ACUTE BIOLOGIC CRISES (24 HOURS) COURSE OUTLINE 1. High Risk Adult (8 hours) A. Respiratory Disorders i. ii. iii. Pulmonary Embolism Acute Respiratory Distress Syndrome (ARDS) Respiratory Failure a. b. iv. B. Acute RF Chronic RF

Mechanical Ventilators

Endocrine/ Metabolic Disorders i. ii. iii. iv. v. Diabetic Ketoacidosis (DKA) Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) Thyrotoxic Crisis (Thyroid Storm) Adrenal Crisis (Peochromocytoma) Hepatic Failure (Hepatic Coma)


Renal Disorders i. Renal Failure a. b. Acute RF Chronic RF


Cardiovascular Disorders i. ii. iii. Angina Pectoris Myocardial Infarction Congestive Heart Failure a. b. iv. v. vi. vii. viii. Right-sided CF Left-sided CF

Cardiogenic Shock Thromboembolism Pericardial Effusion & Cardiac Tamponade Cardiac Arrest Dysrhythmias a. Sinus Node 1. 2. b. Sinus Bradycardia Sinus Tachycardia

Atrial Dysrhythmias 1. 2. 3. Premature Atrial Complex (PAC) Atrial Flutter Atrial Fibrillation


Junctional Dysrhythmias
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008



Ventricular Dsyrhythmias 1. 2. 3. 4. Premature ventricular Complex Ventricular Tachycardia Ventricular Fibrillation Ventricular Asystole



2. High Risk Pregnancy (12 Hours)
Part I. A. Infections i. STDs a. b. c. d. e. f. g. h. i. ii. B. Cndidiasis Trichomoniasis Bacterial Vaginosis (Gardnerella) Chlamydia Trachomatis Syphilis Gonorrhea HPV Group B Streptococci HIV

TORCH infections

Hematologic Disorders i. Anemias a. b. c. ii. Iron Deficiency Folic Acid Deficiency Sickle Cell

Coagulation Disorders a. Idiopathic Thrombocytopenic Purpura


Renal and Urinary Disorders i. ii. UTI Chronic Renal Disease


Respiratory Disorders i. ii. iii. iv. v. vi. Acute Nasopharyngitis Influenza Pneumonia Asthma Tuberculosis Cystic Fibrosis
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008



Rheumatic Disorders i. Juvenile Rheumatoid Arthritis

ii. Systemic Lupus Erythematosus (SLE)
F. Gastrointestinal Disorders i. ii. iii. iv. v. Appendicitis Hiatal Hernia Cholecystitis & Cholelithiasis Viral Hepatitis Inflammatory Bowel Disease

G. Neurologic Disorders i. ii. iii. H. Siezure Myasthenia Gravis Multiple Sclerosis

Musculoskeletal Disorders i. Scoliosis


Cardiovascular Disorders i. ii. iii. iv. v. vi. Left Sided Heart Failure Right Sided heart Failure Peripartal Heart Disease Artificial valve Prosthesis Chronic hypertensive Vascular Disease Venous Thromboembolic Disease


Endocrine Disorders i. Thyroid Dysfunction a. b. ii. iii. iv. Hypothyroidism Hyperthyroidism

Diabetes Mellitus Gestational Diabetes Hyperglycemia

K. L.

Mental Illness Trauma i. ii. iii. Trauma Care Open wounds Battered woman

PART II. COMPLICATIONS OF PREGNANCY A. Bleeding During Pregnancy i. First Trimester Bleeding a. Abortion
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


1. 2. 3. 4. 5. 6. 7. 8.

Spontaneous Threatened Imminent Complete Incomplete Missed Recurrent Complications of Abortion b. Ectopic pregnancy ii. Second Trimester Bleeding a. Gestational Trophoblastic Disease (H. Mole) b. Incompetent Cervix iii. Third Trimester Bleeding a. Placenta Previa b. Abruptio Placenta iv. v. vi. vii. Preterm labor Disseminated Intravascular Coagulation (DIC) Preterm Rupture of Membrane (PROM) Pregnancy Induced Hypertension (PIH) a. Mild Preeclampsia b. Severe Preeclampsia c. Eclampsia

d. HELLP Syndrome viii. ix. x. xi. xii. xiii. Multiple Pregnancy Polyhydramnios Post term pregnancy Psuedocyesis Isoimmunization (RH Incompatibility) Fetal Death


High Risk Newborn (4 hours) A. Part I i. ii. iii. iv. B. Small-for-Gestational-Age Infant Large-for-Gestational-Age Infant Preterm Infant Post Term Infant

Part II: Illness of the Newborn i. Respiratory Distress Syndrome
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


ii. iii. iv. v. vi. vii. viii.

Transient Tachypnea Meconium Aspiration Syndrome Apnea Sudden Infant Death Syndrome (SIDS) Preventricular Leukomalacia (PVL) Hyperbilirubinemia Erythroblastosis Fetalis a. b. RH incompatibility ABO incompatibility

ix. x. xi. C.

Hemorrhagic Disease Twin-to-twin Transfusion Necrotizing Enterocolitis

The Newborn at risk due to: i. Maternal Infection a. b. c. d. e. ii. Group B Hemolytic Streptococcal Infection Congenital Rubella Ophthalmia Neonatorum Hepatitis B Generalized Herpes Virus

Maternal Illness a. b. c. Diabetic Mother Drug Dependent Mother Fetal Alcohol Syndrome (FAS)

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


PULMONARY EMBOLISM  Occurs when a pulmonary embolus [thrombotic (blood clot) or nonthrombotic (fat) emboli] lodges in the pulmonary artery system. This blockage obstructs blood flow to the lung tissue supplied by the affected vessel. Thrombotic emboli mainly originate from the deep veins of the legs, right ventricle of the heart, or pelvis. Nonthrombotic emboli mainly originate from fat release after skeletal injuries, amniotic fluid, air, and foreign bodies. The Virchow’s Triad -three conditions and risk factors that can predispose a patient or that can precipitate the formation of venous thrombi Venous stasis eg. atrial fibrillation, heart failure immobility, polycythemia pregnancy, varicose veins

Vessel wall injury eg. infection, trauma Pathophysiologic Changes

Coagulation problems

embolus lodge in the pulmonary vasculature Pulmonary embolism decreased/nonperfusion of alveoli distal to occlusion infarction of pulmonary vessel impaired gas exchange decreased C02 bronchoconstriction shunting of blood to ventilated areas of the lungs increased pulmonary resistance


release of mediators at the injury site

increased right ventricular workload

pulmonary vasoconstriction pulmonary hypertension

right ventricular failure left ventricular failure decreased cardiac output decreased blood pressure shock death

Clinical Manifestations  Shortness of breath and/or tachypnea- a response to the hypoxia that develops 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

7  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. Other nursing interventions include the following:  Signs and symptoms of DVT are monitored in the lower extremities (calf pain or tenderness, redness, swelling, warmth, pain on dorsiflexion of foot [Homan’s sign]). If Homan’s sign is positive, DO NOT retest it; doing so may dislodge the clot.  Prescribed oxygen therapy is maintained, and the patient is asked to cough and deep breath every 2 hours  Signs and symptoms of respiratory distress or a worsening of pulmonary status (heart failure, pulmonary edema) are monitored, and the physician is notified of any developments.  ABG analysis is monitored and pulse oximetry is continuously taken  Patient is positioned for comfort and maximal oxygenation, as well as to promote the expulsion of secretions.  Signs and symptoms of bleeding are monitored when anticoagulant or thrombolytic therapy is in progress. (eg. blood in stool or urine, pale mucous membranes, petechiae, echymosis, complaints of back or flank pain). ACUTE RESPIRATORY DISTRESS SYNDROME   A clinical syndrome characterized by a sudden and progressive pulmonary edema, increasing bilateral infiltrates, hypoxemia refractory to oxygen supplementation and reduced lung compliance A syndrome with inflammation and increased permeability of the alveollocapillary membrane that occurs as a result of an injury to the lungs. This inflammation causes noncardiogenic pulmonary edema with severely impaired gas exchange.

Etiologic Factors Related to ARDS : 1. Aspiration (gastric secretions, drowning, hydrocarbons) 2. Drug ingestion and overdose 3. Hematologic disorders 4. Prolonged inhalation of high concentrations of oxygen, smoke, or corrosive substances 5. Localized infection (bacterial, fungal, viral pneumonia) 6. Metabolic disorders ( pancreatitis, uremia) 7. Shock (any cause) 8. Trauma ( pulmonary contusion, multiple fractures, head injury) 9. Fat or air embolism 10. Systemic sepsis Pathophysiology lung injury immune system initiates an inflammatory response activation of neutrophils, macrophages, and endotoxins into the lungs and the release of mediators increased alveolomembrane permeability fluid enters into the lung tissue Acute Respiratory Distress Syndrome alveolar collapse narrowing of airways hypoxia hyperventilation pulmonary vasoconstriction pulmonary hypertension right ventricular dysfunction

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

8 respiratory failure Clinical Manifestations: 1. Rapid onset of severe dyspnea 2. Anxiety 3. Labored breathing and tachypnea Assessment: Intercostal retractions and crackles In patients with ARDS, PaO2 will be low, despite oxygen administration, pCO2 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. ACUTE RESPIRATORY FAILURE (ARF)  Defined as a fall in arterial oxygen tension and a rise in arterial carbon dioxide tension.  The ventilation and/or perfusion mechanisms in the lung are impaired.  Respiratory system mechanisms leading to ARF include: 1. Alveolar hypoventilation 2. Diffusion abnormalities 3. Ventilation-perfusion mismatching 4. Shunting Pathophysiology: Common Causes of Acute Respiratory Failure: Decreased Respiratory Drive  May occur with severe brain injury, large lesions of the brain stem (multiple sclerosis), use of sedative medications, and metabolic disorders such as hyperthyroidism. This disorders impair the normal response of chemoreceptors in the brain to normal respiratory stimulation Dysfunction Of The Chest Wall  The impulses arising in the respiratory center travel through nerves that extend from the brain stem down the spinal cord to receptors in the muscles of respiration. Thus, any disease of the nerves, spinal cord, muscles or neuromuscular junction involved in respiration seriously affects ventilation and may lead to ARF Dysfunction Of Lung Parenchyma  Pleural effusion, hemothorax, pneumothorax, and upper airway obstruction are conditions that interfere with ventilation by preventing expansion of the lung. These conditions, which may cause respiratory failure, usually are produced by an underlying lung disease, pleural disease, trauma and injury.  Other diseases and conditions of the lung that lead to ARF include pneumonia, status asthmaticus, lobar atelectasis, pulmonary embolism and pulmonary edema Other Factors  In the postoperative period, esp. after major thoracic or abdominal surgery, inadequate ventilation and respiratory failure may occur. Causes of ARF during this period include the effects of anesthetic agents, analgesics, and sedatives; they may depress respiration and lead to hypoventilation 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 CHRONIC RESPIRATORY FAILURE  Defined as a deterioration in the gas exchange function of the lung that has developed insidiously or has persisted for a long period after an episode of ARF
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

decreased cardiac output

9   Patients develop a tolerance to the worsening hypoxemia and hypercapnia Patient with chronic respiratory failure may develop Acute respiratory failure – seen in COPD patients who develops an exacerbation or infection that causes additional deterioration of the gas exchange mechanism

2 Causes of Chronic Respiratory Failure: 1. COPD 2. Neuromuscular Diseases

What is Mechanical Ventilation?
Mechanical ventilation is a form of artificial ventilation that takes over all 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


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.

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

10 Ventilator Setting Description Ranges VT (Tidal Volume) Amount of oxygen delivered to patient with each preset ventilated breath 5-15 ml/kg (average 10ml/kg) Respiratory rate Number of breaths per minute that ventilator is set to deliver 4-20 breaths/min FiO2 (Fraction of Inspired Oxygen) Percentage of oxygen delivered by ventilator with each breath 21%-100% I/E Ratio ( inspiratory to expiratory) Duration of I/E time 1:2 (unless IRV is used) Sensitivity Determines amount of effort patient must generate before ventilator will give a breath Too low – patient will have to work harder to obtain a breath Too high – patient may fight ventilator Flow rate Determines how fast VT will be delivered during inspiration High – increase airway pressure Low – decrease airway pressure Pressure limits Regulates maximum amount of pressure the ventilator will generate to deliver preset VT Ventilated breath is stopped when pressure limit is reached

Barotrauma occurs when high airway pressures cause overdistention of the alveoli, rupture and leakage of air. Barotrauma can cause pneumothorax, subcutaneous emphysema, or crepitus. Air can leak under the 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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


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. Three Main Clinical Features of DKA: 1. Hyperglycemia 2. Dehydration and electrolyte loss 3. Acidosis Three Main Causes of DKA: 1. Decreased or missed dose of insulin 2. Illness or infection 3. Undiagnosed and untreated diabetes 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 Assessment and Diagnostic Findings : 1. Blood glucose levels may vary from300 to 800 mg/dl 2. The severity of DKA is not necessarily related to the blood glucose level 3. Evidence of DKA is reflected in low serum bicarbonate and low pH values Prevention : 1. Patients must be taught “sick day “rules for maintaining their diabetes when ill. 2. The most important issue is not to eliminate insulin doses when nausea and 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

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC COMA Background: Hyperosmolar hyperglycemic nonketotic coma (HHNC) is a metabolic derangement that occurs principally in patients with adultonset 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. Management: refer to DKA THYROTOXIC CRISIS (THYROID STORM)  A severe form of hyperthyroidism marked by sudden release of thyroid hormone into the blood stream Precipitating Factors : 1. Stress such as injury, infection, thyroidal and non-thyroid surgery, tooth extraction, insulin reaction, diabetic acidosis, pregnancy, digitalis
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

12 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 HEPATIC FAILURE (Hepatic Coma)  An end stage of liver disease, usually arises as a complication of conditions that cause liver dysfunction although it can be idiopathic  Also called Hepatic coma because the patient’s neurologic status gradually deteriorates  Represents the most advanced stage of hepatic encephalopathy  A life threatening crisis may occur if the serum ammonia level rises, causing cerebral ammonia intoxication Causes: 1. Cirrhosis 2. Hepatitis 3. Drug or toxin-induced damage 4. Fatty liver 5. Portal HPN 6. Surgically-created portal systemic shunts that bypass the liver and allow 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

13  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.

