Causes and Incidence Any factor that leads to chronic alveolar inflammation can serve as a precursor for the formation of emphysematous lesions. Common precursors are tobacco smoking; air pollution, particularly in an occupational setting; underlying respiratory disease; and severe respiratory infection in early childhood. A rare congenital alpha1-antitrypsin deficiency also is a precursor. Emphysema is the leading cause of death from respiratory disease in the United States. The incidence increases with age and is highest in white, male, blue-collar workers.

Disease Process Recurrent alveolar inflammation leads to degradation of the elastin in the distal airways because of an imbalance in the elastase-antielastase mechanism. As the degradation proceeds, elastic recoil is lost, the alveolar walls are destroyed, blood vessel density is reduced, the air spaces enlarge, and the peripheral bronchioles collapse; this leads to air trapping and impaired gas exchange.

Symptoms Emphysema is thought to begin in early adulthood and remain asymptomatic until middle age. Gradual progressive exertional dyspnea is the most common presenting complaint. Chronic productive coughing, wheezing, recurrent respiratory infection, and fatigue may also be present. Severe dyspnea and cyanosis are late signs.

Potential Complications Alveolar blebs and bullae may form and rupture, leading to pneumothorax. Cor pulmonale and heart failure may also occur.

Diagnostic Tests

Clinical evaluation
History of smoking, occupational exposure

Radiology
Normal in early disease; localized radiolucency with decreased vascular markings

Pulmonary function
Total lung capacity, residual volume, functional residual capacity, increased compliance; decreased forced vital capacity and forced expiratory volume

Arterial blood gases
Decreased PaO2; normal PaCO2 until late in disease, when it increases

Treatments

Surgery
None.

Drugs
Bronchodilators to promote mucus clearance; antiinfective drugs to treat secondary bacterial infection; flu and pneumonia vaccines for prophylaxis; antitrypsin replacement therapy for individuals with demonstrated deficiency (experimental).

General
Removal of irritants; chest physiotherapy, vaporizer to loosen secretions; lowlevel oxygen to treat hypoxemia, with careful monitoring of blood gases for rise in PaO2 without rise in PaCO2; consistent exercise to improve ventilatory and cardiac function; counseling for depressive episodes.

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Causes and Incidence The cause of primary encephalitis is usually direct invasion by one of several viruses (arbovirus, enterovirus, adenovirus, herpes virus, mumps virus). The mode of transmission is usually a mosquito bite, but ticks and amebae may also transmit the virus. Some forms of the virus (e.g., herpes virus) may be spread by direct contact with nasal excretions or open lesions. A rarer secondary encephalitis may occur as a complication of another primary viral infection such as measles, chicken pox, or rubella. Primary encephalitis occurs worldwide and may be sporadic or epidemic.

Disease Process Within 24 hours of contact, the virus invades the bloodstream, lymph nodes, bone marrow, and most organs. Within 48 hours there is marked lymphocyte destruction and necrosis of lymph nodes. By day 4, macrophages have replaced the destroyed lymph nodes, bone marrow is depleted, and the cytoplasm and megakaryocyte nuclei are degenerating. The viral titer declines in peripheral tissues and increases in the brain. By day 6, there is extensive involvement of the meninges, brain, and spinal cord, with petechial hemorrhages, lymphocytic perivascular cuffing, gliosis, and neuronal necrosis, causing cerebral dysfunction.

Symptoms Subclinical cases of encephalitis do occur and are largely asymptomatic or are accompanied by flulike symptoms such as fever and general fatigue. Common early signs of encephalitis are fever, severe frontal headache, nausea, and vomiting. If encephalitis is untreated, neurologic signs that may manifest 6 to 7 days after initial infection are nuchal rigidity, lethargy, confusion, stupor, coma, seizure activity, and extremity paralysis.

Potential Complications The likelihood of complications is related to the etiologic agent and the person’s general premorbid condition. Complications include permanent neurologic damage and death.

Diagnostic Tests

Clinical evaluation
History of exposure; nuchal rigidity; positive Kernig’s sign; pathologic reflexes; muscle weakness; paralysis

Cerebrospinal fluid
Elevated pressure; WBCs, proteins slightly elevated; glucose normal; clear fluid; occasionally isolation of the virus (mobile amebae can be seen on wet mount)

Serology
Increase in antibody titer early in disease

Immunofluorescent stain of biopsy brain tissue
Positive for specific viruses

Treatments

Surgery
None.

Drugs
Antiinfective drugs for amebic infections: acylovir for herpes infections; sedatives for restlessness; anticonvulsants for seizure activity; mannitol and corticosteroids to reduce cerebral edema and inflammation.

General
Maintenance of fluid and electrolytes; maintenance of the airway: may need mechanical ventilation; oxygen to maintain blood gases; maintenance of nutritional status: may need nasogastric tube; seizure precautions; rest; neurologic assessments; secretion precautions to prevent transmission of some viral agents; prevention of spread through mosquito-ant-tick control.

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Causes and Incidence Acute bacterial endocarditis (ABE) is usually caused by Staphylococcus aureus. Hemolytic streptococcus, pneumococcus, and gonococcus have also been implicated. Subacute bacterial endocarditis (SBE) is usually caused by a streptococcal species but may also be caused by staphylococcal and Haemophilus organisms. Individuals at risk include those with a history of rheumatic heart disease, valvular disease, and congenital heart defects; those with prosthetic valves, pacemakers, or arteriovenous shunts; IV drug abusers; immunosuppressed individuals; and individuals who have had invasive cardiac procedures or surgery. Estimates of the incidence range from 0.16 to 5.4 cases per 100,000 hospital admissions. Men are more susceptible, and the mean age is about 55 years. The overall mortality rate is about 25%, but it rises to as high as 70% in elderly patients.

