Acute Biologic Crisis

Condition that may result to patientmortality if left unattended in a briefperiod of time.

Condition that warrantsimmediateattention for the reversal of diseaseprocess and prevention of furthermorbidity and mortality.

Cardiac Failure Description- 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- Formerly called Congestive Heart Failure

Etiologic Factors :

Increased metabolic rate (eg. fever, thyrotoxicosis) Hypoxia Anemia

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.

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

- Dyspnea on exertion- Cough- Adventitious breath sounds- Restless and anxious- Skin appears pale and ashen and feels cool and clammy- Tachycardia and palpitations- Weak, thready pulse- Easy fatigability and decreased activity tolerance

Right-Sided Cardiac Failure

- 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

- Edema of the lower extremities (dependent edema)- Weight gain- Hepatomegaly (enlargement of the liver)- Distended neck veins- Ascites (accumulation of fluid in the peritoneal cavity)- Anorexia and nausea- Nocturia (need to urinate at night)- Weakness

Diagnostics Chest Xray (may show cardiomegaly or vascular congestion) Echocardiogram (shows decreased ventricular function and decreased ejection fraction) CVP (elevated in right-sided failure)*pulmonary artery pressure monitoring may be used as guide treatment in serious case of pulmonary edema

Nursing Diagnoses- Activity intolerance r/t imbalance between oxygen supply and demand secondary to decreased CO- Excess fluid volume r/t excess fluid/sodium intake or retention secondary to CHF and its medical therapy- Anxiety r/t breathlessness and restlessness secondary to inadequate oxygenation- Non-compliance r/t to lack of knowledge- Powerlessness r/t inability to perform role responsibilities secondary to chronic illness and hospitalization

Nursing Management

a. Acute phase- monitor and record BP, pulse, respirations, ECG and CVP to detect changes in cardiac output- maintain client in sitting position to decrease pulmonary congestion and facilitate improved gas exchange- auscultate heart and lung sounds frequently: increasing crackles, increasing dyspnea, decreasing lung sounds indicate worsening failure- administer O2 as ordered to improve gas exchange and increase oxygenation of blood; monitor arterial blood gases (ABG) as ordered to assess oxygenation- administer prescribed medications on accurate schedule - Monitor serum electrolytes to detect hypokalemia secondary to diuretic therapy- monitor accurate input and output ( may require Foley cathether to allow accurate measurement of urine output) to evaluate fluid status- if fluid restriction is prescribed, spread the fluid throughout the day to reduce thirst- encourage physical rest and organized activities with frequent rest periods to reduce the work of the heart- provide a calm reassuring environment to decrease anxiety; this decreases oxygen consumption and demands on the heartb. Chronic heart failure- educate client and family about the rationale for the regimen- establish baseline assessment for fluid status and functional abilities- monitor daily weights to evaluate changes in fluid status- assess at regular intervals for changes in fluid status or functional activity level

Pharmacologic Therapy - ACE Inhibitors (promotes 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 (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.- Nitroglycerine ( a vasodilator reduces preload) - Morphine to sedate and vasodilate,decreasing the work of the heart - Anticoagulants may be prescribed. Beta-adrenergic blockers maybe indicated in patients with mild or moderate failure

Client Education Include family member or others in teaching as appropriate Weight monitoring: teach client the importance of measuring and recording daily weights and report unexplained increase of 3-5 pounds Diet: sodium restriction to decrease fluid overload and potassium rich foods to replenish loss from medications; do not restrict water intake unless directed Medication regime: explain the importance of following all medication instructions Activity: help client plan paced activity to maximize available cardiac output Symptoms: report to MD promptly any of the following: chest pain, new onset of dyspnea on exertion, paroxysmal and nocturnal dyspnea Report even minor changes to MD as they may be an early sign of decompensation

Acute Myocardial InfarctionDescription - 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. Infarction results from sustained ischemia and is irreversible causing cellular death and necrosis.

Etiologic factors - Physical exertion

- Emotional stress

- Weather extremes

- Digestion after a heavy meal - Valsalva maneuver - Hot baths or showers

- Sexual excitation - Pathophysiologic characteristic (Coronary artery disease)

Pathophysiology- Coronary artery blood flow is blocked by atherosclerotic narrowing, thrombus formation or persistent vasospasm; myocardium supplied by the arteries is deprived of oxygen; persistent ischemia may rapidly lead to tissue death

Clinical Manifestations Chest pain or discomfort ( described as aching or squeezing pain, most common location is substernal, radiating to neck, jaw, back, shoulders, left arm or occasionally the right arm) complain of heartburn or indigestion pallor, diaphoresis, cold skin, shortness of breath, weakness, dizziness, anxiety, and feelings of impending doom

Diagnostics

Laboratory Tests

Imaging Studies - Electrocardiogram (12-lead) capable of diagnosing MI in 80% of patients, making it an indispensable, noninvasive, and cost-effective tool. Reading shows ST elevation, accompanied by T-wave inversion; and later new pathologic Q wave

Cardiac Enzymes elevated CK with MB isoenzymes >5percent (early diagnosis); elevated Troponin (early to late diagnosis); or elevated LDH with flipped isoenzymes (late diagnosis)

WBC count leukocytosis (10,000/mm3 to 20,000/mm3) appears on thesecond day after AMI and dis appears after 1 week

Positron Emission Tomography (PET) is used to evaluate cardiac metabolism and to assess tissue perfusion

Magnetic Resonance Imaging helps identify the site and extent of an MI

Tranesophageal Echocrdiography (TEE) is an imaging technique in which transducer is placed against the wall of the esophagus; the image of the myocardium is clearer when the esophageal site is used.

