Ординатура / Офтальмология / Английские материалы / Clinical Medicine in Optometric Practice_Muchnick_2007

Dietary sodium restrictions and oral diuretics may improve MS symptomology. Mitral valvotomy uses inflation of a balloon seeded across the mitral valve through catheterization to open the valvular orifice.

Mitral Regurgitation

In mitral regurgitation (MR), the mitral valves become hard, deformed, and retracted. This process causes regurgitation of blood from the LV back into the LA. MR can be caused by AMI, trauma, rheumatic heart disease, infective endocarditis, or mitral valve prolapse.

MR is detected on cardiac angiography because contrast material quickly appears in the LA after its injection into the LV.

Patients with MR typically experience fatigue and dyspnea on exertion.

MR is treated by prevention of exertional dyspnea by the restriction of stimulating activities. Sodium intake is reduced and diuretics may help. Surgical treatment for MR is not required unless there are symptoms. In patients with MR who are symptomatic, mitral valve reconstruction (MVR) may maintain LV function and reduce or eliminate symptoms.

Mitral Valve Prolapse

Also known as Barlow’s syndrome or floppy-valve syndrome, mitral valve prolapse (MVP) is a common abnormality of the mitral valve. MVP may be caused by redundant mitral leaflet tissue or degeneration of the valve itself. MVP may be found to be associated with Marfan’s syndrome and osteogenesis imperfecta, but in most cases the cause is never discovered.

Anatomically, MVP causes an increase in the size of the mitral valve annulus. This increase leads to regurgitation of the blood from the LV back into the LA. This process leads to stress and eventual ischemia of the heart muscle, the LV in particular.

MVP is most common in females between the ages of 14 and 30 years of age. This condition is typically benign and never progresses past the auscultated systolic click or murmur. The majority of patients have no symptoms for their entire lives.

Severe MR can result from MVP, however, and often causes arrhythmias, palpitations, syncope, and, rarely, sudden death. Transient ischemic attacks (TIAs) may occur because of emboli from the stenotic mitral valve (Figure 7-1).

Patients with MVP are usually reassured that, in the absence of symptoms, no treatment is necessary. Antiinfective agents may be used as prophylaxis against infective heart disease. Beta-blocking agents may reduce any chest pain experienced because of MVP. Symptomatic tachycardia resulting from MVP is treated with antiarrhythmic agents. Severely symptomatic

FIGURE 7-1 ■ Emboli in the retinal arterial tree causing transient ischemic attacks in a patient with mitral valve prolapse (MVP).

patients with MVP may require surgical mitral valve repair. If the MVP results in TIAs, aspirin or other anticoagulants should be considered.

Aortic Stenosis

Calcification of the aortic cusps leads to valve thickening, increased rigidity, and a narrowed aortic opening. The effect of such stenosis is to obstruct LV outflow into the aorta. When this occurs, the LV becomes hypertrophied.

Aortic stenosis (AS) is caused by a number of conditions, including cardiac degeneration, endocarditis, a congenital malformation of the aortic valve, and inflammation of the aortic valve secondary to rheumatic heart disease.

Symptoms, including dyspnea, angina pectoris, and syncope, might not occur until late in the disease.

Patients with AS should avoid strenuous exercise, and salt intake should be restricted. Surgical treatment mandates aortic valve reconstruction (AVR). But the risks involved in AVR may forestall surgery if the patient is asymptomatic. AVR may improve angina pectoris, syncope, and LV decompensation.

Aortic Regurgitation

Aortic regurgitation (AR) is characterized by thickening, rigidity, and deformity of the aortic valve cusps. Because of this stenosis, the valve cusps lose their proper orientation during systole and diastole. This causes blood from the aorta to regurgitate back into the LV, which may lead to myocardial ischemia.

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AR may occur associated with Marfan’s syndrome or endocarditis. Patients often complain of tachycardia, palpitations, head pounding, dyspnea, and angina pectoris.

AVR may be necessary to relieve the symptoms associated with AR.

