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

be delivered orally or by inhalation. Pills are easy to take but slow to deliver relief. The inhalers are quick to deliver the medication directly to the airways and reduce systemic absorption, but are difficult to time during inspiration. These medications include the beta 2-adrenergic-agonists (i.e., albuterol, salmeterol, and formoterol), anticholinergics (i.e., tiotropium), and theophylline derivatives. The use of glucocorticoids has not been shown to be as effective in the treatment of COPD when compared with its use in asthma. Inhaled corticosteroids have been shown recently to be advantageous in cases of severe COPD, however. Combinations of inhaled steroid and beta 2-adrenergic-agonists have been shown to be more effective than the beta-agonist alone.

Patients with COPD must often be put on chronic oxygen therapy using a nasal cannula and a canister of compressed gas. This therapy helps to reduce depression, improve exercise tolerance and weight gain, and reverse the cellular hypoxia characteristic of COPD.

Three options for surgical therapy are available for patients with COPD: bullectomy, lung volume reduction surgery (LVRS), and lung transplantation. Bullectomy provides benefit in only a small percentage of patients with COPD.

In end-stage COPD, in which emphysema becomes life threatening, lung transplantation is often considered. Half of all lung transplants performed over the last decade have been for COPD.

ASTHMA

Definition

This group of pulmonary diseases is characterized by narrowing of the airways in response to a variety of stimuli. These episodes manifest as acute dyspnea and coughing, and the diseases typically demonstrate periods of exacerbation relieved by long spells of normal respiration. An asthma attack usually lasts from minutes to hours and can occur on a daily basis. Only rarely does an attack lead to death.

whether alone or in combination with other antiglaucoma agents, should be avoided in all patients with glaucoma. The topical use of a beta-blocking agent has been known to cause asthma attacks in previously undiagnosed patients.

Pathophysiology

Asthma involves a state of subacute and chronic inflammation of the tissues of the airways. It is believed that allergens acting as antigens are inspired and activate inflammatory cells on the airway surface epithelium. The release of cellular inflammatory mediators is triggered, including eosinophils and lymphocytes, which release histamine, bradykinin, leukotrienes, and prostaglandins. This process results in lung edema, increased mucus production, and narrowing of the pulmonary airways.

During an asthma attack, airway resistance increases, as does the work of breathing. Air becomes trapped in the lungs and results in a reduction in arterial blood oxygen. This state of hypoxia is typical during an asthma attack. Severe pulmonary obstruction can result in metabolic acidosis.

Symptoms

An asthma attack is typified by wheezing, shortness of breath, and nonproductive coughing. It is episodic and usually occurs on a daily basis, even in a very mild, subclinical form. Often it is characterized by a state of near panic, as the patient begins to gasp for breath and experiences tightness of the chest. It may last for minutes to hours, and often ends with a productive cough.

Diagnosis

A patient whose dyspnea is relieved by the inhalation of a beta-adrenergic agonist has demonstrated a reversible airway obstruction diagnostic of asthma.

Etiology

Most often caused by an allergy, asthma affects tens of millions of people in the United States. A wide variety of antigens have been identified as instigators of an asthmatic attack. The upper airway may become hyperresponsive after an acute viral attack, exposure to toxic levels of gases (i.e., ozone), exercise, emotional stress, and environmental and air pollution.

Exposure to drugs can also exacerbate an asthma attack. Progressive asthma can occur in adults after the consumption of aspirin. Of significant note to the optometrist, the use of topical beta-adrenergic antagonists in the treatment of glaucoma is associated with exacerbations of asthma. The use of topical beta-blockers,

Treatment

The goal of treatment is the prevention of future asthma attacks. To this end, elimination of the stimulating allergen is paramount, but often impossible. Environmental antigens are difficult to identify and often their distribution cannot be adequately controlled. In some cases of cold-induced asthma attacks, the ice skater or skier prone to this condition may have great difficulty in giving up their chosen sport.

Short-term pharmacologic relief is provided by adrenergic stimulants that stimulate beta-adrenergic receptors in the lungs and provide airway dilation by inhibiting smooth muscle contraction. These substances are inhaled to provide maximal bronchodilation with a minimum of systemic absorption.

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Theophylline compounds are medium-potency medications used for longer-term bronchodilation. This medication is taken usually once daily before bedtime to prevent nocturnal attacks.

