Congestive Heart Failure Heart failure can be classified according to a variety of factors (see Heart Failure Criteria and

Classification). The New York Heart Association (NYHA) classification for heart failure comprises 4 classes, based on the relationship between symptoms and the amount of effort required to provoke them, as follows[1] :

Class Class Class Class

I patients have no limitation of physical activity II patients have slight limitation of physical activity III patients have marked limitation of physical activity IV patients have symptoms even at rest and are unable to carry on any physical activity without discomfort

The American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines complement the NYHA classification to reflect the progression of disease and are divided into 4 stages, as follows[2, 3] :

Stage Stage Stage Stage

A patients are at high risk for heart failure but have no structural heart disease or symptoms of heart failure B patients have structural heart disease but have no symptoms of heart failure C patients have structural heart disease and have symptoms of heart failure D patients have refractory heart failure requiring specialized interventions

LABORATORY Laboratory studies for heart failure should include a complete blood cell (CBC) count, electrolytes, and renal function studies. Imaging studies such as chest radiography and 2-dimensional echocardiography are recommended in the initial evaluation of patients with known or suspected heart failure. B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NTproBNP) levels can be useful in differentiating cardiac and noncardiac causes of dyspnea MEDICATIONS Along with oxygen, diuretics, digoxin, inotropes, oxygen, and morphine. *Drugs that can exacerbate heart failure should be avoided (nonsteroidal anti-inflammatory drugs [NSAIDs], calcium channel blockers [CCBs], most antiarrhythmic drugs. SIGNS AND SYMPTOMS : LEFT SIDED HEART FAILURE RIGHT SIDED HEART FAILURE PULMONARY EDEMA HEPATOMEGALY DOB HEPATOJUGULAR RELUX CRACKLES & RALES ANOREXIA INCREASE RR NAUSEA ANXIETY due to decrease O2 supply SPLEENOMEGALY Dizziness, light headedness ASCITES Restlessness, confusion WEIGHT GAIN NOCTURIA

OLIGURIA Treatment : LASIX POTASSIUM LOOSING ( *eat banana )

Heart Failure, also known as Congestive Heart Failure, is a clinical syndrome that results from the progressive process of remodeling, in which mechanical and biochemical forces alter the size, shape, and function of the ventricles ability to pump enough oxygenated blood to meet the bodys metabolic requirements. Compensatory mechanisms of increased heart rate, vasoconstriction, and hypertrophy eventually fail, leading to the characteristic syndrome of heart failure: Elevated ventricular or atrial pressures, sodium and water retention, decreased cardiac output, and circulatory and pulmonary congestion. Systolic dysfunction occurs when the left ventricle is unable to relax and fill sufficiently to accommodate enough oxygenated blood returning from the pulmonary circuit. Systolic dysfunction leads to increased vascular resistance and increased afterload. Diastolic dysfunction leads to pulmonary : Right ventricular failure occurs when the right ventricle is unable to pump blood into the pulmonary circulation. Less blood is oxygenated and pressure increases in the right atrium and systemic venous circulation, which results in edema of the extremities. Left ventricular failure occurs when the left ventricle is unable to pump blood into systemic circulation. Pressure increases in the left atrium and pulmonary veins; then the lungs become congested with blood, causing elevated pulmonary pressure and pulmonary edema. To compensate, the cardiac muscle hypertrophies eventually resulting in decreased ventricular compliance. Decreased compliance requires higher filling pressure to produce the same stroke volume. Increased muscle mass impedes oxygenation of the heart muscle, which leads to decreased contraction force and heart failure. As cardiac output fails, stretch receptors and baroreceptors stimulate the sympathetic nervous system, releasing catecholamines that increase the force and rate of myocardial contraction. This causes increased systemic resistance, increased venous return, and reduced blood flow to the limbs, viscera and kidneys. Sweating results from sympathetic cholinergic fibers, there is extra work for the heart muscle, and there is less systemic blood flow. The renal system responds by releasing renin-angiotensin, which sets off a chain of events vasoconstriction, leading to increased aldosterone release, causing sodium and water retention and, in turn, increasing preload. Finally, sodium and water retention becomes excessive, resulting in signs of systemic venous congestion and fluid overload.

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PREDISPOSING FAXTORS PRECIPITATING FACTORS MYOCARDIUM DSYFUNCTION MYOCARDITIS OBSTRUCTION TO OUTFLOW PULMONARY EMBOLISM VOLUME OVERLOAD SUBSTANCE ABUSE COMPROMISED VENTRICULAR FILLING ALCOHOLIC ABUSE ARTRIAL FIBRILLATION COMMON IN OLDER ADULTS 65 YRS. OLD ABOVE VENTRICULAR ANEURYSM HYPERTENSION

MYOCARDIAL INFARCTION

1 Fluid Volume Excess

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Goals:

Body weight will remain within normal limits Electrolyte levels will be within normal limits Will demonstrate adequate knowledge concerning medical condition. Will maintain optimal fluid balance Will verbalize less dyspnea and be more comfortable.

