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Etiology and pathophysiology 1. Pericarditis

a. Acute or chronic inflammation of the pericardium. b. May be idiopathic or result from; bacterial infection (streptococcal, staphylococcal, gonococcal, meningococcal organisms); viral infection (coxsackievirus ,influenza); mycotic (fungal) infection; rickettsial and parasitic infestation; trauma; collagen disease; rheumatic fever; neoplastic disease secondary to lung and breast metastasis. c. Sequelae: loss of pericardial elasticity or an accumulation of fluid within the sac; heart failure or cardiac tamponade.

1. Sharp pain over sternum radiating to neck, shoulders, back, and arms. 2. Pain increases with deep inspiration, decreases when sitting up or leaning forward (pulls heart away from diaphragmatic pleurae of the lungs). 3. Difficulty in breathing. 4. Tachycardia. 5. Feeling of fullness in chest.

1. Dyspnea, orthopnea 2. Tachycardia 3. Substernal chest pain 4. Pallor; cold, clammy skin 5. Neck vein distention 6. Hypotension

A. Signs of constrictive pericarditis (1) Increase in systemic venous pressure (2) Pericardial friction rub
7. Symptoms similar to right heart failurefluid retention, hepatomegaly, ascites


A pericardial friction rub is diagnostic of pericarditis. The nurse should search diligently for the rub by placing the diaphragm of the stethoscope tightly against the thorax and auscultating the left sternal edge in the fourth intercostal space, the site where the pericardium comes into contact with the left chest wall. A pericardial friction rub has a scratching or leathery sound. The rub is louder at the end of exhalation and may be heard best with the patient sitting and leaning forward.

Cardiac Tamponade
Nursing assessment skills are key to anticipating and identifying the triad of symptoms of cardiac tamponade: (FaRD) o falling arterial pressure - Usually, the systolic pressure falls while the diastolic pressure remains stable; hence, the pulse pressure narrows. o rising central venous pressure o distant heart sounds. - Heart sounds may progress from sounding distant to being imperceptible. /quiet heart sounds

NURSING ALERT Cardiac tamponade is a life-threatening situation, demanding immediate intervention. The signs and symptoms of cardiac tamponade begin with falling arterial pressure. Usually, the systolic pressure falls while the diastolic pressure remains stable; hence, the pulse pressure narrows. Heart sounds may progress from sounding distant to being imperceptible. Neck vein distention/prominent neck veins and other signs of rising central venous pressure are observed. These signs and symptoms occur because, as the fluid-filled pericardial sac compresses the myocardium, blood continues to return to the heart from the periphery but cannot flow into the heart to be pumped back into the circulation. paradoxical pulse

In such situations, the nurse notifies the physician immediately and prepares to assist with pericardiocentesis The nurse stays with the patient and continues to assess and record signs and symptoms while intervening to decrease the patients anxiety.

PERICARDIOCENTESIS The major goal is to prevent cardiac tamponade, which restricts normal heart action. During the procedure
the patient is monitored by ECG and hemodynamic pressure measurements. Emergency resuscitative equipment should be readily available. The head of the bed is elevated to 45 to 60 degrees, placing the heart in proximity to the chest wall so that the needle can be inserted into the pericardial sac more easily. If a peripheral intravenous device is not already in place, one is inserted, and a slow intravenous infusion is started in case it becomes necessary to administer emergency medications or blood products. The pericardial aspiration needle is attached to a 50-mL syringe by a three-way stopcock. Several possible sites are used for pericardial aspiration. o The needle may be inserted in the angle between the left costal margin and the xiphoid, near the cardiac apex; o at the fifth or sixth intercostal space at the left sternal margin; o or on the right sternal margin of the fourth intercostal space. The needle is advanced slowly until it has entered the epicardium and fluid is obtained. The ECG can help determine when the needle has contacted the epicardium. The cable of a precordial lead is attached to the aspirating needle with alligator clamps; contact with the epicardium is seen by ST segment elevation on the ECG. During the procedure, drainage fluid must be checked for clotting. Although not entirely accurate, the guideline is that pericardial blood does not clot readily, whereas blood obtained from inadvertent puncture of one of the heart chambers does clot. A resulting fall in central venous pressure and an associated rise in blood pressure after withdrawal of pericardial fluid indicate that the cardiac tamponade has been relieved. The patient almost always feels immediate relief. If there is a substantial amount of pericardial fluid, a small catheter may be left in place to drain recurrent accumulation of blood or fluid. Pericardial fluid is sent to the laboratory for examination for tumor cells, bacterial culture, chemical and serologic analysis, and differential blood cell count. Complications of pericardiocentesis include o ventricular or coronary artery puncture o dysrhythmias o pleural laceration o gastric puncture o myocardial trauma. After pericardiocentesis, the patients heart rhythm, blood pressure, venous pressure, and heart sounds are monitored to detect any possible recurrence of cardiac tamponade. If it recurs, repeated aspiration is necessary. Cardiac tamponade may require treatment by open pericardial drainage (pericardiotomy). The patient is ideally in an intensive care unit.

CVP Monitoring
To measure the CVP, the transducer (when a pressure monitoring system is used) or the zero mark on the manometer (when a water manometer is used) must be placed at a standard reference point, called the phlebostatic axis (Fig. 26-12). After locating this position, the nurse may make an ink mark on the patients chest to indicate the location. If the phlebostatic axis is used, CVP can be measured correctly with the patient supine at any backrest position up to 45 degrees. The range for a normal CVP is 0 to 8 mm Hg with a pressure monitoring system or 3 to 8 cm H2O with a water manometer system. The most common complications of CVP monitoring are infection and air embolism.

The phlebostatic axis and the phlebostatic level. (A) The phlebostatic axis is the crossing of two reference lines: (1) a line from the fourth intercostal space at the point where it joins the sternum, drawn out to the side of the body beneath the axilla; and (2) a line midway between the anterior and posterior surfaces of the chest. (B) The phlebostatic level is a horizontal line through the phlebostatic axis. The airfluid interface of the stopcock of the transducer, or the zero mark on the manometer, must be level with this axis for accurate measurements. When moving from the flat to erect positions, the patient moves the chest and therefore the reference level; the phlebostatic level stays horizontal through the same reference point. (C) Two methods for referencing the pressure system to the phlebostatic axis. The system can be referenced by placing the airfluid interface of either the in-line stopcock or stopcock on top of the transducer at the phlebostatic level.

2. Myocarditis
a. Inflammation of the myocardium b. May result from: viral, bacterial, mycotic, parasitic, protozoal or spirochetal infections or infestations; rheumatic fever; endocarditis. c. Sequelae, impaired contractility of the heart caused by the inflammatory process; myocardial ischemia and necrosis.