Nursing Diagnoses Acute Pain related to myocardial ischemia resulting from coronary artery occlusion Ineffective Tissue Perfusion related to thrombus in coronary artery Decreased Cardiac Output related to negative inotropic changes in the heart secondary to myocardial ischemia Impaired Gas Exchange related to decreased cardiac output Anxiety and Fear related to hospital admission and fear of death

Nursing Management Assess pain status frequently with pain scale Assess hemodynamic status including BP, HR, LOC, skin color, and temperature (every 5 minutes during with pain;every 15 minutes) Monitor continuous ECG to detect dysrhytmias Perform 12-lead ECG immediately with new pain or changes in level of pain Monitor respirations, breath sounds, and input and output to dtect early signs of heart failure Monitor O2 saturation and administer O2 as prescribed Provide for physiological rest to decrease oxygen demands on heart Keep client NPO or progress to liquid diet as ordered; maintain IV access for medication as needed Provide a calm environment and reassure client and family to decrease stress, fear and anxiety Report significant changes immediately to physician to ensure rapid treatment of complications Maintain bed rest for 24 to 36 hours and gradually increase activity as ordered while closely monitoring CO,ECG and pain status

Pharmacologic Therapy Nitroglycerine (to dilate coronary vessels and increase blood flow) Morphine Sulfate (to relieve chest pain) Anticoagulant (heparin) and Antiplatelet (aspirin) - to prevent additional clot formation Streptokinase (to dissolve clot) Beta blockers (to decrease cardiac work) Anti-dysrhytmic drugs

Surgical Interventions Percutaneous transluminal coronary angioplasty (PTCA) involves the passage of an inflatable balloon catheter into the stenonic coronary 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

Client Education Include appropriate family members whenever possible Explain cardiac rehabilitation program if ordered Explain modifiable risk factors and develop a plan with client including supportive resources to change lifestyle to decrease these factors Explain medication regime as prescribed; identify side effects to report (provide written instructions for later reference) Stress the importance of immediate reporting of chest pain or signs of decreased CO2 Instruct about bleeding precautions if client is on anticoagulant therapy: use soft toothbrush, electric razor, avoid trauma or injury; wear or carry medical alert identification

Acute Pulmonary failureDescription- 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.

Etiologic factors Alveolar hypoventilation Diffusion abnormalities Ventilation-perfusion mismatching Shunting

Pathophysiology progression of pulmonary edema occurs when capillary hydrostatic pressure is increased, promoying movement of fluid into the interstitial space of the alveolar-capillary membrane. Initially, increased lymphatic flow removes the excess fluids, but continued leakage eventually overwhelms this mechanism. Gas exchange becomes impaired by the thick membrane. Increasing interstitial fluid pressure ultimately causes leaks into the alveolar sacs, impairing ventilation and gas exchange

Clinical Manifestations Tachypnea Tachycardia Cold, clammy skin and frank diaphoresis are apparent especially around the forehead and face Percussion reveals hyperresonance in patients with COPD; dull or flat on patients with atelectasis or pneumonia Diminished breath sounds; absence of breath sounds of the affected lung in patients with pneumothorax; wheezes on patients with asthma; ronchi on patients with bronchitis and crackles may reveal suspicion of pulmonary edema

Diagnostics ABG analysis indicates respiratory failure when PaO2 is low and PaCO2 is high and the HCO3 level is normal Chest Xray is used to identify pulmonary diseases such as emphysema, atelectasis, pneumothorax, infiltrates and effusions Electrocardiogram (ECG) can demonstrate arrhytmias, commonly found with cor pulmonale and myocardial hypoxia Pulse oximetry reveals a decreasing SpO2 level WBC count aids detection of an underlying infection;abnormally low hemoglobin and hematocrit levels signal blood loss,indicating decrease oxygen carrying capacity PA catheterization is used to distinguish pulmonary causes from cardiovascular causes of acute respiratory failure

Nursing Diagnoses Impaired Gas Exchange related to capillary membrane obstruction from fluid Excess Fluid Volume related to excess preload

Nursing Management Assess the patients respiratory status at least every 2 hours or more as indicated Position the patient for optimal breathing effort when he isnt intubated. Put the call bell within easy reach to reassure the patient and prevent necessary exertion Maintain the normothermic environment to reduce patients oxygen demand Monitor vital signs, heart rhythm, and fluid intake and output, including daily weights, to identify fluid overload or impending dehydration After intubation, auscultate the lungs to check for accidental intubation of the esophagus or mainstem bronchus. Dont suction too often without identifying the underlying cause of an equipment alarm. Watch oximetry and capnography values because these may indicate changes in patients condition Note the amount and quality of lung secretions and look for changes in the patients status Check cuff pressure on the ET tube to prevent erosion from an overinflated cuff Implement measures to prevent nasal tissue necrosis Be alert of GI bleeding Provide a means of communication for patients who are intubated and alert

