (5 lb, 8 oz) at birth
Infants born weighing 1500-2500g are considered low-birth weight (LBW)
Infants born weighing 1000-1500 g are considered very-low-birth weight (VLBW)
Infants born 500-1000 g are considered extremely-very-low-birth weight (EVLBW)
A lack of lung surfactant makes them extremely vulnerable to respiratory disease syndrome
Preterm babies of every weight need to be differentiated at birth from small-for-gestational-age babies (who also may have low birth weights)
A preterm infant is immature and small but well proportioned for age
Causes:
1. Low socio-economic level
2. Inadequate nutrition before and during pregnancy
3. Lack of prenatal care
4. Multiple pregnancy
5. Prior previous early birth
6. Race (nonwhites have higher percentage than whites)
7. Cigarette smoking
8. Age of mother (highest incidence is mothers younger than 20 years old)
9. Order of birth (early termination is highest in first pregnancies and in those beyond the fourth)
10. Closely spaced pregnancies
11. Abnormalities of the reproductive system such as intrauterine septum
12. Infections (esp. UTI)
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Appearance:
1. Appears small and underdeveloped
2. Head is large (3 cm or more grater than chest size)
3. Skin is unusually ruddy because of little subcutaneous fat
4. Veins are noticeable
5. High degree of acrocyanosis may be present
6. Neonate is covered with vernix caseosa. However, very preterm NB, less than 25 weeks gestation, vernix is absent
7. Lanugo is extensive
8. Anterior and posterior fontanels are small
9. There are few creases on the soles of the feet.
10. Small eyes. Pupillary reaction is present.
11. Ear cartilage is immature and allows the pinna to fall forward. The ears appear large
12. Reflexes are absent if infant’s age is below 33 weeks
13. Much less active and rarely cries. Cry is weak and high pitched
14. (+) Scarf sign – elbow reaches midline
15. When the heel is drawn as near to the ear as possible, little resistance is met
16. Barely visible areola and nipple
17. Males- testes are high in the inguinal canal with the presence of minimal rugae on the scrotum
Female – prominent clitoris, small widely separated labia majora
Potential Complications:
1. Anemia or prematurity
2. Kernicterus (destruction of brain cells by invasion of indirect bilirubin)
3. Persistent patent ductus arteriosus
4. Periventricular/Intraventricular Hemorrhage
5. Respiratory disease syndrome
6. Apnea
7. Retinopathy of prematurity
8. Necrotizing enterocolitis
Interventions:
1. Giving the mother oxygen by mask during birth will provide the infant with optimal oxygen saturation at birth
2. Maternal analgesia and anesthesia to a minimum offers the infant best chance of initiating effective respirations
3. CS has the advantage of reducing pressure on the immature head but may lead to additional respiratory complications because of retained lung
fluid
4. Resuscitate infant within 2 minutes to avoid irreversible acidosis.
5. Prepare preterm size laryngoscopes, endotracheal tubes, suction catheters and synthetic surfactant
6. Infant must be kept warm during resuscitation
7. Continued oxygen administration
Interventions:
1. IVF administration within hours after birth to fulfill fluid replacement and provide glucose to oprevent hypoglycemia
2. Monitor baby’s weight, specific gravity and amount of urine, and serum electrolytes to ensure adequate fluid intake
3. Blood glucose determinations to help determine hypoglycemia or hyperglycemia.
4. Record all blood drawn
5. Check for blood in the stools to determine bleeding from intestinal tract.
Nursing Diagnosis: Risk for altered nutrition; less than body requirement
Nutrition problem arise with the preterm infant because the body is attempting to continue to maintain the rapid rate of intrauterine growth.
Therefore, the NB requires a larger amount of nutrients in the diet than the mature infant..
If nutrients are not supplied, Hypocalcemia or azotemia develops.
Delayed feeding may also add to hyperbilirubinemia
Nutrition problem is compounded with infant’s immature reflexes, which makes swallowing and sucking difficult
Small stomach capacity may affect nutrition, because a distended stomach may cause respiratory distress
Increased activity due to ineffective sucking may increase metabolic rate and oxygen requirements, therefore, increases caloric requirements
even more
Immature cardiac sphincter allows regurgitation to occur readily.
Lack of cough reflex may lead the infant to aspirate regurgitated formula.
Digestion and absorption of nutrients in the stomach and intestine may also be immature.