Disease Process The bacterial agent travels to the heart via the bloodstream after a transient bacteremia. They are attracted to and colonize a fibrin-platelet vegetation that formed as a result of previous endothelial damage. The pathogens are resistant to normal host defense mechanisms because the vegetation prevents access of the defense mechanisms to the microorganisms.

Symptoms

SBE
Onset is insidious with malaise, night sweats, chills, aching, anorexia, weight loss, intermittent fever, headache, and dyspnea over a period of weeks; when embolization occurs, petechiae of the skin and mucous membranes, splinter hemorrhages of the fingernails, macules on the palms and soles, retinal hemorrhage, and neurologic sequelae are also present; late signs include clubbing of the fingers and splenomegaly

ABE
Rapid onset of high fever, chills, and severe aching; rapid course with embolization and manifestations of various complications

Potential Complications The course of endocarditis is progressive and fatal without treatment. Complications include stroke, congestive heart failure, renal failure, meningitis, subarachnoid hemorrhage, and heart failure.

Diagnostic Tests

Clinical evaluation
History of symptoms, risk factors; heart murmur

Complete blood count
Anemia, leukocytosis, elevated erythrocyte sedimentation rate

Blood cultures
To identify causative agent

Echocardiography
To detect vegetations, abscesses, damaged valves, regurgitation

Urinalysis
Proteinuria, hematuria with renal involvement

Rheumatoid factor
Positive in 50% of individuals with SBE of at least 6 weeks’ duration

Treatments

Surgery
Removal of thrombi, valve replacement in cases of uncontrollable sepsis.

Drugs
Antiinfective drugs targeted at causative agent; aspirin for fever, aches.

General
Rest; forcing fluids during temperature elevation; high-calorie supplements; monitoring for complications.

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Causes and Incidence The cause of endometriosis is unclear, but the prevailing hypothesis suggests dissemination and implantation of endometrial cells at local ectopic sites via retrograde menstruation through the fallopian tubes and distant sites via the bloodstream or lymphatics. Sites can be anywhere in the body, but pelvic structures are most common. Another hypothesis suggests transformation of coelomic epithelium into endometrium-like glands. A familial history, late childbearing, and mullerian duct abnormalities are predisposing factors. Approximately 25% of women can expect to develop endometriosis. It is seen most commonly during the childbearing years.

Disease Process After implantation of endometrial cells, primarily on pelvic structures (e.g., the ovaries, ligaments, oviducts, and peritoneal surface of the uterus), the cells grow to form lesions. These lesions are subject to hormonal cycles and bleed during menstruation, causing irritation and inflammation of the surrounding tissue, leading to fibrosis and adhesions.

Symptoms The major symptom is secondary dysmenorrhea, although many individuals are asymptomatic. Other symptoms are abnormal uterine bleeding, dyspareunia, infertility, lower abdominal pain, nausea and vomiting, and pain associated with a full bladder or with defecation.

Potential Complications The primary complication is infertility or spontaneous abortion.

Diagnostic Tests Laparoscopy with biopsy allows visualization and histologic confirmation of the lesions.

Treatments

Surgery
Laparoscopy to remove or vaporize lesions; hysterectomy with bilateral salpingo-oophorectomy for intractable pain.

Drugs
Gonadotropin-releasing hormone agonists, progestins, and antigonadotropic agents to inhibit ovarian function and suppress endometrial growth; prostaglandin synthase inhibitors to relieve dysmenorrhea.

General
Emotional support for depression, altered body image, and possible infertility.

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Causes and Incidence Epistaxis may be caused by a variety of factors, such as irritation, trauma, underlying coagulation disorders, or localized or systemic infections. At least 10% of the population is thought to have suffered at least one episode of epistaxis. Children and men are more susceptible, and winter is the time of most frequent occurrence.

Disease Process Bleeding results when damage interferes with the vascular integrity of the superficial vessels in the fragile mucosa of the nasal passages. Most bleeding originates in the anterior portion of the nose from Kiesselbach’s plexus, a highly vascular network in the anterior nasal septum. Posterior bleeding usually originates from the turbinates or lateral nasal wall.

Symptoms Bleeding from the nostrils.

Potential Complications Pooled blood may cause sinusitis and otitis media. Large blood loss can cause anemia or interfere with cerebral and cardiopulmonary tissue perfusion. In individuals with an altered mental status, aspiration of blood also is a possible complication.

Diagnostic Tests Inspection with a nasal speculum to determine the site of bleeding; x-ray films to locate fracture if trauma is the cause.

Treatments

Surgery
Reduction and fixation of nasal fractures; ligation of the internal maxillary artery for uncontrolled posterior bleeding; split-thickness skin grafts to correct chronic bleeding in Rendu-Osler-Weber syndrome.

Drugs
Analgesics for pain; if posterior chamber is packed, antiinfective drugs to prevent sinusitis and otitis media; if a large amount of blood was swallowed, nonabsorbable antibiotics to prevent breakdown of blood and ammonia absorption.

General
Upright position; pinching of the nose with thumb and forefinger for 5-10 minutes (anterior bleeding); cauterization of site if pressure fails; packing of nasal cavity to apply pressure (posterior bleeding); blood replacement if anemia is evident.

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