Assessment and Diagnostic Findings: 1. Elevated arterial ammonia blood levels 2. The encephalogram shows generalized slowing and an increase in amplitude of brain waves and the appearance of characteristic triphasic waves 3. Occasionally, fetor hepaticus, a characteristic breath odor like freshly mowed grass, acetone, or old wine, may be noticed. 4. In a more advanced stage, there are gross disturbances of consciousness and the patient is completely disoriented with respect to time and place 5. With further progression of the disorder, the patient lapses into frank coma and may have seizures. Intervention: 1. Anti-infective agents – to decrease bacterial action in the colon. 2. Ammonia detoxicants – to reduce ammonia. Lactulose (Duphulac) is administered 3. Cleansing enemas with diluted acetic acid or neomycin 4. Discontinuation of any precipitating substance: Dietary proteins, sedatives, diuretic therapy, analgesics 5. IV administration of glucose to minimize protein breakdown 6. Oxygen administration 7. Correction of any electrolyte imbalance 8. Promote rest, comfort and quiet environment Nursing Diagnosis: 1. Altered thought process 2. Potential impaired skin integrity 3. Impaired skin integrity

RENAL 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. ACUTE RENAL FAILURE  Acute renal failure is a sudden and almost complete loss of kidney function over a period of hours to days. Categories of Acute Renal Failure: 1. Prerenal Condition (hypoperfusion of kidney). Occurs as a result of impaired blood flow that leads to hypoperfusion of the kidney and a drop in the GFR. Common clinical situations are volume-depletion states (hemorrhage or gastrointestinal losses), impaired cardiac performance and vasodilation (sepsis or anaphylaxis) 2. Intrarenal. Intrarenal causes of acute renal failure are the result of actual parenchymal damage to the glomeruli or kidney tubules. Conditions such as burns crush injuries, and infections, as well as nephrotoxic agents, may lead to acute tubular necrosis and cessation of renal function. Severe 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. PHASES OF ACUTE RENAL FAILURE: 1. Initiation period – begins with the initial insult and ends when oliguria develops. 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 Assessment and Diagnostic Findings: 1. Changes in urine. The urinary output varies (from scanty to normal volume). Hematuria may be present and urine has low-specific gravity. Patients with prerenal azotemia have a decreased amount of sodium. Those patients with intrarenal azotemia usually have urinary sodium levels greater than 40 mEq/L. 2. Increased blood urea nitrogen and creatinine levels (Azotemia) 3. Hyperkalemia 4. Metabolic acidosis 5. Calcium and Phosphorus Abnormalities 6. Anemia – due to reduced erythropoietin production, uremic gastrointestinal lesions, reduced Rbc lifespan, and blood loss 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

14 7. Atrial natriuretic peptide – inhibits sodium and water absorption and dilates the afferent arteriole, thus improving blood flow to the glomerulus 8. Correction of acidosis and elevated phosphate levels. When severe acidosis is present, the arterial blood gases or serum bicarbonate levels must be monitored because patient may require sodium bicarbonate therapy or 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. CHRONIC RENAL FAILURE  CRF is a progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia (retention of urea and other nitrogenous wastes in the blood) 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. 4 Stages of Chronic Renal Disease: 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. Signs And Symptoms Of CRF: 1. Neurologic  Weakness and fatigue; confusion; inability to concentrate; disorientation; tremors; seizures; asterixis; restlessness of legs; burning of soles of feet; behavior changes. 2. Integumentary  Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis; purpura; thin, brittle nails; coarse, thinning hair 3. Cardiovascular  HPN; pitting edema (feet , hands, sacrum), periorbital edema; pericardial friction rub; engorged neck veins; pericarditis; pericardial effusion; pericardial tamponade; hyperkalemia; hyperlipidemia 4. Pulmonary  Crackles; thick, tenacious sputum; depressed cough reflex; pleuritic pain; shortness of breath; tachypnea; kussmaul-type respirations; uremic pneumonitis; “ uremic lung 5. Gastrointestinal  Ammonia odor to breath (uremic fetor); metallic taste; mouth ulcerations and bleeding; anorexia; nausea and vomiting; hiccups; constipation or diarrhea; bleeding from GIT 6. Hematologic  Anemia; thrombocytopenia 7. Reproductive  Amenorrhea; testicular atrophy; infertility; decreased libido 8. Musculoskeletal  Muscle cramps; loss of muscle strength; renal osteodystrophy; bone pain; bone fractures; foot drop Assessment And Diagnostic Findings: • Glomerular Filtration Rate. Decreased GFR can be detected by obtaining a 24-hour urine analysis for creatinine clearance. As GFR decreases, the creatinine clearance value decreases, whereas the serum creatinine and BUN levels increase. • Sodium and Water Retention. The kidney is unable to concentrate or dilute the urine normally in ESRD. Some patients retain sodium and water, increasing the risk for edema, CHF, and HPN. • Acidosis. With advanced renal disease, metabolic acidosis occurs because the kidney is unable to excrete increased loads of acid. • Anemia. Anemia develops as a result of inadequate erythoropoietin production, the shortened life span of RBC’s, nutritional deficiencies, and the patient’s tendency to bleed, particularly from GIT • Calcium and Phosphorus Imbalance. The body’s serum calcium and phosphate levels have a reciprocal relationship in the body; as one rises, the other decreases. Complications: 1. Hyperkalemia. Due to decreased excretion, metabolic acidosis, catabolism, and excessive intake (diet, medications, fluids) 2. Pericarditis. Due to retention of uremic waste products and inadequate 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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15  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

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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

16 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. The nurse must ask the following questions:  How severe is the pain? (scale of 1-10)  What does the pain feel like?  Where is the pain? Does it move or radiate? Is it diffused or well localized?  Did the pain start suddenly or gradually?  How long does it last?  How frequently does it occur?  What makes the pain worse? What brings the pain on?  What makes the pain better? What resolves the pain?  Has the pain been increasingly worse with each attack? Another critical nursing function is prompt institution of prescribed medical 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. ACUTE MYOCARDIAL INFARCTION 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

17 infarction. Cardiac Enzyme Laboratory Findings Enzyme Earliest Rise (in hours) Peak (in hours) Return to Baseline Creatinine kinase (CK) CK-MB Myoglobin Troponin 1 2-6 4-8 0.5-1.0 1-6 18-36 15-24 6-9 7-24 3-6 days 3-4 days 12 hours 10-14 days

Troponin 1 is the newest cardiac marker and is a protein found only in myocardial cells. It is a quick, rapid test that, if elevated, indicated MI. First-Line and Initial Treatment for Myocardial Infarction  Provide oxygen  Obtain a 12-lead ECG  Monitor vital signs and pulse oximetry  Monitor continuous cardiac rhythm with ST segment monitoring  Conduct history and physical examinations  Administer medications (thrombolytic therapy and anticoagulant therapy Nursing Interventions: 1. Bedrest must be enforced. 2. The nurse should assist with all position changes and personal hygiene to 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 LEFT-SIDED CARDIAC FAILURE  Pulmonary congestion occurs when the left ventricle cannot pump the blood out of the chamber. This increases pressure in the left ventricle and decreases the blood flow from the left atrium. The pressure in the left atrium increases, which decreases the blood flow coming from the pulmonary vessels. The resultant increase in pressure in the pulmonary circulation forces fluid into the pulmonary tissues and alveoli; which impairs gas exchange 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 RIGHT-SIDED CARDIAC FAILURE
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

18  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 The basic objectives in CHF management are the following: 1. Reducing the workload on the heart 2. Increasing the force and efficiency of myocardial contraction 3. Eliminating the excessive accumulation of body water by avoiding excess fluid, controlling the diet, and monitoring diuretic and angiotensinconverting enzyme (ACE) inhibitor therapy 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) Nursing Process: The Patient With Cardiac Failure 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

19 4. Pericardial effusion and pericardial tamponade Planning And Goals: 1. Promoting activity while maintaining vital signs within identified range 2. Reducing fatigue 3. Relieving fluid overload symptoms 4. Decreasing the incidence of anxiety or increasing patient’s ability to manage anxiety 5. Teaching the patient about the self-care program. 6. Encouraging the patient to verbalize his ability to make decisions and influence outcomes. 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. 3. Managing Fluid Volume  The nurse monitors the patient’s fluid status closely. Auscultating the lungs, comparing daily body weights, monitoring intake and output and assisting the patient to adhere to a low-sodium diet.  The nurse needs to position the patient or teach the patient how to assume a position that shifts fluid away from the heart.  The nurse needs to assess for skin breakdown and institute preventive measures 4. Controlling Anxiety  The nurse should take steps to promote physical comfort and psychological 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 Assessment and Diagnostic Findings: 1. The use of a Pulmonary Artery catheter to measure left ventricular pressures and CO is important in assessing the severity of the problem and planning management. The PA wedge pressure is elevated and the CO is decreased as the left ventricle loses its ability to pump. 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. 6. Arterial blood gas analysis shows metabolic acidosis 7. All laboratory results indicate organ dysfunction. Medical Management: 1. Reduce any further demand on the heart 2. Improve oxygenation and restore tissue perfusion 3. Diuretics, vasodilators, and mechanical devices (filtration and dialysis) 4. Intravenous volume expanders (normal saline, lactated Ringer’s solution, and albumin) are given for hypovolemia or low intravascular volume. 5. Strict bed rest to conserve energy
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20 6. Oxygen administration is increased for hypoxemia 7. Intubation and sedation may be necessary to maintain oxygenation balance. Pharmacologic Therapy:  Most medication are administered IV because of the decreased perfusion to the gastrointestinal system 1. Pressor agents are medications used to raise BP and increase CO. Many pressor medications are catecholamines ( norepinephrine and highdose 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 PERICARDIAL EFFUSION AND CARDIAC TAMPONADE Pathophysiology: Pericardial effusion refers to the escape of fluid into the pericardial sac. Normally, the pericardial sac contains less than 50 ml of fluid, which the heart needs to decrease friction for the beating heart. An increase in pericardial fluid raises the pressure within the pericardial sac and compresses the heart. This results in :  Increased right and left ventricular-end diastolic pressures  Decreased venous return  Inability of the ventricles to distend adequately Pericardial fluid may accumulate slowly without causing noticeable symptoms. A rapidly developing effusion, however, can stretch the pericardium to its maximum size and, because of increased pericardial pressure, and reduce venous return to the heart, and decrease cardiac output. The result is cardiac tamponade. 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 Assessment and Diagnostic Findings: 1. Pericardial effusion is detected by percussing the chest and noting an extension of flatness across the anterior aspect of the chest 2. Echocardiogram to confirm diagnosis Medical Management: 1. Pericardial Fluid Aspiration (pericardiocentesis) – performed to remove fluid from the pericardial sac 2. Pericardiotomy. A portion of pericardium is sliced to permit the pericardial fluid to drain into the lymphatic system. CARDIAC ARREST  Occurs when the heart ceases to produce an effective pulse and blood 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 Maintaining Airway and Breathing  The first step in CPR is to obtain an open airway. Any obvious material in the mouth and throat should be removed. The chin is directed up and back or the jaw (mandible) is lifted forward. The rescuer “looks, listen. and feels” for air movement. An oropharyngeal airway is inserted if available. Two rescue ventilations over 3 to 4 seconds are provided using a bag or mouth-mask device. If the first rescue ventilation entered easily, then the patient is ventilated with 12 breaths per minute and the open airway is maintained. Endotracheal intubation is performed to ensure an adequate airway and ventilation. 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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21 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

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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. Normal Electrical Conduction The electrical impulse that stimulates and paces the cardiac muscle normally originates in the sinus node, located near the vena cava in the right atrium. Normally, the impulse occurs at a rate between 60 and 100 times a minute in the adult. The impulse quickly travels from the sinus node through the atria to the atrioventricular (AV) node causing the atria to contract. The structure of the AV node slows the impulse, which allows time for the atria to contract and the ventricles to fill with blood. From the AV node, the impulse travels quickly along the right and left bundle branches and the Purkinje fibers, located in the ventricular muscle. The electrical stimulation of the ventricles, in turn, causes the ventricles to contract (systole). Then the electromechanical impulse completes the circuit and the cycle begins again. In this way, sinus rhythm promotes cardiovascular circulation. The electrical stimulus causes the mechanical event of the heart.

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Depolarization. The electrical stimulation: the mechanical contraction is called systole.

Repolarization. The electrical relaxation and mechanical relaxation is called diastole. Influences on Heart Rate and Contractility  Heart rate is influenced by the autonomic nervous system, which consists of sympathetic and parasympathetic fibers.  Stimulation of the sympathetic system increases heart rate.  Sympathetic stimulation also causes the constriction of peripheral blood vessels and, therefore, an increase in BP  Parasympathetic stimulation slows the heart rate  Manipulation of the autonomic nervous system may increase or decrease the incidence of dysrhythmias Types of Dysrhythmias 1. Sinus Node Dysrhythmias A. Sinus Bradycardia  Occurs when the sinus node creates an impulse at a slower –than-normal rate.

Etiology: 1. Slower metabolic needs (sleep, athletic training, hypothyroidism) 2. Vagal stimulation (vomiting, suctioning, severe pain, extreme emotions) 3. Medications 4. Increased intracranial pressure and MI Treatment: 1. Atropine 0.5 to 1.0 mg given quickly and IV as bolus – medication of choice 2. Catecholamines and emergency transcutaneous pacing B. Sinus Tachycardia   Occurs when the sinus node creates an impulse at a faster-than-normal rate. It may be caused by acute blood loss, anemia shock, hypovolemia, hypervolemia, CHF, pain, hypermetabolic state, fever, exercise, anxiety or sympathomimetic medications.

