- Physical injury to the brain or other structures in the cranium, which may be open with skull fracture or penetration or closed with impact and rapid jarring. Concussion is the least serious injury and is characterized by a transient loss of consciousness with no gross damage to the brain and no neurologic sequelae. Contusions and lacerations indicate a more serious injury, and there is bruising of brain tissue with bleeding and tearing of the cortical surface.

Causes and Incidence Leading causes of head trauma include falls, industrial accidents, vehicular accidents (particularly involving motorcycles, or automobile accidents with passengers who were not wearing seat belts), assaults, sports injuries (boxing, diving, football), and intrauterine and birth injury. Alcohol use is a common related factor. Traumatic brain injury (TBI) causes more death and disability than any other neurologic disorder in individuals under 50 years of age. It is the leading cause of death in men under age 35. More than 77,000 individuals die of TBI each year in the United States, and 55,000 more are left with permanent neurologic damage.

Disease Process Damage occurs from skull penetration or rapid brain acceleration and deceleration, which injure brain tissue at the point of impact, at its opposite pole (contrecoup), and diffusely in the frontal and temporal lobes. Blood vessels, meninges, and nerves can be ruptured, sheared, and torn. This results in neural disturbances, ischemia, hemorrhage, and cerebral edema. Laceration of meningeal arteries or sinuses can cause subdural or epidural hematomas and leakage of cerebrospinal fluid (CSF).

Symptoms Clinical manifestations vary by the structures and brain tissue involved, by whether the injury was open or closed, and by the severity of the injury. The manifestations listed below are all possible.

Level of consciousness
Ranges from anxiety and irritability to restlessness, confusion, delirium, stupor, and coma; posttraumatic and retrograde amnesia

Pain
Mild to severe headache

Cranial nerve injuries
Anosmia; diplopia, strabismus, nystagmus, or blindness; deafness; vertigo; trigeminal paresthesias

Motor function
Weakness, paresis, paralysis; decorticate and decerebrate posturing; areflexia

Meningeal effects
Nuchal rigidity; positive Kernig’s sign; positive Brudzinski’s sign

Fractures
Linear: no bone displacement, possible epidural hematoma Depressed: focal deficits and cranial nerve injuries Basilar: CSF otorrhea or rhinorrhea; periorbital ecchymosis; conjunctival bleeding

Cerebral edema
Increased intracranial pressure (ICP) with slow respirations, bradycardia, nausea, vomiting, altered or loss of consciousness, seizures, weakness

Hematoma
Epidural: ipsilateral pupil dilation, rapidly increasing ICP Subdural: lethargy, headache, seizures, minimal dilation of pupil on affected side; widening pulse pressure; fixed, dilated pupils; hemiplegia; decorticate rigidity

Vital signs
Decreased blood pressure; pulse slow (intracranial hypertension) or rapid and feeble (hemorrhage); shallow respirations with possible CheyneStokes; hyperthermia with hypothalamic injury

Potential Complications Complications include infection, seizure disorders, hydrocephaly, organic brain syndrome, permanent residual neurologic deficits (memory loss, loss of impulse control, loss of initiation skills, decrease in cognition and abstract reasoning, decrease in judgment and problem solving); physical deficits (paralysis, weakness, spasticity, loss of fine motor abilities); and death.

Diagnostic Tests

Skull xrays
To detect fractures and bone fragments

Computed tomography/ magnetic resonance imaging or angiography
To detect subdural or intracranial hematoma, shift, or cerebral ventricle distortion

Echoencephalography
To detect midline shifts

Cisternography
To detect dural tear

CSF sampling
May be contraindicated with signs of ICP, since it may lead to cerebral herniation; normal findings with cerebral edema and concussion, increased pressure and blood in CSF with laceration and contusion
Treatments

Surgery
Debridement of open injuries; ventriculostomy or shunting procedures for ICP or hydrocephalus; craniotomy to elevate severe skull depressions, to stop hemorrhage from vessel lacerations or to evacuate hematoma; trephine to relieve pressure from hematoma; bolt placement to monitor ICP pressure; tracheostomy if needed for ventilation.