Nursing Management:
1.The infant must be kept under a radiant heat warmer
The infant has difficulty producing phagocytes to localize infection and has a deficiency of IgM antibodies
Nursing Management:
1. Linen and equipment used with the preterm infant must be clean to reduce the chances of infection
2. Hospital staff must be free of infection, and hand washing and gowning regulations must be strictly enforced
Nursing Diagnosis: Diversional activity deficit (lack of stimulation) r/t preterm infant’s rest needs
Preterm infant needs rest to conserve energy for growth and respiratory function, to combat hypoglycemia and infection, to stabilize
temperature and to develop inner balance and attentiveness
Infant needs planned periods of pleasing sensory stimulation
Pathophysiology
- If the placenta continuous to function well, the fetus will continue to grow, which results in an LGA infant who may manifest problems such as
birth trauma and hypoglycemia
- If placental function decreases, the fetus may not receive adequate nutrition. The fetus will utilize its subcutaneous fat stores for energy.
Wasting of subcutaneous fat occurs, resulting in fetal dysmaturity syndrome.
Nursing Management
1. Manage Meconium Aspiration Syndrome
- suction the infant’s mouth and nares while the head is in the perineum and before the first breath is taken to
prevent aspiration of meconium that is in the airway
- once the infant is dry and in the warmer, intubate and do direct tracheal suctioning
- perform chest physiotherapy with suctioning to remove excess meconium and secretions
- provide supplemental oxygen and respiratory support as needed.
2. Obtain serial blood glucose measurements
3. If not contraindicated by respiratory status, provide early feeding to prevent hypoglycemia
4. Maintain skin integrity
- keep the skin clean and dry
- avoid the use of powders, creams and lotions
Cause of RDS: A low level or absence of surfactant, the phospholipid that normally lines the alveoli and resists surface tension on expiration to
keep alveoli from collapsing on expiration.
Pathophysiology:
High pressure is required to fill the lungs with air for the first time and overcome the pressure of lung fluid. It takes a pressure between 40 cm
H2O and 70 cm H2O, to inspire a first breath, but only 15 cm H2O to 20 cm H2O to maintain quiet, continued breathing. If alveoli collapse with
each expiration, as happens when surfactant is deficient, however, it continues to take forceful inspiration to inflate them. With deficient
surfactant, areas of hypoinflation occur and pulmonary resistance is increased. Blood then shunts through the foramen ovale and the ductus
arteriosus. The lungs are poorly perfused, thus affecting gas exchange. As a result, the production of surfactant decrease even further. The
poor oxygen exchange leads to tissue hypoxia. Tissue hypoxia causes the release of lactic acid. This, combined with an increasing carbon
dioxide level resulting from the formation of the hyaline membrane on the alveolar surface, leads to severe acidosis. Acidosis causes
vasoconstriction, and decreased pulmonary perfusion from vasoconstriction further limits surfactant production. With decreased surfactant
production, the ability to stop alveoli from collapsing with each expiration becomes impaired. This vicious cycle continuous until the oxygen-
carbon dioxide exchange in the alveoli is no longer adequate to sustain life without ventilator support.
Assessment:
1. Difficulty initiating respirations at birth
2. Low body temperature
3. Nasal flaring
4. Sternal and subcostal retractions
5. Tachypnea
6. Expiratory grunting
7. On auscultation, fine rales and diminished breath sounds
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8.Seesaw respirations
9. Heart failure evidenced by decreased urine output and edema of the extremities
10. Pale gray skin color
11. Periods of apnea
12. Bradycardia
Therapeutic Management:
1. Surfactant Replacement and Rescue
2. Oxygen administration
3. Ventilation
4. Use of muscle relaxants
5. Extracorpeal Membrane Oxygenation
6. Liquid ventilation
Prevention:
Nursing Diagnosis: Impaired gas exchange r/t immaturity of the NB’s lungs and diminished surfactant
Interventions:
1. Assess NB’s status and note signs of increasing respiratory distress
2. Maintain endotracheal tube, mechanical ventilation and supplemental warm humidified oxygen
3. Prepare to administer surfactant rescue
4. Change the NB’s position during administration and refrain from suctioning the ET tube for up to 1 hour following administration
5. Anticipate administration of indomethacin and pancuronium
6. Maintain a neutral thermal environment and minimize physical activity
7. Plan nursing care to allow for frequent rest periods and attempt to anticipate the NB’s needs
Intervention:
1. Close observation is the priority
2. Oxygen administration
Pathophysiology:
Meconium aspiration syndrome is commonly related to fetal distress during labor. When a neonate becomes hypoxic, peristalsis increases and the
anal sphincter relaxes. Occasionally, healthy neonates pass meconium before birth. In either case, if the neonate gasps or inhales the meconium,
meconium aspiration can develop. The resulting lack of oxygen may lead to brain damage.