Treatment: 1. Calcium channel blockers (ex. Diltiazem) 2. Beta-blockers (ex. Propranolol) C. Sinus Arrhythmia  Occurs when the sinus node creates an impulse at an irregular rhythm; the rate increases with inspiration and decreases with expiration 2. Atrial Dysrhythmias A. Premature Atrial Complex (PAC)  This is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the SA node.  The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium  PAC’s are common in normal hearts. The patient may say “My heart skipped a beat.” A pulse deficit may exist.  If PAC’s are infrequent, no treatment is necessary. B. Paroxysmal Atrial Tachycardia  A term used to indicate a tachycardia characterized by abrupt onset and abrupt cessation and a QRS of normal duration.  Now called AV nodal reentry tachycardia C. Atrial Flutter  Occurs in the atrium and creates impulses at an atrial rate between 250 and 400 times per minute  May cause serious signs and symptoms: chest pain, shortness of breath, and low blood pressure. Treatment: 1. If patient is unstable, electrical cardioversion is indicated 2. If patient is stable, diltiazem, verapamil, beta-blockers or digitalis may be administered IV to slow the ventricular rate. D. Atrial Fibrillation  Causes a rapid, disorganized, and uncoordinated twitching of atrial musculature.  The most common dysrhythmias  Usually associated with advanced age, valvular heart disease, cardiomyopathy, hyperthyroidism, pulmonary disease, moderate to heavy ingestion of alcohol and the aftermath of open heart surgery Treatment:
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22       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 A. Premature Junctional Complex  An impulse that starts in the AV nodal area before the next normal sinus impulse.  Causes include: digitalis toxicity, congestive heart failure, and coronary artery disease  Rarely produce any significant symptoms  Treatment is the same as for frequent PAC’s B. Junctional Rhythm  Occurs when the AV node, instead of the SA node, becomes the pacemaker of the heart.  Junctional rhythm may produce signs and symptoms of reduced cardiac output. If so, the treatment is the same as for sinus bradycardia. C. AV Nodal Reentry Tachycardia  Occurs when an impulse is conducted to an area in the AV node that causes the impulse to be rerouted back into the same area over and over again at a very fast rate.  Factors associated with the development of AV nodal reentry tachycardia include caffeine, nicotine, hypoxemia, and stress  Signs and symptoms vary with the rate and duration of the tachycardia and the patient’s underlying condition. Usually of short duration, resulting only in palpitations. A fast rate may reduce cardiac output, resulting in significant signs and symptoms such as restlessness, chest pain, shortness of breath, pallor, hypotension and loss of consciousness Treatment:  Treatment is aimed at breaking the reentry of the impulse. 1. Vagal maneuvers, such as carotid sinus massage, gag reflex, breath holding, 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 A. Premature Ventricular Complex (PVC)  PVC is an impulse that starts in a ventricle before the next normal sinus impulse.  PVC’s can occur in healthy people, esp. with the use of caffeine, nicotine, and alcohol.  Also caused by cardiac ischemia or infarction, increased workload on the heart (ex. Exercise, fever. Hypervolemia, CHF, and tachycardia), digitalis toxicity, hypoxia, acidosis, and electrolyte imbalances, esp. hypokalemia  In the absence of disease, PVC’s are not serious. In the patient with acute MI, PVC’s may indicate the need for more aggressive therapy.  The following are warning or complex PVC’s (precursors of ventricular tachycardia) : (1) more than 6/minute (2) multifocal (having different shapes), (3) two in a row (pair), and (4) occurring on the T wave (the vulnerable period of ventricular depolarization) 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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

23 Treatment: 1. CPR 2. Rapid assessment to identify possible causes 3. Intubation and establishment of IV access are the first recommended actions 4. Bolus of IV epinephrine and to be repeated at 3-5 minutes intervals 5. Sodium bicarbonate maybe administered IV Nursing Process: The Patient With A Dysrhythmia Assessment  Major areas of assessment include possible causes of the dysrhythmias and the 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. Potential Complications: Ischemic Heart Disease 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 Adjunctive Modalities and Management 1. Cardioversion and Defibrillation  Treatment for tachydysrhythmias.  Used to deliver an electrical current to stimulate a critical mass of myocardial cells. This allows the sinus node to recapture its role as the heart’s pacemaker.  One major difference between cardioversion and defibrillation has to do with the timing of the delivery of electrical current.  Defibrillation is usually performed as an emergency treatment, whereas cardioversion is usually a planned procedure  Cardioversion involves the delivery of a “timed” electrical current to terminate a tachydysrhythmia.  Defibrillation is the treatment of choice for ventricular fibrillation and pulseless ventricular tachycardia. 2. Pacemaker Therapy  An electronic device that provides electrical stimuli to the heart muscle.  Usually used when a patient has a slower-than-normal impulse formation  May also be used to control tachydysrhythmias that do not respond to medication therapy Complications of Pacemakers: 1. Local infection at the entry site of the leads or at the subcutaneous site 2. Bleeding and hematoma at the lead-entry sites or at the subcutaneous sites 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.

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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24 Classification of Burns  Burn injuries are described according to the depth of the injury and the extent of body surface area (BSA) injured. Characteristics of Burns according to Depth Factors to consider in the determination of depth : 1. History of how the injury occurred 2. Causative agent, such as flame or scalding liquid 3. Temperature of the burning agent 4. Duration of contact with the agent 5. Thickness of the skin Extent of Body Surface Area Injured Rule of Nines  An estimation of the total BSA involved in a burn is simplified using the rule of nines Lund and Browder Method  A more precise method of estimating the extent of a burn  Recognizes that the percentage of BSA of various anatomic parts, especially the head and legs, changes with growth.  By dividing the body into very small areas and providing an estimate of the proportion of BSA accounted for by such body parts, one can obtain a reliable estimate of the total BSA burned.  The initial evaluation is made on the patient’s arrival at the hospital. Palm Method  A method to estimate the percentage of scattered burns.  The size of the patient’s palm is approximately 1% of BSA. The size of the palm can be used to assess the extent of burn injury. Local and Systemic Responses to Burns  Burns that do not exceed 25% of the total BSA produce a primarily local response  Burns that exceed 25% BSA may produce both a local and a systemic response, which is considered a major burn injury. Overview of physiologic changes after a major burn injury Cardiovascular Response  Cardiac output decreases before any significant change in blood volume is 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. Effects on Fluids, Electrolytes, and Blood Volume  Circulating blood volume decreases dramatically during burn shock. Evaporative fluid loss through the burn may reach 3 to 5 L or more over a period of 24 hours until the burn surfaces are covered.  During the shock, serum sodium levels vary in response to fluid resuscitation. Usually hyponatremia (sodium depletion) is present, as water shifts from the interstitial to the vascular space.  Immediately after burn injury, hyperkalemia (excessive K) results from massive cell destruction. Hypokalemia may occur later with fluid shifts and inadequate potassium intake.  At the time of burn injury, some red blood cells may be destroyed and/or damaged resulting in anemia. Despite this, patient’s hematocrit may be elevated due to plasma loss  Blood transfusions are required periodically to maintain adequate hemoglobin levels for oxygen delivery.  Abnormalities in coagulation, including a decrease in platelets (thrombocytopenia) and prolonged clotting and prothrombin time, also occur with burn injury. Pulmonary Response  Inhalation injury is the leading cause of death in fire victims.  One third of all burn injuries have a pulmonary problem related to the burn 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. Categories of Pulmonary Injury: 1. Upper Airway Injury  Results from direct heat or edema.  Manifested by mechanical obstruction of the upper airway, including the pharynx and larynx  Because of the cooling effect of rapid vaporization in the pulmonary tract, direct heat injury does not normally occur below the level of the bronchus.  Treated by early nasotracheal or endotracheal intubation. 2. Inhalation below the glottis  Results from inhaling the products of incomplete combustion or noxious gases. These products include carbon monoside, sulfur oxides, nitrogen oxides, aldehydes, cyanide, ammonia, chlorine, phosgene, benzene, and halogens.  The injury results directly from chemical irritation of the pulmonary tissues at the alveolar level.  Inhalation injuries below the glottis cause loss of ciliary action, hypersecretion, severe mucosal edema, and possibly bronchospasm.  The pulmonary surfactant is reduced, resulting in atelectasis (collapse of alveoli). Expectoration of carbon particles in the sputum is the cardinal sign of this injury.  Carbon monoxide is the most common cause of inhalation injury because it is a byproduct of the combustion of organic materials and is
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25 therefore present in smoke. Treatment usually consists of early intubation and mechanical ventilation with 100% oxygen. Using 100% oxygen is essential to accelerate the removal of carbon monoxide from the hemoglobin molecule.

Indicators of possible pulmonary damage: 1. History indicating hat the burn occurred in an enclosed area 2. Burns of the face or neck 3. Singed nasal hair 4. Hoarseness, voice change, dry cough, stridor, sooty sputum 5. Bloody sputum 6. Labored breathing or tachypnea (rapid breathing) and other signs of reduced oxygen levels (hypoxemia). 7. Erythema and blistering of the oral or pharyngeal mucosa Pulmonary Complications secondary to Inhalation Injury: 1. Acute respiratory failure  Occurs when impairment of ventilation and gas exchange is life-threatening.  The immediate intervention is intubation and mechanical ventilation.  If ventilation is impaired by restricted chest excursion, immediate escharotomy is needed. 2. Acute respiratory distress syndrome > May develop in the first few days after injury secondary to systemic and pulmonary responses to the burn and inhalation injury. Other Systemic Responses  Renal function may be altered as a result of decreased blood volume. If there is inadequate blood flow through the kidney, the hemoglobin and myoglobin occlude the renal tubules, resulting in acute tubular necrosis and renal failure.  The immunologic defenses of the body are greatly altered by burn injury. The loss of skin integrity is compounded by the release of abnormal inflammatory factors. Immunosuppression places the patient at high risk for sepsis.  Loss of skin also results in an inability to regulate body temperature. Burn patients may therefore exhibit low body temperature in the early hours after burn injury, but as hypermetabolism resets core temperatures, burn patients becomes hyperthermic for most of the postburn period, even in the absence of infection.  Two potential gastrointestinal complications may occur: paralytic ileus (absence of intestinal peristalsis) and Curling’s ulcer. Decreased peristalsis and bowel sounds are manifestations of paralytic ileus resulting from burn trauma. Gastric distention and nausea may lead to vomiting unless gastric decompression is initiated. Management Of The Patient With A Burn Injury A. Emergent/Resuscitative Phase of Burn Care  The first priority in on-the-scene care for a burn victim is to prevent injury to the rescuer. Airway, Breathing, Circulation  It is important to remember the ABC’s of all trauma care because the systemic effects pose a greater threat to life. 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

Management of Fluid Loss and Shock  Next to respiratory difficulties, the most important is preventing irreversible shock by replacing lost fluids and electrolytes. Survival of burn victims depends on adequate fluid resuscitation. 1. Fluid Replacement  Some combination of fluid categories may be used: Colloids (whole blood, plasma, and plasma expanders) and crystalloids/electrolytes (physiologic sodium chloride or lactated Ringer’s solution)  Formulas have been developed for estimating fluid loss based on the estimated 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.

Nursing Process: Care during the Emergent/Resuscitative Phase  Nursing assessment in the emergent phase of burn injury focuses on the major priorities for any trauma patient; the burn wound is a secondary consideration.  Aseptic management of the burn wounds and invasive line continues.  The nurse checks vital signs frequently. Respiratory status is monitored closely. Apical, carotid, and femoral pulses are evaluated  Cardiac monitoring for patients with cardiac problems, electrical injury or respiratory problems or if the pulse is dysrhythmic or the rate is abnormally slow or rapid.  Determining BP is a problem if all extremities are burned. A sterile dressing under the BP cuff will protect the wound from contamination. A
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

26 Doppler UTZ or a non-invasive electronic BP may be helpful. In severe burns, an arterial catheter is used for BP measurement and for collecting blood specimen Peripheral pulses of burned extremities are checked hourly. Doppler is used. Elevation of burned extremities is crucial to decrease edema. Elevation of the lower extremities on pillows and of the upper extremities on pillows or by suspension using intravenous poles may be helpful. Large-bore IV lines and Indwelling urinary catheter are inserted. Assessment includes monitoring of fluid intake and output. Urine output, an excellent indicator of circulatory status, is monitored carefully. The amount of urine first recorded may assist in determining the extent of preburn renal function and fluid status. Burgundy-colored urine suggests the presence of hemochromogen and myoglobin resulting from muscle damage. This is associated with deep burns caused by electrical injury. Glucosuria results from the release of stored glucose from the liver in response to stress. Infusion pumps and rate controllers are used to deliver a prescribed IV fluids Monitoring IV therapy is a major nursing responsibility. Body temperature, body weight, preburn weight, and history of allergies, tetanus immunization, past medical and surgical problems, current illnesses, and use of medication are assessed. A head-to-toe assessment is performed, focusing on signs/symptoms of concomitant illness, injury, or developing complications. Patients with facial burns should have eye examination for potential injuries to the cornea Assessment should include the time of injury, mechanism of burn, whether the burn occurred in closed space. The neurologic assessment focuses on the client’s level of consciousness, psychological status, pain and anxiety levels, and behavior

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Acute or Intermediate Phase of Burn Care  Begins 48 to 72 hours after the burn injury.  Attention is directed toward continued assessment and maintenance of respiratory and circulatory status, fluid and electrolyte balance, and gastrointestinal function.  Airway obstruction caused by upper airway edema can take as long as 48 hours to develop. Changes may occur as the effects of resuscitative fluid and the chemical reaction of smoke ingredients with lung tissues become apparent. The patient’s arterial blood gas values and other parameters determine the need for intubation and mechanical ventilation.  If cardiac or renal function is inadequate, fluid overload occurs and symptoms of congestive heart failure may result. Vasoactive medications, diuretics, and fluid restriction may be used to support circulatory function and prevent congestive heart failure and pulmonary edema  Cautious administration of fluids and electrolytes continuous because of the shifts in fluid from the interstitial to intravascular compartments. Blood components are administered as needed to treat blood loss and anemia  A resetting of the core body temperature in severely burned patients results in a body temperature slightly higher than normal for several weeks after the burn injury. Bacteremia and septicemia also causes fever in many patients.. Acetaminophen and hypothermia blankets may be required to maintain body temperature to reduce metabolic stress and tissue oxygen demand.  Central venous, peripheral arterial or pulmonary artery thermodilution catheters may be required for monitoring venous and arterial pressures. However, invasive vascular lines are avoided because they provide an additional port for infection.  Infection progressing to septic shock is the major cause of death in patients who have survived the first few days after a major burn injury. The immunosuppression places the patient at high risk for sepsis. The infection that begins within the burn site may spread to the bloodstream. Infection Prevention  Burn wound is an excellent medium for bacterial growth and proliferation.  Bacteria such as Staphylococcus, Proteus, Pseudomonas, Escherichia coli, and 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. Topical Antibacterial Therapy  Topical antibacterial therapy does not sterilize the burn wound; it simply reduces the number of bacteria so that the overall microbial population can be controlled by the body’s host defense mechanisms  The three most commonly used topical agents are Silver sulfadiazine (Silvadene), silver nitrate, and Mafenide acetate (Sulfamylon)  No single agent is universally effective. Using different agents at different times in the postburn period may be necessary. Prudent use and alternation of antimicrobial agents results in less-resistant strains of bacteria, greater effectiveness of the agents.  Before a topical agent is applied, the previously applied topical agent must be thoroughly removed. Wound Dressing  After the wound is cleaned, patted dry and applied topical agent; the wound is then covered with several layers of dressings.  A light dressing is used over joints to allow for motion, light dressing is also applied over areas for which a splint has been designed to conform to the body contour for proper positioning  Circumferential dressings should be applied distally to proximal.  If the hand or foot is burned, the fingers and toes should be individually wrapped to promote adequate healing. Exposure Method
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

27   Occasionally, a wound is treated by exposing it to air. Wound care proceeds in the same manner and a topical agent is applied, but no dressings are applied. The success of exposure method depends on keeping the immediate environment 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)

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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 Debridement has two goals: 1. To remove contaminated tissue, thereby protecting the patient from invasion of bacteria 2. To remove devitalized tissue or burn eschar in preparation for grafting and wound healing. 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). Grafting the Burn Wound  If wounds are deep (full thickness) reepitheliazation is not possible. Therefore coverage of the burn wound is necessary until coverage with a graft of the patient’s own skin (autograft) is possible.  The purpose of wound coverage is to decrease the risk for infection; prevent loss of protein, fluid, and electrolytes through the wound; and minimize heat loss through evaporation.  The main areas for skin grafting include the face, for cosmetic and psychological reasons; the hands and other functional areas such as the feet; and areas that involve joints.  Grafting permits earlier functional ability and reduces contractures (shrinkage of burn scar through collagen maturation).  When burns are extensive, the chest and abdomen maybe grafted first to reduce the burn surface.  During wound healing, granulation tissue develops. It fills the space created by the wound, creates a barrier to bacteria, and serves as a bed for epithelial cell growth.  Richly vascular tissue is pink, firm, shiny, and free of exudates and debris. It should have a bacterial count of less than 100,000 per gram of tissue to optimize graft take.  A preoperative culture is mandatory before grafting, because enzymes of bacteria can dissolve a graft and lead to its failure. Beta hemolytic streptococci are a major factor in graft failure. Biologic Dressings (Homografts And Heterografts)  In extensive burns, biologic dressings can be lifesaving by providing temporary wound closure and protecting the granulation tissue until autografting is possible.  Biologic dressing may also be used to debride untidy wounds after eschar separation.  With each biologic dressing change, debridement occurs.  Once the biologic dressing appears to be taking or adhering to the granulating surface with minimal underlying exudation, the patient is ready for an autograft.  Biologic dressing also provides immediate coverage for clean, superficial burns and decreases the wound’s evaporative water and protein loss.  Biologic dressing decrease pain by protecting nerve endings and are an effective barrier against water loss and entry of bacteria.  When applied to superficial partial-thickness wounds, they seem to speed healing.  Biologic dressings consist of homografts (or allografts) and heterografts(or xenografts).  Homografts are skin obtained from living or recently deceased humans. The amniotic membrane (amnion) from the human placenta may also be used as a biologic dressing.  Heterografts consist of skin taken from animals (usually pigs).  Most biologic dressings are used as temporary coverings of burn wounds and are eventually rejected because of the body’s immune reaction to them as foreign.  Homografts tend to be the most expensive biologic dressings. They are available from skin banks in fresh and cryopreserved (frozen) forms.  Homografts are thought to provide the best infection control. Of all the biologic and bio synthetic dressings available. Revascularization occurs within 48 hours, and the graft may be left place for several weeks.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

28       Amnion is low in cost, however, amnion grafts do not become vascularized by the patient’s vessels and can be left in place only briefly. Pigskin is available from commercial suppliers. Pigskin impregnated with a 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.

