- An acute bacterial infection that may progress rapidly to severe shock.

Causes and Incidence The exact etiologic mechanism of toxic shock is unknown, but all cases have reported infection with exotoxin-producing strains of Staphylococcus aureus. The syndrome was first reported in children and adolescents in 1978. In 1980 a large number of cases occurred in young menstruating women who used tampons. Changes in the composition of tampons and their use have drastically reduced the incidence in this group. Cases have subsequently been detected in postoperative patients, after nasal reconstruction cases with packing, in those with infected insect bites, and in those with burns. Reported mortality rates range from 8% to 15%.

Disease Process It is presumed that those at risk harbor a preexisting colonization of S. aureus in their bodies. The mechanisms that turn the bacteria into a toxin are unclear but seem to be associated with possible mechanical or chemical factors at work on the harbored bacteria. Once the toxin is produced, it is thought to enter the bloodstream through a break in the skin or mucosa and spread systematically.

Symptoms The onset is sudden and marked by high fever, headache, sore throat, nonpurulent conjunctivitis, lethargy, confusion, vomiting, diarrhea, and a sunburnlike skin rash. Within 48 hours the syndrome progresses to syncope, orthostatic hypotension, diminished urine output, and shock. Peripheral and pulmonary edema, hepatitis, and myolysis then occur. After 3 to 7 days, the skin sloughs off on the palms and soles.

Potential Complications Toxic shock syndrome can lead to residual neurologic or psychologic deficit, renal failure, respiratory failure, and death.

Diagnostic Tests The Centers for Disease Control and Prevention has set up diagnostic criteria. At least three of the following conditions must be present on a clinical examination or laboratory test: (1) gastrointestinal effects, including vomiting and profuse, watery diarrhea; (2) muscular effects, with severe myalgia and a fivefold increase in serum creatinine phosphokinase; (3) mucous membrane effects; (4) renal involvement, with blood urea nitrogen or serum creatinine at least double normal levels; (5) hepatocellular damage, with serum bilirubin, alanine aminotransferase, and aspartate aminotransferase double the normal levels; (6) blood involvement, with thrombocytopenia and a platelet count under 100,000/mm3; and (7) central nervous system effects, such as confusion without focal signs.

Treatments

Surgery
Tracheostomy if needed for ventilation.

Drugs
Antiinfective drugs specific to S. aureus to prevent recurrence; antidiarrheal drugs and antiemetics to reduce diarrhea and vomiting; analgesics for pain.

General
Immediate treatment for septic shock if indicated: fluid and electrolyte replacement, packed RBCs, monitoring of intake and output and central venous pressure; universal precautions for secretions and discharges; vital signs, neural vital signs, and reorientation for confusion; safety measures to prevent falls from orthostatic hypotension; mechanical ventilation if necessary; instruction about susceptibility to recurrence and the safe use of tampons.

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- Recurrent, focal neurologic disturbances of sudden onset and brief duration characterized by loss of sensory, motor, or visual function.

Causes and Incidence Most transient ischemic attacks (TIAs) are caused by cerebral emboli that break off from atherosclerotic plaques in the carotid or vertebral arteries in the neck. Hypertension, atherosclerosis, heart disease, diabetes mellitus, and polycythemia serve as predisposing factors. The attacks are most common in adults past middle age and often presage a stroke. Occasionally TIAs are seen in children with severe cardiovascular disease and an elevated hematocrit.

Disease Process An atherosclerotic plaque breaks off from an artery in the neck and travels to the brain, where it temporarily impedes the blood flow in the carotid-middle or vertebral basilar artery in the circle of Willis.

Symptoms TIAs appear suddenly, usually last 2 to 30 minutes, and then subside with no neurologic sequelae. They may occur daily or two or three times a year. The manifestations are specific to the artery occluded.

Carotid
Ipsilateral blindness described as a shade being pulled down over the eye; contralateral hemiparesis; paresthesias; slurred speech

Vertebrobasilar
Confusion; vertigo; diplopia or binocular blindness; unilateral or bilateral muscular weakness and paresthesias; drop attacks with buckling of the legs; slurred speech

Potential Complications TIAs may precede a stroke.

Diagnostic Tests The diagnosis is made on the clinical history with an ultrasound scan or arteriography, which confirms the presence of stenosis and atherosclerosis of the carotid or vertebral arteries.

Treatments

Surgery
Endarterectomy to remove atherosclerotic plaque from the artery is considered if the artery is at least 70% occluded; intracranial anastomosis to revascularize the brain.

Drugs
Antiplatelet agents and anticoagulants for 2 to 3 weeks to interfere with clot formation; aspirin therapy long term to interfere with platelet aggregation.

General
Monitor for bleeding; long-term follow-up.

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