Drugs
Antiinfective drugs to prevent infection with open injury and leaking CSF; osmotic diuretics to control cerebral edema (corticosteroids are contraindicated, since they may increase seizure potential); polar beta-blockers to control transient hypertension; anticonvulsants for seizures; analgesics for pain (medullary depressants are contraindicated, since they may interfere with level of consciousness); muscle relaxants or paralyzing agents for decorticate and decerebrate posturing and restlessness in coma; stool softeners and suppositories to prevent constipation; artificial tears to prevent corneal damage with coma; histamine antagonists and antacids to control gastric reflux with tube feedings and reduce the chance of ulcers developing.

General
Initially: secure airway, control bleeding, stabilize body on backboard and transport; mechanical ventilation if needed with hyperventilation to control intracranial hypertension; central venous and arterial lines; ICP and cardiac monitoring; blood gases; vital signs and neural vital signs; monitoring of intake and output; enteral feedings or hyperalimentation; indwelling Foley catheter; seizure precautions; passive range-of-motion exercises, turning if comatose; cooling blankets for hyperthermia Long term: comprehensive rehabilitation program, including cognitive therapy to address cognitive, memory, and abstract reasoning deficits; speech therapy for communication deficits; physical therapy for residual weakness, paralysis, gait retraining, ataxia; occupational therapy for relearning activities of daily living; respiratory therapy to retain vital capacity; vocational therapy for learning vocational skills; counseling of individual and family to aid in adaptation to residual disabilities and amelioration of behavioral sequelae; transitional living placement to return individual to independent or supervised community living; long-term medical follow-up to reduce complications; instruction of family about the importance of structure and consistency of environment, safety issues arising from impaired judgment and lack of impulse control; instruction in the use of memory books and other memory aids.

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– A recurrent, chronic, infectious pulmonary and extrapulmonary disease characterized by formation of granulomas with caseation, fibrosis, and cavitation.

Causes and Incidence Tuberculosis (TB) is caused by spore-forming mycobacteria (Mycobacterium tuberculosis, M. bovis, or M. africanum). In developed countries the infection is airborne and is spread by inhalation of infected droplets. In underdeveloped countries (Africa, Asia, South America), transmission also occurs by ingestion or by skin invasion, particularly when bovine TB is poorly controlled. The incidence varies widely by country, age, race, sex, and socioeconomic status. Those at greatest risk are children under age 3 and adults over age 65; blacks and Hispanics; males; silicone and asbestos workers (particularly those who smoke); malnourished individuals; people living in unsanitary, crowded conditions; those in institutional settings; drug and alcohol abusers; the chronically ill; and immunosuppressed individuals. The incidence of TB has risen precipitously in the United States with the advent of HIV infection and among certain immigrant populations. The annual incidence in the United States is currently estimated at 14 per 100,000 people.

Disease Process TB has three stages: (1) primary (initial) infection; (2) latent (dormant) infection; and (3) recrudescent (postprimary) disease. During the first stage, the mycobacteria invade the tissues at the port of entry (usually the lungs) and multiply over a period of approximately 3 weeks. They form a small inflammatory lesion in the lung before traveling to the regional lymph nodes and throughout the body, forming additional lesions. The number of lesions formed depends on the number of invading bacteria and the general resistance of the host. This stage is generally asymptomatic.
Lymphocytes and antibodies mount a fibroblastic response to the invasion that encases the lesions, forming noncaseating granulomas. This marks the latent stage, and the individual may remain in this stage for weeks to years, depending on the body’s ability to maintain specific and nonspecific resistance. Stage three occurs when the body is unable to contain the infection, and a necrotic and cavitation process begins in the lesion at the entry port or in other body lesions. Caseation occurs and the lesions may rupture, spreading necrotic residue and bacilli throughout the surrounding tissue. Disseminated bacteria form new lesions, which in turn become inflamed and form noncaseating granulomas and then caseating necrotic cavities. The lungs are the most common site for recrudescent disease, but it may occur anywhere in the body. Untreated disease has many remissions and exacerbations.