Biosynthetic And Synthetic Dressings  Currently, the most widely used synthetic dressing is Biobrane, which is composed of nylon. Silastic membrane combined with a collagen derivative.  Less costly than homograft or pigskin.  Biobrane dressings adhere to donor sites and meticulously clean debrided partial-thickness wounds; they will remain until spontaneous epitheliazation and wound healing occur.  Like biologic dressing, Biobrane protects the wound from fluid loss and bacterial invasion.  Biobrane is also useful for intermediate or long-term closure of a surgically excised wound until an autograft becomes available.  Like Biologic dressing, Biobrane should not be used over grossly contaminated or necrotic wounds.  Several other synthetic dressings are available: Op-site, a thin, transparent, polyurethane elastic film, can be used to cover clean partialthickness wounds and donor sites. This dressing is occlusive and waterproof but permeable to water vapor and air; this permeability provides protection from microbial contamination and allows for the exchange of gases. Other synthetic dressings are Tegaderm, N-Terface, and Duoderm.  Artificial skin (Integra) is the newest type of synthetic dressing. A dermal analogue, Integra is composed of two main layers. The epidermal layer, consisting of Silastic, acts as a bacterial barrier and prevents water loss from the dermis. The dermal layer is composed of animal collagen. It interfaces with the open wound surface and allows migration of fibroblasts and capillaries into the material. 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. Care of the Patient with an Autograft  Occlusive dressings are commonly used initially after grafting to immobilize the graft.  Occupational therapists may be helpful in constructing splints to immobilize newly grafted areas to prevent dislodging the graft  If the graft is dislodged, sterile saline compresses will help prevent drying of the graft until the physician reapplies it.  The patient is positioned and turned carefully to avoid disturbing the graft or putting pressure on the graft site.  If an extremity has been grafted, it is elevated to minimize edema.  The patient begins exercising the area 5 to 7 days after grafting. Care of Donor site  Moist gauze is applied at the time of surgery to maintain pressure and to stop any oozing.  A thrombostatic agent such as thrombin or epinephrine may be applied directly to the site.  The donor site may be applied with a single-layer gauze impregnated with petrolatum, scarlet red, or bismuth to new biosynthetic dressings such as Biobrane.  Donor site must remain clean, dry, and free from pressure.  Because a donor site is usually a partial-thickness wound, it will heal spontaneously within 7 to 14 days with proper care Pain Management  Pain management is the most difficult challenges facing the burn team.  Many factors contribute to the patient’s burn pain experience: severity of the pain, health provider’s pain assessment, the appropriateness and adequacy of pharmacologic treatment of pain, the multiple procedures involved 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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

29    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.

DISORDERS OF WOUND HEALING SCARS  Results from excessive abnormal healing or inadequate new tissue formation.  Hypertrophic scars and wound contractures are more likely to occur if the 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. Nursing Process: Burn Care During The Acute Phase Assessment  Continued assessment focuses on hemodynamic alterations, wound healing, pain and psychosocial responses, and early detection of complications.  Nurse assess VS frequently  Continued assessment of peripheral pulses is essential for the first few post burn days while edema continuous to increase, potentially damaging peripheral nerves and restricting blood flow.  Observation of the electrocardiogram may give clues to cardiac dysrhythmias resulting from potassium imbalance, preexisting cardiac disease, or the effects of electrical injury or burn shock  Assessment focuses on hemodynamic alterations, wound healing, pain and psychosocial responses, and early detection of complications.  Assessment of respiratory and fluid status is the highest priority for detection of complications.  Assess VS  Assessment of peripheral pulses while edema continuous to increase, damaging peripheral nerves and restricting blood flow  ECG may give clues to cardiac dysrhythmias resulting from potassium imbalance, preexisting cardiac disease, or the effects of electrical injury or burn shock  Assessment of residual gastric volumes and pH in the patient with a NGT- gives clues to early sepsis or the need for antacid therapy. Blood in the gastric fluid or stools must also be reported  Important wound assessment include size, color, odor, eschar, exudates, abscess formation under the eschar, epithelial buds (small pearl-like clusters of cells on the wound surface), bleeding, granulation tissue appearance, progress of grafts and donor sites, and quality of surrounding skin  Assessment on pain and psychosocial responses, daily body weights, caloric intake, general hydration, and serum electrolyte and hemoglobin levels and hematocrit  Assessment for excessive bleeding from blood vessels adjacent to areas of surgical site and debridement

Potential Complications: 1. Congestive heart failure and pulmonary edema 2. Sepsis 3. Acute Respiratory Failure 4. Visceral Damage Planning and Goals: The major goals:  restoration of normal fluid balance,  absence of infection,  attainment of anabolic state and normal weight,  improved skin integrity,  reduction of pain and discomfort  optimal physical mobility  adequate patient and family coping  adequate patient and family knowledge of burn treatment  absence of complications Nursing Interventions: Restoring Normal Fluid Balance  Monitor IV and oral intake to reduce risk for fluid overload and consequent CHF 1. Use IV infusion pumps 2. Daily weights are obtained  Low-dose dopamine to increase renal perfusion  Diuretics to increase urine output Preventing Infection  A clean and safe environment  Detect early signs of infection – culture results and WBC counts are monitored  Aseptic technique for wound care procedures. Hand washing before and after each patient contact  Fresh flowers, plants or fresh fruit baskets should not be allowed inside the room because of the risk of microorganism growth  Visitors are screened to avoid exposing the immunocompromised patient to pathogens
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


Maintaining Adequate Nutrition  Oral fluids should be initiated slowly when bowel sounds resumes. If vomiting and abdominal distention do not occur, fluids may be gradually increased  The nurse collaborates with the dietitian to plan a protein-and calorie-rich diet  If caloric goals can not be met by oral feeding, a feeding tube is inserted Promoting Skin Integrity  Assess and record changes or progress in wound healing  Wound care  Topical antibacterial agents Relieving Pain and Discomfort  Pain is more severe in partial-thickness burns than in full-thickness burns because the nerve endings are not destroyed. Cover exposed nerve endings to help reduce pain  Analgesics and anti-anxiety medications  Teach relaxation techniques  Give patient control over wound care  Pain-relieving distractions: video programs/games, hypnosis  Complete treatments and dressings quickly. Analgesics before any painful procedures  Oral anti-pruritic agents, cool environment, frequent lubrication of skin with water or silica-based lotion – to reduce discomfort in itching  Exercise and splinting to prevent skin contracture Promoting Physical Mobility  Early priority is to prevent complications resulting from immobility  Deep breathing, turning, and proper positioning to prevent atelectasis and pneumonia, control edema and to prevent pressure ulcers and contractures.  Early sitting and ambulation  When lower extremities are burned elastic bandage are applied before the patient is placed in an upright position. This bandages promote venous return and minimize swelling  Passive and active ROM to prevent contracture  Splints or other functional devices are used for contracture control. Monitor splinted areas for signs of vascular insufficiency and nerve compression Strengthening Coping Strategies  The patient is facing the reality of burn trauma and is grieving over obvious loss. Depression, regression and manipulative disorders are common problems  Develop effective coping strategies by: 1. Setting specific expectations for behavior 2. Promoting truthful communications to build trust  Patient always ventilates feelings of anger – enlist someone to whom patient can vent feelings without fear of retaliation Monitoring and Managing Potential Complications: Congestive Heart Failure and Pulmonary Edema  Patient is assessed for pulmonary overload – may occur as fluid is mobilized from the interstitial compartment back into the intravascular compartment. If the cardiac and renal system cannot compensate for the excess vascular volume, CHF and pulmonary edema may result.  Crackles in the lungs and increased difficulty with respiration may indicate a fluid buildup in the lungs. 1. Patient is positioned comfortably with the head of the bed raised to promote lung expansion and gas exchange 2. Provide supplemental oxygen 3. Administer IV diuretics Sepsis  Early signs are increased in temperature, increased pulse rate, flushed dry skin, increased pulse rate, widened pulse pressure, and flushed dry skin in unburned areas  Wound and blood cultures  Antibiotics Acute Respiratory Failure and Acute Respiratory Distress Syndrome  Patient is assessed for increased difficulty in breathing, change in respiratory pattern, onset of adventitious (abnormal) sounds  Signs of hypoxia (decreased O2 to the tissues), decreased breath sounds, wheezing, tachypnea, stridor  Patients receiving mechanical ventilation must be assessed for a decrease in tidal volume and lung compliance  Key sign of ARDS is hypoxemia while receiving 100% oxygen, decreased lung compliance and significant shunting  Management includes intubation and mechanical ventilation 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 Rehabilitation Phase Of Burn Care  Rehabilitation begins immediately after the burn has occurred  Wound healing, psychosocial support, and restoring maximal functional activity remain priorities  Continued focus on maintaining fluid and electrolyte balance and improving nutritional status  Reconstructive surgery to improve body appearance and function  Psychological and vocational counseling and referral to support groups

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


Definition: One in which a concurrent disorder, pregnancy-related complication, or external factor jeopardizes the health of the mother and/or fetus.  Many factors enter into the categorization of high risk.  No tool is perfect because the concept of high risk is a very individualized one  The woman identified this way needs close observation during pregnancy to see that pregnancy is progressing well  The infant born of a woman identified this way needs close observation in the neonatal period until it is confirmed that no anomalies exist  The failure to identify risk potential in pregnancy leads to increased perinatal mortality ASSESSMENT FOR A FIRST PREGNANCY VISIT : 1. HEALTH HISTORY Purpose : a. To establish rapport b. To gain information about the woman’s physical and psychosocial health c. To obtain a basis for anticipatory guidance for the pregnancy A. Demographic Data : Name, age, address, telephone number, health insurance B. Chief Concern – Reason why the woman has come to the health care setting. 1. Was the pregnancy planned? 2. Inquire date of last menstruation 3. Ask if she has had a pregnancy test 4. Elicit information about signs of early pregnancy 5. Observe for discomforts of pregnancy 6. Has she been exposed to contagious diseases 7. Has she taken any medicine that might be harmful to fetal growth C. Family Profile – helps to know the woman earlier 1.Identify support persons, Family composition 2.What is her occupation, source of income, Nutrition, sleep pattern, hobbies, living conditions 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

32 2. What is the length and duration of menstrual cycle

F. Obstetric History : 1. Review pregnancy briefly. 2. Determine woman’s status with respect to the number of times she has been 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 G. Typical Day History  Information about a woman’s current nutrition, elimination, sleep, recreation and interpersonal interactions can be elicited best by asking the woman to describe a typical day of her life. H. Review of Systems – Brief review of all body systems a. Head – Ask about headache, head injury, seizures, dizziness b. Eyes – Inquire about vision, eyeglasses, eye diseases c. Ears – Infection, discharges, pain d. Nose – Bleeding, discharges, colds, allergy, sinuses e. Mouth and pharynx –Dentures, teeth, toothache, bleeding, pain, surgery f. Neck – stiffness, masses g. Breast – lumps, secretion, pain, tenderness h. Respiratory – cough, wheezing, asthma, SOB i. Cardiovascular – heart murmur, history of heart disease, HPN j. G.I.T – pre-pregnant weight, diarrhea, constipation, hemorrhoids, ulcer k. Genito-urinary – infection, STD’s l. Extremities – varicose veins, pain or stiffness of joints, fractures m. Skin – rashes, acne, psoriasis I. Support Persons Role  Questions asked to the support person : Current health status, feelings and concern about the pregnancy, knowledge of pregnancy and childbirth 2. PHYSICAL EXAMINATION A. Baseline Data : to establish a baseline for future comparison Weight, Height, BP, PR, RR FHR : 120-160 beats/min 10-12 weeks (Doppler) 18-20 weeks (Stethoscope) Fundic height: 12-14 weeks – Symphysis pubis 20-22 weeks – Umbilicus 36 weeks - Xiphoid process 40 weeks - Xiphoid process B. System Assessment 1. General Appearance and Mental Status  Physical examination always begins with inspection of general appearance to 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 2. Head and Scalp  Examine head for symmetry, normal contour and tenderness  Examine hair for distribution, thickness, excessive dryness or oiliness, cleanliness, or the use of hair dye.  Look for chloasma (extra pigment on the skin) 3. Eyes  Edema in the eyelids  Spots before the eyes  Diplopia (double vision) may indicate PIH 4. Nose  5. Ears  Increased level of estrogen associated with pregnancy may cause nasal congestion. The nasal stuffiness that accompanies pregnancy may lead to blocked Eustachian tubes and therefore a feeling of fullness or dampening of sound during early pregnancy.

