Induced hypothermia in the management of burns encephalopathy

Jeffs, J. V.; Edwards, G.E.; Hoyle, J. R.

doi:10.1016/s0007-1226(66)80079-6

Cited by 6 publications

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“…4 During the next 50 years, multiple case reports and case series described children and adults suffering from severe and sometimes fatal neuropsychiatric symptoms shortly after seemingly successful resuscitation from small to moderate burns (TBSA 5-45%). [5][6][7][8][9][10][11][12] Documented symptoms included delirium, seizures, myoclonus, rigidity, and behavioral aberrations.…”

Section: Discussionmentioning

confidence: 99%

“Burn Catatonia”

Quinn

2014

Journal of Burn Care & Research

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Thermal injuries have been recognized to cause significant neuropsychiatric symptoms and disability in their sufferers since the middle of the 20th century, when Drs. Stanley Cobb and Erich Lindemann of the Massachusetts General Hospital (Boston, MA) studied survivors of the Cocoanut Grove nightclub fire in Boston. Although "burn encephalopathy" or burn-induced delirium is a common occurrence in the acute phase, catatonia in burn patients is not often reported. This report describes a case of malignant catatonia occurring in a 51-year-old male patient acutely suffering from burns acquired in a chemical explosion, effectively treated with reinstitution of a selective serotonin reuptake inhibitor. The literature on burn encephalopathy and catatonia in burns is reviewed. Few examples of burn catatonia exist. Burn encephalopathy is common, and may occur in patients with low TBSA burns such as described in the case above. Descriptions of burn encephalopathy are numerous, but have not included catatonia as a possible etiology. Catatonia in burn patients as an etiology of burn encephalopathy is likely underrecognized. Clinicians should be aware of the possibility of catatonia when a patient's confusional state after a burn does not respond to usual care.

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Section: Discussionmentioning

confidence: 99%

“Burn Catatonia”

Quinn

2014

Journal of Burn Care & Research

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Burn encephalopathy in children

Mohnot

Snead

Benton

1982

Annals of Neurology

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Among 287 children with burns treated over a recent two-year period, 13 (5%) showed evidence of encephalopathy. The major clinical symptoms were an altered sensorium and seizures. The majority of symptoms began later than 48 hours after the burn and were accompanied by multiple metabolic aberrations including hypocalcemia. Three children had a relapsing course, and 1 had temporarily enlarged cerebral ventricles. Eleven children improved to normal. In the majority of instances, burn encephalopathy probably reflects central nervous system dysfunction resulting from complex metabolic, hematological, and hemodynamic abnormalities rather than from a single metabolic abnormality.

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Burns and carbon-monoxide poisoning

Pollard

1970

Journal of British Surgery

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635before death. Irvin, Donaldson, and Smith (1967) studied the ability of gastric juice to sustain the growth of Clostridia, and found that the organisms grew better in aspirate from gastric than from duodenal ulcer patients, and in nitro they showed that the organism did not grow at all if the pH of the media was less than 4.5. In the present case subtotal gastrectomy had been carried out and almost all the acid-secreting area of the stomach removed so that the resultant gastric p H might be expected to permit the growth of CI. welchii, especially with presence of necrotic tissue. I t was to this last factor that Rose and Bukosky (1966) attributed the fatal clostridial septicaemia in a p y e a r -o l d male following perforation of a duodenal ulcer.

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Induced hypothermia in the management of burns encephalopathy

Cited by 6 publications

References 1 publication

“Burn Catatonia”

“Burn Catatonia”

Burn encephalopathy in children

Burns and carbon-monoxide poisoning

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