Myocarditis is an inflammatory process involving the myocardium. Myocarditis can cause heart dilation, thrombi on the heart wall (mural thrombi), infiltration of circulating blood cells around the coronary vessels and between the muscle fibers, and degeneration of the muscle fibers themselves. The incidence of myocarditis is estimated to be 1 to 10 cases per 100,000 persons.

1. Fatigue 2. Difficulty in breathing 3. Feeling of soreness in chest

1. Dyspnea 2. Neck vein distention, tachycardia, fever, arrhythmias (in severe cases)

he, and malaise.

3. Infective subacute bacterial endocarditis

a. Inflammation of the inner lining of the heart and valves. b. May result from; Streptococcus viridans, bacterial, fungal, or rickettsia infections; rheumatic heart disease. c. Sequelae: Structural damage to the valves; pump failure; embolization.

Rheumatic Endocarditis
Acute rheumatic fever, which occurs most often in school-age children, follows 0.3% to 3% of cases of group A beta-hemolytic streptococcal pharyngitis (Chin, 2001). Prompt treatment of strep throat with antibiotics can prevent the development of rheumatic fever (Chart 29-1). The Streptococcus is spread by direct contact with oral or respiratory secretions. Although the bacteria are the causative agents, malnutrition, overcrowding, and lower socioeconomic status may predispose individuals to rheumatic fever (Beers et al., 1999).

Recognizing and Preventing Rheumatic Fever

Rheumatic fever is a preventable disease. Eradicating rheumatic fever would eliminate rheumatic heart disease. Penicillin therapy in patients with streptococcal infections can prevent almost all primary attacks of rheumatic fever. ***A throat culture is the only method by which an accurate diagnosis can be determined.

The signs and symptoms of streptococcal pharyngitis are the following:

Fever (38.9to 40C [101to 104F]) Chills Sore throat (sudden in onset) Diffuse redness of throat with exudate on oropharynx (may not appear until after the first day) Enlarged and tender lymph nodes Abdominal pain (more common in children) Acute sinusitis and acute otitis media (if due to streptococci)

NURSING ALERT A throat culture is the only method by which an accurate diagnosis of streptococcal infection of the
throat can be made.

1. Anorexia, weight loss 2. Malaise, weakness 3. Chest pain 4. Chills 5. Night sweats

1. Low-grade fever (99_102_F)subacute endocarditis 2. High-grade fever (103_104_F)acute infective endocarditis 3. Positive blood cultures 4. Murmurs over valves 5. Clubbing of fingers 6. Petechiae (in 49% of cases) 7. Typical symptoms of complications due to emboli reachingother organs, including spleen, kidney, lungs, peripheral vascular beds. Symptoms include hematuria, pleuritic chest pain, upper left quadrant pain.

B. Clinical findings
a. Oxygen therapy and bed rest. b. Antibiotics to relieve underlying infection; corticosteroids; antidysrhythmics; and salicylates to suppress rheumatic activity. The type of antibiotic used for prophylaxis varies with the type of procedure and the degree of risk. The patient is usually instructed to take 2 g of amoxicillin (Amoxil) 1 hour before dental, oral, respiratory, or esophageal procedures. If the patient is allergic to penicillin (eg, ampicillin [Omnipen, Polycillin], carbenicillin [Geocillin], cloxacillin [Cloxapen], methicillin [Staphcillin], nafcillin [Nafcil, Unipen], oxacillin [Prostaphlin, Bactocill], penicillin G [Bicillin, Permapen]), clindamycin (Cleocin), cephalexin (Keflex), cefadroxil (Duricef), azithromycin (Zithromax), or clarithromycin (Biaxin) may be used. Recommendations for gastrointestinal or genitourinary procedures are ampicillin and gentamicin (Garamycin) for high-risk patients, amoxicillin or ampicillin for moderate-risk patients, and substituting vancomycin (Vancocin) only for patients allergic to ampicillin or amoxicillin. c. Pericardectomy surgical removal of scar tissue and the pericardium). d. Cardiac monitoring.

1. Maintain a tranquil environment and help the client achieve maximum rest; medicate for discomfort as needed. 2. Explain post hospitalization therapy to improve compliance (lifelong doses of penicillin prophylatically when undergoing invasive procedures). 3. Administer IV antibiotics as ordered 4. Monitor temperature and blood cultures to evaluate antibiotic therapy.

Peripheral Vascular System Basic Information

1. The peripheral vascular system includes the branching network of vessels that carry blood from the left side of the heart to tissues and then back to the right side of the heart. 2. Alterations of the vascular system usually occur in adulthood. 3. Peripheral vascular disease refers to vascular disorders other than those specifically affecting the heart. 4. Exercise, diet, and other health promotion practices affect the integrity of the peripheral vascular system. 5. Risk factors for peripheral vascular disease include high fat intake sedentary lifestyle smoking obesity. 6. Females are prone to peripheral vascular disease, particularly in terms of obstruction to the circulation in the lower extremities during pregnancy. 7. Certain disease processes, such as diabetes mellitus, are associated with the development of peripheral vascular impairment. 8. Blood flow is decreased owing to narrowing or obstructed blood vessels. The underlyi ng factor is the arteriosclerotic process. The decreased blood flow causes changes in the tissues.








Data base A. Etiology and pathophysiology

a. Thrombus: a clot composed of platelets, fibrin, clotting factors, and cellular debris attached to the interior wall of an artery or vein. b. Embolus: a clot or solid particle carried by the bloodstream which may interfere with tissue perfusion in an artery or vein. c. Arterial disorders involve depriving oxygen to a body part or tissue. This is affected by blood pressure and presence of collateral circulation. a. Reduced blood flow resulting from atherosclerosis, thrombus, or embolus. b. Buergers disease (thromboangiitis obliterans) 1. Peripheral circulation impaired by inflammatory occlusions of peripheral arteries; thromboses of arteries may occur. 2. Incidence is highest in young adult males who smoke.