Interventions:
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Administer Oxygen as ordered Asess for symptoms such as dizziness, weaknes/fatigue, nausea/vomiting, confusion, sweatiness, cyanosis. Notify physician as appropriate. Assess for presence of edema Check breath sounds and assess for labored breathing. Check Vital Signs Keep head of bed elevated Monitor fluid intake, restrict sodium intake as ordered. Monitor Lab work; K+, NA, BUN, Creatinine Observe for signs and symptoms of malnutrition, Do not force resident to eat. Offer small frequent feedings. Assess food preferences. Weigh patient daily ~~~~~~~~~~~~ 2 (Potential for) Decreased cardiac output

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Goal:

Will maintain optimal cardiac ouput andaeb vital signs within acceptable limits, no s/sx of decreased cardiac output.

Interventions:

Administer medications as ordered by MD and check for side effects. Assess and document breath sounds such as dyspnea, cough, extended expiration, wheezing. Assess and document heart sounds, apical heart rate, presence of any abnormal heart sounds. Check for symptoms related to decreased cardiac output, such as chest pain, dyspnea, orthopnea, dependent edema, JVD, fluid overload. Discourage smoking. Discuss avoiding allergens when possible. Encourage activity as tolerated, rest as needed. Encourage proper posture (stand/sit upright, elevate head as needed) to optimize air exchange and comfort. Monitor breathing pattern; include rate, rhythm, depth, pursed lips, nasal flaring, fatigue. Obtain lab/diagnostic work as ordered and report results to MD. ~~~~~~~~~~~~ 3 Potential for fluid volume overload.

Goals:
Will be free from s/sx or complications related to fluid overload.

Interventions:

Administer diuretics as ordered and monitor for side effects. Encourage adequate fluid intake within fluid restrictions as ordered by MD Ensure that snacks and beverages offered at activities comply with all ordered diet and fluid restrictions. Monitor fluid intake and record Monitor for s/sx of fluid overload (edema, shortness of breath, dyspnea, jugular vein distention, bounding pulses) and report to MD ~~~~~~~~~~~~ 4 Episodes of dyspnea

Goal(s)

Episodes of dyspnea will decrease to less than [daily/weekly/monthly] by ___

Intervention(s)

Administer oxygen at _2_ L/min as ordered. Elevate head of bed as needed to promote comfort Monitor and report signs of dyspnea Reduce stress and anxiety as much as possible Report signs of respiratory distress or infection to MD immediately Speak to patient in calm, low voice to help reduce anxiety. ~~~~~~~~~~~~ 5 Potential for decreased endurance due to decreased cardiac output

Intervention(s)

Allow for periods of rest between activities Determine factors that contribute to intolerance (ie sleep disturbance) Encourage patient to conserve energy If applicable, discourage smoking. Monitor food intake to ensure that activity is supported. Monitor vital signs during activities. Slowly increase activity level. Continue to monitor vitals.

Stroke Cerebrovascular disease; CVA; Cerebral infarction; Cerebral hemorrhage; Ischemic stroke; Stroke - ischemic; Cerebrovascular accident; Stroke hemorrhagic A stroke happens when blood flow to a part of the brain stops. A stroke is sometimes called a "brain attack." Causes, incidence, and risk factors If blood flow is stopped for longer than a few seconds, the brain cannot get blood and oxygen. Brain cells can die, causing permanent damage. There are two major types of stroke: ischemic stroke and hemorrhagic stroke.

Ischemic stroke occurs when a blood vessel that supplies blood to the brain is blocked by a blood clot. This may happen in two ways:

A clot may form in an artery that is already very narrow. This is called a thrombotic stroke. A clot may break off from another place in the blood vessels of the brain, or from some other part of the body, and travel up to the brain. This is called cerebral embolism, or an embolic stroke. Ischemic strokes may be caused by clogged arteries. Fat, cholesterol, and other substances collect on the artery walls, forming a sticky substance called plaque. A hemorrhagic stroke occurs when a blood vessel in part of the brain becomes weak and bursts open, causing blood to leak into the brain. Some people have defects in the blood vessels of the brain that make this more likely. INTRODUCTION Cerebrovascular disease (CVD) includes all disorders in which an area of the brain is transiently or permanently affected by ischemia or bleeding and one or more of the cerebral blood vessels are involved in the pathological process. CVD is the third leading cause of death after heart disease and malignancy and it is estimated that an average of 500,000 new strokes will occur each year in the USA. CVD is the most disabling of all neurologic diseases. Approximately 50% of survivors have a residual neurologic deficit and greater than 25% require chronic care. Stroke incidence and mortality are declining primarily due to the successful treatment of HTN and control of risk factors. II. CLASSIFICATION OF CEREBROVASCULAR DISEASE

III. ISCHEMIC/EMBOLIC STROKE A. ANATOMY 1. Carotid Artery distribution-carotid arteries perfuse the majority of the cerebrum Common Carotid Artery-->splits into the Internal Carotid Artery and the External Carotid Artery, then the Internal Carotid Artery-->divides into the Anterior Cerebral Artery (ACA) and the Middle Cerebral Artery (MCA); both a left and right side are present a. ACA-supplies the medial surface of the frontal lobe, parietal lobe and occipital lobe b. MCA-the largest branch of the internal carotid artery 2. Vertebrobasilar Artery distribution-perfuses base of cerebrum and majority of cerebellum 2 Vertebral Arteries-->join to form the Basilar Artery-->branching from the Basilar Artery are the 2 Posterior Cerebral Arteries (PCA) a. Basilar Artery and PCA-supply the occipital lobe, brain stem and cerebellum B. CLASSIFICATION OF ISCHEMIC EVENTS (These are based on the temporal course and eventual outcome.) 1. Transient Ischemic Attacks (TIAs) a. episodes of a temporary reduction in perfusion to a focal region of the brain causing a short-lived disturbance of function b. the patient experiences a temporary focal neurological deficit such as slurred speech, aphasia, amaurosis fugax (monocular blindness), or weakness or paralysis of a limb c. onset is rapid; usually onset is less than 5 minutes d. duration usually 2-15 minutes; can last up to 24 hours e. symptoms (vary depending on the CNS anatomy involved) 1. 2. 3. sensation of swelling or numbness of the hand, arm, or one side of the face or tongue loss of strength in an arm, hand or leg difficulties in speaking or reading