Long-term medications that reduce pulmonary inflammation include the glucocorticoids and mast-cell stabilizers. Inhaled steroids remain a mainstay of chronic asthma treatment. These reduce inflammation but do not dilate the airway. The mast-cell stabilizers act to reduce mast cell degranulation and thus reduce the histamine and bradykinin levels. This serves to improve lung function and reduce symptoms. Nedocromil and cromolyn sodium are two examples of inhaled mast-cell stabilizers.

Prognosis

Few people die from asthma, although the mortality rate from this disease is rising in the inner-city environment. This rise is most likely the result of limited health care in these regions.

Long-term changes in lung function rarely occur in asthma and it is rare to see other serious systemic alterations in physiology as commonly occur in COPD. In most cases, asthma occurs in childhood and stays mild throughout the lifetime of the patient. It rarely worsens and continues to be characterized by exacerbations and remissions. Approximately half of all children who develop asthma do not have any attacks after 10 years. Only approximately 10% of children with asthma worsen with age.

PNEUMONIA Definition

This group of pulmonary diseases is characterized by infection of the lung tissues.

Etiology

Pneumonia can be caused by various species of bacteria, viruses, chlamydia, fungi, and parasites. Some of the common infective sources of pneumonia include influenza, tuberculosis, and histoplasmosis. The most common cause of pneumonia is the bacteria Streptococcus pneumoniae.

Pathophysiology

Infectious particles gain access to the lung through inhalation, dissemination from the heart, direct inoculation by a tracheal tube, or stab wounds to the chest. In most cases, pneumonia is caused by aspiration of organisms that commonly inhabit the lining of the oropharynx. In some cases the individual inhales infectious aerosols that bypass the upper respiratory

defense mechanisms. Only one infectious particle need be inhaled and deposited in the alveolus to initiate infection.

Symptoms

Pneumonia usually has an acute onset with a sudden production of a fever and a productive cough. The sputum is usually purulent, and chest pain with dyspnea is often present.

Diagnosis

Radiographic analysis reveals pulmonary infiltrates and, in some cases, pulmonary cavities. The key diagnostic test to detect pneumonia is the sputum evaluation and culture. Lower tract secretions for culturing can be safely and effectively sampled by fiberoptic bronchoscopy. Blood testing with culturing of the sample and serology testing can help elucidate the etiology of the pneumonia.

Treatment

The treatment of pneumonia is directed against the offending organism as isolated from the sputum and blood cultures. Antibiotic resistance, as determined by the culture, plays a major role in determining the appropriate antibiotic for treatment. Antimicrobial therapy is usually begun before the radiographic and sputum analysis is available. Because there is a significant amount of resistance to various antibiotic medications, there is no one drug of choice. Preferred antibiotics for the treatment of bacterial pneumonia include penicillin G, amoxicillin, doxycycline, erythromycin, ciprofloxacin, and gatifloxacin.

CYSTIC FIBROSIS Epidemiology

Of cystic fibrosis (CF) patients, 93% are diagnosed in childhood. Slightly more than one third of these patients survive to adulthood, and approximately one tenth of the population with CF live to be older than 30 years of age. Of patients, 15% are diagnosed in the first 24 hours of life because of gastrointestinal obstruction. CF occurs in approximately 1 of every 3000 live births in the Caucasian population. CF is less common in the African-American population, occurring in approximately 1 of every 17,000 live births.

Pathophysiology

CF is a multisystem, primarily pediatric disease characterized by chronic airway infection that leads ultimately to permanent abnormal dilation of the bronchi.

Destruction occurs within the walls of the mediumsized airways, and fibrous tissue replaces the normal wall components. Thick, purulent secretions appear in the airways associated with bronchial wall ulcerations. This inflammation and bronchial wall destruction is known as bronchiectasis, and is a significant component of CF. Multisystem disorders associated with CF include urogenital, sweat gland, and intestinal dysfunction, and pancreatic insufficiency.

Etiology

CF is a monogenetic disease caused by an autosomal recessive trait. This genetic mutation occurs on chromosome 7 and causes an improper processing and degradation of an important protein. The absence of this protein at crucial sites on the cell wall yields a state of improper cellular function. This dysfunction causes cells to alter their water and electrolyte transport systems and leads to pulmonary, intestinal, pancreatic, and sweat gland dysfunction.