Tricuspid Stenosis

Tricuspid stenosis (TS) is rare in the United States and may be caused by rheumatic heart disease. Fatigue is the most common symptom in cases of TS. Poor blood flow from the right atrium (RA) to the right ventricle (RV) because of TS causes severe systemic venous congestion.

Diuretics help reduce total fluid volume and serve to relieve some of the systemic venous congestion. Tricuspid valve replacement (TVR) requires open heart surgery.

Tricuspid Regurgitation

Tricuspid regurgitation (TR) is seen in late tricuspid stenosis, heart failure, ischemic heart disease, and rheumatic heart disease. TR causes venous congestion but usually requires no treatment.

HEART FAILURE

The state of heart failure (HF) exists when the heart muscle no longer can pump blood at a rate appropriate to supply the metabolic needs of the tissues. HF is usually characterized by an inadequate contraction of the heart muscle and may be caused by viral infection, valvular disease, congenital heart disease, and coronary atherosclerosis. HF can be exacerbated by anemia, pregnancy, hypertension, arrhythmias, pulmonary lung infection, and rheumatic heart disease.

Patients in HF complain most often of dyspnea, as well as fatigue, weakness, nausea, confusion (caused by cerebral hypoxia), and anxiety. These patients may report swelling of the ankles and are typically out of breath when attempting to climb stairs. They may seek the counsel of an eye specialist because of fluid retention in the lower eyelids. Any new onset of lid swelling caused by fluid retention should prompt a referral to the primary physician for an evaluation to rule out heart failure.

HF is diagnosed by changes in the heart and lung sounds on auscultation, neck vein distention, enlargement of the heart, and two-dimensional echocardiography.

Treatment of HF involves identifying and eliminating the inciting cause (as in the case of an infective agent), correcting the underlying cause (using medical or surgical intervention), monitoring of the cardiac

function, and control of progressive congestive heart failure. In general, the left ventricular load is controlled by use of ACE-inhibitors. Excessive fluid levels are controlled by the restriction of salt intake, weight reduction, and the use of diuretics. Cardiac glycosides, such as digitalis, can increase myocardial contractility and helps control HF. Topical beta-blockers for use as intraocular pressure-lowering agents should be avoided in HF, because systemic absorption of the drug may worsen the heart condition.

ACUTE PERICARDITIS

The pericardium is a serous membrane that surrounds the heart muscle. This membrane prevents sudden expansion of the chambers during exercise and helps atrial filling during ventricular systole. The pericardium also reduces friction between the moving heart and the surrounding tissues.

Inflammation of the pericardium is known as pericarditis and may be caused by infection, noninfectious entities, and autoimmune reactions.

Infectious pericarditis may be caused by viruses such as HIV and adenovirus infections. Bacteria, such as tuberculosis, and fungal infections are also known causes of infectious pericarditis.

Noninfectious pericarditis may be caused by AMI, neoplasm, elevated cholesterol levels, trauma and sarcoidosis, among others.

Rheumatic fever, ankylosing spondylitis, and certain drugs may contribute to the autoimmune basis of pericarditis.

The most common symptom of pericarditis is chest pain. Auscultation of the heart may reveal a pericardial frictional rub, a high-pitched grating sound heard on expiration. The ECG findings may reveal the presence of pericarditis.

Treatment of pericarditis is designed to eliminate the cause, such as an infectious agent, and control any effusion (or fluid leakage) from the swollen pericardium.

BIBLIOGRAPHY

Braunwald E: Disorders of the heart. In Braunwald E, et al, eds:

Harrison’s principles of internal medicine, ed 16, New York, 2005, McGraw-Hill.

Carabello BA, Crawford FA:Valvular heart disease, N Engl J Med 337:32, 1997.

Colucci WS: Heart failure: cardiac function and dysfunction. In Braunwald E, ed: Atlas of heart diseases, ed 2, Philadelphia, 1999, Current Medicine.