6. Sinuses  Sinuses should feel nontender 7. Mouth, Teeth and Throat  Pregnant woman is prone to vitamin deficiency because of the rapid growth of the fetus.  Assess carefully for cracked corners of the mouth that would reveal vitamin A deficiency.  Assess carefully for pinpoint lesions with an erythematous base on the lips; these suggest a herpes infection  Gingival hypertrophy may result from estrogen stimulation during pregnancy.  Teach all women not to neglect good dental hygiene while pregnant 8. Neck   Slight thyroid hypertrophy may occur with pregnancy because the overall 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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33 for thyroxine production with this increased rate. 9. Lymph Nodes  No palpable lymph nodes should be present. 10. Breasts  As pregnancy begins, the breast undergo the following : Breast areola darkens; Montgomery’s tubercles become prominent; Breast size increases; breast tone affirms; secondary areola may develop surrounding 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. 15. Extremities and Skin  Assess the upper extremities. Many women develop palmar erythema and itching early in pregnancy from a high estrogen level and perhaps subclinical jaundice.  Assess the lower extremities carefully for varicosities, filling time of the toenails (should be under 5 seconds) and edema.  Assess the gait of pregnant women to see that they are keeping their pelvis tucked under the weight of their abdomen. MEASUREMENT OF FUNDAL HEIGHT AND FETAL HEART SOUNDS  12-14 weeks of pregnancy – uterus is palpable over the symphysis pubis as a firm globular sphere  20-22 weeks – reaches umbilicus  36 weeks – xiphoid process  40 weeks – often return to 4 about 4 cm below the xiphoid due to lightening  Auscultate for fetal heart sounds (120 to 160 beats/minute. These can be heard at 10 to 12 weeks if Doppler is used. 18 to 20 weeks if regular stethoscope is used.  Palpate for fetal outline and position after the 28th week. PELVIC EXAMINATION > Reveals information on the health of both internal and external reproductive organs a. EXTERNAL GENITALIA – note for : 1.Signs of inflammation 2.Irritation 3.Infection 4.Herpes simplex II virus infection 5.Rectocele 6.Cystocele b. INTERNAL GENITALIA 1. Cervix should be in the center and color should be almost purple when 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). e. EXAMINATION OF PELVIC ORGANS  A bimanual (two-handed) examination is performed to assess the position, contour, consistency, and tenderness of pelvic organs  Abnormalities that can be noted by bimanual examination include ovarian cysts, enlarged fallopian tubes (perhaps from pelvic Inflammatory Disease) and an enlarged uterus.
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34  An early sign of pregnancy (Hegar’s sign) is elicited on bimanual examination.

f. RECTOVAGINAL EXAMINATION  To assess the strength and irregularity of the posterior vaginal wall e. ESTIMATING PELVIC SIZE  It is hard to see from the outward appearance of a woman whether her pelvis is adequate for the passage of a fetus.  Pelvic measurements should be taken if the woman is pregnant and if she has never given birth vaginally  In sonogram, estimations may be made by a combination of pelvic pelvimetry and fetal sonogram  Estimation of pelvic adequacy must be done at least by the 24 th week of pregnancy, because by this time, there is danger that the fetal head will reach a size that will interfere with safe passage and birth if the pelvic measurements are small  Once a woman has given birth vaginally, her pelvis has been approved adequate, and it is not necessary to take pelvic measurements. Types of Pelvis > Categorized into 4 groups : • Gynecoid : normal female pelvis • Anthropoid : Ape-like pelvis • Platypelloid : Flattened pelvis • Android : Male pelvis PELVIC MEASUREMENTS  Internal pelvic measurements give the actual diameters of the inlet and outlet through which the fetus must pass. The following measurements are made most commonly : 1. The Diagonal Conjugate – The distance between the anterior surface of the 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. 2. The True Conjugate – Conjugate Vera. The measurement between the anterior surface of the sacral prominence and the posterior surface of the inferior margin of the symphysis pubis. 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

   Some women enter pregnancy with a chronic illness that, when superimposed on the pregnancy, makes it high risk. Other women enter pregnancy in good health but then develop a complication of pregnancy that causes it to become high risk. A combination of particular instances – poverty, lack of support people, poor coping mechanisms, genetic inheritance, or past history of pregnancy complications can cause a pregnancy to be categorized as high risk.

Maternal infections during pregnancy may contribute significantly to fetal morbidity and mortality. Infections in this category may be caused by various viruses. Other organisms like bacteria, spirochetes, protozoa, or yeast may also cause maternal infections, which are harmful to the developing fetus. Even though the infection in the mother may be very mild, the effects on the fetus may be catastrophic. • Most organisms cross the placenta and infect the fetus, causing birth anomalies. The fetus may also acquire the organism as it travels the birth canal during labor, causing illness after birth. SEXUALLY TRANSMITTED DISEASES AND PREGNANCY  Spread through sexual contact with an infected partner.  All STD’s can be prevented to some extent by the use of safer sex practices.  Treatment begins with determining the causative organism so the appropriate antibiotic or antifungal medication can be prescribed. Nursing Diagnosis : Pain related to vulvar irritation secondary to existence of STD 1. THE WOMAN WITH CANDIDIASIS  Candidiasis causes a vaginal infection spread by the fungus Candida. Assessment : 1. Thick, cream cheeselike vaginal discharge and extreme pruritus. 2. Vagina appears red and irritated Etiology : 1. Occurs more frequently during pregnancy because of the increased estrogen 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 Dx : Diagnosed by microscopic analysis 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. 2. THE WOMAN WITH TRICHOMONIASIS  A single-cell protozoan spread by coitus. Assessment :
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• •

35 1. 2. A yellow-gray, frothy, odorous vaginal discharge. Vulvar itching, edema, and redness

Dx: Diagnosed by examination of vaginal secretions on a wet slide that has been treated with Potassium Hydoxide (KOH). Treatment : Topical clotrimazole instead of metronidazole because of its possible 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 3. THE WOMAN WITH BACTERIAL VAGINOSIS (GARDNERELLA INFECTION)  Local infection of the vagina by the invasion, most commonly, of Gardnerella organisms. 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 6.THE WOMAN WITH GONORRHEA  A sexually transmitted disease caused by the gram-negative coccus Neisseria gonorrhea. 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 7.THE WOMAN WITH HUMAN PAPILLOMA VIRUS INFECTION  The Human papilloma virus (HPV) causes fibrous tissue overgrowth on the external vulva (condyloma acuminatum) 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


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. 8.THE WOMAN WITH A GROUP B STREPTOCOCCI INFECTION Etiology : 1. Occurs at a higher incidence during pregnancy Assessment : 1. Patient usually experiences no symptoms. Complications : 1. Urinary Tract Infection (UTI) 2. Intra-amniotic Infection leading to preterm birth 3. Postpartal endometritis 4. 40 % to 70% of neonates whose mothers have an active infection will become 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 Dx: Women are screened at 35 to 38 weeks of pregnancy by a vaginal culture. Treatment : 1. Broad spectrum penicillin such as ampicillin 2. Women who experience rupture of membranes at less than 37 weeks of pregnancy are treated with Ampicillin IV 9.THE WOMAN WITH HUMAN IMMUNODEFICIENCY VIRUS (HIV) INFECTION  The HIV virus, which leads to AIDS, is the most serious of the STD’s because it may be fatal to both mother and child. Etiology : 1. Multiple sexual partners of the individual or sexual partner 2. Bisexual partners 3. IV drug use by the individual or sexual partner 4. Blood transfusions Assessment : 1. Initial invasion of the virus, which may be accompanied by mild, flu-like 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 trimethroprimsulfamethoxazole to prevent P. carinii pneumonia Nursing Diagnosis: Risk for opportunistic infections

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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37 Herpes can be transmitted at birth if active lesions are present at that time in the vagina or vulva. When infection in the NB occurs, Congenital Herpes can result. To avoid transmission, CS may be scheduled. If no lesions are present, a vaginal birth is preferable. Dx : Appearance of lesions, PAP smear, enzyme Immunosorbent Assay (ELISA) Treatment : 1. Drug of choice is acyclovir (Zovirax) in an ointment or oral form 2. Women can reduce the pain of infection by sitz baths or applying warm. Moist tea bags to the lesions. Assessment : Painful, small, pinpoint vesicles surrounded by erythema on the vulva or in the vagina 3-7 days after exposure. B.  HEMATOLOGIC DISORDERS AND PREGNANCY Hematologic disorders during pregnancy involve either blood formation or coagulation disorders.

Anemia And Pregnancy  Because the blood volume expands during pregnancy, most women have a pseudoanemia of early pregnancy. This is normal and should not be confused with the true anemia that can occur as a complication of pregnancy. Nursing Diagnosis: Risk for altered tissue perfusion 1. THE WOMAN WITH IRON DEFICIENCY ANEMIA  Most common anemia of pregnancy  Iron deficiency anemia is characteristically a microcytic (small-sized red blood cell), hypochromic (less Hgb than the average red blood cell) anemia, because when an adequate supply of iron is not ingested, iron is unavailable for incorporation into red blood cells and so cells are not as large or as rich in hemoglobin as normally. Both Hgb and Hct will be reduced. Therapeutic Management : 1. All women should take prenatal vitamins that contain an iron supplement of 60 mg of elemental iron as prophylactic therapy. 2. Advise women to take iron supplements with orange juice or a Vitamin C supplement. 3. They need to eat diet high in iron and vitamins 3. For severe iron deficiency anemia, and patient is noncompliant with oral iron therapy, Iron Dextran IM or IV can be administered. Etiology : 1. Diet low in iron 2. Heavy menstrual periods 3. unwise weight-reducing programs 4. Low socio-economic status Complications : 1. Low fetal birth weight 2. Preterm birth Assessment : 1. Extreme fatigue and poor exercise tolerance. 2. THE WOMAN WITH FOLIC ACID DEFICIENCY ANEMIA  Folic acid or Folacin is necessary for both the normal formation of red blood cells in the mother.  Associated with a decrease in neural tube defects in the fetus. Etiology : 1. Occurs most often in multiple pregnancies because of the increased fetal 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. Megaloblastic anemia (enlarged red blood cells) – anemia that develops.  The mean corpuscular volume will be elevated.  May be a factor in early abortion or abruptio placenta 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 3. THE WOMAN WITH SICKLE CELL ANEMIA  Sickle cell anemia is a recessively inherited hemolytic anemia caused by an abnormal amino acid in the beta chain of hemoglobin. (The amino acid valine is substituted for glutamic acid in the sixth position of the beta chain causing the hemoglobin structure to change.) It is a congenital hematologic disease that causes impaired circulation, chronic ill health, and premature death. Patients who suffer from this disease inherit the sickling gene from both parents, although some parents may only be carriers and don’t experience the symptoms. If both parents are carriers, chances are that one in four of their children will be affected.  Infection, exposure to cold, high altitudes, overexertion or other situations that cause cellular oxygen deprivation may trigger a sickle cell crisis. The deoxygenated, sickle-shaped red blood cells stick to the capillary wall and each other, blocking blood flow and causing cellular hypoxia. The crisis worsens as tissue hypoxia and acidic waste products cause more sickling and cell damage. 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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38 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. COAGULATION DISORDERS AND PREGNANCY  Most coagulation disorders are sex linked, or only occurs in males, so have little effect on pregnancies.  Von Willebrand’s disease is a coagulation disorder inherited as an autosomal dominant trait that does occur in women. Signs/Symptoms : 1. Menorrhagia 2. Frequent episodes of epistaxis 3. Prolonged bleeding time IDIOPATHIC THROMBOCYTOPENIC PURPURA :  A decrease in number of platelets Etiology: - unknown but assumed to be autoimmune illness Signs/Symptoms : 1. Miniature petechiae or large ecchymoses appear on the woman’s body. 2. Frequent nose bleeds may occur 3. Marked thrombocytopenia Therapeutic Management : 1. Platelet transfusion to temporarily increase platelet count 2. Oral prednisone is effective C. RENAL AND URINARY DISORDERS AND PREGNANCY  Adequate kidney function is important to successful pregnancy outcome; any condition that interferes with kidney or urinary function is therefore potentially serious. 1. THE WOMAN WITH A URINARY TRACT INFECTION  The organism most commonly responsible for UTI is Escherichia coli Causes : 1. In pregnant woman, because of the dilated ureters from the effect of 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. Nursing Diagnosis: Risk for infection Common Measure to prevent UTI : 1. Voiding frequently (at least every two hours) 2. Wiping front to back after bowel movements 3. Wearing cotton, not synthetic fiber underwear 4. Voiding immediately after sexual intercourse 2. THE WOMAN WITH CHRONIC RENAL DISEASE  Pregnancy increases the work load of the kidneys because the woman’s kidneys must excrete waste products not only for herself but for the fetus for 40 weeks.  Many women with renal disease take a corticosteroid at a maintenance level. An effect that may occur is that the infant may be hyperglycemic at birth because of the suppression of insulin activity by corticosteroid.  Infants of women with renal disease tend to have intrauterine growth restriction from lessened placental perfusion.  Women may develop severe anemia because their diseased kidneys do not produce erythropoietin  Many women with renal disease have elevated blood pressure.  Women with kidney disease who normally have an elevated serum creatinine level more than 2.0 mg/dl may be advised not to undertake a pregnancy or the increased strain on already damaged kidneys could lead to kidney failure  Women with kidney transplants should be considered individually to determine whether they will be able to carry a pregnancy to term before a pregnancy is initiated.  Women with severe renal disease may require dialysis to aid kidney function during pregnancy. This is associated with a risk of preterm labor because progesterone is removed with the dialysis. To prevent this complication Progesterone IM may be administered before dialysis D. RESPIRATORY DISORDERS AND PREGNANCY  Chronic respiratory conditions may worsen in pregnancy because the rising uterus compresses lung space.  Any respiratory disorder can pose serious hazards to the fetus if allowed to progress to the point where the mother’s oxygen-carbon dioxide exchange is altered. Nursing Diagnosis: Risk for ineffective breathing pattern 1. THE WOMAN WITH ACUTE NASOPHARYNGITIS
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39  Acute nasopharyngitis (common colds) tends to be more severe during pregnancy because during this period estrogen stimulation normally causes some degree of nasal congestion.

2. THE WOMAN WITH INFLUENZA  Influenza is caused by a virus that is identified as Type A, B or C.  Type A causes most infections. Assessment : 1. Disease spreads in epidemic form 2. High fever 3. Extreme prostration 4. Aching pains in the back and extremities 5. A sore, raw throat.    Correlate with preterm labor and abortion Treated with antipyretic to control fever and perhaps a prophylactic antibiotic to prevent a secondary infection such as pneumonia. Exposure to influenza while in utero was associated with the development of schizophrenia in later life. Later studies do not show this association.