Risk factors for meconium aspiration syndrome include:
Maternal diabetes
Maternal hypertension
Difficult delivery
Fetal distress
Intrauterine hypoxia
Advanced gestational age (greater than 40 weeks)
Poor intrauterine growth
Signs and symptoms of meconium aspiration syndrome include:
Dark greenish staining or streaking of the amniotic fluid
Obvious presence of meconium in the amniotic fluid
Skin with a greenish stain (if the meconium was passed long before delivery)
Limp appearance at birth
Cyanosis
Rapid and labored breathing. retractions
Low heart rate before birth
Low APGAR score
Nursing Interventions:
1. Infant should be suctioned with a bulb syringe while at the perineum to avoid meconium aspiration
2. Infant should be intubated and meconium should be suctioned from the trachea and bronchi as soon as the infant is born
Therapeutic Management:
1. Amniotransfusion may be used to dilute the amount of meconium in amniotic fluid and reduce risk of aspiration
2. Oxygen adminitration
3. Antibiotic Therapy
4. Maintain a thermal neutral environment
5. Chest physiotherapy with clapping and vibration to facilitate removal of remnants of meconium from the lungs
4. APNEA
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Tx Management:
1. Gently shake or flick the sole of the foot to stimulate the baby
2. Apnea monitors to detect failing respiration
3. Ventilator to provide respiratory coordination
4. Maintain a neutral thermal environment
5. Always suction gently
6. Careful burping after feeding
7. Theophylline or caffeine sodium benzoate may be administered to stimulate respirations
Etiology:
Occur usually in infants of adolescent mothers, infants of closely spaced pregnancies and underweight and preterm infants.
Also prone to SIDS are infants with bronchopulmonary dysplacia, twins, siblings of another child with SIDS
Infants of narcotic-dependent mothers
Peak ages of incidence are between 2 weeks and 1 year of age
Viral respiratory or botulism infection
Distorted familial breathing patterns
Possible lack of surfactant in alveoli
Sleeping prone rather than on the side or back
7. HYPERBILIRUBINEMIA
Hyperbilirubinemia is an excess of bilirubin in the blood that results in elevated serum bilirubin levels and mild jaundice. Hyperbilirubinemia can be
physiologic (with jaundice being the only symptom) or pathologic (resulting from an underlying disease).
Physiologic hyperbilirubinemia is self-limiting. It usually resolves in 7-10 days. Prognosis for pathologic hyperbilirubinemia varies, depending on
the cause. If left untreated, hyperbilirubinemia may result in kernicterus, a neurologic syndrome caused by unconjugated bilirubin depositing in
the brain cells. Survivors may develop cerebral palsy, epilepsy, or mental retardation, or they may have only minor effects, such as perceptual-
motor disabilities and learning disorders.
Pathophysiology:
As erythrocytes break down at the end of their neonatal life cycle, hemoglobin separates into globin (protein) and heme (iron and protoporphyrin)
fragments.
Heme fragments (protoporphyrin component) form unconjugated bilirubin. Unconjugated bilirubin is fat soluble and cannot be excreted by the
kidneys in this state. Instead unconjugated bilirubin binds with albumin and is transported to the liver. In the liver, it is converted by the liver
enzyme glucuronyl transferase into direct bilirubin, which is water soluble and is incorporated into stool and then excreted in the feces.
Many newborns have such immature liver function that indirect bilirubin can not be converted into direct form and, therefore, remains indirect. Other
factors include:
- certain drugs (such as aspirin, tranquilizers and sulfonamides) or conditions ( such as hypothermia, anoxia,
hypoglycemia, and hypoalbuminemia) can disrupt conjugation and usurp albumin-binding sites
- Increased erythrocyte production or breakdown (like in the resolution of cephalhematoma), or Rh or ABO
incompatibility
- Maternal enzymes and hormones (pregnanediol) present in breast milk can inhibit the neonate’s
glucuronyltransferase conjugating activity
Manifestations:
The predominant sign of hyperbilirubinemia is jaundice in which the usual pattern of progression is from head to feet. Blanch skin over bony
prominence or look at conjunctiva and buccal membranes in dark-skinned infants. Jaundice doesn’t become clinically apparent until serum bilirubin
levels reach about 7mg/100ml. Around this serumlevel, unconjugated bilirubin escape to the extravascular tissues.