Colucci WS, et al: Clinical aspects of heart failure. In Braunwald E, ed: Heart disease: a textbook of cardiovascular medicine, ed 6, Philadelphia, 2001, Saunders.

Colucci WS, Braunwald E: Pathophysiology of heart failure. In Braunwald E, ed: Heart disease: a textbook of cardiovascular medicine, ed 6, Philadelphia, 2001, Saunders.

Gillis AM: Pacing to prevent atrial fibrillation, Cardiol Clin 18:25, 2000.

Groh SS, Zipes DP: Cardiac pacemakers. In Braunwald E, ed:

Heart disease: a textbook of cardiovascular medicine, ed 6, Philadelphia, 2001, Saunders.

Katz AM: Heart failure, New York, 2000, Raven.

Kim EJ: Index of suspicion. Diagnosis: acute rheumatic fever (ARF), Pediatr Rev 21:21-26, 2000.

Levy S: Classification system of atrial fibrillation, Curr Opin Cardiol 15:54, 2000.

Wyse DG: Pharmacologic therapy in patients with ventricular tachyarrhythmia, Cardiol Clin 11:65, 1993.

Zipes DP: Specific arrhythmias: diagnosis and treatment. In Braunwald E, ed: Heart disease: a textbook of cardiovascular medicine, ed 6, Philadelphia, 2001, Saunders.

The excretory function of the kidney helps to regulate the volume and composition of the plasma.

The individual must excrete the end products of nitrogen metabolism, nonmetabolized dietary solutes, and excessive water volume, to preserve the internal environment of the body. In situations in which a deficit of water or solute exists, the kidneys act to conserve fluid and specific substances to prevent dehydration and preserve the intracellular and extracellular fluid compartments.

The processes of plasma ultrafiltration and reabsorption of the resulting filtrate occurs in the kidney and produces the volume and composition of excreted urine. Ultrafiltration of the plasma occurs at the glomerulus, and glomerulotubular balance is maintained by the reabsorption of filtered water and sodium salts by the renal tubules.

This chapter discusses the biological consequences of renal disease, including acute and chronic renal failure, proteinuria, systemic diseases and nephrology, injury, and nephrolithiasis. In addition, the effects of

genetic disease and diabetes on kidney functioning will be explored. Renal therapy, including dialysis and transplantation, is an integral part of this discussion.

ACUTE RENAL FAILURE

In acute renal failure (ARF) a reduction in glomerular filtration rate (GFR) occurs within hours to days. This rapid inability to process plasma, water, and solutes results in the retention of nitrogenous waste products, most notably urea and creatinine. This disturbance of physiological homeostasis produces changes in the extracellular fluid volume and the acid-base balance of the internal environment.

ARF typically occurs without symptoms and is discovered when biochemical lab tests reveal a rise in plasma creatinine and urea concentrations. Usually characterized by oliguria, or a reduced urine output, ARF is reversible.

ARF is responsible for approximately one third of all admissions to intensive care units. It is a

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complication of many serious conditions and contributes to significant in-hospital morbidity and mortality rates. ARF is associated with diseases that do not affect the renal tissues (prerenal ARF), diseases that do involve the renal tissues (intrinsic ARF), and, rarely, in cases of diseases associated with urinary tract obstruction (postrenal ARF).

Prerenal Acute Renal Failure

Accounting for slightly more than half of all ARF cases, prerenal ARF is characterized by mild-to-moderate renal hypoperfusion without kidney damage. This condition is typically caused by hypoperfusion caused by low blood volume (from trauma, hemorrhage, gastrointestinal fluid loss, and use of diuretics), low cardiac output, or systemic vasodilation. Prerenal ARF can complicate any disease that causes it. Renal hypoperfusion can be aggravated by the use of nonsteroidal antiinflammatory drugs (NSAIDs), although their topical use with punctal occlusion should limit this serious systemic side effect.