3. THE WOMAN WITH PNEUMONIA  Pneumonia is the bacterial or viral invasion of lung tissue.  Pneumonia poses a serious complication of pregnancy because fluid collects in alveolar spaces causing limited oxygen-carbon dioxide exchange in the lungs.  After the invasion, an acute inflammatory response occurs with exudates of red blood cells, fibrin, and polymorphonuclear leukocytes into the alveoli. This process confines the bacteria or virus within segments of the lobes of the lungs. Treatment : 1. Appropriate antibiotic 2. Oxygen administration 3. Ventilation support maybe necessary in severe cases.  There is tendency of preterm labor late in pregnancy

4. THE WOMAN WITH ASTHMA  Asthma is paroxysmal wheezing and dyspnea in response to an inhaled allergen.  With inhalation of allergen, there is an immediate histamine release from IgE immunoglobulin interaction. This results in constriction of the bronchial smooth muscle, marked mucosal swelling, and the production of thick bronchial secretions. These 3 processes reduce the lumen of air passages markedly. 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. 5. THE WOMAN WITH TUBERCULOSIS  With TB, lung tissue is invaded by mycobacterium tuberculosis, an acid-fast bacillus 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. 6. THE WOMAN WITH CYSTIC FIBROSIS  Cystic Fibrosis is a recessively inherited disease in which there is generalized dysfunction of the exocrine glands. This dysfunction leads to mucus secretions, particularly in the pancreas and lungs, so thick that normal secretion is blocked.  Women may have lessened fertility from inability of sperm to migrate through viscid cervical mucus. Symptoms : 1. Chronic respiratory 2. Over inflation of lungs from the thickened mucus 3. Inability to digest fat and protein because the pancreas cannot release amylase. 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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40 Treatment : 1. Pancrelipase – to supplement pancreatic enzymes 2. Bronchodilator 3. Antibiotic 4. Postural drainage daily – to reduce a buildup of lung secretions 5. Iron supplement – because panrelipase interferes with iron absorption 6. Monitor for serum glucose to detect development of gestational diabetes  It is not usually recommended for postpartum women with cystic fibrosis to breastfeed because their breast milk contains more fatty acid.

E. RHEUMATIC DISORDERS AND PREGNANCY Nursing Diagnosis : Pain related to rheumatic disorder during pregnancy 1. THE WOMAN WITH JUVENILE RHEUMATOID ARTHRITIS  Juvenile Rheumatoid Arthritis is a disease of connective tissue with joint inflammation and contracture, probably the result of an autoimmune response. 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. 2. THE WOMAN WITH SYSTEMIC LUPUS ERYTHEMATOSUS  SLE is a multisystem chronic disease of connective tissue that can occur in women of childbearing age.  Highest incidence is in women ages 20 to 40 years  Widespread degeneration of connective tissue occurs with the onset of illness Assessment : 1. Marked skin change is erythematous “butterfly-shaped” rash on the face.  Most serious of the kidney changes are fibrin deposits that plug and block the glomeruli, leading to necrosis and scarring.  The thickening of collagen tissue in the blood vessels causes vessel obstruction, blood flow to the vital organs become compromised and to the fetus if blood flow to the placenta is obstructed Treatment : 1. Corticosteroid, NSAID’s and salicylate therapy to reduce symptoms of joint pain and inflammation. Complication : 1. Acute nephritis with glomeruli destruction 2. Higher incidence of abortion and preterm births. 3. Infants may be born with lupuslike rash, anemia and thrombocytopenia. 4. Congenital heart block can occur in the NB.      With nephritis, BP will rise. Patient will develop hematuria and decreased 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.

F. GASTROINTESTINAL DISORDERS AND PREGNANCY  Minor gastrointestinal disorders are common in pregnancy (nausea, heartburn, constipation). Acute abdominal pain or vomiting are causes for concern  Women who have colostomies can complete pregnancy without difficulties. Nursing Diagnosis: Risk for altered nutrition, less than body requirements 1. THE WOMAN WITH APPENDICITIS  Appendicitis is inflammation of the appendix. Assessment : 1. Nausea 2. Generalized abdominal discomfort 3. Vomiting 4.Sharp, peristaltic, lower right quadrant pain 5. Leukocytosis 6. Elevated temperature 7. Ketones in the urine  In the pregnant woman, the appendix is often displaced so far upward in the 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 2. THE WOMAN WITH A HIATAL HERNIA  Hiatal Hernia is a condition in which a portion of the stomach extends and protrudes up through the diaphragm into the chest cavity. Symptoms : 1. Heartburn 2. Gastric regurgitation 3. Indigestion 4. Dysphagia 5. Possible weight loss due to inability to eat 6. Hematemesis in extreme cases Dx : Diagnosed by direct endoscopy or sonogram Therapeutic Management :
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

41 1. Antacids to relieve pain 2. Elevate head when sleeping 3. THE WOMAN WITH CHOLECYSTITIS AND CHOLELITHIASIS Etiology : 1. Associated with women older than 40 years 2. Obesity 3. Multiparity 4. High fat diet 5. Gallstones are formed from cholesterol Symptoms : 1. Aching and pressure in the right epigastrium 2. Jaundice 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 4. THE WOMAN WITH VIRAL HEPATITIS  Hepatitis is liver disease that may occur from invasion of the A, B, C, or D virus.  Hepatitis A is spread mainly by contact with another person or by ingestion of fecally contaminated water or shellfish  Incubation period 2 to 6 weeks.  Prophylactic gamma globulin to prevent the disease after exposure.  Hepatitis B (serum hepatitis) is spread by transfusion of contaminated blood or blood products; it can be spread by semen or vaginal secretions and thus considered STD.  Incubation period 6 weeks to 6 months  Hepatitis B vaccine may be administered to those who are at high risk Assessment : 1.Nausea, vomiting 2. Liver is tender to palpation 3. Dark yellow urine 4. Light colored stools 5. Jaundice 6. On physical examination, liver is enlarged 7. Elevated bilirubin 8. Increased liver enzymes Dx : Liver Biopsy 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. 5. THE WOMAN WITH INFLAMMATORY BOWEL DISEASE  Crohn’s Disease (inflammation of the terminal ileus) and ulcerative colitis (inflammation of the distal colon) Etiology : 1. Occurs most often in young adults Between ages 12 and 30 years 2. Cause is unknown but an autoimmune process may be responsible Symptoms : 1. Shallow ulcers 2. Chronic diarrhea 3. weight loss 4. Occult blood in stool 5.Nausea and vomiting 6. Obstruction and fistula formation with peritonitis can occur in extreme 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. G. NEUROLOGIC DISORDERS AND PREGNANCY  Any neurologic disease with symptoms of seizures must be carefully managed during pregnancy because anoxia caused by severe seizures could deprive the fetus with oxygen, with serious outcomes. Nursing Diagnosis : Risk for Injury (maternal) 1. THE WOMAN WITH A SEIZURE DISORDER Etiology : 1. Head trauma
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42 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. Nursing Diagnosis : Risk for altered placental perfusion 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 Nursing Diagnosis: Risk for altered parenting   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.

2. THE WOMAN WITH MYASTHENIA GRAVIS  Myasthenia Gravis is an autoimmune disorder characterized by the presence of an IgG antibody against acetylcholine receptors in striated muscle.  It produces sporadic but progressive weakness and abnormal fatigue in striated (skeletal) muscles. This weakness and fatigue are exacerbated by exercise and repeated movement but improved by anticholinesterase drugs. Usually, myasthenia gravis affects muscles innervated by the cranial nerves (face, lips, tongue, neck, and throat), but it can affect any muscle group.  Other common signs of myasthenia gravis include weak eye closure, ptosis and diplopia, blank masklike facial expression, difficulty chewing and swallowing, a hanging jaw, bobbing motion of the head, and symptoms of respiratory failure if respiratory muscles are involved 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. 3. THE WOMAN WITH MULTIPLE SCLEROSIS  Nerve fibers become demyelinated and lose function. Pregnant women with this disorder grow increasingly fatigued as pregnancy progresses.  Other signs and symptoms include visual disturbances such as optic neuritis, diplopia and blurred vision, sensory impairment such as paresthesia, urinary disturbances such as incontinence, frequency, urgency, and infections, emotional lability such as mood swings, irritability and euphoria and other associated signs like poorly articulated speech and dysphagia 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

H. MUSCULOSKELETAL DISORDERS AND PREGNANCY 1. THE WOMAN WITH SCOLIOSIS  Scoliosis is lateral curvature of the spine Etiology : 1. Often in women approximately 12 years of age Complications : 1. Cosmetic deformity 2. Because of chest compression, interferes with respiration and heart action 3. Pelvic distortion 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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43 1. THE WOMAN WITH LEFT-SIDED HEART FAILURE  Occurs with conditions such as mitral stenosis, mitral insufficiency and aortic coarctation.  Occurs when the left ventricle is unable to move forward the volume of blood received by the left atrium from the pulmonary circulation 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 2. THE WOMAN WITH RIGHT-SIDED FAILURE  Congenital heart defects such as pulmonary valve stenosis and atrial and ventricular septal defects may result in right-sided heart failure.  Occurs when the output of the right ventricle is less than the blood volume the heart receives at the right atrium from the vena cava or venous circulation. Back pressure from this results in congestion of the systemic venous circulation and decreases cardiac output to the lungs.  Blood pressure falls in the aorta because less blood is reaching it ;  Pressure is high in the vena cava  Both jugular venous distention and increased portal circulation occur.  Both the liver and spleen become distended  Distention of abdominal vessels can lead to exudates of fluid from the vessels into the peritoneal cavity (ascites). Fluid moves from the systemic circulation into interstitial spaces (peripheral edema).  Liver enlargement can cause extreme dyspnea and pain because it will put extreme pressure on the diaphragm.  Eisenmenger’s syndrome – congenital anomaly most apt to cause right-sided failure (A right-to-left atrial or ventricular septal defect with accompanying pulmonary stenosis). They need oxygen administration and frequent arterial gases to ensure fetal growth. 3. THE WOMAN WITH PERIPARTAL HEART DISEASE 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 Assessment Of The Woman With Cardiac Disease : 1.Fatigue 2. Cough 3. Increased respiratory rate 4. tachycardia 5. Poor fetal heart tone variability from poor tissue perfusion 6. Decreased amniotic fluid from intrauterine growth retardation 7. Edema from poor venous return 8. Irregular pulse 9. Chest pain on exertion Diagnostic Assessment : Chest x-ray, ECG Fetal Assessment : 1. Low birth weights 2. Severe fetal distress Nursing Diagnosis : Knowledge deficit regarding the effects of maternal cardiovascular disease Nursing Interventions : 1. Promote rest 2. Promote healthy nutrition 3. Educate regarding medication 4. Educate regarding avoidance of Infection 4. THE WOMAN WITH AN ARTIFICIAL VALVE PROSTHESIS  Many women with valve prosthesis take oral anticoagulants to prevent formation of blood clots at valve site. However, these medications increase the risk of congenital anomalies in infants  Women are placed on heparin therapy before becoming pregnant  Observe for signs of premature separation of the placenta during pregnancy and labor because anticoagulant in the mother may cause placental dislodgement. 5. THE WOMAN WITH CHRONIC HYPERTENSIVE VASCULAR DISEASE  Women with chronic hypertensive vascular disease come into pregnancy with elevated BP. This kind of HPN is usually associated with arteriosclerosis or renal disease  Fetal well-being is compromised by poor placental perfusion during pregnancy  Management is similar with PIH 6. THE WOMAN WITH VENOUS THROMBOEMBOLIC DISEASE  Incidence increases during pregnancy due to acombination of stasis of blood in the lower extremities from uterine pressure and hypercoagulability (effect of increased estrogen) Signs/symptoms : 1. Chest pain
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44 2. Sudden onset of dyspnea 3. Cough with hemoptysis 4. Tachycardia or missed beats 5. Severe dizziness or fainting from lowered blood pressure Therapeutic Management : 1. Avoid use of constrictive knee-high stockings, 2. Do not cross legs 3. Bed rest 4. Heparin IV administration J. ENDOCRINE DISORDERS AND PREGNANCY 1. THE WOMAN WITH A THYROID DYSFUNCTION  Thyroid gland enlarges slightly due to increased vascularity, as a normal effect of pregnancy Nursing Diagnosis: Risk for maternal and fetal injury A. THE WOMAN WITH HYPOTHYROIDISM  A rare condition in pregnancy because women with symptoms of untreated hypothyroidism are anovulatory and often unable to conceive Signs/symptoms : 1. Easy fatigability 2. Obese 3. dry skin 4. Little tolerance for cold 5. Extreme nausea and vomiting 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 C. THE WOMAN WITH HYPERTHYROIDISM

Symptoms : 1. Rapid heart rate 2. Exophthalmos 3. Heat Intolerance 4. Nervousness 5. Heart palpitation 6. Weight loss  If undiagnosed, woman may develop heart failure during pregnancy because her 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. 2. THE WOMAN WITH DIABETES MELLITUS  DM is an endocrine disorder in which the pancreas is unable to produce adequate insulin to regulate body glucose Pathophysiology :  The pancreas has both endocrine and exocrine types of tissue. The Islets of 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.

3. THE WOMAN WITH GESTATIONAL DIABETES  Pregnant woman becomes diabetic usually at the midpoint of pregnancy when insulin resistance become noticeable – Gestational Diabetes Mellitus Risk Factors for gestational diabetes : 1. Obesity 2. Age over 30 years 3. History of large babies 4. History of unexplained fetal loss 5. History of congenital anomalies in previous pregnancies 6. History of unexplained perinatal loss 7. Family history of diabetes
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


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 K. MENTAL ILLNESS AND PREGNANCY  Mental illness may precede or occur with pregnancy. Depression is the most common mental illness seen.  Lithium, a mainstay of therapy for bipolar disorders is a known teratogen. L. TRAUMA AND PREGNANCY  Trauma occurs at high incidence in childbearing years because for this age group, automobile accidents, homicide, and suicide are among the three leading causes of death.  High incidence occurs during the last trimester due to clumsiness, fainting and hyperventilation.  Orthopedic injuries occur because the pregnant woman’s sense of balance is altered PHYSIOLOGIC CHANGES IN PREGNANCY THAT AFFECT TRAUMA CARE  After a traumatic injury, a woman’s body will maintain her own homeostasis at the expense of the fetus.  The woman’s total plasma volume increases during pregnancy at term. This increase serves as a safeguard tot the woman if trauma with bleeding should occur.  Fluid replacement volume would be high in case of injury because pregnant woman needs more fluid to restore fully her circulatory volume.  Peripheral venous pressure in pregnant woman is unchanged, it tends to be higher in the lower extremities because of the compression of the vena cava and back pressure. This causes lacerations of the legs or perineum to bleed much more profusely than usual.  During pregnancy, leucocyte count rises so it is difficult to use this determination as a sign of infection after an open wound.  Serum albumin level decreases during pregnancy, making the large loss that normally occurs with burns a more serious than usual response.  Serum liver enzyme levels remain the same during pregnancy, so if these are elevated during trauma, liver trauma can be detected.  Bleeding into the abdominal cavity with an abdominal injury is apt to be forceful and extreme because of the increased pressure in the pelvic vessels.  Paracentesis is dangerous because the bowel, dislocated from its usual position, can be easily punctured.  Culdocentesis may be done  Peritoneal lavage may reveal bleeding or bladder rupture best.  Bladder of pregnant woman is susceptible to rupture because it is the most anterior organ and is elevated abnormally.  After abdominal trauma, an indwelling bladder catheter is inserted to assess for blood in the urine.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

46 Emotional Considerations :  A feeling of guilt lowers self-esteem and increases the level of stress.  People under stress do not process well and so may not perceive correctly the information given to them. Initial Assessments After Trauma During Pregnancy > With multiple trauma, a nasogastric tube is usually passed to empty the stomach. A foley catheter is inserted to assess for urine output and to rule out ruptured bladder.  To prevent supine hypotension syndrome, be sure the woman does not lie supine for an examination. If it is necessary for her to lie supine, manually displace the uterus from the vena cava by placing rolled towels or a blanket under her right side to tip her body approximately 15 o to the side Nursing Diagnosis : 1. Fear related to threat of injury to the fetus 2. Risk for fetal injury 3. Altered tissue perfusion r/t to severed artery 4. Ineffective breathing pattern related to lung lacerated by gunshot wound 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. Nursing Diagnosis : Risk for altered tissue perfusion OPEN WOUNDS: 1. LACERATIONS  Bleeding should be halted by pressure on the edge of the laceration 2. PUNCTURE WOUNDS  If the woman has had tetanus immunization within the past 10 years, tetanus 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

47 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 oxygencarbon 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.