Symptoms Manifestations vary with the systems involved. Symptoms are rarely seen until the recrudescent stage. Individuals are communicable whenever bacilli are present in the sputum.

Pulmonary
Weight loss, fatigue, generalized weakness, anorexia; slight fever with chills and night sweats; nonproductive cough that eventually becomes productive with mucopurulent sputum; tachycardia; dyspnea on exertion; hemoptysis

Cardiovascular
Pericarditis with precordial chest pain, fever, ascites, edema, and distention of neck veins

Gastrointestinal
Peritonitis with acute abdominal pain, abdominal distention, vomiting, anorexia, weight loss, night sweats; gastrointestinal bleeding, bowel obstruction

Neurologic
Meningitis with headache, vomiting, fever, declining consciousness, and neurologic deficit

Musculoskeletal
Joint pain, swelling, tenderness, deformities; limitation of motion

Genitourinary
Urgency, frequency, dysuria, hematuria, pyuria; infertility, amenorrhea, vaginal bleeding and discharge; salpingitis with lower abdominal pain

Lymphatics
Enlarged lymph nodes

Potential Complications Complications include massive destruction of lung tissue, leading to pneumothorax, pleural effusion, pneumonia, and respiratory failure; brain abscess; cardiac tamponade; vertebral collapse and paralysis; liver failure; renal failure; and generalized, massive dissemination of disease that usually is fatal. New drug-resistant strains of tuberculosis are emerging, leading to more frequent progression to complications.

Diagnostic Tests

Skin tests (purified protein derivative/Mantoux)
Positive reaction indicates past infection and presence of antibodies; it is not indicative of active disease

Sputum culture
Positive for causative agent within 2 to 3 weeks of onset of active disease; it is not positive during latency

Acid-fast sputum smear
Positive for acid-fast bacillus

Tissue biopsy/culture
Positive for causative agent

Pleural needle biopsy
Positive for causative agent

Chest x-ray
May reveal cavitation, calcification, parenchymal infiltrate; not diagnostically definitive

Treatments

Surgery
Drainage of pulmonary abscesses; correction of complications such as intestinal obstruction or urethral stricture.

Drugs
Antiinfective drugs in combinations of primary drugs or primary and secondary drugs to combat causative agent (new strains of bacillus are occurring that are resistant to traditional primary drugs); antiinfective drugs (isoniazid) as chemoprophylaxis in individuals who have converted from a negative to a positive skin test, particularly those with HIV or other immune-suppressed conditions, insulindependent diabetics, those on prolonged corticosteroid therapy, small children, and health care workers who are regularly exposed.

General
Sputum precautions until negative sputums are evident (10 to 14 days after start of drug therapy); management usually on an outpatient basis unless the disease is in an advanced state with complications; instruction about the importance of uninterrupted drug therapy and the need for periodic recultures of sputum throughout drug therapy, which may last a year or longer; skin testing and examination of close contacts at the time of initial diagnosis and again in 2 to 3 months; long-term medical follow-up to prevent recurrence.

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- A chronic inflammatory mucosal disease of the colon and rectum characterized by bloody diarrhea.
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- A circumscribed excavation of the gastric or duodenal mucosal wall that penetrates the muscularis mucosae and exposes it to acid and pepsin.

Causes and Incidence The precise etiologic mechanisms of peptic ulcer formation are unclear. However, recent research points to infection by Helicobacter pylori bacteria as the major factor in ulcer formation. Other factors that have been implicated include use of certain drugs (e.g., aspirin and other nonsteroidal antiinflammatory agents ([NSAIDs]); use of alcohol, cigarettes, and caffeine; and a familial history of ulcers. Those at risk of a duodenal ulcer have increased acid production and type O blood. Risk factors for a gastric ulcer include type A blood and underlying disease processes such as pancreatitis, gastritis, and hepatic disorders. About 80%of all peptic ulcers are duodenal in origin, and the remain-ing 20% are gastric. Gastric ulcers strike men and women equally, with the peak incidence occurring between ages 55 and 65. There are 40,000 to 80,000 cases reported annually in the United States. Duodenal ulcers occur in men two to three times as often as in women, and the incidence increases with age. The annual incidence is 200,000 to 300,000, but it has been steadily decreasing since the 1950s.