Buergers Disease
(Thromboangiitis Obliterans) Description 1. Buergers disease is an inflammatory occlusive condition involving the small and medium arteries in decrease in blood flow to feet and legs. 2. Pain is the result of ischemia, which occurs with inflammation of vessel layers. 3. Condition causes segmental lesions and eventual thrombus formation. 4. It may produce ulcerations and eventually gangrene. 5. Incidence is highest among males of Jewish ancestry aged 2040. 6. Causesunknown 7. Predisposing factorassociated with smoking (hypersensitivity to nicotine)

(sometimes veins), resulting

Buergers Disease
Assessment SUBJECTIVE 1. History of cigarette smoking, exposure to cold, stress 2. Pain in fingers and feet at rest (aggravated by arm elevation and hyperextension) 3. Pain in neck, shoulder, and hand due to compression of brachial plexus 4. Instep claudication (pain) with exercise 5. Numbness or tingling 6. Cold extremities OBJECTIVE 1. Diminished or absent pulses 2. Skin ulceration 3. Changes in appearance of extremities 4. Skin colorwhite (pallor at first) changes to cyanotic, then red 5. Redness and hardness along vesselsindication of recurring superficial phlebitis 6. Muscle atrophy 7. Slow-healing cuts 8. Presence of ischemic ulcers or blisters on toes 9. Gangrene

c. Raynauds disease 1. Spasms of digital arteries thought to be caused by abnormal response of the sympathetic nervous system to cold or emotional stress, usually bilateral and primarily occur in young females. 2. Raynauds phenomenon is episodic arterial spasm of the extremities secondary to another disease of abnormality. 2. Venous disorders involve a problem with transportation of blood back to the heart from the capillary beds as a smooth muscle around vessels. result to changes in

Raynauds disease is characterized by episodic vasospasm in small peripheral arteries and arterioles, resulting in interruption of blood flow to distal parts of affected extremities. 2. It occurs bilaterally, usually affects hands; feet are less often affected. 3. It is characterized by triphasic color change from white to blue to red of involved body parts. 4. It is most prevalent in females, especially between puberty and age 40. 5. Over time, disease may progress to occlusion of the arteries, resulting in digital gangrene; eventually amputation may be required. 6. Causeunknown 7. Precipitating factors A. Cold, stress, smoking B. Associated with collagen diseases in women 8. Predisposing factors A. Pressure to fingertipsaffects typists, pianists, users of hand-held vibrating equipment 9. Raynauds phenomenon may occur with no underlying or concomitant disease and is associated with connective tissue disease, which is considered to be an early indicator of these conditions when it occurs in well individuals.

Raynauds disease Assessment SUBJECTIVE 1. Numbness, coldness of hands or feet 2. Pain in hands or feet OBJECTIVE 1. Hands or feet feel cold to touch 2. Color changespallor, cyanosis, rubor 3. Numbness and tingling 4. Dryness and atrophy of nails 5. Ulcerations or gangrene, especially on fingertips

b. Thrombophlebitis: Inflammation of a vein associated with clot formation; risk factors include immobilization, venous stasis, vessel trauma, pregnancy, obesity, and pelvic surgery. Thrombophlebitis (Venous Thromboembolic Disease) Description 1. Thrombophlebitis is characterized by inflammation and thrombus formation. It may occur in deep or 2. Phlebothrombosis is a clot in the vein without accompanying inflammation. 3. Superficial thrombophlebitis begins with localized inflammation alone (phlebitis); thrombus formation is frequently provoked by the inflammatory process. Platelets, RBC, and fibrin form a clot within the vein, which potentially can break loose and lead to emboli. A. Causes (1) Trauma or irritation of a vein from an IV catheter or administration of an irritating solution (2) IV administration of potassium chloride and antibiotics (3) IV drug abuse 4. Deep vein thrombophlebitis A. Presence of unilateral edema in affected limb. B. Edema may be mild or severe. C. Pain on dorsiflexion of foot (Homans sign) when leg is affected. This sign is accurate less than 1/3 of the time. D. Condition may frequently lead to pulmonary embolism. E. Causes (1) Damage to vessel lining (2) Venous pooling and stasis (3) Increased clotting ability of blood F. Predisposing factors (1) Immobilization such as paralysis, being bedridden or chairfast, long plane or car rides (2) Disease processes such as sepsis, hematological disorders, malignancy, CHF, MI (3) Increased abdominal pressure due to obesity, pregnancy, or tumor (4) Trauma such as fractures, venipuncture (5) Clotting deficiencies such as antithrombin III deficiency, disorders of plasminogen activators, and abrupt heparin withdrawal (6) Surgical procedures such as hip pinning, craniotomy, transurethral resection, hysterectomy G. Other factors (1) Dehydration (2) Advancing age (3) Prior thrombosis or thromboembolic event (4) Use of oral contraceptives

superficial veins.

a. Subjective: pain on dorsiflexion of affected extremity (Homans sign) --- only about 10% of clients with phlebitis manifest this sign and there are a lot of false positive results; may be asymptomatic until embolus is released and occludes organ b. Objective: swollen limb with hard veins that are sensitive to pressure; redness and warmth of area along the vein; Doppler studies/flow studies of lower extremities indicate obstruction or decreased flow to the area suggest thrombus formation

1. Pain in affected extremity 2. History of causes and contributing factors

1. Warmth and redness of extremitysuperficial thrombophlebitis 2. Elevation of temperature 3. Swelling 4. Pain elicited by palpation of calf muscle for deep vein thrombosis 5. Area sensitive to touch 6. Quality of pulse in affected extremity

Varicose veins
Occur when veins in lower extremities become dilated, congested, and tortuous as result of weakness of valves or loss of elasticity of vessel walls: risk factors include family history, prolonged standing, pregnancy, leg trauma, and thrombophlebitis.

Varicose Veins Description

1. Varicose veins are dilated, tortuous leg veins due to backflow of blood caused by incompetent venous valve closure. Results in venous congestion and further enlargement of veins. 2. Condition usually affects subcutaneous leg veins (saphenous veins and branches). 3. Classification

A. Primary varicosities
(1) Venous valve insufficiency. (2) Incompetence of superficial veins resulting in reflux of blood from deep to superficial veins. (3) Increased hydrostatic pressure from long column of blood extending from inferior vena cava to the saphenous vein. (4) Veins become dilated and tortuous with characteristic bulging appearance of varicose veins. (5) Varicosities usually found in greater saphenous vein along thigh, but may extend laterally.

B. Secondary varicosities
(1) Deep venous disease (2) May produce postphlebitic syndromechronic problem that cannot be cured by the removal of the superficial veins

4. Causesunknown 5. Predisposing factors

A. Congenital weakness of venous valves or venous wall B. Diseases of venous system such as thrombophlebitis C. Conditions that produce venostasispregnancy, prolonged standing, obesity D. Familial tendency

Varicose veins Manifestations a. Subjective: heaviness and fatigue in legs with cramping that increases at night b. Objective: positive venogram; positive trendelenburg test is diagnostic of varicose veins; brown skin discoloration; stasis ulcers. Assessment SUBJECTIVE 1. Aching 2. Cramping and pain 3. Heavy feeling in legs OBJECTIVE 1. Palpable nodulesprimary varicose veins 2. Foot and ankle edema exacerbated by prolonged standing or immobility 3. Edema relieved by bed rest and elevation of legs 4. Dilated veinsprimary varicose veins 5. Status pigmentation of calves and ankles

A. GENERAL CLINICAL FINDINGS 1. Peripheral arterial disorders a. Subjective: paresthesia; aching to severe or burning pain b. Objective: pallor or cyanosis; gangrenous ulcers, and diminished pulses in Buergers disease. Assessment SUBJECTIVE 1. Aching calves 2. Numbness in legs 3. Leg cramps