Intrinsic Acute Renal Failure

Characterized by kidney damage, intrinsic ARF can be caused by toxins, allergy, infection, neovascular obstruction, glomerular disease, and tubular ischemia. The most common cause of intrinsic ARF is tubular sclerosis, and intrinsic ARF may result from cases of advanced atherosclerosis. Intrinsic ARF is characterized by renal hypoperfusion and may in rare cases lead to irreversible renal failure. The initial hypoperfusion usually occurs within hours to days of the instigating event, most commonly trauma, hemorrhage, volume depletion, or major cardiovascular surgery. Renal blood flow falls off and reduces the glomerular filtration process. Necrotic debris obstructs the kidney tubules because of the resulting ischemia. This obstruction disrupts ion transport and membrane integrity, leading to cellular death. Restoration of renal blood flow during this period may limit kidney tissue injury, and cell rejuvenation may occur in one to two weeks.

Diagnosis of Acute Renal Failure

ARF is diagnosed on the basis of laboratory testing that reveals elevated urea and creatine levels with anemia. Patients may experience thirst and dizziness, but ARF is typically asymptomatic. Physical examination may reveal tachycardia, dry mucous membranes, and reduced sweating. Retention of sodium, potassium, and water occur with ARF, with a consequent increase in volume with tissue swelling and weight gain. Eventual brain-tissue swelling with seizure activity may occur.

Treatment of Acute Renal Failure

ARF is treated best by avoiding the onset of renal hypoperfusion. Hypovolemia is treated by restoration of the intravascular volume after major surgery or trauma. As long as the primary hemodynamic abnormality is corrected, and fluid management is maintained, ARF is readily reversible. Approximately half of all patients with ARF die, but in most cases death is caused by the underlying disease and not the kidney involvement. The vast majority of patients who survive an episode of ARF recover renal function and live normal lives.

CHRONIC RENAL DISEASE

Chronic renal disease (CRD) is a long-term process of nephron destruction that results in a reduction in kidney mass and function. Early in this disease some kidney nephrons die, and the rest hypertrophy and sclerose. This process causes a reduction in GFR and, although asymptomatic, patient’s urea and creatine serum levels rise. During the progression of the disease, severe renal insufficiency occurs when GFR drops even further. At this point, the patient is prone to urinary or respiratory infection and systemic hypertension. When GFR falls even further, permanent and widespread nephron destruction results in end-stage renal disease (ESRD), and the survival of the patient depends on renal replacement therapy.

As CRD progresses, nitrogenous waste products such as urea and creatine are retained, resulting in apothecia. Progressive renal insufficiency can cause functional derangement of multiple organ systems because of retention of toxins. Uremia results from failure of the kidneys to excrete toxins that are the products of protein and amino acid metabolism. Symptoms of uremia are variable but include anorexia, vomiting, headache, and fatigue.

Laboratory diagnosis will reveal fluid retention and acid-based disorders, metabolic acidosis, and abnormalities of bone, calcium, and phosphate. Other complications of CRD include anemia, congestive heart failure, peripheral vascular disease, and coronary artery disease.

The most common causes of CRD are systemic hypertension and diabetes mellitus, and the treatment of CRD is aimed at the underlying cause with the goal of avoiding ESRD. To avoid hyperfiltration injury, dietary protein is restricted and pharmaceuticals may be used.

Protein is degraded by the kidney to form urea, which must be excreted. CRD causes urea and other nitrogenous waste compounds to accumulate, thus resulting in uremia. Nephron injury may be slowed by the dietary restriction of protein-rich foods.

Medications to treat CRD are aimed at controlling systemic hypertension and offering nephron protection. The ACE inhibitors are particularly effective at performing these functions. With widespread renal destruction, eventual renal replacement therapy options include dialysis and kidney transplantation.

Dialysis

Dialysis serves to extend the life of the patient with ESRD. Patients with ESRD are candidates for dialysis if they have uremia, or other laboratory evidence of abnormalities caused by CRD. Hemodialysis aims to remove solutes from the sera. Blood from the patient flows through the dialyzer and urea is cleared from the system. Usually 12 hours per week of dialysis for a patient, divided into three equal visits, is needed for adequate treatment. The most common side effects of hemodialysis include systemic hypertension and muscle cramps.

