- Enteric or neural intoxication following ingestion of bacterially contaminated food.

Causes and Incidence Food poisoning is caused by one of the following organisms: staphylococcal enterotoxins, Clostridium botulinum, Clostridium perfringens, Vibrio parahaemolyticus, or Bacillus cereus. The resulting illness is noncommunicable.

Disease Process The causative organism multiplies in the food before ingestion; the pathogenesis is organism specific. Staphylococcal enterotoxins form in foods held at room temperature. They act on the gastric mucosa, producing hyperemia, erosion, petechiae, and purulent exudate. C. perfringens reproduces rapidly in cooled and reheated food and acts on the epithelial layer of the ileum, increasing absorption of fluid, sodium, and chloride and inhibiting glucose absorption. V. parahaemolyticus multiplies in uncooked seafood and invades the intestinal tissue, producing necrosis, ulceration, and granulocytic infiltration of the mucosa. B. cereus, an aerobic spore, multiplies in foods held at room temperature and attacks either the gastric or intestinal mucosa. C. botulinum forms a toxin in improperly processed foods in anaerobic conditions; it is a neurotoxin that impairs autonomic and voluntary neurotransmission and causes muscular paralysis.

Symptoms The signs and symptoms depend on the causative agent.

Staphylococci
Symptoms appear within 7 hours of ingestion: weakness, acute nausea and vomiting, intestinal cramps, diarrhea

Enteric type (C. perfringens, V. parahaemolyticus, B. cereus)
Symptoms appear within 24 hours of ingestion: nausea, vomiting, abdominal pain, diarrhea

C. botulinum
Symptoms appear within 36 hours of ingestion: dry mouth, diplopia, loss of pupillary light reflex; nausea, vomiting, cramps, and diarrhea precede dysphagia, dysarthria, and progressive descending muscular paralysis

Potential Complications The complication of enteric manifestations is dehydration, and infants and small children are most susceptible. Botulism is fatal in about 10% of cases, usually because of respiratory failure.

Diagnostic Tests

Cultures
Stomach contents, feces, or suspected food for causative organism.

Serum
Positive for botulinal toxins.

Treatments

Surgery
Tracheostomy if necessary for airway with botulism.

Drugs
Trivalent botulinal antitoxin as soon as possible after onset of botulism.

General
Botulism: gastric lavage, mechanical ventilation if necessary, nasogastric tube feedings, fluid and electrolyte replacement, prevention of skin breakdown and contractures during paralysis, minimization of stimuli, precise communication because of altered vision and loss of speech, allaying anxiety about paralysis and treatment.
Other causes: fluid and electrolyte replacement, instruction in prevention.

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- Localized cold injury.

Causes and Incidence Frostbite is caused by exposure to damp cold temperatures around freezing or to dry cold temperatures well below freezing. Susceptibility is increased by dehydration, exhaustion, hunger, substance abuse, impaired circulation, and impaired consciousness. Factors that promote heat loss (e.g., wet clothing, contact with wet metal, wind chill, radiation) increase the severity of injury, as does prolonged exposure to cold. The very young and the elderly are more prone to frostbite, as are those from warmer climates who are not acclimated to cold.

Disease Process Cold exposure can cause cellular injury either by direct formation of ice crystals in the cells or by vascular spasm and occlusion, which result in inadequate tissue perfusion. Cell dehydration leads to vasoconstriction and increased blood viscosity, with sludge and thrombus formation. As thawing takes place, venous stasis occurs at the sites of injury, obstructing the vascular bed and causing edema and tissue necrosis. Tissue damage may range from superficial (skin and subcutaneous tissue) to deep (muscle, tendon, and neurovascular structures).

Symptoms

Superficial
Injured area is white, waxy, soft, and numb while still cold; as thawing occurs, area becomes flushed, edematous, and painful, and may become mottled and purple; in 24 hours, large blisters form that remain about 2 weeks before turning into a hardened eschar that remains for about a month before separating, leaving painful, sensitive new skin that often sweats excessively

Deep
Injured part remains hard, cold, mottled, and blue-gray after thawing; edema forms in entire limb and may remain for months; blisters may not form or may form after a delay of several weeks; after several weeks, dead tissue blackens and sloughs off; a line demarcates dead from live tissue

Potential Complications Loss of digits, ears, nose, and extremities is possible, as is secondary infection.