4. Loss of sensation in legs 5. Pain in legs during exercise (intermittent claudication) 6. History of diabetes mellitus, thrombophlebitis, hypertension, alcoholism OBJECTIVE 1. Arterial Insufficiency A. Pain in region of the affected vessel, very painful, occur on lateral legs, toes, heels; demarcated edges, necrotic not edematous -- pain is sharp, increases with walking and elevation; intermittent claudication (relieved by rest) -- smooth skin, shiny skin, loss of hair, thickened nails -- cool temp B. Numbness in affected limb C. Pallor or mottling in the affected limb (on elevation); rubor when dependent D. Muscle spasms E. Pulselessness in distal limb (due to blockage); decrease or absent F. Possible paralysis 2. Venous Insufficiency A. Lower leg edema, marked edema, slightly painful; occur on medial legs, ankles; uneven edges; superficial -- persistent, aching, full feeling, dull sensation pain; relieved when horizontal (elevate and use elastic stockings) -- brown pigment around ankles -- warm temp -- normal B. Discolored skin in affected lower limb; cyanotic when dependent C. Affected subcutaneous tissue feels hard D. Stasis ulcers over the ankle E. Redness of leg in dependent position 3. Other A. Sparse hair distribution B. Varicose veins C. Delay in capillary filling D. Bruits heard in major arteries E. Difference in circumference of legs

Assessment criteria
Presenting history, physical and social risk factors

Venous disease
Previous history of DVT Varicose veins Reduced mobility Traumatic injury to the lower leg Obesity Pregnancy Non-healing ulceration Recurrent phlebitis Previous vein surgery

Arterial disease
Diabetes Hypertension Smoking Previous history of vascular disease Obesity Inability to elevate limb

Position of ulceration

Gaiter area of the leg Common site is medial aspect

Lateral malleolus and tibial area are common sites as well as toes and feet Over pressure points


Throbbing, aching, heavy feeling in legs Improves with elevation and rest

Intermittent claudication Can be worse at night and at rest Improves with dependency

Ulcer characteristics

Shallow with flat margins Often presents with slough at the base with granulation tissue Moderate to heavy exudate

Punched out, occasionally deep Irregular in shape Unhealthy appearance of wound bed Presence of necrotic tissue or fixed slough Low exudate unless ulcers infected

Condition of the lower leg

Haemosiderin staining Thickening and fibrosis Dilated veins at the ankle Crusty, dry, hyperkeratotic skin Eczematous, itchy skin Pedal pulses present Normal capillary refill (less than three seconds) Limb edema is common

Thin, shiny, dry skin Reduced or no hair on lower leg Skin feels cooler to touch Pallor on leg elevation Absence or weak pedal pulses Delayed capillary refill (greater than

B. Therapeutic Intervention
1. Peripheral vascular disease a. Sympathectomy to sever the sympathetic ganglia supplying the area; there is local vasodilation with improved circulation b. Femoropopliteal bypass grafting c. Amputation if vascular supply is severely impaired (see Neuromuscoloskeletal System) 2. Varicose veins a. Sclerotherapy involves injection of a chemical irritant to the vein b. Surgical intervention involves ligation of vein above the varicosity and removal of the involve vein; the great saphenous vein may be ligated near the femoral junction. c. Postoperatively early ambulation is essential to prevent formation of thrombi

3. Thrombophlebitis a. Prophylactic antiembolytic stockings and exercise to promote venous return b. Warm moist heat to promote vasodilation c. Elevation of extremity to reduce edema d. Anticoagulants to prevent recurrence of deep vein involvement e. Vasodilators to prevent vascular spasm f. Thrombolytic therapy to dissolve clot g. Transvenous filter or thrombectomy PLANNING/IMPLEMENTATION 1. Observe frequently for signs of vascular impairment (e.g. Pallor, cyanosis, coolness of involve extremities and amplitude and symmetry of peripheral pulses) 2. Apply antiembolism stockings before ambulating and remove and replace as ordered; if thrombophlebitis is suspected maintain bed rest and notify physician 3. Instruct the client to avoid tight and constricting clothing that can affect peripheral vessels, cigarette smoking, massaging legs, maintaining one position for long periods, and to reducing weight when indicated 4. In arterial disease, keep extremities warm; instruct the client to wear gloves when exposed to cold, apply lubricants to keep skin supple 5. Observe for signs of pulmonary embolism (e.g. Sudden pain, cyanosis, hemoptysis, shock) 6. Provide specific care if undergoing vascular surgery: monitor for hemorrhage, notify physician if bleeding is suspected; asses circulatory status of extremity; keep extremity elevated,; allow out of bed as ordered; avoid prolonged hip flexion 7. Provide specific care for the client following a vein ligation: elevate the foot of the bed for the first 24 hours; observe for signs of hemorrhage; maintain compression dressing; assist with ambulation 8. Provide specific care for the client following endarterectomy and femoropopliteal bypass grafting a. Assess circulation of involved area by checking pulses, color, temperature, and neurotic function b. Observe blood pressure frequently because, hypotension increases the possibility of thrombus formation c. Observe for signs of hemorrhage, including pain, change in skin color, and alteration of vital signs d. Ambulate as ordered: sitting should be avoided in femoropopliteal bypass surgery.

Data Base A. Etiology and pathophysiology
1. Distention at the site of a weakness in the arterial wall a. Saccular aneurysm: pouch like projection at one side of the artery b. Fusiform aneurysm: entire circumference of the artery walls is dilated c. Mycotic aneurysm: tiny weakness is arterial walls resulting from infection d. Dissecting aneurysm: tear in the lining of an arteriosclerotic aortic wall causes blood to form a hematoma between layers of the artery compressing the lumen 2. Causes: congenital weakness; syphilis; trauma; atherosclerosis (most common cause of both thoracic and abdominal aortic aneurysms) 3. Represent surgical emergency if ruptured 4. Occur most frequently in middle-aged white males 5. Risk factors include history of hypertension, obesity, stress, hypercholesterolemia, cigarette smoking, familial tendency

B. Clinical Findings 1. Thoracic aortic aneurysm

a. Subjective: may be asymptomatic; dyspnea; dysphagia; pain resulting from pressure against the nerves or vertebrae b. Objective: hoarseness, cough, and laryngeal nerve, unequal pulses and arterial pressure in upper extremities; trachea may be displaced from midline because of adhesions between trachea and aneurysm

2. Abdominal aortic aneurysm

a. Subjective: may be asymptomatic; lower back or abdominal pain (severe if aneurysm is leaking); sensory changes in the lower extremities if aneurysm ruptures b. Objective: hypertension; pulsating abdominal mass; mottling of the lower extremities if aneurysm ruptures, increased abdominal girth if aneurysm ruptures