    

THE BATTERED WOMAN  Abused women may be pregnant because they were unable to resist sexual advances from their abusive partner.  Beatings may increase during pregnancy because stress is often a “trigger” to beatings, and pregnancy can increase the stress. 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. Tasks the woman could accomplish to meet goals of care : 1. Client carries phone number for home for abused women with her. 2. Client and abusive partner continue to attend counseling sessions. 3. Client states she has filed restraining order against abusive partner 4. Client states she feels secure living at safe house

 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

  Vaginal bleeding is a deviation from the normal that may occur at anytime during the pregnancy Primary causes of bleeding during pregnancy

1. BLEEDING AND THE DEVELOPMENT OF SHOCK  A woman with any degree of bleeding needs to be evaluated for hypovolemic shock. Process of shock due to blood loss Therapeutic Management Assessment : 1. Confusion 2. Pallor 3. Increased Pulse 4. Tachypnea 5. Decreased BP 6. Decreased cardiac output 7. Fetal bradycardia 8. Peripheral vasoconstriction 9. Decreased urinary output 10. Cold extremities Nursing Diagnosis : Risk for fluid volume deficit CONDITIONS ASSOCIATED WITH FIRST TRIMESTER BLEEDING 1. ABORTION A. SPONTANEOUS ABORTION  Abortion-any interruption of a pregnancy before the fetus is viable. A non-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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

48 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. C. IMMINENT (INEVITABLE) ABORTION  A threatened abortion becomes an imminent or inevitable abortion if uterine contractions and cervical dilatation occur. Symptoms: 1. Cramping or uterine contractions Dx: UTZ Tx: 1. D & C – to ensure all products of conception are removed. 2. Suction Curettage 3. Any tissue fragments should be saved to be examined for possible 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. Cx: DIC (Disseminated Intravascular Coagulation) G.  RECURRENT ABORTION 3 spontaneous abortions that occurred in same gestational age.

Possible Causes: 1. defective spermatozoa or ova 2.endocrine factors 3.deviations of uterus 4.infection 5.autoimmune disorders

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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

49 2. Septicemia 3. Kidney Failure 4. Infertility Laboratories: 1. CBC, Serum Electrolytes, 2. BT, Xmatching 3. Cultures of vaginal, cervical & urine specimen Treatment: 1. Hydration 2. Antibiotic 3. D&C 4. TT or HTIG for Tetanus    A CVP or pulmonary artery catheter may be inserted to monitor left atrial 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 Signs & Symptoms: a. Bleeding – growing zygote ruptures the site of implantation which results to tearing & destruction of blood vessels which results to bleeding b. Sharp, stabbing pain c. Vaginal spotting – placental detachment, uterine deciduas sloughs thus bleeding occurs d. Severe shock – evidenced by rapid pulse, rapid respirations and falling blood pressure e. Leucocytosis due to trauma f. Rigid abdomen due to peritoneal irritation g. positive Cullen’s Sign h. Pain in the shoulders from blood in the peritoneal cavity causing irritation to the phrenic nerve. i. On vaginal examination, a tender mass is usually palpable in Douglas’ cul-de-sac j. Extensive or dull vaginal and abdominal pain k. Excruciating pain on the cervix during pelvic examination 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

CONDITIONS ASSOCIATED WITH SECOND TRIMESTER BLEEDING 1. GESTATIONAL TROPHOBLASTIC DISEASE (HYDATIDIFORM MOLE) > Proliferation and degeneration of the trophoblastic villi. As the cells degenerate, they become filled with fluid, appearing as fluid-filled, grape-sized vesicles. Embryo dies.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


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. CONDITIONS ASSOCIATED WITH THIRD-TRIMESTER BLEEDING 1. PLACENTA PREVIA: Low implantation of the placenta. Occurs in 4 Degrees: (1) Implantation in the lower rather than in the upper portion of the uterus (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: Immediate Care Measures: 1. Place woman immediately on bed rest in a side-lying position to ensure an adequate blood supply to the woman and fetus. 2. Determine vaginal blood loss 3. Never attempt a pelvic or rectal examination with painless bleeding late in pregnancy because any agitation of the cervix may initiate a massive hemorrhage. 3. Obtain baseline vital signs to determine whether symptoms of shock are present 4. Monitor BP every 5 to 15 minutes 5. IVF therapy using a large gauge catheter 6. Monitor urine output frequently as an indicator of blood volume adequacy 7. Monitor fetal heart sounds and uterine contraction 8. Hgb, Hct. PT, PTT, fibrinogen, platelet count, type and xmatch or antibody screen should be assessed to establish baselines, detect a possible clotting disorder 9. Prepare BT if necessary 10. Prepare oxygen equipment in case of fetal distress. Complications: 1. Postpartal Hemorrhage – because the placental site is in the lower uterine 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.

2. PREMATURE SEPARATION OF THE PLACENTA (ABRUPTIO PLACENTAE) Predisposing Factors: 1. High parity 2. Chronic hypertensive disease
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

51 3. Hypertension of pregnancy 4. Direct trauma 5. Vasoconstriction from cocaine use 6. Cigarette smoking Assessment: 1. Sharp, stabbing pain high in the uterine fundus 2. Tenderness on uterine palpation 3. Heavy bleeding 4. Hard, board-like uterus in cases of couvelaire uterus (Blood infiltrates 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 Labor That Cannot Be Halted > Labor is too far advanced that it cannot be halted. 1. The rupturing of membranes is a point of no return in stopping or delaying labor because of the increased risk of infection. 2. If the cervix is more than 50% effaced and 3-4 cm dilated Management: 1. If the fetus is very immature, a CS maybe planned to reduce pressure on the 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. DISSEMINATED INTRAVASCULAR COAGULATION (DIC)  Acquired disorder of blood clotting.  Also known as consumptive coagulopathy  A diffuse, pathologic form of clotting, secondary to underlying disease/pathology  Occurs in critical maternity problems such as abruptio placenta, intrauterine fetal death, amniotic fluid embolism, pre-eclampsia/eclampsia, hydatidiform mole and hemorrhagic shock 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 causative or precipitating mechanism injury to vessel endothelium or blood cell injury to tissue with tissue factor or thromboplastin release
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


intrinsic production of microthrombi consumption of clotting factors thrombosis continues


activation of fibrinolytic system (lysis of clots) digestion of fibrin clots release fibrin split or degradation products


vascular occlusion tissue or organ ischemia or infarction hemorrhage DIC

shock and circulatory collapse

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 PRETERM RUPTURE OF MEMBRANES (PROM)  A spontaneous rupture of fetal membranes with loss of amniotic fluid before onset of regular contractions that results in progressive cervical dilation. 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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

53 Changes associated with PIH: Vasospasm

Effects on the vascular system

Effects on the renal system Reduced glomerular filtration rate; Increased glomerular membrane permeability

Effects on the interstitial Tissues

Vasoconstriction Impaired organ perfusion Increased serum blood urea nitrogen And creatinine levels Oliguria and proteinuria

Fluid diffusion from vascular space Into interstitial space



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 Medical Management: Magnesium Sulfate Magnesium sulfate acts upon the myoneural junction, diminishing neuromuscular transmission It promotes maternal vasodilation, better tissue perfusion, and has anticonvulsant effect. Keep in mind that for magnesium to be effective as an anticonvulsant, serum magnesium levels should be between 5 and 8 mg/dl. Levels above 8 mg/dl indicate toxicity and place the patient at risk for respiratory depression, cardiac arrhythmias, and cardiac arrest. Monitor client’s respirations, blood pressure, and reflexes, as well as urinary output frequently. Assess the client’s patellar reflex. If the client has received epidural anesthesia, test the biceps or triceps reflex. Diminished or hypoactive reflexes suggest magnesium toxicity. Assess for ankle clonus (alternating contractions and relaxations of the muscles) by rapidly dorsiflexing the client’s ankle three times, then removing your hand and observing the foot’s movement. If no further motion is noted, ankle clonus is absent; if the foot continues to move involuntarily, clonus is present. Moderate (3-5 movements) or severe (6 or more movements) suggests possible magnesium toxicity. Antidote for excess levels of magnesium sulfate is calcium gluconate or calcium chloride Interventions promote complete bedrest, left side lying carefully monitor maternal/fetal vital signs monitor intake and output take daily weights institute seizure precautions ( restrict visitors, minimize all stimuli, monitor for hyperreflexia, administer sedatives as ordered) instruct client about appropriate diet continue monitoring for up to 48 hours post delivery
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

54 administer medications as ordered, vasodilator of choice is usually hydralazine (apresoline)

ECLAMPSIA  The most severe classification of hypertension of pregnancy Assessment: increased hypertension precedes convulsion followed by hypotension, seizure may recur coma may ensue labor may begin, putting fetus in great jeopardy Complications: 1. Cerebral hemorrhage 2. Circulatory collapse 3. Renal failure Interventions minimize all stimuli monitor vital signs have airway, oxygen, and suction equipment available administer medications as ordered prepare for caesarian section when seizures stabilize continue observations 48 hours post delivery HELLP SYNDROME  is a category of PIH that involves changes in blood components and liver 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

55 4. Fetus may suffer from lack of oxygen, fluid and nutrients 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 ISOIMMUNIZATION (RH INCOMPATIBILITY)  Occurs when an Rh (-) mother is carrying a fetus with an Rh (+) blood 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 Diagnosis: Powerlessness related to fetal death Nursing Intervention: A. Healthy process of grieving 1. Give woman opportunities to express feelings 2. Encourage support person to stay with the woman during labor 3. Present the baby if parents wished to in a manner like she were a well 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

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

56   A neonate is considered to be high risk if he has an increased chance of dying during or shortly after birth or has a congenital or perinatal problem that requires prompt intervention Being able to predict that an infant is high risk allows for advanced 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.

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

57 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). HEAD TO TOE ASSESSMENT 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.

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.

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 812 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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


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.

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.

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.

Mouth and Pharynx.
The neonate’s mouth usually has scant saliva and pink lips. Inspect the mouth for its existing structures. The palate is usually narrow and highly arched. Inspect the hard and soft palates for clefts. Epstein pearls (pin-head sized, white or yellow, rounded elevations) may be 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.

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.

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.

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.

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.

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.

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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

59 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.
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.

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.

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 Eight (8) Priorities In First Days Of Life : 1. Initiating and maintaining respirations  Resuscitation  Establishing an airway  Expanding the lungs  Drug Therapy  Maintaining effective ventilation 2. Establishing intrauterine circulation 3. Fluid and Electrolyte Balance 4. Thermometer Regulation  Radiant heat sources  Isolettes  Kangaroo Care 5. Preventing Infection 6. Establishing Parent-Infant Bonding  Following High-Risk Infants At Home  High-Risk Infants and Child Abuse
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60  Providing for Growth and Development 7. Intake of adequate nourishment 8. Developmental care or care that balances physiologic needs and stimulation for mental development 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 THE SMALL-FOR-GESTATIONAL-AGE INFANT  Birth weight is below the 10th percentile on an intrauterine growth curve for that age (based on a postnatal growth chart).  Infant may be born preterm, post term or term.  They are small for their age because they have experienced intrauterine growth restriction (IUGR) or failed to grow at the expected rate in utero Causes: 1. Lack of adequate nutrition 2. Pregnant adolescents 3. Placental anomaly  Placenta is unable to obtain sufficient nutrients from the uterine arteries or it is inefficient at transporting nutrients to the fetus

4. Placental damage 5. Women with systemic diseases that decrease blood flow to the placenta 6. Smoking or use of narcotics 7. Infants with intrauterine infections such as rubella or toxoplasmosis 8. Infants with chromosomal abnormalities Assessment: A. Prenatal Assessment 1. Fundal height during pregnancy is less than what is expected. Dx Procedures: 1. Sonogram 2. Biophysical profile including nonstress test, placental grading , UTZ add 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  In contrast, the child may have: 1. Better developed neurologic responses, sole creases, and ear cartilage 2. Skull may be firmer 3. Unusually active and alert for that weight that could be attributed to prolonged prenatal hypoxia  SGA infant needs careful assessment for possible congenital anomalies

Laboratory Findings: 1. High hematocrit level at birth 2. Increase in total number of red blood cells 3. Decrease serum glucose Nursing Diagnosis: Ineffective breathing pattern related to underdeveloped body system  Birth asphyxia is a common problem for SGA because they have underdeveloped 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 THE LARGE-FOR-GESTATIONAL-AGE INFANT  An infant is large for gestational age (Macrosomia) if the birth weight is above the 90% percentile on an intrauterine growth chart for that gestational age Causes: 1. Mothers with diabetes mellitus 2. Multiparous women 3. Transposition of the great vessels 4. Beckwith’s Syndrome, a rare condition characterized by overgrowth 5. Congenital anomalies such as omphalocele Assessment:
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61      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 Specific Criteria For Initial Or Continuing Assessment 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 Nursing Diagnosis: Ineffective breathing pattern r/t possible birth trauma Outcome Identification: Newborn will initiate and maintain respirations at birth Outcome Evaluation: NB initiates breathing at birth; maintains normal NB respiratory rate at 30 to 60 breaths per minute     SGA infants have difficulty establishing respirations because of birth trauma Increase intracranial pressure from birth may lead to pressure on the respiratory center, in turn, causes a decrease in respiratory function A diaphragmatic paralysis may occur due to cervical nerve trauma as the head is bent laterally to allow for birth of the large shoulders. This prevents active lung motion on the affected side. During CS, transient fluid can remain in the lungs and interfere with effective gas exchange

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   As a rule, the LGA infants need to be breastfeed immediately to prevent hypoglycemia Infant may need supplemental feeding after breastfeeding to supply enough fluid and glucose for the larger than normal size for the first few days.

Nursing Diagnosis: Risk for altered parenting 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      Educate parents regarding status of infant Allow mother to express resentments or fear she may feel toward the infant A LGA infant needs the same developmental care as normal infants do. Infant stimulation are important for infant’s development Encourage parents to treat their baby as a fragile NB who needs warm nurturing Remind parents that infant’s birth weight is not a correlation of the child’s projected adult size.