Symptoms and Signs

The most prominent symptoms are cough and chronic sinusitis. The sputum produced is typically green, viscous, and purulent. Blood is often found in the sputum sample (hemoptysis). Associated signs include weight loss, increased sputum production, and worsening dyspnea. Ultimately, there may be respiratory failure. Associated signs of the multisystem characteristics of CF include lower right quadrant pain with failure to pass food, and late onset of puberty.

such as recombinant human DNAse. Antibiotics are used to mitigate pulmonary infections. Short-term bronchodilation can be achieved with inhaled betaadrenergic agonists or anticholinergics. Pancreatic enzyme replacement therapy will aid digestion and improve weight gain.

PULMONARY THROMBOEMBOLISM Pathophysiology

Patients inherit a predisposition to pulmonary thromboembolism (PTE) that initiates the sequence of vessel wall damage, hypercoagulation of blood, and venous stasis. An instigating factor, known as a stressor, precipitates this sequence in genetically prone individuals. Such stressors include trauma, surgery, pregnancy, obesity, and the use of oral contraceptives. Often immobile patients, such as pregnant women on long airplane flights, will be prone to the development of PTE. Genetics plays a role in that patients inherit a predisposition to hypercoagulability. The thrombi in these patients tend to develop in the pelvic vein or veins of the leg. Embolization occurs to the pulmonary arterial circulation. Pulmonary embolism then causes increased pulmonary vascular resistance, impaired gas exchange, bronchoconstriction, and lung edema. Death usually results from right ventricular dysfunction, known as right heart failure. Right ventricular failure causes the interventricular septum bulges into the left ventricle. Left ventricular output falls, leading to a decrease in blood pressure, a compromised coronary artery perfusion, and eventual myocardial ischemia.

Diagnosis

The diagnosis of CF is made primarily on clinical signs and symptoms and the analysis of the chloride ion in sweat. Sputum microbiology reveals characteristic infections associated with CF including Staphylococcus aureus and Haemophilus influenzae. Chest x-rays may reveal small airway obstruction with hyperinflation. DNA analysis is being performed more frequently but remains challenging because of the high rate of CF mutations.

Diagnosis

Patients with PTE are seen with significant dyspnea. Lung pain, coughing, and hemoptysis may occur. Large PTEs may provoke syncope, fever, chest pain, cyanosis, and tachycardia. Enzyme-linked immunosorbent assay (ELISA) testing for plasma D-dimer is often positive in PTE. Electrocardiogram results reveal sinus tachycardia. Chest x-rays are typically normal in cases of PTE, but chest CT, lung scanning, echocardiography, and pulmonary angiography are the principal tests to diagnose PTE.

Therapy

Treatment of CF aims to control pulmonary infections, clear airway secretions, prevent intestinal obstruction, and provide nutritional support for appropriate weight management. Pulmonary complications of CF are managed with respiration exercises that help to preserve lung function. Secretions are often removed by using hypertonic saline aerosols. Mucus clearance is also aided by the use of appropriate pharmaceuticals,

Treatment

The goal of PTE treatment is the dissolving of the clot, pain relief, and the prevention and management of deep vein thrombosis (DVT). Treatment of the primary blood clot consists of thrombolysis with a pharmaceutical agent such as recombinant tissue plasminogen activator (TPA), or removal of the PTE by embolectomy. Long-term management includes the use of anticoagulating agents such as heparin and

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warfarin for the treatment of DVT. Nonsteroidal antiinflammatory agents (NSAIDS) may be helpful for pain relief. Beta-adrenergic agonists may be used to treat right heart failure. Insertion of a vena cava filter may be necessary in cases that do not respond to pharmaceutical intervention.

BIBLIOGRAPHY

Barnes PJ, Adcock IM: Transcription factors and asthma, Eur Respir J 12:221, 1998.

Bartlett JG, et al: Community-acquired pneumonia in adults: guidelines for management, Clin Infect Dis 26:811, 1998.

Dinwiddie R: Pathogenesis of lung disease in cystic fibrosis,

Respiration 67:3, 2000.

Drazen JM, Weinberger SE: Disorders of the respiratory system. In Braunwald E, et al, eds: Harrison’s principles of internal medicine, ed 15, New York, 2001, McGraw-Hill.

Hanania NA, et al:The efficacy and safety of fluticasone propionate (250 microg)/ salmeterol (50 microg) combined in the diskus inhaler for the treatment of COPD, Chest 124:834-843, 2003.

Madison J, Irwin R: Chronic obstructive pulmonary disease, Lancet 352:467, 1998.

