What cardiovascular abnormalities occur with uremia?

Patients with chronic kidney disease (CKD) are the highest risk group of individuals for cardiovascular disease, and cardiovascular events are the major cause of death among dialysis patients. Death from cardiovascular disease is 10 to 30 times higher in dialysis patients than in the general population. The cardiovascular mortality risk is increased twofold to fourfold in patients with diabetes (National Diabetes Information Clearinghouse, 2007).

Hypertension is the most common cardiovascular complication seen in patients with CKD and affects the majority of patients (Table 5-1). Hypertension causes CKD and CKD causes hypertension. Strict blood pressure control can delay the progession of CKD. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends a target blood pressure of less than 130/80 mm Hg in patients with CKD (Snively & Gutierres, 2004). Hypertension is associated with the progression of left ventricular hypertrophy (LVH), which places the patient at an increased risk for cardiovascular morbidity. Expanded extracellular fluid volume from fluid overload associated with sodium retention is the most prevalent cause. Many patients have increased plasma renin activity. Nephrectomy is an option to assist in the control of resistant hypertension, but is rarely seen today with the current pharmacologic agents available for treatment.

Table 5-1 Classification of Blood Pressure for Adults 18 Years and Older

Fluid volume and sodium regulation by diet, antihypertensive medications, and ultrafiltration help in the management of hypertension. Patients are also encouraged to exercise with their physician’s approval, and stop smoking programs or literature should be offered.

Atherosclerosis is a major factor in morbidity and mortality. A defect in liver lipoprotein lipase is a likely cause of increased serum triglycerides. Coronary artery disease, stroke, and peripheral arterial disease are increased.

Myocardial dysfunction presents as LVH resulting from hypertension, anemia, and atherosclerosis. With LVH the left ventricle grows abnormally thick, causing an interference with the normal pumping action of the heart. Signs and symptoms of LVH depend on the cause, but can include shortness of breath, chest pain, arrhythmias, dizziness, and congestive heart failure. The symptoms of LVH can be controlled or improved with the correction of hypertension, anemia, and fluid volume control. Some patients experience no symptoms at all, but progression to cardiac failure is not unusual.

Coronary artery calcification may occur as a result of imbalances in calcium phosphorus metabolism. Calcification of blood vessels, including the coronary arteries, which bring blood to the heart muscle, can place the patient at risk for heart attack and stroke.

Congestive heart failure (CHF) may be acute but is usually a chronic manifestation related to the retention of sodium and water. Symptoms of CHF include edema of the lower extremities, shortness of breath, and often fatigue, weakness, and the inability to perform physical activities. Weight gain from the excess fluid is another common symptom.

Pericarditis is a cardiovascular complication seen in the patient with CKD. The heart is surrounded by a double-membrane sac containing approximately 15 to 20 mL of fluid. This fluid provides lubrication, allowing the layers of the pericardium to glide smoothly over one another during the contraction of the heart. Uremic toxins, fluid overload, or bacterial/viral infections can all irritate the pericardial membrane, causing inflammation of the lining around the heart (the pericardium), which may trigger chest pain and fluid accumulation around the heart (pericardial effusion).

Patients often present with the classic triad of symptoms: chest pain, low-grade fever, and pericardial friction rub. The chest pain is intensified by deep inspiration, swallowing, and coughing and improves when sitting and leaning forward. The pericardial friction rub is harsh and leathery and heard best at the lower left sternal border during systole as the inflamed layers of the pericardial sac rub together. Aggressive dialysis therapy (daily dialysis) with ultrafiltration to minimize uremic toxins and excess fluids is necessary. Heparin therapy during the dialysis treatment is either decreased or not administered to the patient to minimize bleeding into the pericardial space. Antiinflammatory agents, both steroidal and nonsteroidal, may be prescribed to reduce inflammation.

Pericardial effusion can develop when increased fluid invades the pericardial space. Chest pain and elevated temperature will continue but the pericardial friction rub may be absent on auscultation. Hypotension and shortness of breath may also be seen. The fluid is usually bloody; if volume is large, tamponade may result.

Pericardial tamponade occurs when a large volume of fluid fills the pericardial space, compressing the cardiac muscle. Pericardial tamponade may have a slow or immediate onset and is associated with a high degree of mortality.

What integumentary changes are seen with chronic kidney disease?

Patients with CKD stage 5 present with very brittle hair, nails, and skin due to a decrease in the size and activity of the sweat and sebaceous glands. Calcium may deposit in the skin, causing intractable pruritus leading to excoriations of the skin from the itching. Uremic frost is rarely seen today and only in the patient with advanced uremia that is left untreated. Whitish precipitates of urea crystals deposit on the skin, giving it a “frosty” appearance. The skin color may appear tan-yellow from the pallor of anemia coupled with the retention of urinary pigments called urochromes. Ecchymosis is commonly seen due to platelet dysfunctions.

Why are infections a problem?