Pharmacologic Therapy Reversal agents such as Naloxone (Narcan) are given if drug overdose is suspected Bronchodilators are given to open airways Antibiotics are given to combat infection Corticosteroids may be given to reduce inflammation Continuous IV solutions of positive inotropic agents may be given to increase cardiac output, and vasopressors may be given to induce vasoconstrictions to improve or maintain blood pressure Diuretics may be given to reduce fluid overload and edema

Client Education- Include family member or others in teaching as appropriate Weight monitoring: teach client the importance of measuring and recording daily weights and report unexplained increase of 3-5 pounds Diet: sodium restriction to decrease fluid overload and potassium rich foods to replenish loss from medications; do not restrict water intake unless directed Medication regime: explain the importance of following all medication instructions Instruct client and family to maintain elevation of the head of the client at least 45 degrees ; position increases chest expansion and mobilizes fluid from the chest into more dependent areas

Acute Renal FailureDescription a sudden loss of kidney function caused by failure of renal circulation or damage to the tubules or glomeruli

Etiologic factora. Prerenal - caused by decrease blood flow to kidneys like severe dehydration,diuretic therapy,circulatory collapse,hypovolemia or shock;readily reversible when recognized and treatedb. Intrarenal caused by disease process, ischemia, or toxic conditions such as acute glomerulonephritis,vascular disorders,toxic agents, or severe infectionc. Postrenal caused by any condition that obstructs urine flow such as benign prostatic hyperplasia,renal or urinary tract calculi, or tumors

Pathophysiology Acute renal failure is classified as prerenal, intrarenal or postrenal. All conditions that lead to prerenal failure impair blood flow to the kidneys (renal perfusion), resulting in a decreased glomerular filtration rate and increased tubular resorption of sodium and water. Intrarenal failure results from damage to the kidneys. Postrenal failure results from obstructed urine flow.

Clinical Manifestations *A change in blood pressure and volume signals pre renal failure, the patient may have the following: Oliguria Tachycardia Hypotension Dry mucous membranes Flat jugular veins Lethargy progressing to coma Decreased cardiac output and cool, clammy skin in patient with heart failure *As renal failure progresses, the patient may manifest the following signs and symptom: - uremia - confusion - GI complaints - fluid in the lungs - infection

Diagnostics Blood studies reveal elevated BUN, serum creatinine, and potassium levels and decreased blood pH, bicarbonate, HCT, and Hb levels Urine studies show cats, cellular debris, decreased specific gravity and, in glomerular diseases, proteinuria and urine osmolality close to serum osmolality. Creatinine clearance testing is used to measure the GFR and estimate the number of remaining functioning nephrons Electrocardiogram (ECG) shows tall, peaked T waves, a widening QRS complex, and disappearing P waves if increased potassium is present *other studies used to determine the cause of renal failure: - kidney ultrasonography - plain films of the abdomen - KUB radiography - excretory urography - renal scan - retrograde pyelography - computed tomography scan and nephrotomography

Nursing Diagnoses Excess Fluid Volume Imbalanced Nutrition: Less than Body Requirements Deficient Knowledge Risk for Infection

Nursing Management Monitor intake and output Observe for oliguria followed by polyuria Weigh daily and observe for edema Monitoring of complications of electrolyte imbalances, such as acidosis and hyperkalemia Allow client to verbalize concerns regarding disorder Encourage prescribed diet: moderate protein restriction, high in carbohydrates, restricted potassium Once diuresis phase begins, evaluate slow return of BUN, creatinine, phosphorus, and potassium to normal

Pharmacologic Therapy use volume expanders are prescribed to restore renal perfusion in hypotensive clients and Dopamine IV to increase renal blood flow Loop diuretics to reduce toxic concentration in nephrons and establish urine flow ACE inhibitors to control hypertension Antacids or H2 receptor antagonists to prevent gastric ulcers Kayexelate to reduce serum potassium levels and sodium bicarbonate to treat acidosis* avoid nephrotoxic drugs

Client Education Dietary and fluid restrictions, including those that may be continued after discharge Signs of complications such as fluid volume excess, CHF, and hyperkalemia Monitor weight, blood pressure, pulse, and urine output Avoid neprotoxic drugs and substances: NSAIDs, some antibiotics, radiologic contrast media, and heavy metals; consult care provider prior to taking any OTC drugs Recovery of renal function requires up to 1 year; during this period, nephrons are vulnerable to damage from nephrotoxins

Stroke/Cerebrovascular accidentDescription is a condition where neurological deficits occur as a result of decreased blood flow to a localized area of the brain thrombosis of the cerebral arteries supplying the brain or of the intracranial vessels occluding blood flow embolism from a thrombus outside the brain, such as in the heart, aorta, or common carotid artery hemorrhage from an intracranial artery or vein, such as from hypertension, ruptured aneurysm, AVM, trauma, hemorrhagic disorder, or septic embolism

Pathophysiology the underlying event leading to stroke is oxygen and nutrient deprivation; if the arteries become blocked, auto regulatory mechanisms maintain cerebral circulation until collateral circulation develops to deliver blood to the affected area; if the compensatory mechanisms become overworked or cerebral blood flow remains impaired for more than a few minutes, oxygen deprivation leads to infarction of brain tissue