NHLBI/WHO: Global initiative for chronic obstructive lung disease workshop report: global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. 2004, GOLD: the global initiative for chronic obstructive lung disease (website): www.goldcopd.com. Accessed December 12, 2005.

Pedullo PF: Pulmonary thromboembolism, In Murray JF, Nadle JA, eds: Textbook of respiratory medicine, ed 3, Philadelphia, 2000, Saunders.

Sethi JM, Rochester CL: Smoking and chronic obstructive pulmonary disease, Clin Chest Med 21:67, 2000.

Sin DD, et al: Contemporary management of chronic obstructive pulmonary disease: scientific review, JAMA 290: 2301-2312, 2003.

Taylor DO, et al: Registry of the International Society for Heart and Lung Transplantation: twenty-second official adult heart transplant report-2005, J Heart Lung Transplant 24: 945-955, 2005.

Weinberger SE: Principles of pulmonary medicine, ed 3, Philadelphia, 1998, Saunders.

CHARACTERISTICS OF LIVER DISEASE

In general, liver disease may manifest as one of two distinct clinical entities. The condition may be obstructive, as in cholestatic disease, or hepatocellular. A patient with a liver that is inflamed, injured, or necrotic is considered to have hepatocellular disease. The causes of hepatocellular disease include alcoholism and viral hepatitis. Cholestatic liver disease is characterized by obstruction of bile flow and can be caused by such entities as gallstones, drugs, and neoplasm.

The symptomology will implicate one of these two clinical categories, and the physical examination with laboratory testing will usually pinpoint the diagnosis. Additional testing includes radiographic analysis of the liver and surrounding structures and liver biopsy.

Symptoms

Jaundice

Also known as icterus, jaundice represents an elevated serum bilirubin. Bilirubin is a breakdown product of hemoglobin that is produced in the spleen and liver. The state of hyperbilirubinemia results from a diseased liver that overproduces bilirubin, or from an impairment in the excretion of bilirubin. Elevated bilirubin causes a darkening of the urine. The large quantity of elastin in the sclerae tends to accumulate bilirubin resulting in yellow-appearing eyes, or scleral icterus. Jaundice also causes a yellowishorange discoloration of the skin that remains the

most reliable method of assessing the severity of liver disease.

Pruritus

Acute liver disease typically causes body-wide itching. Pruritus often occurs in association with acute hepatitis, biliary obstruction, and cirrhosis. Although typical in acute conditions, chronic liver disease can also cause itching.

Right Upper Quadrant Pain

Tenderness experienced by the patient when the area over the liver is palpated is a typical presenting symptom in liver disease. Severe right upper quadrant pain occurs in gallbladder disease and acute hepatitis.

Abdominal Distention

Abdominal swelling may be caused by liver disease. Cirrhosis may cause fluid retention within the abdomen known as ascites. The patient with abdominal distention may at first notice an enlarging flank that makes normal fitting clothes difficult to button or fasten.

Fatigue

A feeling of tiredness and a lack of energy is the single most common presenting symptom of liver disease. Unfortunately this symptom is very nonspecific, because so many disorders can cause lethargy. When associated with liver disease, fatigue tends to be worse in the afternoon and after exercise.

Palmar Erythema

Also known as “liver palms,” this clinical sign of chronic liver disease is characterized by a red discoloration of the palms of the hands (Figure 10-1).

Spider Angioma

This nevus of the cheek represents dilated vascular lesions under the epidermis that resemble spiders. This condition is the result of chronic liver disease and is most often found associated with hepatic cirrhosis (Figure 10-2).

FIGURE 10-1 ■ Palmar erythema (“liver palms”). A clinical sign of chronic liver disease is this red discoloration of the palms. (From Goldman L, Ausiello D: Cecil textbook of medicine, ed 22, Philadelphia, 2004, Elsevier.)

FIGURE 10-2 ■ Spider angioma (cheek nevus). Dilated vascular lesions of the cheek that resemble spiders due to chronic liver disease (hepatic cirrhosis). (From Goldman L, Ausiello D: Cecil textbook of medicine, ed 22, Philadelphia, 2004, Elsevier.)

Evaluation of the Patient with Liver Disease

The majority of patients with liver disease seen in the physician’s office are there because of the clinical sign of jaundice. Patients will notice the yellowing of their sclera, particularly if they are contact lens wearers. In addition, many report that friends or relatives notice the yellowing of the patient’s eyes.

