Multiple hornet stings with features of Reye's syndrome

Weizman, Zvi; Mussafi, Huda; Ishay, Jacob S.; Shvil, Yigal; Goitein, K. J.; Livni, Nelly; Deckelbaum, Richard J.

doi:10.1016/0016-5085(85)90662-6

Cited by 21 publications

(11 citation statements)

References 15 publications

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“…Intravascular hemolysis has been reported in most reports discussing wasp sting complications in the literature [4,8,9,11,13,14,22] as in our reviewed patients, in which six had anemia, three of which in turn had a hematocrit of less than 25 which could not be explained only from a dilutional effect due to volume overload; hemolysis has previously been noted as a major reaction in ARF [3,11]. Thrombocytopenia has also been found in one patient reported from India, and the authors believed that the thrombocytopenia was a direct result of the effect of the venom on the platelets [21].…”

Section: Discussionmentioning

confidence: 98%

Acute renal failure following wasp sting in children

Vachvanichsanong

Dissaneewate

2009

Eur J Pediatr

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The medical records of patients admitted between 1985 and 2007 with wasp stings were retrospectively analyzed. Among the 45 children, seven developed acute renal failure. Classical clinical and laboratory data pointed to hemolysis and rhabdomyolysis as the underlying pathophysiology. All patients had hyponatremia and hyperkalemia as well as metabolic acidosis. Six patients had anemia. Five patients were oliguric for 9 to 15 days. Maximum serum creatinine was 4.0 to 11.9 mg/dl. Peritoneal dialysis was performed for 3 to 15 days. One patient died due to hyperkalemia, the remaining ones recovered completely. This paper wants to remind pediatricians to watch for acute renal failure in children with wasp stings.

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Section: Discussionmentioning

confidence: 98%

Acute renal failure following wasp sting in children

Vachvanichsanong

Dissaneewate

2009

Eur J Pediatr

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“…Subsequent investigations have been unrewarding. Exposure to a variety of agents including salicylates, valproic acid, the unripe fruit of the Akee tree, margosa oil, chlordane, pyrrolizidine, camphor, methyl bromides and multiple stings by the Oriental hornet may produce clinical manifestations quite similar to Reye's syndrome (3,(78)(79)(80)(81)(82)(83)(84)(85). However, none have had sufficiently similar laboratory, histopathologic or ultrastructurd pathologic features to make them serious candidates as the cause of Reye's syndrome.…”

Section: Toxinsmentioning

confidence: 99%

Reye's syndrome: Current concepts

1987

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Despite greater than 23 years of study, an incomplete understanding of the etiology, epidemiology and pathogenesis of Reye's syndrome persists. Better understanding of the disease has been hampered by the lack of a good animal model on which hypotheses of its pathogenesis could be tested. Human studies indicate that a primary mitochondrial injury may lead to complex metabolic disturbances that produce the observed pathophysiology. Specific directions regarding avenues for future research should pursue two lines: a good animal model still needs to be developed in which the biochemical and morphologic alterations identified in Reye's syndrome are duplicated. This model should include an antecedent viral illness but may not require aspirin exposure as an essential ingredient. With the identification of a satisfactory model, specific questions about the roles of environmental toxins or medications may be answered. Study of noncomatose cases of Reye's syndrome should continue. The specific emphasis should be to delineate what factors (NH3, free fatty acids and dicarboxylic acids) may be implicated in the pathogenesis of the CNS disease with the hopes of devising strategies for more effective treatment of encephalopathy and its attendant morbidity and mortality.

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“…Hepatic damage has also been reported [2,5,13]. Weizman et al [13] reported a girl who had encephalopathy, hepatomegaly, elevated transminase levels, low prothrombin time, hyperammonemia, and microvesicular fatty infiltration with diffuse mitochondrial changes. Franca et al [5] reported manifestation of acute respiratory distress/pulmonary edema which resulted from shock alone or from the effects of venom on the pulmonary capillary membrane, either acting directly or through leukocytes.…”

Section: Discussionmentioning

confidence: 94%

“…One example is a skin eruption such as edema, erythema, or giant urticaria which can later become septic or even gangrenous [6,15]. Hepatic damage has also been reported [2,5,13]. Weizman et al [13] reported a girl who had encephalopathy, hepatomegaly, elevated transminase levels, low prothrombin time, hyperammonemia, and microvesicular fatty infiltration with diffuse mitochondrial changes.…”

Section: Discussionmentioning

confidence: 95%

Non-fatal acute renal failure due to wasp stings in children

1997

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We report two children who developed acute renal failure after multiple wasp stings. Each case involved intravascular hemolysis which caused acute renal failure, volume overload, hypertension, anemia, hyponatremia, hyperkalemia, and metabolic acidosis. Peritoneal dialysis was required for short periods. The children recovered completely with blood urea nitrogen and creatinine returning to normal within 3 months. One child had a renal biopsy which showed mild tubulointerstitial nephritis. Although there is no specific treatment or antivenom, dialysis and supportive care have proved to be successful.

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Multiple hornet stings with features of Reye's syndrome

Cited by 21 publications

References 15 publications

Acute renal failure following wasp sting in children

Acute renal failure following wasp sting in children

Reye's syndrome: Current concepts

Non-fatal acute renal failure due to wasp stings in children

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