Transplantation

The most effective renal replacement therapy for ESRD is kidney transplantation. It is least effective in elderly patients, those with metastatic cancer, or those with cardiopulmonary disease. Donor kidneys may come from living family members or cadavers, and the transplanted organ must have matching antigens of the human leukocyte antigen (HLA) major histocompatibility gene complex. After transplantation, immunosuppressive therapy is mandatory to prevent graft rejection but increases the risk of infection and malignancy. Such agents include azathioprine and, more recently, mycophenolate mofetil. Prednisone is a valuable adjunct in immunosuppressive therapy regimens, but use of this medication may increase the risk of glaucoma and posterior subcapsular cataracts. Cyclosporine is a powerful immunosuppressive agent usually used in conjunction with glucocorticoids to prevent renal tissue rejection.

SYSTEMIC DISEASE–RELATED NEPHROPATHY

Diabetic Nephropathy

The leading cause of ESRD is diabetic disease of the kidney. When diabetes causes kidney damage, hyperfiltration is present at first. Within 5 years of the onset of renal hyperfiltration a proteinuria becomes detectable on dipstick testing. Enlargement of the kidneys may result within a decade of onset. In patients who develop such nephropathy, more than two thirds develop diabetic retinopathy.

To slow the progression of diabetic nephropathy diet control, oral hypoglycemic agents and insulin are administered to control blood sugar. ACE inhibitors are used to control systemic hypertension. Poorly controlled diabetic nephropathy may yield ESRD, thus mandating the use of dialysis or transplantation.

Systemic Lupus Erythematosus Nephritis

Systemic lupus erythematosus (SLE) may cause isolated low-grade renal disease and CRD. The etiology of lupus nephritis is the deposition of immune complexes in the glomerular capillary wall. Diagnosis is made by renal biopsy. Blood laboratory studies may reveal a positive ANA and a positive anti–double-stranded DNA (dsDNA) antibody test. Some lupus nephritis cases do not require treatment. Advanced lupus nephritis cases may require glucocorticoids and cyclosporine therapy. This treatment usually controls acute glomerular inflammation.

Sjögren’s Syndrome Nephropathy

Renal disease can occur in association with dry eyes in Sjögren’s syndrome. Interstitial inflammation of the kidney tubules is the most common renal disease associated with Sjögren’s syndrome. Glucocorticoids and cyclosporine have been used successfully to mitigate the Sjögren’s nephropathy.

PROTEINURIA

Proteinuria is an elevated serum protein level secondary to reduced protein renal excretion. The vast majority of the cases are benign, asymptomatic, and have an excellent prognosis. These cases can occur spontaneously during fever or exposure to environmental stress. All other diagnostic renal tests are normal. Benign proteinuria resolves without treatment.

If the proteinuria is persistent, then a renal lesion may be present. Proteinuria may be caused by diseases of the glomerulus and, in particular, glomerulonephritis.

Nonsteroidal Antiinflammatory Drug—Related Glomerular Disease

Systemically ingested NSAIDs may produce ARF, kidney necrosis, and ESRD. If the oral administration of the NSAIDs is discontinued, then renal rejuvenation results in a return to normal kidney function. Topical NSAIDs pose little risk to patients of renal complications caused by poor systemic absorption and the typically short course of topical treatment. Patients with kidney disease who require topical NSAID therapy should use punctal occlusion while on these eye drops.

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Sickle Cell Anemia Nephropathy

As many as one third of homozygotes for sickle cell anemia (SCA) have glomerular disease, with kidney hyperfiltration occurring in the first five years of life. Within 30 years approximately one third of survivors typically demonstrate proteinuria, and some develop ESRD. CRD may occur in patients with anemia and systemic hypertension. SCA-related retinopathy is a common association in SCA nephropathy.