Body-wide itching is another common clinical sign of liver disease that motivates patients to seek medical care. The itching can be relentless and distracting. It is not as specific a sign of liver disease as jaundice, however, and may occur from such wide-ranging conditions as allergy and pancreatic cancer.

Patients with right upper quadrant pain, or tenderness over the liver, often seek medical help. Often, however, they may delay medical intervention, because this symptom may be interpreted as a stomach virus or muscular cramp.

Because they are such nonspecific symptoms, fatigue and nausea rarely motivate the patient to seek medical help.

Clinical History

The patient should be asked about nausea, fatigue, pain in the right upper quadrant, and body-wide itching. The history should also include the major risk factors for liver disease, including sexual activities, the use of alcohol and intravenous drugs, exposure to jaundiced individuals or needle stick, recent surgeries or blood transfusions, and family history of liver disease.

Physical Examination

The physical examination is oriented towards the detection of icterus, or yellowing of the skin and eyes. Palpation of the right upper quadrant may uncover hepatic pain and tenderness. The optometrist should inspect for scleral icterus under natural light.

Laboratory Testing

Serum testing for liver disease includes serum alanine (ALT) and aspartate aminotransferases (ALT). Other valuable liver serum tests include alkaline phosphatase (AP) and serum bilirubin. In addition, viral serology can help detect and diagnose viral hepatitis.

Imaging

Computed axial tomography (CAT) scan imaging is useful in the evaluation of obstructive jaundice. The hemodynamics of the liver can be evaluated by Doppler ultrasonography and magnetic resonance imaging (MRI). Liver masses can be evaluated by CT and MRI.

Liver Biopsy

Chronic liver disease is best evaluated by liver biopsy. This method allows for the most accurate diagnosis and staging of liver disease possible. The biopsy also helps evaluate the effectiveness of treatment and helps to form the prognostic opinion.

CLASSIFICATION OF LIVER DISEASE

Liver disease can be classified as either hepatocellular or cholestatic. Hepatocellular diseases include viral hepatitis, drug toxicity, alcoholism and chronic cirrhosis. Cholestatic liver conditions include gallstones and malignant obstructions.

Hepatocellular Diseases

Viral Hepatitis

Acute viral hepatitis is caused by a systemic viral infection that affects the liver. Five viruses can cause hepatitis; each has its own characteristics yet all have fairly similar clinical presentations. Symptoms and signs of viral hepatitis range from nonexistent to fulminate and disabling disease. The disease state may be subclinical for the lifetime of the patient, or it can be persistent and complicated and lead to destruction of the liver. Liver destruction occurs because of the immune response of the host and not by direct injury from the hepatovirus. Serologic testing is necessary to determine which virus is causing the liver damage.

Hepatitis A

Caused by an RNA virus, hepatitis A (HAV) incubates for one month and replicates only in the liver. For 2 to 4 months after infection, HAV causes an immunoglobulin M (IgM) antibody response that converts to an immunoglobulin G (IgG) response after 5 months. Acute HAV infection is diagnosed by detection of an IgM response. The IgG response is detectable for the life of the patient. Early on, virus sheds into the feces, and so the fecal-oral route is the primary means of transmission. HAV outbreaks occur in areas of overcrowding and filth. The disease has been linked to poor personal hygiene and the failure of food employees to wash their hands after defecating. Improved sanitation will reduce the incidence of HAV infection. In rare cases HAV has been linked to the consumption of contaminated shellfish. HAV causes a mild presentation and may cause jaundice. The disease is detected early in the infection by an elevated anti-HAV IgM. Almost all patients with HAV infection fully recover with no significant sequelae. Some patients may have a recurrence of the hepatitis months after the initial infection. HAV is not associated with cancer, and the prognosis without treatment is excellent. Liver de-

struction is almost never seen in HAV infection. Therapy for acute viral hepatitis is limited and not necessary in HAV infection. Immunization against HAV infection is safe and effective for as long as four months. Immunization is often recommended to tourists traveling to areas of poor sanitation, daycare workers, and family members of patients with HAV infection. Vaccination against HAV infection is effective for as long as 20 years and is often recommended to military personnel, daycare workers, laboratory workers, and Alaskan natives.