f. no neurological deficit remains after the attack g. one episode in a lifetime to > 20 in one day h. may be the only warning of an impending stroke 2. Reversible Ischemic Neurological Deficit (RIND) a. focal brain ischemia in which the deficit improves over a maximum of 72 hours b. deficits may not completely resolve in all cases 3. Cerebral Infarction a. permanent neurological disorder; the patient presents with fixed deficits b. can present in 3 forms: 1. stable-the neurological deficit is permanent and will not improve or deteriorate 2. improving-return of previously lost neurological function over several days to weeks 3. progressing-the neurological status continues to deteriorate following the initial onset of focal deficits; may see a stabilization period, followed by further progression C. PATHOPHYSIOLOGY 1. Atherosclerosis and subsequent plaque formation results in arterial narrowing or occlusion and is the most common cause of arterial stenosis. 2. Thrombus formation is most likely to occur in areas where atherosclerosis and plaque deposition have caused the greatest narrowing of vessels. 3. Platelet Aggregation a. exposed subendothelium after injury to vessel b. vessel collagen is exposed to blood triggering "activation" of platelets c. release of ADP from activated platelets causes platelet aggregation d. consolidation of platelet-plug by RBCs, coagulation factors, and formation of fibrin network e. Thromboxane A2 (TX A2) is produced by platelets and endothelium promoting platelet aggregation and vasoconstriction 4. Coagulation Cascade a. a series of enzyme complexes located on the surface of platelets and endothelium which lead to thrombin production b. Thrombin (IIa) then converts Fibrinogen to Fibrin D. CLINICAL PRESENTATION Clinically, symptoms depend on the area of cerebral circulation affected and on the extent to which it is affected. 1. Internal Carotid Artery occlusion: a. no characteristic clinical picture b. may range from a TIA to infarction of a major portion of the ipsilateral (on the same side) hemisphere c. if adequate intracranial collateral circulation is present, may see no signs or symptoms d. Neurological symptoms: 1. 2. 3. monoparesis to hemiparesis with or without a defect in vision impairment of speech or language transient monocular blindness 2. Middle Cerebral Artery occlusion: a. most occlusions in the first portion of this artery are due to emboli and typically produce a neurological deficit b. opportunity for collateral circulation is restricted to anastomotic blood flow from the anterior and posterior cerebral arteries on the surface of the brain c. Neurological symptoms: 1. 2. 3. 4. hemiplegia (paralysis of one side of the body) hemisensory deficit hemianopsia (blindness in 1/2 of the visual field) aphasia (if infarct is in the dominant hemisphere) 3. Anterior Cerebral Artery occlusion: a. Neurological symptoms:

1. 2. 3.

weakness of the opposite leg with or without sensory involvement apraxia (particularly of gait) possible cognitive impairment 4. Vertebrobasilar system: a. Neurological symptoms:

1. 2. 3.

severe vertigo, nausea, vomiting, dysphagia, ipsilateral cerebellar ataxia decreased pain and temperature discrimination diplopia, visual field loss, gaze palsies E. RISK FACTORS 1. Hypertension-most important risk factor for all stroke types; no defined BP indicating increased stroke risk, but risk increases proportionately as BP increases. 2. Heart Disease

1. 2. 3. 4. 5.

CHF CAD AFib Rheumatic Heart Disease LVH 3. 4. 5. 6. TIAs, prior stroke, carotid bruits Increased hematocrit, increased fibrinogen Sickle Cell Disease Lifestyle Factors

1. 2. 3. 4. 5. 6.

Age (older) Alcohol abuse Cigarette smoking Drug abuse Genetic factors Males 7. Diabetes Mellitus 8. Migraine HAs 9. Retinal emboli IV. TREATMENT OF CEREBROVASCULAR DISEASE A. GOALS OF THERAPY 1. Stroke prevention through risk-factor reduction. 2. Prevention of initial or recurrent stroke by modifying the underlying pathologic process. 3. Reduction of secondary brain damage by maintaining adequate perfusion to marginally ischemic areas and decreasing edema. B. TREATMENT OF TRANSIENT ISCHEMIC ATTACKS 1. Eliminate or control risk factors. 2. Education of patient regarding risk-factor reduction and signs and symptoms of TIAs and mild stroke. 3. Surgical Interventions a. Carotid Endarterectomy (CEA)

1. 2. 3.

surgical removal of the atheromatous plaque reserved for patients with an ulcerated lesion or clot that occludes > 70% of blood flow in the carotid artery may decrease risk of stroke by 60% over the two years following the procedure

4.

vertebral endarterectomy no longer used 4. Endovascular procedures a. Balloon Angioplasty

1. 2. 3.

consists of placing a small deflated balloon in the stenosed vessel the balloon is then inflated pressing the atheromatous plaque against the wall has a risk of dislodging emboli that can be carried to the brain or retina b. Stent Placement

1. 2.

experimental procedure consists of placing a stainless steel coil into the vessel which then sticks to wall of artery 5. Antiplatelet Agents a. Aspirin 1.Mechanism of Action

1. 2. 3.

inhibition of platelet aggregation decreases release of vasoactive substances from platelets irreversible inactivation of platelet cyclooxygenase; effect lasts for the life of the platelet (5-7 days) 2. Efficacy

1. 2. 3. 4. 5.