Physiologic hyperbilirubinemia
- Typically develops within 2-3 days after birth in 50% of term neonates and within 3-5 days after birth in 80% of preterm neonates. It generally
disappears by day 7 in term neonates and by day 9 or 10 in preterm neonates. Throughout physiologic jaundice, the serum unconjugated bilirubin
level doesn’t exceed 12mg/100ml.
Pathologic hyperbilirubinemia
-May appear anytime after the first day of life and persists beyond 7 days with serum bilirubin levels greater than 12mg/100ml in a term neonate,
15mg/100ml in a preterm neonate, or increasing more than 5mg/100ml in 24 hours.
Treatment:
Depending on the underlying cause, treatment may include:
*exchange transfusion – replaces the neonate’s blood with fresh blood (blood that is less than 48 hours old), thus removing some of the
unconjugated bilirubin in serum
*phototherapy - uses fluorescent light to decompose bilirubin in the skin by oxidation. Implemented after the initial exchange
transfusion, phototherapy is usually discontinued after bilirubin levels fll below 10mg/100ml and continue to
decrease for 24 hours
Performing Phototherapy
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Set up the phototherapy unit about 18” above the neonate’s crib and verify the placement of the
light-bulb shield. If the neonate is in the incubator, place the phototherapy unit at least 3” above
the incubator and turn on the light. Place a photometer probe in the middle of the crib to measure
the energy emitted by the lights.
Explain the procedure to the parents.
Record the neonate’s initial bilirubin level and his axillary temperature.
Place the opaque eye mask over the neonate’s closed eyes and fasten securely.
Undress the neonate and place a diaper under him. Cover male genitalia with a surgical mask or
small diaper to catch urine and prevent possible testicular damage from the heat and light waves.
Take the neonate’s axillary temperature every 2 hours and provide additional warmth by adjusting
the warming unit’s thermostat
Monitor elimination and weigh the neonate twice daily. Watch for signs of dehydration (dry skin,
poor turgor, depressed fontanels) and check urine specific gravity with a urinometer to gauge
hydration status.
Take the neonate out of the crib, turn off the phototherapy lights, and unmask his eyes at least
every 3-4 hours with feedings. Assess his eyes for inflammation and injury.
Reposition the neonate every 2 hours to expose all body surfaces to the light and to prevent head
molding and skin breakdown from pressure.
Check the bilirubin level at least once every 24 hours – more often if levels rise significantly. Turn
off the phototherapy unit before drawing venous blood for testing because the lights may degrade
bilirubin in the blood. Notify the doctor if the bilirubin level nears 20mg/dl in full-term neonates or
15mg/dl in premature neonates.
and albumin infusion -(1g/kg of 25% salt-poor albumin) which provides additional albumin for binding unconjugated bilirubin.
E. Nursing Interventions
determine blood type and Rh early in pregnancy
determine results of indirect Coomb’s test early in pregnancy and again at 28-32 weeks
determine results of direct Coomb’s test on cord blood
administer Rhogam IM to mother as ordered
do careful monitoring
implement phototherapy or exchange transfusion for any hyperbilirubinemia
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Symptoms:
1. Petechiae from superficial bleeding into the skin
2. Conjuntival, mucous membrane or retinal hemorrhage
3. May vomit fresh blood or pass black, tarry stools because of bleeding into the GIT
Therapeutic Management:
1. Hemorrhagic disease of the NB can be prevented by Vit K 1 mg IM immediately after birth
2. Blood transfusion of fresh whole blood in severe bleeding to increase the prothrombin level
B. Medical Management
- parenteral antibiotics
- gastric decompression
- correction of acidosis and fluid and electrolyte imbalance
- surgical removal of the diseased intestine
C. Assessment Findings
-history indicating high-risk group
-findings related to sepsis (temperature instability, apnea and labored respiration, cardiovascular collapse, lethargy or irritability)
-gastrointestinal symptoms (abdominal distention and tenderness, vomiting and poor feeding, hematest positive stools, x-rays showing air in the
bowel wall, adynamic ileus, and bowel wall thickening)
D. Nursing Interventions
-carefully assess infants at risk for early recognition of symptoms
-discontinue oral feedings, insert nasogastric tube
-prevent trauma to abdomen by avoiding diapers and planning care for minimal handling
-maintain acid base balance by administering fluid and electrolytes as ordered
-administer antibiotics as ordered
-inform parents of progress and support them in expressing their fears and concerns
Assessment:
1. Tachypnea
2. Apnea
3. Symptoms of shock such as decreased urine output, extreme paleness, or hypotonia
4. Lethargy
5. Fever
6. Loss of appetite
7. Bulging fontannels
Therapeutic Management:
1. Antibiotics. Gentamicin, ampicillin and penicillin.
2. Immunization of all childbearing age women against streptococcal organisms
2. CONGENITAL RUBELLA
Rubella virus is capable of causing extensive congenital fetal malformations if the mother is infected during the first trimester of pregnancy
The greatest risk to an embryo from rubella virus is during weeks 2 to 6 of intrauterine life.
Assessment:
1. Thrombocytopenia
2. Cataracts
3. Heart Disease
4. Deafness
5. Microcephaly
6. Motor and cognitive impairment
Therapeutic Management:
1. Treatment is symptomatic, depending on the congenital defects present
2. Contact precautions
3. Susceptible pregnant women should avoid contacts with the NB still having the virus
4. Women with low rubella titers should be given rubella vaccine to ensure that rubella infection does not occur in future pregnancies
3. OPHTHALMIA NEONATORUM
Ophthalmia neonatorum is eye infection at birth or during the first month
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Prevention:
1. Prophylactic instillation of erythromycin ointment into the eyes of NB’s
Therapeutic Management:
1. Therapy is individualized depending on the organism cultured from the exudate
2. If gonococci is identified, Ceftriaxone and penicillin IV are effective drugs
3. If chlamydia is identified, Erythromycin ophthalmic solution is used
4. The eyes are irrigated with sterile saline solution to clear the copious discharge
5. The mother of the infected infant needs treatment for gonorrhea or chlamydia
Prevention:
1. Routine vaccination of infants at birth
2. If mother is identified as HbsAg+. The infant is administered immune serum globulin (HBIG) within 12 hours of birth to decrease possibility of
infection
3. The infant should be bathed immediately after birth to remove HBV-infected blood and secretions
4. Suctioning should be with gentle technique to avoid possible trauma to the mucous membrane which could allow HBV invasion
Assessment:
1. Vesicles covering the skin if the infection was acquired during pregnancy
2. Loss of appetite
3. Low-grade fever
4. Lethargy
5. Stomatitis (ulcers of the mouth) or a few vesicles in the skin
6. Herpes vesicles are always clustered, pinpoint in size and surrounded by a reddened base
7. After vesicles appear, infants become extremely ill. They develop dyspnea, jaundice, purpura, convulsions, and shock
Complications:
1. Death may occur within hours or days
2. Some who survived the infection may have permanent central nervous system sequelae
Therapeutic Management:
1. Drugs that inhibit viral deoxyribonucleic acid synthesis (acyclovir and vidaribine) are effective in combating this infection
2. Women with active herpetic vulvar lesions are often delivered by caesarian to minimize the NB’s exposure
3. Infants with this infection are separated from other infants
4. Women with lesions on their face should not feed or hold their NB’s until lesions are crusted and no longer contagious
Assessment:
1. Infants of a diabetic mother whose illness was poorly controlled during pregnancy is typically longer and weighs more thatn other babies
(macrosomia)
2. Infant has a greater chance of having congenital anomaly
3. Caudal regression syndrome or hypoplasia of the lower extremities is a syndrome that occurs almost exclusively in such infants
4. Cushingoid (fat and puffy) appearance
5. Lethargic or limp in the first days of life, effects of hyperglycemia
6. Lungs may be immature
7. RDS occurs frequently
Complications:
1.Greater chance of birth injury if infant is macrosomic
2. Infants tend to be hyperglycemic immediately after birth
3. Hyperbilirubinemia
4. Hypocalcemia
5. Infants will be small for gestational age (SGA) because of poor placental perfusion
Therapeutic Management:
1. To prevent hypoglycemia, infants are fed early with formula or administered a continuous infusion of glucose
2. It is important not to give bolus of glucose to avoid rebound hypoglycemia
Assessment:
1. Infants tend to be small for gestational age
2. Irritability
3. Disturbed sleep patterns
Constant movement possibly leading to abrasions on their elbows, knees or nose
4. Tremors
5. Frequent sneezing
6. Shrill, high –pitched cry
7. Possible hyperplasia and clonus (neuromuscular irritability)
8. Convulsions
9. Tachypnea
10. Vomiting and diarrhea leading to large fluid losses and secondary hydration
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Therapeutic Management:
