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It is stated that four people die in the United Kingdom every year from anaphylactic reactions to wasp and bee stings.1However, long term sequelae, including neurological complications, are rare. We report on a young woman who sustained a stroke after a wasp sting and review the literature with particular reference to possible underlying mechanisms of stroke.
A 30 year old woman was seen in a casualty department, 45 minutes after a wasp sting on her left arm. She complained of immediate localised itch, followed by facial and arm swelling and widespread pruritis. She was noted to have a normal conscious level and widespread urticaria and her blood pressure at admission was 90/50. An intravenous infusion of gelofusine was started and she was given subcutaneous adrenaline (1 mg), intravenous hydrocortisone (100 mg), and intramuscular chlorpheniramine (10 mg). Her blood pressure responded and she had no further recorded hypotension. However, after infusion of gelofusine (3 l) over 2 hours she developed respiratory distress and hypoxia. Examination and a chest radiograph showed acute pulmonary oedema and she was intubated and ventilated for 36 hours. She received intravenous frusemide (150 mg in total over 8 hours), but did not require inotropic support. Chlorpheniramine (10 mg thrice daily) and hydrocortisone (100 mg thrice daily) were continued for 48 hours. After extubation she complained of difficulty seeing objects in her right upper visual field and a right homonymous quadrantinopia was demonstrated. Brain CT showed a left occipital infarct (figure).
She subsequently made a full recovery from the quadrantinopia. She was shown to have IgE antibodies to both wasp and bee venom and a positive skin test to wasp venom and underwent successful desensitisation to wasp venom.
Cerebral infarction in this woman occurred in the setting of anaphylaxis to a wasp sting. There was only a single recorded episode of hypotension which was rapidly corrected and was not thought to be sufficient to cause her stroke. The infarct was an occipital cortical lesion and not in a typical border zone distribution.
Vascular complications of bee and wasp stings are rare. Cerebral infarction has only been reported in three other people.2 3 In one three wasp stings were followed by collapse and a tonic-clonic seizure. Hypotension was not recorded. He was treated with adrenaline, barbiturates, and steroids. It is unclear whether the development of a hemiparesis preceded or followed this treatment. Brain CT confirmed cerebral infarction. Both other patients died after bee or wasp stings. At postmortem cerebral infarction was found in both.3 The mechanism of cerebral infarction was not alluded to.
Acute myocardial infarction has been reported four times.4It has been suggested that this may be due to a combination of coronary vasoconstriction secondary to mediators released after wasp sting, aggravated by exogenous adrenaline given as part of the treatment and by platelet aggregation.4 5 It is likely that the mechanism of cerebral infarction in this patient was similar. Wasp venom contains vasoactive, inflammatory, and thrombogenic peptides and amines, including histamine, leucotrienes, and thromboxane. The venom also contains allergenic proteins such as phospholipases which elicit an IgE response, resulting in mast cell activation.6 Mast cell activation results in release of preformed substances such as histamine as well as de novo synthesis of other mediators. Constriction of coronary arteries has been shown to occur in response to histamine.7 Both thromboxane and leucotrienes have been shown to be vasoconstrictors.8 The adrenaline that the patient was given may also have been implicated in vasoconstriction, resulting in her cerebral infarct. Many of the factors released, including thromboxane and leucotrienes, cause platelet aggregation resulting in a prothrombotic state.
The other neurological complications of stings which have been reported are individual cases of ocular myasthenia gravis,9 optic neuritis, limb numbness, and trigeminal neuralgia10 and three cases of encephalopathy, one of which was fatal.11Postulated mechanisms include both a toxic effect of venom9 and hypersensitivity to venom.10 11