ASA has shown clinically significant reductions (22-24%) in stroke risk and death in randomized trials in patients who have experienced a previous TIA or stroke (secondary prevention) doses have ranged from 50 to 1500 mg/day more recent trials have evaluated lower doses (30 to 325 mg/day); results indicate that lower doses may be as beneficial with less adverse effects some studies suggest that ASA is more effective in men than in women (due to small number of women in studies??) role in primary prevention unclear

b. Dipyridamole (PERSANTINE) 1. Mechanism of Action 1. 2. weak inhibitor of platelet aggregation inhibits platelet phosphodiesterase 2. Efficacy 1. 2. clinical trials have not supported the use of dipyridamole in cerebral ischemia no additive effect found with aspirin c. Sulfinpyrazone (ANTURANE) 1. Mechanism of Action 1. reversible inhibition of cyclooxygenase 2. Efficacy

1.

clinical trials have not supported use Ticlopidine (TICLID) 1. Mechanism of Action

1. 2. 3. 4.

inhibits ADP-induced platelet aggregation inhibits platelet aggregation induced by collagen, PAF, epinephrine and thrombin bleeding time prolonged minimal effect on cyclooxygenase 2. Efficacy

1. 2. 3. 4. 5.

has been shown to reduce the incidence of stroke by approximately 22% in patients who have experienced previous TIAs or stroke may be more effective than aspirin with less GI effects no gender difference seen with ticlopidine as with ASA dosed at 500 mg/day divided into 2 doses (250 mg PO BID) adverse effects: 1. diarrhea 2. rash 3. increased total serum cholesterol (ratio of HDL:TChol unchanged) 4. neutropenia occurred in 1-2% of patients; must monitor CBC every 2 weeks for the first 3 months of therapy RECOMMENDATIONS

1. 2. 3. 4.

ASA has been proven to be beneficial in the secondary prevention of TIAs and in decreasing major cerebrovascular events and death; however, the correct dosage is still unknown. The currently recommended dose of aspirin is 325-975 mg/day. The role of aspirin in the primary prevention of TIAs and stroke is still unclear. Ticlopidine has been proven to be effective in the secondary prevention of TIAs and stroke. Due to side effects and cost, it should be reserved for those patients who fail or cannot tolerate ASA. 6. Anticoagulation a. Warfarin 1. no studies that prove the superiority of anticoagulants over antiplatelet agents 2. may reduce the risk of stroke in patients with a prior MI 3. may be useful in those patients who continue to be symptomatic despite antiplatelet therapy 4. the major exception is in patients with cerebral embolism of cardiac origin a. chronic anticoagulation with warfarin has been shown to prevent cerebrovascular events in patients with NVAF b. INR adjusted to between 2.0-3.0 C. Treatment of Acute Cerebral Infarction/Ischemic Stroke 1. Accurate diagnosis is key! A CT Scan must be done to rule out a hemorrhagic stroke before initiation of any treatment.

1. 2.

most patients do not have impaired consciousness in the first 24 hours if consciousness is impaired, suspect a stroke-related seizure, hemorrhage, hypoxia or increased intracranial pressure 2. Supportive care

1. 2.

Maintain adequate tissue oxygenation: May require airway support and ventilatory assistance. Check for possible aspiration pneumonia. BP: In most cases, BP should not be lowered. If severe HTN, lower BP cautiously as neurological status may worsen when BP is lowered.

3. 4. 5. 6.

Volume status: Correct for hypovolemia and keep electrolytes in the normal range. Fever: treat and look for source of fever. Hypoglycemia/hyperglycemia: Keep under control. Hyperglycemia may worsen the ischemic injury. DVT Prophylaxis: This is a must as stroke patients have a high risk for DVT! It is important to use either sc heparin 5,000 IU q. 8 or 12 hrs. or sc enoxaparin 30 mg q. 12 hrs. plus early ambulation! 3. Pharmacologic Therapy

1.

Recombinant Tissure Plasminogen Activator (r-tPA) Protocol--(For Select Patients Only!!) 1. efficacy is influenced by the length of time between the onset of the stroke and the initiation of treatment 2. rapid diagnosis and immediate administration of tPA increases its efficacy and may limit the potential for hemorrhagic conversion of ischemic stroke 3. Inclusion Criteria:

1. 2.

ischemic stroke within 3 hours SBP < 185; DBP < 110 4. Exclusion Criteria:

1. 2. 3. 4. 5. 6.

isolated neurological deficit another stroke or serious head injury within the previous 3 months INR > 1.7 use of heparin in the prior 48 hours major surgery in the prior 14 days platelet count < 100,000/mm3 5. tPA dose:

1. 2. 3.