3. Dissecting aortic aneurysm

a. Subjective: restlessness; anxiety; severe pain b. Objective: diminished pulses; signs of shock

PLANNING/IMPLEMENTATION 1. 2. 3. 4. 5. 6. Perform neurovascular assessment of extremities Monitor hemodynamic status Record intake and output, because renal failure may occur after surgery Administer narcotics as ordered to alleviate pain Apply abdominal binders to provide support when the client is coughing, deep breathing and ambulating Prevent flexion of hip and knees to eliminate pressure on the arterial wall

SHOCK A. Etiology and pathophysiology

1. Hypovolemic: occurs when there is loss of fluid resulting in inadequate tissue perfusion; caused by excessive bleeding, diarrhea; or vomiting; fluid loss from fistulas or burns 2. Cardiogenic: occurs when pump failure causes, inadequate tissue perfusion; caused by congestive heart failure; myocardial infarction, cardiac tamponade 3. Neurogenic: caused by rapid vasodilation and subsequent pooling of blood within the peripheral vessels; caused by spinal anesthesia; emotional stress; drugs that inhibit the sympathetic nervous system 4. Anaphylactic: caused by an allergic reaction that causes a release of histamine and subsequent vasodilation 5. Septic (similar to anaphylaxis) reaction to bacterial toxins (generally gram-negative infections), which results in the leakage of plasma into tissues

B. Clinical findings
1. Subjective: apprehension; restlessness; paresis of extremities 2. Objective: weak, rapid, thready pulse; diaphoresis; cold, clammy skin; pallor; decreased urine output, progressive loss of consciousness; decreased mean arterial pressure (normal 80 to 120 mm Hg)

C. Therapeutic interventions
1. 2. 3. 4. Aimed at correcting the underlying cause Fluid and blood replacement Oxygen therapy, ventilator Vasoconstricting drugs to increase blood pressure


1. 2. 3. 4. Constrict peripheral blood vessels through alpha-adrenergic stimulation. Elevate blood pressure Indication: Shock, increased perfusion; hypotension Available in parenteral (IV) preparations.

B. Examples: levarterenol bitartrate (Levophed); metaraminol bitartrate (Aramine); phenylephrine HCI (Neo- Synephrine); dopamine (Depostat,
Dopamine HCl, Intropin). levarterenol bitartrate (Levophed, Levarternol) Action: Vasopressor; stimulates the alpha and beta adrenergic receptors to cause vasoconstriction maintaining BP Indication: Management of shock Undesirable effects: angina, hpn, tachycardia, dysrhythmias, extravasation may cause severe irritation, necrosis, and sloughing of tissues infiltrate area with 10 15 ml of 0.9 % NACl with 5 10 mg of phentolamine (Regitine), an alphaadrenergic blocking agent that reverses vasoconstriction and restore blood flow, readily available in any setting where IV adrenergic drugs are used; Phentolamine is most effective if injected within 12 h after extravasation

C. Major side effects: hypertension (compression of cerebral blood vessels); headache (increase in blood pressure); GI disturbance
(autonomic dysfunction); palpitations, tachycardia, wide QRS complex

D. Nursing care. 1. Assess vital signs; monitor blood pressure frequently; titrate IV depending on blood pressure readings to prevent hypertension. 2. Assess for IV infiltration; may lead to tissue necrosis. 3. Encourage intake of high-fiber foods to reduce the potential of constipation. 4. Do not use within 2 weeks of MAOIs, phenytoin hypertensive crisis may result; Decrease action of dopamine with beta-blockers; increased BP with oxytoxics Dopamine
**Do not confuse dopamine with dobutamine. **Dopamine is a unique drug and different from the other adrenergic agonists because its actions depends on the dose. ** 5 to 10 mcg/kg/min stimulate alpha receptors (constrict peripheral blood vessels) ** 2 to 3 mcg/kg/min stimulate dopaminergic receptors causing dilation of the mesenteric and renal arteries Dopamine is frequently used to increase blood flow to the kidneys when renal insufficiency is present or to prevent renal failure from shock

DOPAMINE D ilation of pupil R ate of Heart will increase A rterioles constrict (increase BP) G I contractility Dobutamine (Dobutrex)
**stimulates beta, adrenergic receptors (myocardial) to increase contractility but with relatively minor effect on heart rate **Indication: short term management of heart failure due to decreased contractility **Undesirable effects: increase BP, dysrhythmias, tachycardia, headache, angina pectoris, dyspnea, NV **increased risk of dysrhythmias with MAOI, oxytoxics or tricyclics antidepressants, halothane, cyclopropane **monitor BP, PR, RR, ECG, PCWP, CVP, Cardiac output, Urine output

DOBUTAMINE F ailure (Heart) A ngina, arrhythmia undesirable effect I ncreases contractility, BP L ook for an increase in cardiac and urine output

5. Cardiac and hemodynamic monitoring 6. Cardiotonics for cardiogenic shock 7. Antihistamines for anaphylactic shock 8. Antibiotics for septic shock based on blood cultures 9. Elevation of lower extremities to ensure circulation to vital organs 10. Intraaortic balloon pump may be used to aid the failing heart PLANNING/IMPLEMENTATION
1. 2. 3. 4. 5. 6. Keep the client warm, place in supine position Monitor hemodynamic status and vital signs Monitor urine output and specific gravity Allay clients anxiety Administer intravenous fluid as ordered Monitor oxygen saturation and provide oxygen therapy as indicated

ANEMIAS AND BLOOD DISORDERS A. Etiology and pathophysiology 1. Iron deficiency anemia: inadequate dietary intake of iron needed for hemoglobin formation, vitamin B12 and/or folic acid which is needed for erythrocyte synthesis - results when the intake of dietary iron is inadequate for hemoglobin synthesis. Cause:

In children, adolescents, and pregnant women, the cause is typically inadequate iron in the diet to keep up with increased growth. However, for most adults with iron deficiency anemia, the cause is blood loss. The most common cause of iron deficiency in men and postmenopausal women is bleeding (from ulcers, gastritis, inflammatory bowel disease, or gastrointestinal tumors). The most common cause of iron deficiency anemia in premenopausal women is menorrhagia (excessive menstrual bleeding) and pregnancy with inadequate iron supplementation. Patients with chronic alcoholism often have chronic blood loss from the gastrointestinal tract, which causes iron loss and eventual anemia. Other causes include iron malabsorption, as is seen after gastrectomy or with celiac disease.