Fabry’s Disease

Glomerulosclerosis occurs as a late feature in Fabry’s disease. Patients in their late teens to early 20s develop elevated urine lipids and proteins with high blood pressure and renal insufficiency. Corneal and lenticular opacities are a common feature of Fabry’s disease. Kidney transplantation has been successful in some cases.

turia. If the stone breaks loose it may enter the ureter and cause excruciating back pain with fever. The passing of a stone is associated with pain and bleeding.

Stone removal is mandatory if pain, obstruction, or bleeding is present. Treatment involves the use of shock waves to fragment the stone and allow for passage (lithotripsy). Various therapeutic medications may prevent reformation of the stone.

OPHTHALMIC MANIFESTATIONS OF KIDNEY DISEASE

Patients with kidney disease may have manifestations in both the anterior and posterior chamber. Anterior chamber disorders associated with renal disease include band-shaped keratopathy and posterior-subcapsular cataract. The posterior manifestations include renal retinopathy, retinal detachment, Seigert’s streaks, and Elschnig spots.

Gouty Nephropathy

Chronically elevated serum uric acid concentration may yield uric acid crystal deposits in the kidney. Such deposits cause inflammation of the kidney with lymphocyte proliferation. Renal fibrosis follows and results in insufficiency. Treatment with allopurinol will reduce serum acid levels and uric acid stone formation.

VASCULAR INJURY

The renal blood vessels may be compromised by systemic hypertension, atherosclerosis, embolism, and inflammation. If the lumen of the large renal vessels narrows, inadequate delivery of blood to the glomerular capillary network occurs. This process results in a reduced GFR.

Atherosclerosis or embolism may cause thrombosis of the major renal arteries. Acute onset of thrombosis causes trunk, side or back pain and fever. Blood tests show an elevation in renal enzymes (LDH is most reliable).

Surgical intervention may relieve the renal blood vessel occlusion, but approximately one quarter of patients die during an acute renal thrombosis.

Atherosclerosis of the renal artery may cause a shower of microemboli to occlude small kidney vessels, which may cause renal ischemia. Renal vein thrombosis may also occur.

Band-Shaped Keratopathy

This uncommon anterior chamber manifestation of renal disease occurs because of elevated serum calcium levels. This state of hypercalcemia can result from renal failure, in which an elevated serum phosphorus level causes an alteration in the systemic calciumphosphorus ratio. Calcium carbonate salts may deposit in the cornea near Bowman’s membrane and extend across the interpalpebral zone. This hazy band can cause symptoms of halos, blurred vision, and foreign body sensation. Treatment of band-shaped keratopathy in symptomatic individuals involves removal of the deposition at the slit-lamp by using a scalpel and 2% to 3% sodium–ethylenediaminetetraacetic acid (NaEDTA) to expedite debridement. Phototherapeutic keratectomy with use of an eximer laser has been shown to be an effective technique to remove band keratopathy in some cases.

Posterior Subcapsular Cataract

This form of cataract is particularly detrimental to vision and is associated with the use of steroids and azathioprine in cases of renal transplantation. These immunosuppressive agents are used after transplantation to prevent or curtail tissue rejection. Cataract surgery is preferable to discontinuation of the immunosuppressive agent.

KIDNEY STONES

Nephrolithiasis, or kidney stones, are composed of cysteine, uric acid, calcium salts, and struvite. Stones may be associated with gout. Stones may cause hema-

Renal Retinopathy

Patients in renal failure may exhibit a retinopathy consisting of atherosclerotic changes to the retinal arterioles, crossing changes, cotton-wool spots, and flameshaped hemorrhages. This retinopathy is similar in

appearance to hypertensive retinopathy. Blood pressure readings will help to differentiate the true hypertensive retinopathy from renal retinopathy. Resolution of the retinopathy may occur with appropriate treatment of the renal disease.

Elschnig Spots

Elschnig spots of the retina are small, white spots or circular areas of hyperpigmentation surrounded by depigmentation. These spots are areas of serous detachment that resolve slowly because of elevated blood pressure. If the detachment resolves fairly quickly, a small depigmented area remains. If the detachment resolves slowly, hyperpigmented spots occur. The production of Elschnig spots occurs at the level of the pigment epithelium and is exacerbated by renal disease.