0.9 mg/kg body weight; max. dose 90 mg give 10% of the dose as a bolus over 1-2 minutes and the rest as a continuous infusion over 1 hour No antiplatelets or anticoagulants within 24 hours!! 6. Results:

1. 2. 3.

improved outcome with regard to disability and death that persists 3 months after therapy there is a higher incidence of intracerebral hemorrhage (6.4% vs. 0.6%) Intra-arterial Thrombolysis 1. 2. 3. 4. 5. early clot lysis and recanalization in about 50% of the patients with intra-arterial streptokinase and urokinase intra-arterial r-pro UK 6 mg given within 6 hours of the stroke resulted in a 58% recanalization rate vs. 14% with placebo main concern is hemorrhagic transformation of the ischemic lesion risk of bleeding may increase with concomitant heparin should still be considered investigational until further data collected

1.

Heparin 1. useful for progressing stroke; questionable role in stable or improving stroke 2. dosing: 50-70 U/kg as a loading dose, followed by 10-25 U/kg/hour; goal PTT 1.5-2.0X control 3. may opt to not use a loading dose in these patients

10

4. major concerns are conversion of an ischemic stroke into a hemorrhagic stroke secondary to heparin, bleeding and thrombocytopenia 5. careful selection of patients is important 1. Low-Molecular Weight Heparin (LMWH) 1. 2. 3. 4. 5. 1. Org 10172 has been studied in acute stroke patients synthetic low-molecular-weight fraction of heparin undergoing investigation in several clinical trials less risk of hemorrhage(?) and thrombocytopenia(?) cannot be recommended for treatment until the results of an ongoing multicenter study are reported

Ancrod (ARVIN) 1. derived from the venom of the Malayan pit viper snake 2. enzyme that breaks down fibrinogen to a soluble ancrod-fibrin complex without allowing stabilization of fibrin (fibrin is not cross-linked) 3. may stimulate tPA activation from vascular endothelium 4. causes fibrinolysis soon after administration; low risk of hemorrhagic complications 5. dose: 0.5 U/kg in NS over 6 hours; administered for 7 days following stroke in the clinical trials; titrate to a fibrinogen level of 0.5-1.0 g/L 6. cannot recommend for use until further clinical trials are completed; role in therapy not yet established 4. Investigational Therapies for Acute Ischemic Stroke

1.

Dextran Infusion 1. decreased blood viscosity by volume expansion 2. decreased platelet function 3. decreased blood interaction with endothelium

1.

Prostacyclin 1. potent vasodilator and platelet suppressant 2. has fibrinolytic activity

1.

Calcium Channel Blockers 1. 2. 3. 4. may increase CBF by smooth muscle relaxation may preserve neuronal function by preventing the calcium influx into neurons that occurs during ischemia nimodipine 30 mg PO every 6 hours for 28 days used in clinical trials; nicardipine also evaluated role in therapy not fully known at this time; seems to work best if initiated within 6-8 hours of symptom onset

1.

Hemodilution 1. utilize albumin and fluids to decrease hematocrit to 30- 35% which decreases blood viscosity 2. questionable role in therapy

1.

21-Aminosteroids (Tirilazad Mesylate-FREEDOX) 1. during ischemia, free radicals are formed which initiate lipid peroxidation 2. 21-aminosteroids are potent inhibitors of lipid peroxidation

11

3. doses up to 6.0 mg/kg/day divided into 4 doses IV x 5 days have been shown to be beneficial in clinical trials 4. role in therapy not yet defined; studies still ongoing V. HEMORRHAGIC STROKE (SAH) Subarachnoid hemorrhage occurs in approximately 26,000 North Americans per year. Most patients range in age from 20-70 years old; however, SAH occurs most frequently in those who are 50-60 years old. The initial hemorrhage is fatal in 20-30% of patients and will ultimately be fatal in 50% of patients. SAH causes permanent neurological disability in 20-50% of survivors. Two-thirds of patients with successful aneurysm clipping never return to the same quality of life as before the SAH. Unlike other types of cerebrovascular diseases, the incidence of SAH has remained about the same for the last 20 years. A. PATHOPHYSIOLOGY 1. SAH occurs when blood is released into the subarachnoid space surrounding the brain and spinal cord. B. ETIOLOGY 1. trauma 2. ruptured intracranial aneurysms (75-80%) 1. 2. 3. Associated with disorders such as congenital weakening of blood vessels, bacterial or fungal infections and hypertension. The walls of the cerebral blood vessels become weak and an aneurysm forms. Blood can leak out slowly if the vessel wall is fragile or rapidly if the aneurysm ruptures. The escape of blood into the subarachnoid space causes irritation and damage to brain tissue. 3. arteriovenous malformation (AVM) (4-5%) 1. An abnormal collection of blood vessels where arterial blood flows directly into draining veins. 4. vasculitis 5. tumor 6. anticoagulants 7. coagulation disorders (ie. hemophilia) 8. no known cause (14-22%) C. RISK FACTORS FOR SAH 1. hypertension 2. cigarette smoking (3-10X greater risk than in nonsmokers) 3. oral contraceptive use/estrogen use 4. alcohol consumption (binge drinking) 5. pregnancy and parturition/straining exercises 6. drug abuse (cocaine) D. CLINICAL PRESENTATION 1. Symptoms 1. 2. 3. 4. 5. 6. severe headache-"the worst headache of my life" nausea and vomiting neck pain nuchal rigidity photophobia, diplopia seizures 2. Grading of the severity of SAH 1. 2. 3. relates to the clinical status of the patient and to the outcome Hunt and Hess Scale frequently used in clinical practice Hunt and Hess Scale for Rating Severity of SAH

12

1. 2. 3. 4. 5. 3. 1. 2. 3.