Manifestations: Patients with iron deficiency primarily have the symptoms of anemia. (Pallor, Fatigue, Dyspnea, Anginal pain,
Blurred vision, Vertigo, Irritability, Depression, Nausea, Anorexia, Weight loss, Bone pain, Numbness, tingling of feet)

Decreased reticulocytes, iron, ferritin, iron saturation, MCV; increased TIBC If the deficiency is severe or prolonged, they may also have a smooth, sore tongue, brittle and ridged nails, and angular cheilosis (an ulceration of the corner of the mouth). o These signs subside after iron-replacement therapy. The health history may be significant for multiple pregnancies, gastrointestinal bleeding, and pica (a craving for unusual substances, such as ice, clay, or laundry starch).

The most definitive method of establishing the diagnosis of iron deficiency anemia is bone marrow aspiration. o The aspirate is stained to detect iron, which is at a low level or even absent. o However, few patients with suspected iron deficiency anemia undergo bone marrow aspiration.


to assess the quantity and quality of each type of cell produced within the marrow. Normal bone marrow is in a semifluid state and can be aspirated through a special large needle. Normal: Yellow marrow fat cells and connective tissue; Red marrow hematopoetic cells, fat cells and connective tissue

In adults, bone marrow is usually aspirated from the iliac crest and occasionally from the sternum. The aspirate provides only a sample of cells. Aspirate alone may be adequate for evaluating certain conditions, such as anemia. However, when more information is required, a biopsy is also performed. Biopsy samples are taken from the posterior iliac crest; occasionally, an anterior approach is required. A marrow biopsy shows the architecture of the bone marrow as well as its degree of cellularity. Before aspiration, the skin is cleansed as for any minor surgery, using aseptic technique. Then a small area is anesthetized with a local anesthetic through the skin and subcutaneous tissue to the periosteum of the bone. It is not possible to anesthetize the bone itself. The bone marrow needle is introduced with a stylet in place. When the needle is felt to go through the outer cortex of bone and enter the marrow cavity, the stylet is removed, a syringe is attached, and a small volume (0.5 mL) of blood and marrow is aspirated. Patients typically feel a pressure sensation as the needle is advanced into position. The actual aspiration always causes sharp but brief pain, resulting from the suction exerted as the marrow is aspirated into the syringe; the patient should be forewarned about this. Taking deep breaths or using relaxation techniques often helps ease the discomfort.

In many patients, the diagnosis can be established with other tests, particularly in patients with a history of conditions that predispose them to this type of anemia. There is a strong correlation between laboratory values measuring iron stores and levels of hemoglobin. After the iron stores are depleted (as reflected by low serum ferritin levels), the hemoglobin level falls. The diminished iron stores cause small RBCs. Hematocrit and RBC levels are also low in relation to the hemoglobin level. Normal: Yellow marrow fat cells and connective tissue; Red marrow hematopoetic cells, fat cells and connective tissue

2. Pernicious anemia: lack of intrinsic factor in the stomach prevents the absorption of B12 which reduces the number of erythrocytes formed Causes:
A deficiency of vitamin B12 can occur in several ways. - Inadequate dietary intake is rare but can develop in strict vegetarians who consume no meat or dairy products. - faulty absorption from the gastrointestinal tract is more common. o This occurs in conditions such as Crohns disease, or after ileal resection or gastrectomy. Another cause is the absence of intrinsic factor, as in pernicious anemia.

Symptoms of folic acid and vitamin B12 deficiencies are similar, and the two anemias may coexist. However, the neurologic manifestations of vitamin B12 deficiency do not occur with folic acid deficiency, and they persist if B12 is not replaced. Therefore, careful distinction between the two anemias must be made. Serum levels of both vitamins can be measured. In the case of folic acid deficiency, even small amounts of folate will increase the serum folate level, sometimes to normal. Measuring the amount of folate within the RBC itself (red cell folate) is therefore a more sensitive test in determining true folate deficiency. After the body stores of vitamin B12 are depleted, patients may begin to show signs of the anemia. However, because the onset and progression of the anemia are so gradual, the body can compensate very well until the anemia is severe, so that the typical manifestations of anemia (weakness, listlessness, fatigue) may not be apparent initially. The hematologic effects of deficiency are accompanied by effects on other organ systems, particularly the gastrointestinal tract and nervous system. a. Patients with pernicious anemia develop a smooth, sore, red tongue and mild diarrhea. They are extremely pale, particularly in the mucous membranes. Beefy red tongue, lack of intrinsic factor, positive Romberg test (loss of balance with eyes closed) with pernicious anemia They may become confused; more often they have paresthesias in the extremities (particularly numbness and tingling in the feet and lower legs). They may have difficulty maintaining their balance because of damage to the spinal cord, and they also lose position sense (proprioception). These symptoms are progressive, although the course of illness may be marked by spontaneous partial remissions and exacerbations. Without treatment, patients can die after several years, usually from heart failure secondary to anemia. The classic method of determining the cause of vitamin B12 deficiency is the Schilling test: - in which the patient receives a small oral dose of radioactive vitamin B12, followed in a few hours by a large, nonradioactive parenteral dose of vitamin B12 (this aids in renal excretion of the radioactive dose). - If the oral vitamin is absorbed, more than 8% will be excreted in the urine within 24 hours; therefore, if no radioactivity is present in the urine (ie, the radioactive vitamin B12 stays within the gastrointestinal tract), the cause is gastrointestinal malabsorption of the vitamin B12. - Conversely, if the urine is radioactive, the cause of the deficiency is not ileal disease or pernicious anemia. - Later, the same procedure is repeated, but this time intrinsic factor is added to the oral radioactive vitamin B12. If radioactivity is now detected in the urine (ie, the B12 was absorbed from the gastrointestinal tract in the presence of intrinsic factor), the diagnosis of pernicious anemia can be made.

The Schilling test is useful only if the urine collections are complete; therefore, the nurse must promote the patients understanding and ability to comply with this collection. Another useful, easier test is the intrinsic factor antibody test. A positive test indicates the presence of antibodies that bind the vitamin B12intrinsic factor complex and prevent it from binding to receptors in the ileum, thus preventing its absorption. Unfortunately, this test is not specific for pernicious anemia alone, but it can aid in the diagnosis.

3. Aplastic (hypoplastic) anemia: bone marrow is depressed or destroyed by a chemical or drug leading to leucopenia, thrombocytopenia, decreased erythrocytes, and decreased leukocytes (agranuclocytosis) Aplastic anemia is a rather rare disease caused by a decrease in or damage to marrow stem cells, damage to the microenvironment within the marrow, and replacement of the marrow with fat. *It results in bone marrow aplasia (markedly reduced hematopoiesis). *Therefore, in addition to severe anemia, significant neutropenia and thrombocytopenia (a deficiency of platelets) are also seen. Substances Associated With Aplastic Anemia
Analgesics Antiseizure agents (mephenytoin, triethadione*) Antihistamines Antimicrobials* Antineoplastic agents (alkylating agents, antitumor antibiotics, antimetabolites) Antithyroid medications Benzene* Chloramphenicol* Gold compounds* Heavy metals Hypoglycemic agents Insecticides Organic arsenicals* Phenylbutazone* Phenothiazines Sulfonamides* Sedatives

o o o
Aplastic anemia can be congenital or acquired, but most cases are idiopathic (ie, without apparent cause). Infections and pregnancy can trigger it, or it may be caused by certain medications, chemicals, or radiation damage (Chart 33-3). Agents that regularly produce marrow aplasia include benzene and benzene derivatives (eg, airplane glue). Certain toxic materials, such as inorganic arsenic and several pesticides (including DDT, which is no longer used or available in the United States), have also been implicated as potential causes.