Risk factors hypertension family history of stroke history of TIA cardiac disease, including arrhythmias, coronary artery disease, acute myocardial infarction, dilated myopathy, and valvular disease diabetes mellitus familial hyperlipidemia cigarette smoking increased alcohol intake obesity, sedentary lifestyle use of hormonal contraceptives

Clinical Manifestations hemiparesis on the affected side ( may be more severe in the face and arm than in leg) unilateral sensory defect (such as numbness, or tingling) generally on the same side as the hemiparesis slurred or indistinct speech or the inability to understand speech blurred or indistinct vision, double vision, or vision loss in one eye (usually described as a curtain coming down or gray-out of vision) mental status changes or loss of consciousness (particularly if associated with one of the above symptoms) very severe headache (with hemorrhagic)*A stroke in the left hemisphere produces symptoms on the right side of the body; in the right hemisphere, symptoms on the left side

Diagnostics CT scan discloses structural abnormalities, edema, and lesions, such as nonhemorrhagic infarction and aneurysms MRI is used to identify areas of ischemia, infarction and cerebral swelling DSA is used to evaluate patency of the cerebral vessels and shows evidence of occlusion of the cerebral vessels, a lesion or vascular abnormalities Cerebral angiography shows details of disruption or displacement of the cerebral circulation by occlusion or hemorrhage Carotid Duplex scan is a high frequency ultrasound that shows blood flow through the carotid arteries and reveals stenosis due to atherosclerotic plaque and blood clots Transcranial Doppler studies are used to evaluate the velocity of blood flow through major intracranial vessels, which can indicate vessel diameter Brain scan shows ischemic areas but may not be conclusive for up to 2 weeks after stroke Single photon emission CT scanning and PET scan show areas of altered metabolism surrounding lesions that arent revealed by other diagnostic tests Lumbar puncture reveals bloody CSF when stroke is hemorrhagic EEG is used to identify damaged areas of the brain and to differentiate seizure activity from stroke A blood glucose test shows whether the patients symptoms are related to hypoglycemia Hemoglobin and hematocrit level may be elevated in severe occlusion Baseline CBC, platelet count, PTT, PT, fibrinogen level and chemistry panel are obtained before thrombolytic therapy

Nursing Diagnoses Ineffective Tissue Perfusion related to decreased cerebral blood flow Risk for Prolonged Bleeding related to use of thrombolytic agents Increased Risk for Aspiration related to depressed gag reflex, Impaired swallowing Impaired Physical Mobility related to loss of muscle tone

Nursing Management Encourage active range of motion on unaffected side and passive range of motion on the affected side Turn client every 2 hours Monitor lower extremities for thrombophlebitis Encourage use of unaffected arm for ADLs Teach client to put clothing on affected side first Resume diet orally only after successfully completing a swallowing evaluation Collaborate with occupational and physical therapists Try alternate methods of communication with aphasia patients Accept clients frustration and anger as normal to loss of function Teach client with homonymous hemianopsia to overcome the deficit by turning the head side to side to be able to fully scan the visual field

Pharmacologic Therapy Thrombolytics for emergency treatment of ischemic stroke Aspirin or Ticlopidine (Ticlid) as an antiplatelet agent to prevent recurrent stroke Benzodiazepines to treat patients with seizure activity Anticonvulsants to treat seizures or to prevent them after the patients condition has stabilized Stool softeners to avoid straining, which increase ICP Antihypertensives and antiarrhythmics to treat patients with risk factors for recurrent stroke Corticosteroids to minimize associated cerebral edema Hyperosmolar solutions (Mannitol) or diuretics are given to clients with cerebral edema Analgesics to relieve the headaches that may follow a hemorrhagic stroke

Surgical Intervention Craniotomy to remove hematoma Carotid endarterectomy to remove atherosclerotic plaques from the inner arterial wall Extracranial bypass to circumvent an artery thats blocked by occlusion or stenosis

Client Education Educate client and family about CVA and CVA prevention Educate client and family about community resources Educate client and family about physical care and need for psychosocial support Educate client and family about medication

Increased Intracranial PressureDescription- prolonged pressure greater than 15mmHg or 180mmH2O measured in the lateral ventricles

Etiology Cerebral Edema is an increase in volume of brain tissue due to alterations in capillary permeability, changes in functional or the structural integrity of the cell membrane or an increase in the interstitial fluids Hydrocephalus is an increase in the volume of CSF within the ventricular system; it may be noncommunicating hydrocephalus where the drainage from the ventricular system is impaired

Pathophysiology Blood flow exerts pressure against a weak arterial wall, stretching it like an overblown balloon and making it to rupture; rupture is followed by a subarachnoid hemorrhage, in which blood spills into space normally occupied by CSF. Sometimes, blood spills into brain tissue, where a clot can cause potentially fatal increased ICP and brain tissue damage

Clinical manifestations blurring of vision, decreased visual acuity and diplopia are the earliest signs of increased ICP headache, papilledema or the swelling of optic disk and vomiting change of LOC