THE PRE TERM INFANT         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

DIFFERENTIATING CHARACTERISTICS OF SGA INFANTS AND PRETERM INFANTS: 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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62 13.Obstetric complications such as PROM or premature separation of placenta 14. Early induction of labor 15.Elective CS 16.Chronic Diseases – DM, renal, cardiovascular, respiratory 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 Nursing Diagnosis: Impaired gas exchange related to immature pulmonary functioning  Preterm infants have difficulty initiating respirations at birth because the pulmonary capillary bed is immature  A fetus usually turns to a vertex position late in pregnancy, the preterm infant may still be in a breech position at birth 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 Nursing Diagnosis: Risk for fluid volume deficit  Preterm babies have a high insensible loss due to the large body surface as compared with total body weight.  The infant is unable to concentrate urine well because of immature kidney function and thus excretes a high proportion of fluid from the body.  It is important that the preterm baby receive up to 160 to 200 ml of fluid/kg of body weight daily 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 Diagnosis: Ineffective thermoregulation r/t immaturity  A preterm baby has difficulty maintaining body temperature because of the large surface area per pound of body weight  Rapid cooling from evaporation occurs due to extended position  The preterm infant has little subcutaneous fat for insulation and because of poor muscular development the child does not move actively to produce body heat.  The preterm infant has limited amount of brown fat, the special tissue present in NB’s to maintain body temperature  Because of an immature central nervous system and hypothalamic control, the child is unable to sweat thereby reducing body temperature and unable to shiver, a useful mechanism to increase body temperature Nursing Management: 1.The infant must be kept under a radiant heat warmer Nursing Diagnosis: Risk for infection  The skin of preterm infant is easily traumatized therefore has less resistance to infection  Preterm infant has lowered resistance to infection
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63  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 THE POST TERM INFANT  Infant born after the 42nd week of a pregnancy  Infant who stays in utero past week 42 of pregnancy is at special risk because a placenta appears to only function effectively for 40 weeks. Fetus may die or develop post term syndrome 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. Stages of Fetal Dysmaturity Syndrome 1. Stage 1 – Chronic Placental Insufficiency  Dry, cracked, peeling, loose, and wrinkled skin  Malnourished appearance  Open-eyed and alert 2. Stage 2 – Acute Placental Insufficiency  Dry, cracked, peeling, loose, and wrinkled skin  Malnourished appearance  Meconium staining  Perinatal depression 3. Stage 3 – Subacute Placental Insufficiency  Dry, cracked, peeling, loose, and wrinkled skin  Malnourished appearance  Meconium staining  Green staining of skin, nails, cord, and placental membrane  A higher risk of intrapartum and neonatal death -The newborn is at increased risk for developing complications related to compromised uteroplacental perfusion and hypoxia (eg. Meconium aspiration syndrome [MAS]) - Chronic intrauterine hypoxia causes increased fetal erythropoietin and red blood cell production resulting in polycythemia - Post-term infants are susceptible to hypoglycemia because of the rapid use of glycogen stores 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

1. RESPIRATORY DISTRESS SYNDROME  RDS most often occurs in preterm infants, infants of diabetic mothers, infants born by CS, those who have decreased blood perfusion of the lungs Pathologic Feature: A hyaline-like (fibrous) membrane comprised of products formed from an exudates of the infant’s blood that lines the terminal bronchioles, alveolar ducts, and alveoli. This membrane prevents exchange of oxygen and carbon dioxide at the alveolar-capillary membrane. 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 oxygencarbon 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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64 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: 1. Preventing preterm labor by using tocolytic agents 2. Administer 2 injections of a glucocorticosteroid to the mother at 12 and 24 hours before birth. Steroids quickens the formation of lecithin production pathways 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 2. TRANSIENT TACHYPNEA OF THE NEWBORN Signs and Symptoms: 1. Mild retractions but not marked cyanosis 2. Mild hypoxia and hypercapnia 3. Feeding is difficult because infant cannot suck and breathe this rapidly at the same time 4. Chest x-ray reveals fluid in the lungs  Transient tachypnea results from slow absorption of lung fluid

Intervention: 1. Close observation is the priority 2. Oxygen administration 3. MECONIUM ASPIRATION SYNDROME Meconium is a thick, sticky, greenish black substance that constitutes the neonate’s first feces. It is present in the bowels of the fetus as early as 10 weeks gestation. Meconium aspiration syndrome results when the neonate inhales meconium that is mixed with amniotic fluid. It typically occurs while the neonate is in utero or with the neonate’s first breath. The meconium partially or completely blocks the neonate’s airways so that air becomes trapped during exhalation. Also, the meconium irritates the neonate’s airways, making breathing difficult. The severity of meconium aspiration syndrome depends on the amount of meconium aspirated and the consistency of the meconium. Thicker meconium generally causes more damage. Neonates with meconium aspiration syndrome increase their respiratory efforts to create greater negative intrathoracis pressures and improve airflow to the lungs. Hyperinflation, hypoxemia, and academia cause increased peripheral vascular resistance. Right to left shunting often follows. 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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65    A pause in respirations longer than 20 seconds with accompanying bradycardia Many preterm infants have periods of apnea as a result of fatigue or the immaturity of their respiratory functions Babies with secondary stresses, such as infection, hyperbilirubinemia, hypoglycemia or hypothermia tend to have high incidence of apnea

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 5. SUDDEN INFANT DEATH SYNDROME (SIDS)  SID is the sudden unexplained death in infancy 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 Apparent Life-Threatening Event (ALTE)  Infants discovered cyanotic and limp in their beds but have survived after mouth-to-mouth resuscitation by parents 6. PERIVENTRICULAR LEUCOMALACIA (PVL)  PVL is abnormal formation of the white matter of the brain  Occurs most frequently in preterm infants who experience cerebral ischemia  Ischemic episode interferes with circulation to a portion of the brain. Phagocytes and macrophages invade the area to clear away necrotic tissue, what is left is an area in the white matter of the brain that is revealed on sonogram as a hollow space.  No therapy is identified.  Infants may die from the original insult; thay may be left with long term effects such as learning disabilities. 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 perceptualmotor 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

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

66  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.

8. HEMOLYTIC DISEASE OF THE NEWBORN (Erythroblastosis Fetalis) A. General Information characterized by RBC destruction in the newborn, with resultant anemia and hyperbilirubinemia possibly caused by Rh or ABO incompatibility between the mother and the fetus (antigen-antibody reaction) mechanisms of Rh incompatibility sensitization of Rh-negative woman by transfusion of Rh-positive blood sensitization of Rh-negative woman by presence of Rh-positive RBCs from her fetus conceived with Rh-positive man approximately 65% of infants conceived by this combination of parents will be Rh-positive mother is sensitized by passage of fetal Rh-positive RBCs through placenta either during pregnancy (break/leak in the membrane) or at the time of separation of placenta after delivery this stimulates the mother’s immune response system to produce anti-Rh positive antibodies that attack fetal RBCs and cause hemolysis if this sensitization occurs during pregnancy, the fetus is affected in utero; if sensitization occurs at the time of delivery, subsequent pregnancies may be affected. ABO incompatibility same underlying mechanism mother is blood type O; infant A, B, or AB reaction in ABO incompatibility is less severe compared to Rh-incompatibility B. Rh- Incompatibility first pregnancy, mother may become sensitized, baby rarely affected Indirect Coomb’s test (tests for anti-Rh positive antibodies in mother’s circulation) performed during pregnancy at first visit and again at 28 weeks gestation. If indirect Coomb’s test is negative at 28 weeks, a small dose (Mic Rhogam) is given prophylactically to prevent sensitization in the third trimester ( Rhogam may also be given after the 2nd trimester amniocentesis) If positive, levels are titrated to determine extent of maternal sensitization and potential effect on the fetus Direct Coomb’s test is done on cord blood at delivery to determine presence of anti-Rh positive antibodies on fetal RBCs. If both direct and indirect Coomb’s tests are negative (no formation of anti-Rh positive antibodies) and infant is Rh-positive, then Rhnegative mother can be given Rhogam (Rho human immune globulin) to prevent development of anti-positive antibodies as the result of sensitization from present pregnancy In each pregnancy, an Rh-negative mother who carries an Rh-positive fetus can receive Rhogam to protect future pregnancies if the mother has had negative indirect Coomb’s test and the infant has had a negative direct Coomb’s test If the mother has been sensitized (produced anti Rh-positve antibodies), Rhogam is not indicated. She may be given high doses of gamma globulin to help reduce fetal involvement, hoping to interfere with the rapid destruction of fetal RBCs. The fetus may receive a blood transfusion in utero via an injection of RBCs directly into a vessel in the fetal cord or instillation in the fetal abdomen via amniocentesis. After birth, the neonate may receive an axchange transfusion to remove hemolyzed RBCs and replace them with healthy blood cells. Rhogam may be injected (IM in the gluteal area) into unsensitized mother’s system within 72 hours of delivery of Rh-positive infant. C. ABO Incompatibility Reaction less severe than with RH incompatibility First born may be affected because type O mother may have anti-A and anti-B antibodies even before pregnancy Fetal RBCs with A, B, or AB antigens evoke less severe reaction on part of mother, thus fewer anti-A, anti-B, or anti-AB antibodies are produced Clinical manifestations of ABO incompatibility are milder and of shorter duration than those of Rh compatibility D. Assessment Findings jaundice and pallor within the first 24-36 hours anemia and hyperbilirubinemia – due to RBC destruction erythropoiesis enlarged placenta and enlarged fetal liver and spleen – due to the attempt to produce and supply new red blood cells edema and ascites – resulting from fluid shift because the blood in the intravacular space is hypotonic relative to the interstitial * Hydrops fetalis – “fatal edema”, old term for the appearance of a severely involved infant at birth 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

67 9. HEMORRHAGIC DISEASE OF THE NEWBORN  Results from a deficiency of Vit. K  Vit K is essential for the formation of prothrombin by the liver  Babies born to mothers on anticonvulsive medication are at high risk 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 10. TWIN-TO-TWIN TRANSFUSION  A phenomenon that can occur if twins are monozygotic (identical; share the same placenta) and if abnormal arteriovenous shunts occur that direct more blood to one twin than the other  Can be identified through sonogram  One twin is larger than the other 11. NECROTIZING ENTEROCOLITIS A. General Information - an ischemic attack to the intestines resulting in thrombosis and infarction of affected bowel, mucosal ulcerations,, pseudomembrane formation, and inflammation - bacterial actions (E. coli, Klebsiella) complicates the process, producing sepsis - may be precipitated by any event in which blood is shunted away from the intestines to more vital organs like the heart and brain (e.g. fetal distress, low APGAR score, RDS, prematurity, neonatal shock, and asphyxia). - average age of onset is 4 days - now that severely ill infants are surviving, NEC is encountered more frequently - may ultimately cause bowel perforation and death 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

1. BETA-HEMOLYTIC, GROUP B STREPTOCOCCAL INFECTION  Beta-hemolytic, group B streptococcal organism is the major cause of infection in NB infants 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

68 Most common causative organisms include Neisseria gonorrhea or Chlamydia trachomatis N. gonorrhea if left untreated could progress to corneal ulceration and destruction, resulting in opacity of the cornea and severe vision impairment Assessment: 1. Ophthalmia neonatorum is generally bilateral 2. Eye conjunctivae become fiery red, there is thick pus and the eyelids are edematous   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 4. HEPATITIS B VIRUS INFECTION  The hepatitis B virus can be transmitted to the NB through contact with infected vaginal blood at birth  70 to 90% of infected infants become chronic carriers of the virus.  A number of these NB’s will develop liver cancer later in life 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 5. GENERALIZED HERPESVIRUS INFECTION  A herpes simplex virus type 2 (HSV-2) infection can be contracted by a fetus across the placenta if the mother has a primary infection during pregnancy.  Most often, the virus is contracted from the vaginal secretions from the mother who has active herpetic vulvovaginitis at the time of birth 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 6. THE INFANT OF A DIABETIC MOTHER 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 7. THE INFANT OF A DRUG-DEPENDENT MOTHER 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
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008


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 8. THE INFANT WITH FETAL ALCOHOL SYNDROME (FAS) - A cluster of birth defects that are caused by in utero exposure to alcohol referred to as FAS. - Although prenatal alcohol exposure doesn’t always result in FAS, the safe level of alcohol consumption during pregnancy isn’t known. - Alcohol crosses through the placenta and enters fetal blood supply, and it can interfere with the healthy development of the fetus. In fact, birth defects associated with prenatal alcohol exposure can occur in the first 3-8 weeks of pregnancy, before a woman even knows she is pregnant. Variables that affect the extent of damage caused by the fetus by alcohol include the amount of alcohol consumed, the timing of consumption, and the pattern of alcohol use. 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.


1. 2.

Quizzes – pretest and post-test 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.
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

70 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. B. C. D. E. Set 2: A. B. C. D. E. Set 3: A. B. C. D. E. Set 4: following, related) A. B. C. D. E. Set 5: following, related) A. B. C. D. E. Set 6: A. B. C. D. E. Set 7: A. B. Pulmonary embolism ARDS Acute and Chronic Respiratory Failure DKA HHNC Thyrotoxic Crisis Adrenal Crisis Hepatic Coma Acute and Chronic Renal Failure Myocardial Infarction

Right-sided Heart Failure, to include Eisenmenger’s Syndrome Left-Sided heart Failure Pericardial Effusion Cardiac Tamponade Burns (General pathophysio of the not necessarily pregnancy TORCH infections Sickle Cell Anemia Idiopathic Thromocytopenic Purpura Cystic Fibrosis SLE (General pathophysio of the not necessarily pregnancy Juvenile Rheumatoid Arthritis Myasthenia Gravis Multiple Sclerosis Hypothyroidism Hyperthyroidism Abortion (all) Ectopic Pregnancy H. Mole Placenta Previa Abruptio Placenta

C. D. E. Set 8: A. B. C. D. E.

DIC PIH, to include: Mild preeclampsia, Severe preeclampsia, eclampsia, HELLP Syndrome Polyhydramnios RH incompatibility ABO incompatibility RDS MAS Hyperbilirubinemia Infant born to a Diabetic Mother Fetal Alcohol Syndrome

GRADING POLICY: Output: Completeness/ Comprehensiveness To include: • Definition • Etiology • Predisposing/Precipitating Factors • Manifestations • Complications Accuracy Neatness & organization

10 pts

10 pts 5 pts
Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008

71 ===================================================== Total 25 pts for each Flow Chart/ 125 pts total output REFERENCE MATERIALS: 1. Books

a. b.
c. d. e. f. g. Internet: • •

The Lippincott Manual of Nursing Practice, 7th edition, 2001. Luckmann and Sorensen Medical and Surgical Nursing: A Psychophysiologic Approach, 4th edition, 2002 Maternal and Child Health Nursing: Care of the Childbearing and Childrearing Family. Adele Pilliteri.1999. Maternal and Child Health Nursing. Koniak. Maternal and Neonatal Nursing Made Incredibly Easy. 2004 Medical-Surgical Nursing books Critical Care and Emergency Nursing. Schumacher and Chernecky. 2006 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.

Amanuel/Pslidasan/Ksjuliano/MRCueno NCM 104 1st sem S.Y. 2007-2008