Manifestations: The manifestations of aplastic anemia are often insidious. Complications resulting from bone marrow failure may occur before the diagnosis is established. Typical complications are infection and symptoms of anemia (eg, fatigue, pallor, dyspnea). Purpura (bruising) may develop later and should trigger a CBC and hematologic evaluation if these were not performed initially. If the patient has had repeated throat infections, cervical lymphadenopathy may be seen. Other lymphadenopathies and splenomegaly sometimes occur. Retinal hemorrhages are common. Fever, bleeding from mucous membranes, decreased leukocytes, erythrocytes, and platelets with aplastic anemia ***A bone marrow aspirate shows an extremely hypoplastic or even aplastic (very few to no cells) marrow replaced with fat.

4. Polycythemia vera: a sustained increased in the number of erythrocytes , leukocytes, and platelets, with an increased viscosity of the blood
Polycythemia refers to an increased volume of RBCs. It is a term used when the hematocrit is elevated (to more than 55% in males, more than 50% in females). Dehydration (decreased volume of plasma) can cause an elevated hematocrit, but not typically to the level to be considered polycythemia. Polycythemia is classified as either primary or secondary. Polycythemia vera, or primary polycythemia, is a proliferative disorder in which the myeloid stem cells seem to have escaped normal control mechanisms. The bone marrow is hypercellular, and the RBC, WBC, and platelet counts in the peripheral blood are elevated. However, the RBC elevation is predominant; the hematocrit can exceed 60%. This phase can last for an extended period (10 years or longer).

Clinical Manifestations Patients typically have a ruddy complexion and splenomegaly (enlarged spleen). The symptoms result from the increased blood volume (headache, dizziness, tinnitus, fatigue, paresthesias, and blurred vision) or from increased blood viscosity (angina, claudication, dyspnea, and thrombophlebitis), particularly if the patient has atherosclerotic blood vessels. Another common and bothersome problem is generalized pruritus, which may be caused by histamine release due to the increased number of basophils. Erythromelalgia, a burning sensation in the fingers and toes, may be reported and is only partially relieved by cooling. Increased hemoglobin, purple-red complexion with polycythemia vera

Assessment and Diagnostic Findings

Diagnosis is made by finding an elevated RBC mass (a nuclear medicine procedure), a normal oxygen saturation level, and an enlarged spleen. 5. Thrombocytopenia purpura: appears to result from the production of an antiplatelets and facilitates their destruction by phagocytic leukocytes


ITP is a disease that affects people of all ages, but it is more common among children and young women. There are two forms of ITP: acute and chronic. ***The acute form, which occurs predominately in children, often appears 1 to 6 weeks after a viral illness. This form is self-limited; remission often occurs spontaneously within 6 months. Occasionally, corticosteroids are needed for a brief time. ***Chronic ITP is often diagnosed by exclusion of other causes of thrombocytopenia.

Although the precise cause remains unknown, viral infections sometimes precede ITP in children. Occasionally medications such as sulfa drugs can induce ITP. Other conditions, such as systemic lupus erythematosus (SLE) or pregnancy, can also induce ITP.

Clinical Manifestations
Many patients have no symptoms, and the low platelet count (often less than 20,000/mm3, and less than 5000/mm3 is not uncommon) is an incidental finding. Common physical manifestations are easy bruising, heavy menses, and petechiae on the extremities or trunk. Patients with simple bruising or petechiae (dry purpura) tend to have fewer complications from bleeding than those with bleeding from mucosal surfaces, such as the gastrointestinal tract (including the mouth) and pulmonary system (eg, hemoptysis), which is termed wet purpura. Patients with wet purpura have a greater risk for intracranial bleeding than do those with dry purpura. Despite low platelet counts, the platelets are young and very functional. They adhere to endothelial surfaces and to one another, so spontaneous bleeding does not always occur. gum bleeding and epistaxis with thrombocytopenic purpura Low platelet count, ecchymotic areas, hemorrhage petechiae with thrombocytopenic purpura

Assessment and Diagnostic Findings

Patients may have an isolated decrease in platelets (less than 20,000/mm3 is common), but they may also have an increase in megakaryocytes (platelet precursors) within the marrow, as detected on bone marrow aspirate.

B. Therapeutic interventions
1. Improve diet; include ascorbic acid, which stimulates iron uptake 2. Vitamin supplements: iron, B12, folic acid Iron supplementation is usually given in oral form, typically as ferrous sulfate, or FeSO4. Many patients have difficulty tolerating iron supplements, primarily due to gastrointestinal toxicities (eg, nausea, abdominal discomfort, constipation). Here are some helpful guidelines for taking iron supplements: Take iron on an empty stomach (1 hour before or 2 hours after a meal). Iron absorption is reduced with food, especially dairy products.

To prevent gastrointestinal distress, the following schedule may work better if more than one tablet a day is prescribed: Start with only one tablet per day for a few days, then increase to two tablets per day, then three tablets per day. This method permits the body to adjust gradually to the iron. Increase the intake of vitamin C (citrus fruits and juices, strawberries, tomatoes, broccoli), to enhance iron absorption. Eat foods high in fiber to minimize problems with constipation. Remember that stools will become dark in color. Polysaccharide iron complex forms are better tolerated but are more expensive. Liquid forms of iron supplementation may be better tolerated than solid forms, although they are more expensive. The liquid forms can discolor teeth. Use a straw or place the spoon at the back of the mouth to take the supplement; rinse mouth thoroughly afterward. ***Food sources high in iron include organ meats (beef or calfs liver, chicken liver), other meats, beans (black, pinto, and garbanzo), leafy green vegetables, raisins, and molasses. Taking iron-rich foods with a source of vitamin C enhances the absorption of iron.