Hepatitis B

A small DNA virus, hepatitis B (HBV) replicates in the liver but can live elsewhere in the body. These extrahepatic sites include the spleen, lymph nodes, and pancreas. HBV can cause acute or chronic hepatitis and is associated with liver carcinoma. Serologic and virologic markers are detectable after HBV infection to aid diagnosis, prognosis, and help determine length of infection. The HBV virus incubates for 2 to 3 months, and its onset can be either acute or insidious. HBV occurs most often in babies, toddlers, children and young adults. Spread by percutaneous inoculation, fetal delivery, or sexual activity, the HBV disease is occasionally severe. People at highest risk for HBV infection include hospital workers, spouses of HBV-infected individuals and prisoners. Hepatic necrosis is a rare complication of HBV infection. Antiviral therapy is not necessary in cases of HBV because almost all cases of HBV infection recover completely. Vaccination against HBV infection is recommended for hemophiliacs, prisoners, health care workers exposed to blood, intravenous drug users, sexually active individuals, and children younger than 18 years.

Hepatitis C

An RNA virus, hepatitis C (HCV) provokes a cellmediated response that results in liver injury. It incubates for an average of two months and results in a disease of insidious onset. In the past, HCV infection typically occurred as the result of percutaneous inoculation of contaminated blood, particularly during blood transfusions. Laboratory testing has virtually eliminated this route of transmission. However, HCV is still transmitted through percutaneous injection by IV drug abusers. Exposure to blood products is another route of transmission. The liver disease associated with HCV infection is moderate in presentation and commonly progresses to a chronic state of hepatitis. No known prophylaxis exists against HCV infection, and therapy consists of interferon and lamivudine. A HCV vaccine is still considered impractical, and prevention of HCV involves the alteration of behavior and the appropriate use of precautions against exposure to infected individuals.

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Hepatitis D

The RNA virus hepatitis D (HDV) has a one to three month incubation period and causes either acute or insidious-onset liver disease. HDV is spread by close personal contact and exposure to bloodborne products, and is prominent among intravenous drug abusers and certain ethnic populations. HDV infection is often superimposed over HBV infection and can contribute to chronic hepatitis. No treatment exists for HDV infection, and it can be prevented by HBV vaccine. The only therapy for HDV infection is the use of interferon.

Hepatitis E

The RNA virus hepatitis E (HEV) has a 2 week to 2 month incubation period and causes an acute liver disease in the infected, who typically are young adults. The major route of HEV transmission is fecal-oral and results in a mild disease state. Outbreaks throughout the world often occur after major floods because of contamination of the water supply. HEV is rarely spread by person-to-person contact. This virus does not progress to chronic liver disease and it has a good prognosis without treatment. No established prophylaxis or therapy exists for HEV infection.

Hepatovirus Prophylaxis in the Office

The optometrist faced with examining a patient with known viral hepatitis should establish safeguards against contamination. The appropriate use of barrier precautions is essential in preventing spread from the patient to the doctor. Certain challenges prompt the physician to use latex gloves when examining patients who report a positive history of hepatoviral infection. Although it is rare for the optometrist to encounter bodily secretions or blood from the patient, the fingers of the optometrist may be exposed to a significant amount of tears. This mandates the use of latex, or appropriate nonlatex, allergy-free, examination gloves, in all cases of patients with known, active viral hepatitis. The optometrist need not wear gloves in cases of patients with resolved viral hepatitis, unless there is a chronic condition. In this case, and when the patient is unsure whether the condition is resolved, the optometrist should wear gloves. In addition, the optometrist should always wear gloves if any risk of bleeding on the part of the patient exists, even if no known hepatovirus infection is present.

Alcoholic Liver Disease and Cirrhosis

Excessive alcohol consumption is a leading cause of cirrhosis, alcoholic hepatitis, and fatty liver disease. Severe liver disease typically occurs after the patient has consumed approximately five beers per day during a 10-year period. Three beers per day during a

10-year period are enough to produce a fatty liver. Seven beers per day during a 10-year period may result in hepatitis or cirrhosis. Women are more susceptible to developing alcoholic liver disease than men. Patients who test positive for hepatitis C infection are more prone to develop accelerated liver disease.