Diagnostic Tests The diagnosis is made by clinical examination plus a history of exposure to cold.

Treatments

Surgery
Escharotomy; sympathectomy for severe vasospasm; debridement after retraction of viable tissue (34 months after injury; amputation of nonviable extremities several months after injury).

Drugs
Immunologic agents (tetanus) and antiinfective drugs for prophylaxis; analgesics for pain; plasma expanders to reduce sludge and thrombus formation.

General
Rapid rewarming by immersion in water (37.8o to 43.3o C [100o to 110o F]); fluid and electrolyte replacement; whirlpool baths; precautions with injured area to prevent dislodgment of eschar and further damage; counseling for altered body image from loss of limbs; exercise to prevent joint restriction.

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- An acute or chronic inflammation of the gastric mucosa.

Causes and Incidence Many factors can cause acute gastritis, including alcohol ingestion; drugs (e.g., aspirin, non-steroidal antiinflammatory agents [NSAIDs], cortico-steroids, cytotoxins, antimetabolites); ingested poisons (e.g., DDT, ammonia, mercury, carbon tetrachloride); ingestion of corrosive agents; trauma; burns; and endotoxins. Chronic gastritis is associated with peptic ulcer disease, renal disease, alcoholic cirrhosis, ulcerative colitis, and diabetes mellitus. Chronic use of NSAIDs, radiation treatments, genetics, diet, prolonged emotional stress, and gastrectomy may also be predisposing factors in chronic gastritis. Type B chronic gastritis is caused by a specific infection with Helicobacter pylori. Gastritis occurs five times more often in those who abuse alcohol than in the general population.

Disease Process In acute gastritis the stomach mucosa erodes because of hydrochloric acid and one or more predisposing factors, which serve as irritants. The erosions, which are caused by back diffusion of the hydrogen ion and mucosal ischemia, involve the granular layer and lead to submucosal hemorrhage and inflammation. Spontaneous remission occurs if the irritant is removed.
Chronic gastritis begins as an inflammatory infiltration of the lamina propria by plasma cells and leukocytes. The surface epithelial cells become flattened and necrotic in what is labeled the superficial gastritis phase. In the atrophic gastritis phase, the plasma cells and leukocytes also invade the fundic glands and intraglandular spaces, and the glands atrophy as mucous thickness decreases and the muscularis mucosae hypertrophies. Finally, in the gastric atrophy phase, the fundic glands lose the parietal and chief cells as metaplasia occurs, with thinned mucosa and minimum inflammation with marked gland loss. If chronic gastritis involves the fundus, it is labeled type A. If it involves primarily the antrum with some fundic involvement, it is labeled type B.

Symptoms

Acute
Rapid onset of epigastric pain,

indigestion, feeling of early fullness, anorexia, weight loss, cramping, nausea, vomiting, hematemesis, melena, general malaise

Chronic
Often asymptomatic; dyspepsia, flatulence, diarrhea, intolerance of spicy and fatty foods, no relief from antacids

Potential Complications Individuals who have gastric atrophy often develop pernicious anemia. Untreated gastric disease can lead to obstruction, perforation, and peritonitis. Individuals with metaplasia have a higher risk of gastric cancer.

Diagnostic Tests

Clinical evaluation
History of exposure to one or more predisposing factors or agents

Endoscopy with biopsy/cytology
To visualize lesions, erosions, and bleeding sites and to rule out carcinoma

Stool guaiac
Positive

Nasogastric aspiration
Frank blood

Serum gastrin
Elevated in type A chronic gastritis

Intrinsic factor antibodies
Present in type A

Antibodies to gastrin-producing cells
Present in type B

Treatments

Surgery
Partial or total gastrectomy, pyloroplasty, vagotomy for major uncontrollable bleeding associated with acute gastritis.

Drugs
Antacids; histamine receptor antagonists and vasoconstrictors for acute gastritis; vitamins C and B12 in chronic gastritis with accompanying pernicious anemia; antibacterial agents in type B gastritis.

General
Removal of causative agents; ice water lavage to control bleeding; laser therapy by endoscopy; blood transfusions; with acute gastritis: NPO, then bland diet.

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