Diagnostics skull radiography CT scan MRI* Lumbar puncture is not performed because of brain herniation caused by sudden release of pressure*Laboratory tests are performed to augment and monitor treatment approaches; serum osmolarity monitors hydration status and ABGs measure pH, oxygen and carbon dioxide

Nursing Diagnoses Ineffective Cerebral Tissue Perfusion related to Increased ICP Risk for Infection Impaired Physical Mobility Risk for Ineffective Airway Clearance

Nursing Management Assess neurological status every 1 to 2 hours and report any deterioration; include LOC, behavior, motor/sensory function, pupil size and response, vital signs with temperature Maintain airway; elevate head of 30 degree or keep flat as prescribed; maintain head and neck in neutral position to promote venous drainage Assess for bladder distention and bowel constipation; assist client when necessary to prevent Valsava maneuver Plan nursing care so it is not clustered because prolonged activity may increase ICP; provide quiet environment and limit noxious stimuli; limit stimulants such as radio, TV and newspaper; avoid ingesting stimulants such as coffee, tea, cola drinks and cigarette smoke Maintain fluid restriction as prescribed Keep dressings over catheter dry and change dressings as prescribed; monitor insertion site for CSF leakage or infection; monitor clients for signs and symptoms of infection; use aseptic technique when in contact with ICP monitor

Pharmacologic therapy Osmotic diuretics such as Mannitol and loop diuretics such as Furosemide ( Lasix) are mainstays used to decrease ICP Corticosteroids are effective in decreasing ICP especially with tumors

Surgical Intervention A drainage catheter, inserted via ventriculostomy into lateral ventricle, can be done to monitor ICP and to drain CSF to maintain normal pressure; if used the system is calibrated with transducer is leveled 1 inch above the ear; sterile is of utmost importance

Client Education Teach the client at risk for increased ICP to avoid coughing, blowing the nose, straining for bowel movements, pushing against the bed side rails, or performing isometric exercises Advice the client to maintain neutral head and neck alignment Encourage the family to maintain a quiet environment and minimize stimuli Educate the family that upsetting the client may increase ICP

METABOLIC EMERGENCIESDKADescription Life threatening metabolic acidosis resulting from persistent hyperglycemia and breakdown of fats into glucose, leading to presence of ketones in blood; can be triggered by emotional stress, uncompensated exercise,infection, trauma, or insufficient or delayed insulin administration

Etiology Decreased or missed dose of insulin Illness or infection Undiagnosed and untreated diabetes

Pathophysiology In the absence of endogenous insulin, the body breaks down fats for energy. In the process, fatty acids develop too rapidly and are converted to ketones, resulting to severe metabolic acidosis. As acidosis worsens, blood glucose levels increase and hyperkalemia worsens. The cycle continues until coma and death occur

Clinical manifestations - Acetone breath - Poor appetite or anorexia - Nausea and vomiting - Abdominal pain - Blurred vision - Weakness - Headache - Dehydration - Thirst or polydipsia - Orthostatic hypotension - Hyperventilation (Kussmaul respirations) - Mental status changes in DKA vary from patient to patient - weight loss - muscle wasting - leg cramps - recurrent infections

Diagnostics Serum glucose is elevated (200 to 800 mg/dl) Serum Ketone Level is increased Urine acetone test is positive Arterial Blood Gas analysis reveals metabolic acidosis ECG findings shows tall tented T waves and widened QRS complex changes related to hyperkalemia; later with hypokalemia, shows flattened T wave and the presence of U wave Serum osmolality is elevated

Nursing Diagnoses Deficient Fluid Volume Risk for Injury Risk for Skin Impaired Integrity Ineffective Breathing Pattern Disturbed Sensory Perception Knowledge Deficit Anxiety

Nursing Management Restore fluid, electrolyte and glucose balance with IV infusions and medications, analyze intake and out, blood glucose, urine ketones, vital signs, oxygenation and breathing pattern Maintain skin integrity; promote healing of impaired skin; prevent infection by turning and positioning client every 2 hours; provide pressure relief as indicated; manage incontinence and perspiration with skin protective barriers and cleansing; provide appropriate nutrition and oxygen support Promote safety by analyzing vital signs, client communication, LOC and emotional response, and activity tolerance; implement falls prevention measures Assist client to verbalize concerns and cope effectively with illness and fears Assist client to update Medic-Alert bracelet information as appropriate

Pharmacotherapy Administer IV Insulin and fluid and electrolyte replacements based on laboratory test results

Client Education Instruct client about the nature and causes of DKA (such as excess glucose intake, insufficient medications or physiological and/or psychological stressors) any new medications

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC COMA Description Life threatening metabolic disorder of hyperglycemia usually recurring with DM type 2 medications, infections, acute illness, invasive procedure, or a chronic illness

Etiology Medications Infections acute illness invasive procedure chronic illness

Pathophysiology glucose production and release into the blood is increased or glucose uptake by the cells is decreased; when the cells dont receive glucose, the liver responds by converting glycogen to glucose for release into the bloodstream; when all excess glucose molecules remain in the serum, osmosis cause fluid shifts.; the cycle continues until fluid shifts in the brain cause coma and death