Disease Process The pathology is unclear, but it is hypothesized that H. pylori or other factors may upset the balance between ulcer-promoting factors, such as secretion of acid and pepsin and factors that serve as protectors of the mucosal lining, such as mucus production and replacement of damaged mucosal cells. This sets up an inflammatory process, with resultant ulceration, thrombosis, fibrosis, and scarring of the muscularis mucosae layer of the stomach or duodenum.

Symptoms Manifestations vary with location, and ulcers are often asymptomatic or associated with vague symptoms. Only about 50% of individuals have a characteristic pattern of symptoms. The characteristic pain is described as burning, gnawing, or aching and is located in a well-circumscribed epigastric area. In duodenal ulcers the pain usually appears midmorning, is relieved by food, and then reappears 2 to 3 hours after eating. It also wakens the individual 2 to 3 hours after falling asleep. It occurs daily for 1 week or longer and may then disappear without treatment. With a gastric ulcer the pain usually occurs after eating food, is located in the left midgastric area, and often radiates to the back. Epigastric pain occurs with an empty stomach. Pain in both instances is typically relieved by antacids or milk.

Potential Complications Complications include hemorrhage and perforation of the stomach or duodenum, with resulting peritonitis and obstruction of the pylorus or gastric outlet.

Diagnostic Tests

Endoscopy/biopsy
To establish presence of ulcer and determine whether malignancy is present

Upper gastrointestinal series
May reveal ulcers overlooked on endoscopy

Gastric analysis
Increased output with duodenal ulcer; decreased or normal output with gastric ulcer

Carbon 13 urea breath test
Low levels of 13C in exhaled breath indicative of H. pylori infection

Treatments

Surgery
Gastrectomy, gastroduodenostomy, gastrojejunostomy to remove gastrin-producing portion of stomach in intractable cases with complications; fundic vagotomy with chronic duodenal ulcer disease.

Drugs
Histamine receptor antagonists to block gastric acid output; antacids to reduce pain; cytoprotectives (Sucralfate) to form a protective coating in the base of the ulcer; bismuth preparations in combination with antiinfective drugs for H. pylori (not yet approved in the United States); omeprazole is a proton pump inhibitor in clinical trials in the United States; prostaglandins are in clinical trials for treatment associated with NSAID use.

General
Avoidance of alcohol and tobacco products; avoidance of pepper, coffee (caffeinated and decaffeinated), and foods that cause epigastric distress; avoidance of NSAIDs.

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- Involuntary leakage of urine classified as instability incontinence (sudden urgent desire or detrusor contraction with immediate loss of control), stress incontinence (loss of control on sneezing, coughing, laughing, or straining), overflow incontinence (chronic overdistention of the bladder that results in dribbling), and constant incontinence (continual dribbling).

Causes and Incidence Causes vary by classification. Instability incontinence is often associated with disease or trauma of the central nervous system (e.g., cerebrovascular accident, parkinsonism, brain tumors, spinal cord injury); bladder outlet obstructions (e.g., benign prostatic hypertrophy); bladder infection; and bladder irritation (e.g., calculi). Other causes of instability incontinence remain unclear and are labeled idiopathic.
Stress incontinence is caused by pelvic relaxation or sphincter incompetence. Pelvic relaxation leads to cystocele, rectocele, or uterine prolapse. Factors associated with relaxation include multiparity, aging, peripheral neuropathy and diabetes, and extensive pelvic surgery. Sphincter incompetence is associated with any factor that loosens the sphincter, such as prostate or urinary surgery or repeat urinary procedures, infection, or a reduction in mucus production.
The two causes of overflow incontinence are deficient detrusor function and bladder outlet obstruction. Detrusor function deficiency is associated with cauda equina syndrome, multiple sclerosis, tabes dorsalis, polio, herpes zoster, pelvic trauma, diabetes, and chronic overdistention. Obstruction is associated with inflammation, benign prostatic hypertrophy, adenocarcinoma of the bladder, urethral stricture in men, and urethral distortion in women.
Constant incontinence results from bypassing of normal sphincter function and failure of the bladder to store urine. Associated factors include urinary fistula, epispadias, urethral etopia, and surgical conduit.
It is estimated that at least 10 million individuals suffer from incontinence in the United States. It occurs in both men and women and increases with age. As many as 50% of institutionalized elderly individuals experience chronic incontinence, and 20% more experience intermittent incontinence.