Grade I -----minor headache, minor neck stiffness Grade II ----severe headache, severe neck stiffness, cranial nerve signs, photophobia Grade III ---drowsiness, confusion, mild paresis, mild dysphagia Grade IV ---stuporous, moderate to severe hemiparesis, dysphagia Grade V ----coma, decerebrate rigidity, symptoms of acute midbrain syndrome Diagnosis

Computed Tomography (CT Scan)-used to demonstrate the presence of blood in the subarachnoid space. Lumbar Puncture (LP)-look for bloody CSF that does not clear. Angiography-used to establish the presence of an aneurysm and precisely locate it for surgery. E. COMPLICATIONS AND TREATMENT MEASURES IN SAH 1. Rebleeding

1. 2. 3. 4.

Usually occurs within 2 weeks of the SAH; however, the maximal frequency of rebleeding is in the first day after SAH. Rebleeding within 2 days occurs in 20% of patients and is associated with 60-70% mortality. The cause is usually due to rupture of the clot that surrounds the original hemorrhage site. Symptoms 1. sudden onset of severe headache 2. rapid rise in BP 3. decreased level of consciousness

1.

Prevention of Rebleeding 1. General

1. 2. 3.

Avoid anticoagulants and antiplatelet drugs including salicylates, nonsteroidal anti-inflammatory drugs, ticlopidine, heparin and warfarin. Avoid rapid reduction of intracranial pressure. Keep BP low, but avoid a rapid reduction. 2. Surgery

1. 2.

Early surgery-surgical intervention within 3 days of SAH. Eliminates the risk of rebleeding and removal of the clot may decrease the risk of delayed cerebral ischemia. Late surgery-intervention more than 3 days after SAH. 3. Antifibrinolytic Therapy (controversial)

1. 2.

Aminocaproic acid (Amicar)-blocks activation of plasminogen to plasmin and inhibits the activity of plasmin on the fibrin clot. Dose: 5 grams IV bolus, followed by a continuous infusion of 1-2 gms/hour for 14-21 days 2. Hydrocephalus

1. 2. 3.

May develop within 1 day or may be delayed for weeks after the initial hemorrhage. The risk of hydrocephalus is associated with the volume and location of blood within the subarachnoid space and ventricular system. Acute hydrocephalus occurs within 24 hours of the initial hemorrhage and causes a decreased level of consciousness and focal neurological deficits. Late hydrocephalus causes dementia, gait disturbances, and incontinence. Treatment of Hydrocephalus

13

1. Surgery 1. 2. 1. 2. 3. Surgery is the only treatment for hydrocephalus. A drain is placed to allow CSF to flow outward. External Ventricular Drain (EVD) Intraventricular Shunt to the peritoneum (VPS) Intraventricular Shunt to the aorta (VAS) 3. Delayed Cerebral Ischemia (secondary to vasospasm) 1. 2. 3. Primary cause of permanent neurological deficits. Cerebral vasospasm develops in 20-40% of patients during the 2-3 weeks following a SAH and most commonly develops 512 days after the initial hemorrhage. The cause is not well understood; however, it may result from compromised autoregulation causing portions of the brain to become ischemic. It may also result from vasoactive substances that are released from degrading red blood cells (epinephrine, serotonin, and oxyhemoglobin) which may cause arterial narrowing. Treatment of Delayed Cerebral Ischemia 1. Volume expansion and induction of hypertension ("Triple H Therapy"-hydration, hypertension, hemodilution) 1. 2. Volume expansion: 0.9% NaCl and 5% serum albumin solutions are used. Endpoint is to maintain PAWP of 15-20 mmHg without causing pulmonary edema. Induction of hypertension: Dopamine and norepinephrine are used to elevate BP. The goal is to elevate SBP to 200-220 mmHg and maintain it for 7 to 14 days. 2. Calcium Channel Blockers (Nimodipine and Nicardipine) 1. 1. 2. 3. 4. Mechanism of Action May improve clinical outcome by limiting fixed neurological deficits. May inhibit the rapid influx of calcium into ischemic neurons and prevent calcium-induced damage. May dilate penetrating blood vessels allowing blood to be shunted back to ischemic areas of the brain and re-establish some autoregulation of cerebral blood flow. Dose Nimodipine 60 mg PO/NGT every 4 hours for 21 days. Must be initiated within 3 days of SAH. 3. Angiography with Papaverine 1. Papaverine, a non-selective muscle relaxant, is injected intra-arterially directly at the site of vasospasm. It is still considered experimental. 4. Angioplasty 4. Seizures 1. 2. Occur in 5 to 15% of patients with SAH. Prevention of Seizures 1. Anticonvulsants 1. 2. Phenytoin is preferred acutely as there is an IV dosage form available and it has minimal effects on mental status. Dose

4.