Clinical Manifestations severe dehydration hypotension and tachycardia diaphoresis tachypnea polyuria, polydipsia and polypahgia lethargy and fatigue vision changes rapid onset of lethargy stupor and coma neurologic changes

Diagnostics Serum glucose is elevated, sometimes 800 to 2,000 mg/dl Ketones are absent, urine and serum ketones are absent Urine glucose levels are positive Serum osmolality is increased Serum Sodium levels are elevated and the serum potassium level is usually normal ABG results are usually normal, without evidence of acidosis

Nursing Diagnoses Decreased Cardiac Output Deficient Fluid Volume Hyperthermia Disturbed Sensory Perception Risk for Impaired Skin Integrity Risk for Aspiration Deficient Knowledge

Nursing Management Assess the patients LOC, respiratory status and oxygenation Monitor the patients VS; changes may reflect the patients hydration status Monitor patients blood glucose and serum electrolytes Administer regular insulin IV as ordered, by continuous infusion and titrate dosage based on the patients blood glucose levels Maintain intact skin integrity by turning every 2 hours, use of pressure relief aids, nutritional support, use of skin moisturizers and barriers, and management of incontinence Prevent aspiration by using appropriate feeding precautions, elevate head of bed 15 to 30 degrees during and after feeding for 1 hour; if BP is too unstable to elevate head of bed with feeding, then withhold oral feedings

Pharmacotherapy IV infusion of NS to replace fluids and sodium, regular insulin IV to manage the hyperglycemia, and potassium to replace losses and shifts

Client Education Instruct client and family about HHNK, symptoms to report, and administration of new medications Provide patient and family education to foster prevention of future episodes

Massive BleedingDescription Uncontrolled bleeding

Etiology Result of blunt or penetrating trauma Gastrointestinal or genitourinary bleeding Hemoptysis

Pathophysiology Due to the lack of adequate circulating blood volume causing dcreased tissue perfusion and metabolism resulting in hypoxia, vasoconstriction and shunting of the available circulating blood volume to the vital organs(heart and brain);Symphathetic nervous system stimulation, hormonal release of antidiuretic hormone and the angiotensin-renin mechanisms and neural responses attempt to compensate for the loss of circulating volume but eventually metabolic acidosis, multi organ system failure occurs

Clinical Manifestations cool, clammy, pale skin (esp. distal extremities) delayed capillary refill (>3 seconds) weak, rapid pulses decreased blood pressure (systolic pressure 28/ min) restless, anxious, decreased LOC cardiac dysrhtymias (abnormalities of cardiac rhythm) decreased urinary output

Diagnostics evidence of bleeding from thorocostomy that indicates bleeding from chest area abdominal or pelvic CT scan, abdominal ultrasound or peritoneal lavage indicate intra abdominal bleeding Endoscopy indicates upper or lower GI bleeding Angiography procedures diagnose severe vascular damage Extremity radiographs show long bone fractures Hemoglobin and hematocrit from the CBC are decreased due to blood loss Elevated serum lactate if bleeding continues and client becomes acidotic ABGs show metabolic acidosis as blood loss continues Baseline coagulation studies should be reviewed; initial PT/PTT and platelet counts will be within normal limits but as coagulation factors become depleted, clotting times will increase and platelet counts will decrease Serum electrolytes to assess renal function

Nursing Diagnoses Impaired Tissue Perfusion Deficient Fluid volume Decreased cardiac Output

Nursing Management Establish an adequate airway, breathing pattern, and applying supplemental oxygen Give priority interventions to control bleeding such as direct pressure to wound site, or assisting with surgical interventions Establish IV access and begin with fluid replacement Draw blood specimens as ordered to assist in evaluation of hemoglobin, hematocrit, electrolyte, oxygenation andhydration status Insert an indwelling catheter and NG tube to assist in accurate recording of fluid balance status Perform and document continuous serial assessments of hemodynamic parameters such as VS, capillary refill, CVP, cardiac rhythm, LOC, urinary output and laboaratory findings

Pharmacotherapy Crystalloids and blood products to maintain adequate circulating volume status Sodium Bicarbonate to correct acidosis state Vasopressor such as Dopamine

Client Education Explain procedures to the client Support the family by explaining emergency measures and interventions

BurnsDescription An alteration in skin integrity resulting in tissue loss or injury caused by heat, chemicals, electricity or radiation

EtiologyTypes of burn injurya. Thermal: results from dry heat (flames) or moist heat (steam or hot liquids); it is the most common type; it causes cellular destruction that results in vascular, bony, muscle, or nerve complications; thermal burns can also lead to inhalation injury if the head and neck area is affectedb. Chemical burns are caused by direct contact with either acidic or alkaline agents; they alter tissue perfusion leading to necrosisc. Electrical burns; severity depends on type and duration of current and amount of voltage; it follows the path of least resistance(muscles, bone, blood vessels and nerves); sources of electrical injury include direct current, alternating current and lightningd. Radiation burns: are usually associated with sunburn or radiation treatment for cancer; are usually superficial; extensive exposure to radiation may lead to tissue damage