1. Infants are most comfortable when firmly swaddled.
2. Infants should be kept in an environment free from excessive stimuli
3. Infants must be gavage fed if infants have poor sucking ability and may have difficulty getting enough fluid intake
4. Maintenance of electrolyte and fluid balance is essential
5. IVF administration is necessary if infant has vomiting or diarrhea
6. Drugs used to counteract withdrawal symptoms include paregoric, Phenobarbital, methadone, chlorpromazine and diazepam
7. Infants should not be breastfeed to avoid passing narcotics to the child
Characteristics:
1. Pre and postnatal growth restriction
2. Central nervous system involvement such as cognitive impairment, microcephaly and cerebral palsy
3. Facial features such as short palpebral fissures, thin upper lip, strabismus, low nasal bridge, flat midface, flat or absent groove in the upper lip,
short nose and receding jaw
4. Infant may be tremulous, fidgety, irritable, and may have a weak sucking reflex during neonatal period
5. Sleep disturbances are common
6. Behavior problems such as hyperactivity may occur in school-age children
7. Growth deficiencies may remain through life
Supportive treatment is implemented.
Emphasis on management of respiratory problems, nutrition, and maternal-neonate bonding should be made.
2. Output- The class will be divided into 4 groups, who shall submit in long bond paper a comprehensive pathophysiology flowchart of
each of the 5 different ABC conditions assigned to them by the instructor. Each condition/illness must be introduced with a brief definition.
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The output must be computerized, with the name of the group members listed on the front sheet, and be collected in a secured paperback
folder.
THE ASSIGNMENT OF TOPICS WILL BE DONE WHEN WE MEET.
Set 1:
A. Pulmonary embolism
B. ARDS
C. Acute and Chronic Respiratory
Failure
D. DKA
E. HHNC
Set 2:
A. Thyrotoxic Crisis
B. Adrenal Crisis
C. Hepatic Coma
D. Acute and Chronic Renal Failure
E. Myocardial Infarction
Set 3:
A. Right-sided Heart Failure, to
include Eisenmenger’s Syndrome
B. Left-Sided heart Failure
C. Pericardial Effusion
D. Cardiac Tamponade
E. Burns
Set 6:
A. Abortion (all)
B. Ectopic Pregnancy
C. H. Mole
D. Placenta Previa
E. Abruptio Placenta
Set 7:
A. DIC
B. PIH, to include: Mild
preeclampsia, Severe
preeclampsia, eclampsia, HELLP
Syndrome
C. Polyhydramnios
D. RH incompatibility
E. ABO incompatibility
Set 8:
A. RDS
B. MAS
C. Hyperbilirubinemia
D. Infant born to a Diabetic Mother
E. Fetal Alcohol Syndrome
GRADING POLICY:
Output:
Completeness/ Comprehensiveness 10 pts
To include:
• Definition
• Etiology
• Predisposing/Precipitating Factors
• Manifestations
• Complications
Accuracy 10 pts
Neatness & organization 5 pts
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=====================================================
Total 25 pts for each Flow Chart/ 125 pts total output
REFERENCE MATERIALS:
1. Books
a. The Lippincott Manual of Nursing Practice, 7th edition, 2001.
b. Luckmann and Sorensen Medical and Surgical Nursing: A Psychophysiologic Approach, 4th edition, 2002
c. Maternal and Child Health Nursing: Care of the Childbearing and Childrearing Family. Adele Pilliteri.1999.
d. Maternal and Child Health Nursing. Koniak.
e. Maternal and Neonatal Nursing Made Incredibly Easy. 2004
f. Medical-Surgical Nursing books
g. Critical Care and Emergency Nursing. Schumacher and Chernecky. 2006
2. Internet:
• www.Emedicine.com
• http://health.discovery.com/tools/blausen/blausen.html
NB: Students enrolled in NCM 104 are required to bring a copy of this Acute Biologic Crisis Module and
Practice Tests when coming to class.
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