Fatty Liver

Fatty liver represents the earliest histological response to alcohol-induced injury. In this condition, the liver accumulates fat in the cells responsible for producing an enzyme responsible for alcohol metabolism. Extensive drinking results in further fat accumulation throughout the entire liver lobule. Cessation of drinking allows the liver to regenerate and return to normal, however. Fatty liver is therefore benign and reversible. If the patient continues to drink, a consequential transition from fatty liver to alcoholic hepatitis will occur. Fatty liver is detected on routine physical examination by the discovery of an enlarged liver in a known alcoholic. Rarely, an associated jaundice may be present. Laboratory findings include mild elevations in liver enzyme tests, and elevated cholesterol levels and hyperbilirubinemia. Ultrasound studies of the liver will assess liver size and help in the diagnosis of fatty liver. The treatment of fatty liver disease involves complete cessation of alcohol use. Patient education is necessary to allow the alcoholic to learn about appropriate nutritional alternatives to their previous life style. Psychosocial therapy is mandatory to help the alcoholic through the symptoms of withdrawal. To prevent a relapse, the alcoholic must learn to confront his or her dependency on a daily basis for the rest of his or her life.

Alcoholic Hepatitis

When alcohol-damaged liver cells swell and degenerate, the result is isolated areas of necrosis and fibrosis. Excessive alcohol intake results in a release of cytokines that initiates an immunologic process of liver damage. This state of hepatitis represents a transition from fatty liver to cirrhosis. This form of hepatitis is reversible with cessation of drinking. Clinically, alcoholic hepatitis may be associated with fever, jaundice, and abdominal pain. Laboratory testing reveals significant elevations in liver enzyme levels and significant hyperbilirubinemia. Ultrasound studies can help determine the presence of significant liver disease by detecting ascites, reversal of blood flow in the portal vein, and intra-abdominal collaterals. Mortality rates in cases of severe alcohol hepatitis approach 70%, and these patients often have anemia, low serum protein, and hyperbilirubinemia. Death is often associated with ascites, hemorrhage within the liver, and encephalopathy. Treatment of the hepatitis involves alcohol cessation and the use of glucocorticoids to suppress the immunologic basis of hepatocellular damage.

Alcoholic Cirrhosis

Once the chronic injury to the liver is irreversible a state of cirrhosis is said to exist. Cirrhosis is characterized by fibrosis of the liver, liver cell necrosis and scarring, a loss of liver cells, and a distorted vascular supply. Liver injury induces the deposition of collagen from fibroblasts. Finally, the liver shrinks and becomes hard and nodular. The result is a condition clinically characterized by ascites, jaundice, and encephalopathy. Cirrhosis is often associated with anorexia, weight loss, poor nutritional intake, easy bruising, and fatigue. Alcoholic cirrhosis is the end result of untreated fatty liver and alcoholic hepatitis. This is the most common cause of cirrhosis in North and South America. Laboratory findings in advanced alcoholic cirrhosis include anemia, hyperbilirubinemia, and elevated liver enzymes. No association is known to exist between chronic alcoholism and the development of diabetes mellitus. Cessation of alcohol ingestion may result in a reversal of the cirrhosis. Alcohol counseling is recommended for these patients, because the strict prohibition of alcohol ingestion is necessary to prevent further liver damage. Once liver cirrhosis occurs, aspirin should be avoided, because aspirin metabolism is altered and this in turn affects blood coagulability.

Ocular Evaluation

Chronic alcohol consumption may cause reduced visual acuity in the range of 20/50 to 20/200. Color testing may reveal red-green defects. Visual field testing typically demonstrates central and cecocentral scotomata. The optic nerve heads may appear normal in the early stages of alcohol optic neuropathy, but in the later stages optic nerve swelling may occur with splinter hemorrhages. Eventually, optic atrophy ensues resulting in a pale, atrophic disc. Acute ingestion of alcohol may result in inebriation. An ocular characteristic of the intoxicated patient is endpoint nystagmus on lateral gaze. Commonly, acne rosacea with an associated keratitis results from alcohol consumption (Figure 10-3). Acne rosacea may be treated with either tetracycline, 250 mg four times a day by mouth (prohibited in children), or doxycycline 300 mg three times per day by mouth. With sensitivity to these medications, erythromycin may be substituted at a dosage of 250 mg four times per day by mouth.