Pathophysiology It depends on the cause and classification of the burn; the injuring agents denatures cellular proteins; some cells die because of traumatic or ischemic necrosis; loss of collagen cross-linking also occurs with denaturation, creating abnormal osmotic and hydrostatic pressure gradients that cause intravascular fluid to move into interstitial spaces; Cellular injury triggers the release of mediators of inflammation, contributing to local and in the case of major burns , systemic increases in capillary permeability

Clinical Manifestations Localized pain and erythema, usually without blisters in the first 24 hours (first degree burn) Chills, headache, localized edema, nausea and vomiting (most severe first degree burn) Thin-walled, fluid filled blisters appearing within minutes of the injury, with mild to moderate edema and pain (second degree superficial partial thickness burn) White, waxy appearance to damaged area(second degree partial-thickness burn) White, brown or black leathery tissue and visible thrombosed vessels due to destruction of skin elasticity(dorsum of hand, most common site of thrombosed veins), without blisters (third-degree burn) Silver-colored, raised or charred area, usually at the site of electrical contact

Diagnostics*Rule of Nines chart determines the percentage of body surface area (BSA)covered by the burn - ABG levels may be normal in the early stages but may reveal hypoxemia and metabolic acidosis Carboxyhemoglobin level may reveal the extent of smoke inhalation due to the presence of carbon monoxide

Complete blood count may reveal a decrease hemoglobin due to hemolysis, increased hematocrit and leukocytosis

Electrolyte levels show hyponatremia and hyperkalemia,other laboratory tests reveals elevated BUN,decreased total protein and albumin

Creatinine kinase (CK) and myoglobin levels may be elevated

Presence of myoglobin in urine may lead to acute tubular necrosis

Nursing Diagnoses Risk for Deficient Fluid Volume Risk for Infection Impaired Physical Mobility Imbalanced Nutrition: Less than Body Requirements Ineffective Breathing Pattern Impaired Tissue Perfusion Risk for Impaired Gas Exchange Anxiety Risk for Ineffective Thermoregulation Pain Impaired Skin Integrity

Nursing Management Assess patients ABCs; monitor arterial oxygen saturation and serial ABG values and anticipate the need for ET intubation and mechanical ventilation Auscultate breath sounds Administered supplemental humidified oxygen as ordered Perform oropharyngeal or tracheal suctioning as indicated by the patients inability to clear his airway Monitor the patients cardiac and respiratory status Assess LOC for changes such as confusion, restlessness or decreased responsiveness

Irrigate the wound with amounts of water or normal saline solution for chemical burns Place the patient in semi-Fowlers position to maximize chest expansion; keep patient as quiet and comfortable to minimize oxygen demand Prepare the patient for an emergency escharotomy of the chest and neck for deep burns Administer rapid fluid replacement therapy as ordered*For burn patient in shock - Monitor VS and hemodynamic parameters - Assess patients intake and output every hour, insert an indwelling cathether

Assess the patients level of pain, including nonverbal indicators and administer analgesics such as Morphine Sulfate IV as ordered Keep the patient calm, provide periods of uninterrupted rest between procedures and use nonpharmacologic pain relief measures as appropriate Obtain daily weights and monitor intake, including daily calorie counts; provide high calorie, high protein diet Administer histamine 2 receptor antagonists as ordered to reduce risk of ulcer formation Assess the patients sign and symptoms of infection; may obtain wound culture and administer antimicrobials an antipyretics as ordered Administer tetanus prophylaxis if indicated Perform burn wound care as ordered; prepare patient for grafting as indicated Assess the neurovascular status of the injured area, including pulses, reflexes, paresthesia, color and temperature of the injured area at least 2 to 4 hours or more frequently as indicated Assist with splinting, positioning, compression therapy and exercise to the burned area as indicated; maintain the burned area in a neutral position to prevent contractures and minimize deformity Explain all procedures to the patient before performing them

Pharmacotherapy Antibiotic prophylaxis will eradicate bacterial component Pain therapy Tetanus prophylaxis Topical antimicrobial Enzymatic debriding agents such as collagenase, fibrinolysin-desoxyribonuclease, papin or sutilins are used with a moisture barrier to protect surrounding tissue Recommended dressings include polyurethane films(Op-site, Tegaderm), absorbent hydrocolloid dressings (Duoderm)

Client Education Environmental safety: use low temperature setting for hot water heater, ensure access to and adequate number of electrical cords/outlets, isolate household chemicals, avoid smoking inbed Use of household smoke detectors with emphasis on maintenance Proper storage and use of flammable substances Evacuation plan for family Care of burn at home Signs and symptoms of infection How to identify risk of skin changes Use of sunscreen to protect healing tissue and other protective skin care

PoisoningDescription Substances that are harmful to humans that are inhaled, ingested (food, drug overdose) or acquired by contact

Etiology Carbon monoxide inhalation Food poisoning Drug overdose Insecticide surface absorption

Pathophysiology The pathophysiology of poisons depends on the substance thats inhaled or ingested. The extent of damage depends on the pH of the substance, the amount ingested, its form and the length of exposure to it. Substances with an alkaline pH cause tissue damage by liquefaction necrosis, which softens the tissue. Acids produce coagulation necrosis. Coagulation necrosis denatures proteins when substance contacts tissue. This limits the extent of the injury by preventing penetration of the acid into the tissue. *The mechanism of action for inhalants is unknown, but theyre believed to act on the CNS similarly to a very potent anesthetic. Hydrocarbons sensitize the myocardial tissue and allow it to be sensitize to cathecolamines, resulting in arrhythmias