Nonrhegmatogenous Retinal Detachment

Nonrhegmatogenous retinal detachment is most often inferiorly located and bilateral. Associated with Elschnig spots, it is a localized serous detachment that looks like a white spot of retinal pigment epithelial necrosis. The resolution of this detachment causes an Elschnig-type atrophic spot or a hyperpigmented area. It is exacerbated by renal failure.

Seigert’s Streaks

Seigert’s streaks appear as radiating streaks extending from the posterior pole into the periphery at the level of the choroid. These are deep to the retinal epithelium. These occur as a result of occlusion of the choroidal artery leading to necrosis of the choroids. The etiology is atherosclerosis secondary to systemic hypertension. This condition is associated with detachment, and immediate referral for blood pressure control is mandatory. Prompt treatment may allow for healing of the choroidal vascular endothelium.

BIBLIOGRAPHY

Brady, et al:Acute renal failure. In Brenner BM, ed: Brenner and Rector’s the kidney, ed 6, Philadelphia, 2000, Saunders.

Brady HR, Wilcox CS, eds: Therapy in nephrology and hypertension, Philadelphia, 1999, Saunders.

Brenner BM: Disorders of the kidney and urinary tract. In Braunwald E, et al, eds: Harrison’s principles of internal medicine, ed 15, New York, 2001, McGraw-Hill.

Burton C, Harris KP:The role of proteinuria in the progression of chronic renal failure, Am J Kidney Dis 27:765, 1996.

Denker BM, et al: Hemodialysis. In Brenner BM, ed: Brenner and Rector’s the kidney, ed 6, Philadelphia, 2000, Saunders.

Heilberg IP: Update on dietary recommendations and medical treatment of renal stone disease, Nephrol Dial Transplant 15:117, 2000.

Meyer MM: Renal replacement therapies, Crit Care Clin 16:29, 2000.

Parving HH, et al: Diabetic nephropathy. In Brenner BM, ed:

Brenner and Rector’s the kidney, ed 6, Philadelphia, 2000, Saunders.

Price SR, Mitch WE: Metabolic acidosis and uremic toxicity: protein and amino acid metabolism, Lemin Nephrol 14: 252, 1994.

Star RA:Treatment of ARF, Kidney Int 54:1817, 1998.

Yaded M, Llach F: Vascular complications involving the renal vessels. In Brenner BM, ed: The kidney, ed 6, Philadelphia, 2001, Saunders.

SYMPTOMOLOGY

The most common symptom of lung disease is dyspnea, or shortness of breath. Acute dyspnea that occurs within hours to days may indicate asthma, infection, pulmonary edema, pneumothorax, or pulmonary embolism. Dyspnea that occurs during a period of days to weeks is most often the result of bronchitis. Chronic shortness of breath that occurs during a period of months to years typically indicates chronic obstructive pulmonary disease (COPD).

Coughing is also a common symptom associated with pulmonary disease, but is not useful in the differential diagnosis because it is so nonspecific. The coughing up of blood, or hemoptysis, is a rare symptom associated with disease of the lung tissue or vas-

culature. Such disorders include bronchitis, cystic fibrosis, neoplasm, pneumonia, or tuberculosis.

DIAGNOSIS

After the intake interview and a thorough history, the physician will perform a physical examination that includes inspection, palpation, percussion, and auscultation. The inspection qualifies the pattern of breathing and quantifies its rate. Any asymmetry of lung expansion is noted. Other abnormalities that can be isolated during inspection include rapid or labored breathing and dyspnea.

The symmetry of lung expansion can also be evaluated by palpation. Asymmetry may occur because of pleural fluid trapped between the lung and chest wall.

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Percussion can further evaluate this condition; pleural effusion will cause a dull sound. Emphysema, or air in the pleural space, causes a sharp percussive sound.