Anemia in Renal Disease

The availability of recombinant erythropoietin (epoetin alfa [Epogen, Procrit] erythrocyte growth factor) has dramatically altered the management of anemia in end-stage renal disease by decreasing the need for RBC transfusion, with its associated risks. Erythropoietin, in combination with oral iron supplements, can raise and maintain hematocrit levels to between 33% and 38%. This treatment has been successfulwith dialysis patients. Many patients report decreased fatigue, increased energy, increased feelings of well-being, improved exercise tolerance, better tolerance of dialysis treatments, and improved quality of life. Hypertension is the most serious side effect in this patient population when the hematocrit rapidly increases to a high level. Therefore, the hematocrit should be checked frequently when a patient with renal disease begins erythropoietin therapy. The dose of erythropoietin (epoetin alfa) should be titrated to the hematocrit. In some patients, the elevated hematocrit and associated hypertension may necessitate antihypertensive therapy.

SE: Fever, fatigue, weakness, bone pain, diarrhea, dizziness, nausea, edema, shortness of breath 3. Blood transfusions (except for polycythemia vera) 4. Corticosteroids and androgens to stimulate bone marrow function; bone marrow transplant; splenectomy when formed elements of the blood are destroyed (aplastic anemia); thrombocytopenic purpura 5. Phlebotomy, low iron diet, radioactive phosphorus, busulfan (Myleran)Alkylating Agents - (polycythemia vera) busulfan (Myleran)Alkylating Agent - Alter DNA structure by misreading DNA code, initiating breaks in the DNA molecule,cross-linking DNA strands

SE: Bone marrow suppression, nausea, vomiting, cystitis (cyclophosphamide, ifosfamide), stomatitis, alopecia, gonadal suppression, renal toxicity (cisplatin) PLANNING/IMPLEMENTATION
1. Teach client about dietary modifications and medication administration 2. Explain the need for prevention of hemorrhage and phlebotomies (polycythemia vera) 3. Provide postoperative care if splenectomy is performed

HODGKINS DISEASE A. Etiology and pathophysiology

1. 2. 3. 4. 5. Cause unknown Higher incidence in males and young adults Proliferation of malignant cells (Reed-Sternberg cells) within lymph nodes All tissues may eventually be involved, but chiefly lymph nodes, spleen, liver, tonsils, and bone marrow Classification by standings and the presence or absence of systemic symptoms

B. Clinical Findings
Facts About Hodgkins Lymphoma
The lymphatic system is a network of thin tubular vessels that branches out to almost all parts of the body. Scattered in between these vessels are lymph nodes. The job of the lymphatic system is to fight infection and disease. Cancer of the lymphatic system is called lymphoma. Hodgkins is one of two main types of lymphoma with non-Hodgkins being the other. Hodgkins lymphoma (Hodgkins disease) commonly affects lymph nodes in the neck or in the area between the lungs behind the breastbone. It can also begin in groups of lymph nodes under the arms, in the abdomen or in the groin. It's named after the British doctor Thomas Hodgkin who first described the disease in 1832. According to the American Cancer Society, nearly 64,000 new cases of lymphoma will be diagnosed this year. This includes 7,350 cases of Hodgkins lymphoma. Hodgkins lymphoma is very treatable and often curable. Eighty-five percent of patients with Hodgkins live longer than five years after diagnosis.

Risk Factors for Hodgkins Lymphoma

The cause of Hodgkins lymphoma is unknown. However, doctors believe immune system problems as well as age may increase a person's chance of developing this disease. Hodgkins lymphoma has two peak time frames: between the ages of 15 and 40 and in people over age 55. However, the disease can affect anyone. Males are typically more at risk of developing Hodgkins lymphoma. Those who have been infected with the Epstein-Barr virus are more likely to develop Hodgkins lymphoma. Having a parent or sibling with Hodgkins lymphoma also increases risk of the disease.

Staging of Hodgkins Lymphoma

The stage of cancer is a term used to describe its size and whether it has spread. Knowing this helps doctors plan the best treatment. Stage I: Single lymph node or non-lymph node region is affected. Stage II: Two or more lymph node or non-lymph node regions are affected on the same side of the diaphragm (the muscle under the lungs). Stage III: Lymph node or non-lymph node regions above and below the diaphragm are affected. Stage IV: The cancer has spread outside the lymph nodes to organs such as the liver, bones or lungs. Stage IV can also refer to a tumor in another organ and/or tumors in distant lymph nodes.

B symptoms are so called because lymphoma staging includes both a number (I-IV) and a letter (A or B). "A" indicates the absence of systemic symptoms, while "B" indicates their presence. B symptoms include:
Fever greater than 38C. Pel-Ebstein fever, the classic intermittent fever associated with Hodgkin disease, occurs at variable intervals of days to weeks and lasts for 1-2 weeks before resolving. However, fever associated with lymphoma can follow virtually any pattern. Drenching sweats, especially at night. Unintentional weight loss of >10% of normal body weight over a period of 6 months or less.

1. Subjective: pruritus; anorexia; dyspnea and dysphagia caused by pressure from enlarged nodes 2. Objective a. Enlarged lymph nodes (generally cervical nodes are involved first) b. Diagnosis confirmed by histologic examination of the lymph node c. Progressive anemia d. Elevated temperature e. Enlarged spleen and liver may occur f. Pressure from enlarge lymph nodes may cause symptoms of edema and obstructive jaundice g. Thrombocytopenia if spleen and bone marrow involved


1. 2. 3. 4. 5. 6. Provide emotional support for the client and family Protect from infection Monitor temperature Observe for signs of anemia; provide adequate rest Examine sclera and skin for signs of jaundice Encourage high nutrient density foods; observe for anorexia and nausea

Assessment and Diagnostic Findings

Because many manifestations are similar to those occurring with infection, diagnostic studies are performed to rule out an infectious origin for the disease. The diagnosis is made by means of an excisional lymph node biopsy and the finding of the Reed-Sternberg cell. Once the diagnosis is confirmed and the histologic type is established, it is necessary to assess the extent of the disease, a process referred to as staging. During the health history, the nurse should assess for any B symptoms. Physical examination requires a careful, systematic evaluation of the lymph node chains, as well as the size of the spleen and liver. A chest x-ray and a CT scan of the chest, abdomen, and pelvis are crucial to identify the extent of lymphadenopathy within these regions. Laboratory tests include CBC, platelet count, ESR, and liver and renal function studies. A bone marrow biopsy is performed if there are signs of marrow involvement, and some physicians routinely perform bilateral biopsies. Bone scans may be performed to identify any involvement in these areas. A staging laparotomy and lymphangiography are no longer considered mandatory, primarily because of the accuracy of CT.

It is important to know the stage of a cancer in order to plan treatment. Stages of Adult Hodgkin's Lymphoma Stages of adult Hodgkin's lymphoma may include A, B, E, and S.

A: The patient has no symptoms. B: The patient has symptoms such as fever, weight loss, or night sweats. E: "E" stands for extranodal and means the cancer is found in an area or organ other than the lymph nodes or has spread to tissues beyond, but near, the major lymphatic areas. S: "S" stands for spleen and means the cancer is found in the spleen.