14

1. Loading Dose: 15-20 mg/kg 2. Maintenance Dose: 5-7 mg/kg/day, based on side effects and serum concentrations 1. 2. If patients do not experience a seizure, may discontinue the anticonvulsant after 3-12 months. Phenobarbital and Valproic Acid are alternative agent

Enlarged prostate The prostate is a male reproductive gland that produces the fluid that carries sperm during ejaculation. It surrounds the urethra, the tube through which urine passes out of the body. An enlarged prostate means the gland has grown bigger. Prostate enlargement happens to almost all men as they get older. As the gland grows, it can press on the urethra and cause urination and bladder problems. An enlarged prostate is often called benign prostatic hyperplasia (BPH) or benign prostatic hypertrophy. It is not cancer, and it does not raise your risk for prostate cancer. Causes The actual cause of prostate enlargement is unknown. Factors linked to aging and the testicles themselves may play a role in the growth of the gland. Men who have had their testicles removed at a young age (for example, as a result of testicular cancer) do not develop BPH. Similarly, if the testicles are removed after a man develops BPH, the prostate begins to shrink in size. Some facts about prostate enlargement:

The likelihood of developing an enlarged prostate increases with age. BPH is so common that it has been said all men will have an enlarged prostate if they live long enough. A small amount of prostate enlargement is present in many men over age 40 and more than 90% of men over age 80. No risk factors have been identified other than having normally functioning testicles. Symptoms Less than half of all men with BPH have symptoms of the disease, which include:

Dribbling at the end of urinating Inability to urinate (urinary retention) Incomplete emptying of your bladder Incontinence Needing to urinate two or more times per night Pain with urination or bloody urine (these may indicate infection) Slowed or delayed start of the urinary stream Straining to urinate Strong and sudden urge to urinate Weak urine stream Exams and Tests After taking a complete medical history, your doctor will perform a digital rectal exam to feel the prostate gland. The following tests may also be performed:

Urine flow rate Post-void residual urine test to see how much urine is left in your bladder after urination Pressure flow studies to measure the pressure in the bladder as you urinate Urinalysis to check for blood or infection Urine culture to check for infection

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Prostate-specific antigen (PSA) blood test to screen for prostate cancer Cystoscopy In addition, you may be asked to complete a form to evaluate the severity of your symptoms and their impact on your daily life. Your score may be compared to past records to determine if the condition is getting worse.

Treatment The choice of a treatment is based on the severity of your symptoms, the extent to which they affect your daily life, and the presence of any other medical conditions. Treatment options include "watchful waiting," lifestyle changes, medication, or surgery. If you are over 60, you are more likely to have symptoms. But many men with an enlarged prostate have only minor symptoms. Self-care steps are often enough to make you feel better. If you have BPH, you should have a yearly exam to monitor the progression of your symptoms and determine if any changes in treatment are necessary. SELF-CARE For mild symptoms:

Urinate when you first get the urge. Also, go to the bathroom when you have the chance, even if you don't feel a need to urinate. Avoid alcohol and caffeine, especially after dinner. Don't drink a lot of fluid all at once. Spread out fluids throughout the day. Avoid drinking fluids within 2 hours of bedtime. Try NOT to take over-the-counter cold and sinus medications that contain decongestants or antihistamines. These medications can increase BPH symptoms. Keep warm and exercise regularly. Cold weather and lack of physical activity may worsen symptoms. Learn and perform Kegel exercises (pelvic strengthening exercises). Reduce stress. Nervousness and tension can lead to more frequent urination. MEDICATIONS

Alpha 1-blockers (doxazosin, prazosin, tamsulosin, terazosin, and alfuzosin) are a class of medications also used to treat high blood pressure. These medications relax the muscles of the bladder neck and prostate. This allows easier urination. Most people treated with alpha 1-blocker medication find that it helps their symptoms. Finasteride and dutasteride lower levels of hormones produced by the prostate, reduce the size of the prostate gland, increase urine flow rate, and decrease symptoms of BPH. It may take 3 to 6 months before you notice much improvement in your symptoms. Potential side effects related to the use of finasteride and dutasteride include decreased sex drive and impotence. Antibiotics may be prescribed to treat chronic prostatitis (inflammation of the prostate), which may accompany BPH. Some men note relief of their BPH symptoms after a course of antibiotics. SAW PALMETTO Many herbs have been tried for treating an enlarged prostate. Saw palmetto has been used by millions of men to ease BPH symptoms and is often recommended as an alternative to medication. Some studies have shown that it helps with symptoms, but there is evidence that this popular herb is no better than a dummy pill in relieving the signs and symptoms of BPH. Further studies are needed. If you use saw palmetto and think it works, ask your doctor if you should still take it.

SURGERY Prostate surgery may be recommended if you have:

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Incontinence Recurrent blood in the urine Inability to fully empty the bladder (urinary retention) Recurrent urinary tract infections (UTI) Kidney failure Bladder stones The choice of a specific surgical procedure is usually based on the severity of your symptoms and the size and shape of your prostate gland.