Leukocyte abnormalities include reduced white blood cell (WBC) count in some patients. Granulocytes have reduced response to infection and low bactericidal activity. In fact, infection is the second most common cause of death in CKD stage 5 patients. Susceptibility is enhanced by malnutrition, age, diabetes mellitus, immune system defects, and the frequency of cannulation and other invasive procedures. The use of central venous catheters is a major source of infection in the dialysis patient and efforts should be made to have them removed as soon as possible and replaced with an internal vascular access, such as a fistula. Caution must be taken when assessing body temperature because hypothermia is common and responses to infection may not be accompanied by fever. Elevated uremic levels impair phagocytosis and suppress the inflammatory response as well as hypersensitivity reactions.

Urea has an antipyretic effect and patients present with subnormal body temperatures. Poor nutrition plays a role in the diminished activity of WBC production.

Good nutrition, handwashing, and hygiene should be encouraged to help minimize infectious processes. It is recommended that all dialysis patients receive the pneumococcal, influenza, and hepatitis B vaccines.

What are some gastrointestinal manifestations of uremia?

Uremic individuals have a poor appetite and are often nauseated. The nausea will often diminish after dialysis is initiated and the circulating uremic toxins are reduced. Altered taste and dry mouth are common. Patients often complain of a metallic taste in the mouth, which leads to decreased appetite. The circulating uremic toxins cause nausea and vomiting, which can also be aggravated by intradialytic hypotension. Gastrointestinal bleeding, often occult, is aggravated by medications (aspirin, heparin) and by the platelet defects. Uremic fetor is characteristic of the patient with kidney disease and is the smell of urine or ammonia on the breath from decomposing urea. Gastrointestinal bleeding is seen from irritation of the gastrointestinal mucosa from the uremic environment and from capillary fragility as urea in the gastrointestinal tract breaks down, releasing the irritant ammonia. Diarrhea may be seen from intestinal irritation or hyperkalemia.

Functional constipation is frequent in patients on dialysis due to medications, fluid restrictions, low-potassium and low-fiber diet, and decreased activity levels. Discretion must be used in the choice of laxatives because many products used to manage constipation contain magnesium, phosphorus, or potassium.

Why is prevention of constipation important?

Because of a restricted diet, limited fluid intake, and regular ingestion of phosphate binders, CKD patients tend to become constipated or develop fecal impactions. As older patients are taken into dialysis programs, there is more functional constipation. Such patients have a high incidence of diverticula of the colon. In addition, diverticulitis or perforation is not rare. Hematomas of the bowel and perforation caused by injudicious enemas have occurred. Cathartics and laxatives should be avoided. Stool softeners seem to work well, although they are often required in larger than usual doses. Patients should be encouraged to eat a high-fiber diet, to adhere to a program of regular exercise, and to plan a regularly scheduled time for bowel movements to reduce the problems of constipation. Severe constipation may also cause hyperkalemia because stool potassium losses account for up to 40% of total body potassium losses per day in dialysis patients (see Chapter 14).

Is peptic ulcer disease common in dialysis patients?

Some reports cite an increased incidence of peptic ulcer disease in dialysis patients; others do not. There are reports of higher than normal gastric acidity related to high blood levels of gastrin, which may relate to parathyroid overactivity. Other studies indicate low gastric acidity related to increased urea and ammonia content of gastric juice. Literature suggests that the incidence of ulcer disease is about the same as for the nonuremic general population.

Does ascites occur in chronic kidney disease patients?

Ascites (a massive fluid collection in the peritoneal cavity) is an infrequent problem that is very troublesome. Most cases are related to repeated fluid overload, poor nutrition, and cardiomyopathy. Although some patients overcome ascites, deterioration and death are frequent outcomes.

What are the hematologic abnormalities?

Bleeding tendencies are seen as a result of a decrease in the quality and quantity of platelet production.

Anemia is the most common and severe hematologic defect. The hematocrit for normal men is 46% to 52%; for women it is 40% to 45%. People with uremia or who are on maintenance dialysis are anemic and have considerably lower hematocrit values. Anemia from diminished erythropoietin secretion occurs and results in fatigue, pallor, shortness of breath, and chest pain. The hostile uremic environment decreases the survival of red blood cells (RBCs) from 120 to 70 days.

What causes anemia?

Causes of anemia include (1) failure of production, or inhibition of action, of erythropoietin, a hormone produced by the kidney that stimulates the bone marrow to produce red blood cells; (2) a shortened life span of the red blood cells; (3) impaired intake of iron; (4) blood loss, including a tendency to bleed from the nose, gums, gastrointestinal tract, uterus, or skin, caused by platelet abnormalities; (5) blood loss related to the dialysis procedure itself; (6) elevated levels of parathyroid hormone (PTH), which has a suppressive effect on erythropoiesis in the bone marrow; and (7) poor nutrition and diet.

How does dialysis influence anemia?

Incomplete blood recovery after dialysis, dialyzer leaks, and frequent blood sampling contribute to anemia. The patient who is receiving adequate dialysis, is in a good nutritional state, and has adequate iron stores and intake will usually stabilize with a hematocrit between 20% and 30%. It is unusual for the hematocrit to go much higher except in people with polycystic kidney disease, in whom there may be greater than normal production of erythropoietin.

To minimize blood loss related to dialysis, particular care must be taken to (1) pretest dialyzers to prevent leaks; (2) monitor heparinization to prevent clotting; (3) return blood as completely as possible; (4) prevent damage to blood cells from incorrect pump occlusion or equipment malfunction; and (5) minimize the volume and number of blood samples drawn.