Reye’s Syndrome. A fatty liver in a child younger than 15 years that results in encephalopathy is known as Reye’s syndrome. Although the cause remains unknown, it is postulated that viral pathogens and drugs may be associated with this form of liver disease. One definitive association is the use of aspirin and other salicylates by children. For this reason, the use of aspirin is always prohibited in children younger than 15 years. Symptoms appear soon after the ingestion of aspirin or

FIGURE 10-3 ■ Acne rosacea. The face shows red papules and pustules and the lids reveal an associated blepharitis. (Courtesy the Department of Dermatology, University of North Carolina at Chapel Hill. From Goldstein BG, Goldstein AO: Practical dermatology, ed 2, St Louis, 1997, Mosby.)

an upper respiratory condition and include stupor, coma, vomiting, and convulsions. Jaundice is not usually present, but the liver is enlarged and hypoglycemia is typically discovered on laboratory testing. Any child who ingests aspirin accidentally should be taken to an emergency room immediately to watch for signs of Reye’s syndrome. Treatment includes infusions of glucose, plasma, and mannitol. Only approximately half of all children with Reye’s syndrome survive.

Cholestatic (Obstructive) Diseases

The hallmark of cholestatic disease is an inhibition of bile flow resulting in jaundice. Associated clinical signs and symptoms include itching, fatigue, and right upper quadrant pain.

Gallstone Obstruction

A gallstone is a concretion of bile that consists of cholesterol, calcium bilirubinate, and other salts, protein, and fatty acids. Gallstones form most often among North American Indians and the obese. These obstructions also commonly form in people who are undergoing weight loss programs, women, the elderly, and those eating a high-fat diet. Symptoms are induced by obstruction of the cystic duct and include nausea, vomiting, and severe pain in the right upper quadrant of the abdomen. Stones are diagnosed on radiographic imaging and ultrasound. Treatment involves the use of medication to slowly dissolve the stone during a 6-month period and prevent further stone development (lithogenesis). Some gallbladder stones are amenable to fragmentation by the generation of shock waves. Known as lithotripsy, the use of stone fragmentation negates the use of long-term medication. In cases of severe symptomology, previous gallbladder disease, or very large gallstones, cholecystectomy may

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be necessary. Often approached by a laparoscopic method, the gallbladder in this case is entirely removed. Most cases of symptomatic cholelithiasis are now treated by laparoscopic cholecystectomy.

Primary Biliary Cirrhosis

Primary biliary cirrhosis (PBC) appears to be autoimmune in nature, because approximately 90% of patients with this condition have circulating IgG antimitochondrial antibodies. PBC occurs mostly in women. The disease is usually asymptomatic and is detected by an elevation in the alkaline phosphatase level. The earliest symptom is itchiness (pruritus) of the palms and soles of the feet. Jaundice may occur after several months and hyperpigmentation of the skin may be present. As the condition progresses, ascites and hypertension may develop. No effective treatment for PBC exists at this time. The use of ursodiol may increase the lifespan and reduce the symptoms of the patient, but this has yet to be confirmed. The eventual liver destruction mandates a liver transplant and results have been excellent in these cases.

Drug-Induced Hepatitis

Liver injury may result from the ingestion of drugs because of cellular membrane distortion or the blocking of biochemical pathways. Necrosis follows and the bile ducts become injured, and this in turn blocks lipid

movement and causes fat accumulation. The effect may be the result of a direct toxic effect on the liver, as in tetracycline-induced hepatitis, or idiosyncratic, as in isoniazid and chlorpromazine-induced hepatitis. Medications known to cause cholestasis include erythromycin, rifampin, oxacillin, methimazole, and cyclosporine.

BIBLIOGRAPHY

Bismuth H, ed: Consensus conference on indication of liver transplantation, Hepatology 20(suppl ):1, 1994.

DiBisceglie AM: Hepatitis C, Lancet 351:351, 1998.

Ghany M, Hoofnagle JH: Liver and biliary tract disease. In Braunwald E, et al, eds: Harrison’s principles of internal medicine, ed 15, New York, 2001, McGraw-Hill.

Hoofnagle JH, DiBisceglie AM: The treatment of chronic viral hepatitis, N Engl J Med 336:347, 1997.

Hurwitz ES, et al: Public Health Service Study on Reye’s syndrome and medications, N Engl J Med 313:842, 1985.

Johnston DE, Kaplan MM: Medical progress: pathogenesis and treatment of gallstones, N Engl J Med 328:412, 1993.

Lee WM: Drug-induced hepatotoxicity, N Engl J Med 333:1118, 1995.

McCullough AJ, O’Connor JFB: Alcoholic liver disease: recommendations of the American College of Gastroenterology,

Am J Gastroenterol 93:2022, 1998.

Ransohoff DF, Gracie WA: Treatment of gallstones, Ann Intern Med 119:606, 1993.

Runyon BA, et al: Management of adult patients with ascites caused by cirrhosis, Hepatology 27:264, 1998.