Some abnormal breath sounds include wheezes, rales, and rhonchi. Wheezes occur during expiration and indicate the narrowed bronchial lumen that can occur with airway edema, pulmonary neoplasm, or airway secretions. Rales, or crackles, occur during inspiration, and indicates interstitial lung disease. Rhonchi occur when fluid is present in the lumen of the airway that produces a vibratory sound.

Radiographic analysis of the chest may provide valuable initial information on respiratory disease. X-ray analysis of the lungs may show typical radiographic patterns of disease including a diffuse nodular pattern characteristic of neoplasm or tuberculosis, a diffuse alveolar disease typical of sarcoidosis, a diffuse interstitial disease, or a localized infiltrate indicative of pneumonia. Computed tomography (CT) and magnetic resonance imaging (MRI) may further define respiratory disease.

More specialized lung testing includes pulmonary angiography, needle aspiration for culturing, and bronchoscopy for direct visualization of the bronchial tree.

Laboratory testing may be used to measure the arterial blood gases and determine the presence and amount of hypoxemia (hypoxia), which is a reduction in O2 saturation of the arterial blood. The laboratory may also be used to collect and culture the sputum sample.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE Definition

As a category, the COPDs represent lung disorders characterized by a slow progression of reduced expiration. COPD is an inflammation of the airways and distal airspaces. A COPD with normal lung architecture but permanent enlargement of airspaces is diagnosed as emphysema. A COPD with a productive cough of at least 3 months’ duration during a 2-year period is diagnosed as chronic bronchitis.

nal respiratory units. These small airways are obscured by edema, fibrosis, smooth muscle cell infiltration, and goblet cell hyperplasia.

Symptoms

The primary symptom of COPD is dyspnea, and airway obstruction is always found in both emphysema and chronic bronchitis. This obstruction occurs mostly in the small airways when the patient’s workload increases and breathing becomes difficult and labored.

Hypoxemia may result if inspired gases are poorly distributed to the plasma (maldistribution of inspired gases is detected on arterial blood gases). The pulmonary circulation becomes adversely affected. When pulmonary hypertension occurs and results in elevations in cardiac output, changes in circulating biochemicals and hormones (including renin, aldosterone, norepinephrine, and antidiuretic hormone) lead to renal dysfunction.

As COPD advances, cachexia, or weight loss, occurs because of alterations in the levels of specific biochemicals. Skeletal muscle and protein are lost which results in a consequential reduction in strength. As wasting of arm and chest muscles advances, dyspnea is worsened, and this leads to worsening of the hypoxemia.

COPD occurs most commonly among smokers who have smoked for at least two decades. The earliest symptoms usually occur in the fifth decade and start as a productive cough. Within a decade, dyspnea may occur and exercise becomes severely limited.

As the disease advances, periods of marked exacerbations occur that can be life-threatening. These episodes usually occur once yearly and can be triggered by cardiac arrhythmia and lung infections. Advanced COPD is characterized by morning headaches caused by increased CO2 retention.

Diagnosis

Factors that point to a diagnosis of COPD include a history of chronic smoking, wheezing on forced expiration, increased chest diameter, the finding of emphysema on x-ray, and positive pulmonary function testing.

Etiology

COPD is exacerbated by dust, cigarette smoke, air pollution, toxic gases, pulmonary infections, and reduced antioxidant intake.

Pathophysiology

These environmental stresses, as well as genetic predisposition and influences, cause the epithelium of the airways to undergo squamous metaplasia and hypertrophy of the mucous glands. These changes cause the airways to narrow as mucous plugs obstruct the termi-

Treatment

The goals of treatment of COPD includes preservation of the airflow and lung capacity, enhancement of pulmonary function, management of hypoxemia, heart, and kidney complications, prevention of further progression of the disease, and avoidance of episodic exacerbations.

Treatment begins with smoking cessation, which serves to reduce malignancy rates, improve cardiovascular health, and improve airflow. Pharmacotherapy includes the use of bronchodilators that reduce dyspnea and improve exercise tolerance. These medications can