Disease Process Stress incontinence occurs when the bladder pressure exceeds the urethral closure pressure. This happens when the urethra is no longer maintained in a normal anatomic position, resulting in inefficient transmission of abdominal pressures along the length of the urethra. Thus sudden increases in abdominal pressure from coughing, sneezing, or straining are not transmitted to the sphincter, and it does not tighten.
Instability incontinence is a result of inappropriate contraction of the detrusor muscle, with loss of coordination between bladder contraction and sphincter release. Overflow incontinence results when the detrusor muscle fails to contract, allowing the bladder to overfill, or when the bladder outlet is blocked and urine backs up and overfills the bladder. Constant incontinence occurs when the sphincter is bypassed and the urine has a new channel or outlet, such as a fistula between the bladder or urethra and the vagina or rectum.

Symptoms Involuntary loss of urine is the chief manifestation, and the pattern varies by classification of the incontinence. Abdominal distention and associated urinary tract infection (UTI) are also seen in overflow incontinence.

Potential Complications Complications include UTI, kidney infection, and skin breakdown.

Diagnostic Tests

Voiding cystourethrography
Stress incontinence: pelvic descent below the pubis, urethral excursion, and leakage of contrast material with straining Instability: detrusorsphincter dyssynergia Overflow: large bladder capacity, possible blockage Constant: leakage of contrast material through fistula or ectopic structure

Urodynamic testing
Stress: normal capacity, sensations, and compliance; stable detrusor; normal electromyographic (EMG) explosive flow with low-pressure detrusor contraction Instability: decreased functional capacity, early sensation, normal compliance, unstable detrusor, normal EMG findings Overflow with detrusor dysfunction: enlarged capacity, delayed sensations, abnormal compliance, poor stream, residuals Overflow with obstruction: normal or enlarged capacity, normal or delayed sensation, normal or impaired compliance, high detrusor contraction with poor flow Constant: impaired urine storage with fistulous tract

Treatments

Surgery
Stress: vesicourethral suspension to elevate anatomic structures; artificial urinary sphincter, pubovaginal sling to replace or reinforce damaged sphincter Instability: urinary diversions (e.g., suprapubic catheter or ileoconduit) Overflow: transurethral resection of enlarged prostate; urethrotomy to correct urethral stricture; reconstruction of bladder or urethra Constant: repair or removal of ectopic structures or fistulas.

Drugs
Autonomic drugs, spasmolytics to increase detrusor contractility and tone; autonomic drugs to increase or decrease bladder neck tone; muscle relaxants to diminish external muscle tone; antispasmodics to decrease detrusor spasms.

General
Stress: Kegel exercises to strengthen periurethral muscles; electrostimulation therapy to strengthen pelvic muscles; use of pessary to alter anatomic structure Instability: use of a timed voiding schedule; manipulation of fluid intake, avoiding largevolume intake periods; intermittent catheterization Overflow: double voiding techniques; intermittent catheterization; voiding schedules with manual Crede’s maneuvers Other: good skin care with use of barrier cream to protect irritated skin from moisture and urine; use of incontinence aids (e.g., pads, adult diapers, odor elimination substances, external catheters); referral to continence support group; instruction in intermittent catheterization techniques if needed.

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