Suddent death after phosphorus burns: experimental observations of hypocalcemia, hyperphosphatemia, and electrocardiographic abnornalities following production of a standard white phosphorus burn

Bowen, Thomas; Whelan, Thomas J.; Nelson, Thomas

doi:10.1097/00006534-197206000-00039

Cited by 5 publications

(8 citation statements)

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“…8,9 In addition, hypocalcaemia results by preferential binding of calcium by phosphorus in serum. 10 Later reports have, however, proposed that toxicity may be the result of changes in ribosomal function and protein synthesis, failure of regulation of blood glucose, alteration of lipoprotein synthesis and secretion of triglycerides, leading to intracellular accumulation and fatty degeneration of multiple organs, especially the liver, the kidney, the heart and brain. [11][12][13][14] Clinical manifestations have been divided into three phases.…”

Section: Discussionmentioning

confidence: 99%

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Clinical spectrum of yellow phosphorous poisoning in a tertiary care centre in South India: a case series

et al. 2016

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Rodenticides such as yellow phosphorus are highly toxic compounds which are commonly used for pest control. Reports of yellow phosphorus poisoning from tropical nations is scanty. In this retrospective study, we report the clinical features, mortality and predictors of mortality among nine patients at a tertiary care centre in south India. Yellow phosphorus consumption was common among a younger age group of patients. The mean duration of presentation after consumption was five days. The most common clinical manifestations seen were abdominal pain and vomiting followed by a depressed sensorium. Features of acute liver failure including coagulopathy were seen in all patients. Despite all patients receiving supportive therapy, a poor outcome or death resulted in the majority. Early referral to a tertiary care centre, meticulous monitoring and supportive measures are key elements of patient management as there are no specific antidotes available at present. Increase in public and physician awareness to the toxin and implementation of preventive policies is of utmost importance.

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Section: Discussionmentioning

confidence: 99%

“…8,9 In addition, hypocalcaemia results by preferential binding of calcium by phosphorus in serum. 10…”

Section: Discussionmentioning

confidence: 99%

Clinical spectrum of yellow phosphorous poisoning in a tertiary care centre in South India: a case series

et al. 2016

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“…Similar to other burns discussed, phosphorus burns of Ͻ 10% can have associated mortality (33). Three stages of systemic toxicity exist.…”

Section: White Phosphorusmentioning

confidence: 88%

“…Symptoms of headache, seizures, and coma, as well as the potential for cardiovascular collapse, may occur in the initial phase. Decreasing serum calcium concentrations during this stage have been demonstrated to lead to electrocardiographic abnormalities of prolonged QT and ST intervals as well as T wave changes (33). Stage two is the symptom-free period, which is followed by stage three (4 to 8 days post-exposure), characterized by neurological toxicity, bleeding diathesis, hepatic failure, renal failure, and shock (35).…”

Section: White Phosphorusmentioning

confidence: 99%

Special Considerations in Hazardous Materials Burns

Robinett

Shelton

Dyer

2010

The Journal of Emergency Medicine

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“…10 It should be noted that white phosphorus (which can be highly flammable) can cause hypocalcemia, resulting in a prolonged QT interval on electrocardiogram; intravenous calcium may be required. 11 Because it will react with ambient oxygen, tissue debridement to remove the solid particles and irrigation with water is important. Similarly, hydrofluoric acid (HF) can result in refractory hypocalcemia along with hypomagnesemia and hyperkalemia.…”

Section: Corrosive Chemicalsmentioning

confidence: 99%