Clinical Manifestationsa. Carbon monoxide inhalation: mild exposure nausea, vomiting, mild throbbing headache, flu-like symptoms; moderate exposure dyspnea, dizziness, confusion, increased severity of mild symptoms; severe/prolonged exposure seizures, coma, respiraotory arrest, hypotension and dysrhytmias b. Food poisonings: nausea, vomiting, diarrhea, abdominal cramps, fever , chills, dehydration, headachec. Drug overdose: depends upon the substance ingested; symptoms may include nausea, vomiting, CNS depression or agitation, altered pupil response, respiratory changes such as tachypnea or bradypnea, alterations in temperature control, seizures or cardiac arrestd. Surface absorption of insecticides( organophosphates or carbamates): nausea, vomiting, diarrhea, headache, dizziness, weakness or tremors, mild to severe respiratory distress, slurred speech, seizures, and cardio-pulmonary arrest

Diagnostics*The diagnosis of many poisonings is based on a thorough client history and clinical manifestations - laboratory toxicology screens (serum,vomitus, stool and urine) determine the extent of the absorption

- baseline blood work such as CBC, electrolytes, renal and hepatic studies enable future determination of organ and tissue damage

- Chest Xray may show aspiration pneumonia in inhalation poisoning Abdominal Xrays may reveal iron pills or other radiopaque substances ABG analysis used to evaluate oxygenation

Nursing Diagnoses Risk for Ineffective Airway Clearance Risk For Decreased Cardiac Output Deficient Fluid Volume Ineffective Breathing Pattern Impaired Tissue Perfusion Risk for Injury Anxiety Risk for Self-directed Violence Hopelessness

Nursing Management Assist with the management of an effective airway, breathing pattern and circulatory status Give treatment of life-threatening dysrhythmias and conditions as ordered; continual monitoring of vital signs, cardiac rhythm and neurological status and supportive care is essential Assist in the hastening in the elimination of the medication or poison, decrease the amount of absorption and administer antidotes as ordered for specific treatment contact the poison center

Pharmacotherapy*antidotes will vary with medication ingested - Ipecac syrup 30ml PO followed by 240ml water is used for adults - Activated charcoal powder slurry 30 to 100g PO or per NG tube - Magnesium Citrate will be used for GI evacuation - Naloxone (Narcan) for respiratory depression caused by narcotic overdose Flumazanil (Romazicon) for benzodiazepine ingestions

Client Education Assist the client and family in seeking the appropriate referrals and provide client education to further complications or incidence of overdose Ensure that the client and family understand discharge instruction for follow up care or reason for admission

Multiple InjuriesDescription Is a physical injury or wound thats inflicted by an external or violent act; it may be intentional or unintentional; involve injuries to more than one body area or organ

Etiology Weapons Automobile collision Physical confrontation Falls Unnatural occurrence to the body*Type of trauma which determines the extent of injury Blunt trauma leaves the body intact Penetrating trauma disrupts the body surface Perforating trauma leaves entrance and exit

Pathophysiology A physical injury can create tissue damage caused by stress and strain on surrounding tissue which results to infection, pain , swelling and potential compartment syndrome or it can be life threatening if it affects a highly vascular or vital organ

Diagnostics Chest Xray detect rib and sterna fractures, pneumothorax, flail chest, pulmonary contusion and lacerated or ruptured aorta Angiography studies performed with suspected aortic laceration or rupture Ct scan, cervical spine Xrays, skull Xrays, Angiogram test for a patient with head trauma ABG analysis to evaluate respiratory status and determine acidotic and alkalotic states CBC to indicate the amount of blood loss Coagulation studies to evaluate clotting ability Serum electrolyte levels to indicate the presence of electrolyte imbalances

Nursing Diagnoses Ineffective Airway Clearance Ineffective Breathing Pattern Impaired Gas Exchange Deficient Fluid Volume Decreased Cardiac Output Impaired Tissue Perfusion Impaired Skin Integrity Risk for infection Anxiety Pain Disturbed Body Image

Nursing Management Assess the patients ABCs and initiate emergency measures Administer supplemental oxygen as ordered Immobilize the patients head and neck with an immobilization device, sandbags, backboard and tape Assist with cervical Xrays Monitor VS and note significant changes Immobilize fractures Monitor the patients oxygen saturation and cardiac rhythm for arrhythmias Assess the patients neurologic status, including LOC and papillary and motor response Obtain blood studies, including type and crossmatch Insert large bore IV catheter and infuse normal saline or lactated Ringers solution Assess the patient for multiple injuries Assess the patients wounds and provide wound care as appropriate; cover open wounds and control bleeding by applying pressure and elevating extremities Assess for increased abdominal distention and increased diameter of extremities Administer blood products as appropriate Monitor the patient for signs of hypovolemic shock Provide pain medication as appropriate Provide reassurance to the patient and his family

Pharmacotherapy Tetanus immunization Antibiotics for infection control Analgesics for pain

Client Education Provide explanations of all procedures done Families usually require emotional support and honest discussions about therapeutic interventions and plans