Transurethral resection of the prostate (TURP): This is the most common and most proven surgical treatment for BPH. TURP is performed by inserting a scope through the penis and removing the prostate piece by piece. Transurethral incision of the prostate (TUIP): This procedure is similar to TURP, but is usually performed in men who have a smaller prostate. It is usually performed without the need for a hospital stay. Like TURP, a scope is inserted through the penis until the prostate is reached. Then, rather than removing the prostate, a small incision is made in the prostate tissue to enlarge the opening of the urethra and bladder outlet. Simple prostatectomy: An open prostatectomy is usually performed using general or spinal anesthesia. An incision is made through the abdomen or perineum (the area behind the scrotum). Only the inner part of the prostate gland is removed. The outer portion is left behind. This is a lengthy procedure, and it usually requires a hospital stay of 5 to 10 days. Most men who have prostate surgery have improvement in urine flow rates and symptoms. See prostate removal for a description of complications. Other, less-invasive procedures are available. These use different forms of heat to destroy prostate tissue, including:

Radiofrequency energy -- transurethral needle ablation (TUNA) Microwave energy -- transurethral microwave thermotherapy (TUMT) Electrical current -- transurethral electrovaporization (TUVP) Hot water -- water-induced thermotherapy (WIT) Laser -- interstitial laser coagulation (ILC) and holmium laser enucleation of the prostate (HoLEP) None of these techniques have been proven to be better than TURP. Patients who receive these less-invasive procedures are more likely to need surgery again after 5 or 10 years. However, these procedures may be a choice for:

Younger men (many of the less-invasive procedures carry a lower risk for impotence and incontinence than TURP, although the risk with TURP is not very high) Elderly patients Patients with severe medical conditions, including uncontrolled diabetes, cirrhosis, alcoholism,psychosis, and serious lung, kidney, or heart disease Men who are taking blood-thinning drugs Robot-guided prostatectomy is another newer technique. However, the technology is not widely available, and surgeon experience should be taken into consideration. In addition, there are no long-term studies of this surgery. Another form of treatment is prostatic stents. For more information, see prostate surgery. Support Groups See: BPH support groups Possible Complications Men who have had long-standing BPH with a gradual increase in symptoms may develop:

Sudden inability to urinate

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Urinary tract infections Urinary stones Damage to the kidneys Blood in the urine Even after surgical treatment, a recurrence of BPH may develop over time. When to Contact a Medical Professional Call your doctor right away if you have:

Less urine than usual Fever or chills Back, side, or abdominal pain Blood or pus in your urine Also call your doctor if:

Your bladder does not feel completely empty after you urinate You take medications that may cause urinary problems, like diuretics, antihistamines, antidepressants, or sedatives. Do NOT stop or adjust your medications on your own without talking to your doctor You have taken self-care measures for 2 months without relief

ACUTE PYELONEPHRITIS One of the most common renal diseases, acute pyelonephritis is a sudden inflammation caused by bacteria. It primarily affects the interstitial area and the renal pelvis or, less often, the renal tubules. Chronic pyelonephritis is persistent kidney inflammation that can scar the kidneys and may lead to chronic renal failure. This disease is most common in patients who are predisposed to recurrent acute pyelonephritis, such as those with urinary obstructions or vesicoureteral reflux.

Risk Factors for Complicated Acute Pyelonephritis Age Infants Elderly (> 60 years of age) Anatomic/functional abnormality Polycystic kidney disease Horseshoe kidney Double ureter Ureterocele Vesicoureteric reflux Foreign body

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Urinary, ureteric, or nephrostomy catheters Calculus Immunosuppressed state Diabetes mellitus Sickle cell disease Transplantation Malignancy Chemoradiation HIV infections Corticosteroid use Male sex Anatomic abnormalities Prostatic obstruction Obstruction Foreign body Calculi Bladder neck obstruction Posterior urethral valve Benign prostatic hypertrophy Neurogenic bladder Pregnancy Miscellaneous Inappropriate antibiotics Resistant organisms Instrumentation

HIV = human immunodeficiency virus.

Symptoms

Back pain or flank pain Chills with shaking Severe abdominal pain (occurs occasionally) Fatigue Fever

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Higher than 102 degrees Fahrenheit Persists for more than 2 days General ill feeling Chills with shaking Mental changes or confusion* Skin changes Flushed or reddened skin Moist skin (diaphoresis) Warm skin Urination problems Blood in the urine Cloudy or abnormal urine color Foul or strong urine odor Increased urinary frequency or urgency Need to urinate at night (nocturia) Painful urination Vomiting, nausea * Mental changes or confusion may be the only signs of a urinary tract infection in the elderly. Exams and Tests A physical exam may show tenderness when the health care provider presses (palpates) the area of the kidney.

Blood culture may show an infection. Urinalysis commonly reveals white or red blood cells in the urine. Other urine tests may show bacteria in the urine. An intravenous pyelogram (IVP) or CT scan of the abdomen may show swollen kidneys. These tests can also help rule out underlying disorders. Additional tests and procedures that may be done include:

Kidney biopsy Kidney scan Kidney ultrasound Voiding cystourethrogram

Prevention Prompt and complete treatment of bladder infections may prevent development of many cases of pyelonephritis. Chronic or recurrent urinary tract infection should be treated thoroughly. You can help preventing kidney infections by taking the following steps:

Keep the genital area clean. Wiping from front to back helps reduce the chance of introducing bacteria from the rectal area to the urethra. Urinating immediately after sexual intercourse. This may help eliminate any bacteria that may have been introduced during sexual activity. Drink more fluids (64 to 128 ounces per day). This encourages frequent urination and flushes bacteria from the bladder. Drink cranberry juice. Doing so prevents certain types of bacteria from attaching to the wall of the bladder and may lessen your chance of infection.

Possible Complications

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Acute kidney failure Kidney infection returns Infection around the kidney (perinephric abscess) Severe blood infection (sepsis) When to Contact a Medical Professional Call your health care provider if you have symptoms of pyelonephritis. Call your health care provider if you have been diagnosed with this condition and new symptoms develop, especially:

Decreased urine output Persistent high fever Severe flank pain or back pain

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