|Year : 2021 | Volume
| Issue : 2 | Page : 95-97
Cerebral infarction following bee sting
Krishnan Balagopal1, Anand Muraleedharan2, Ansa Grace Koshy1, Jerin Peter Jacob1
1 Department of Neurology, MOSC Medical College, Kochi, Kerala, India
2 Department of Radiology, MOSC Medical College, Kochi, Kerala, India
|Date of Submission||03-Dec-2020|
|Date of Acceptance||13-Jan-2021|
|Date of Web Publication||17-Mar-2021|
Dr. Krishnan Balagopal
Department of Neurology, MOSC Medical College, Kolenchery, Kochi, Kerala
Source of Support: None, Conflict of Interest: None
Although bee stings can cause local reactions, neurovascular complications are rare. The venom toxins of honeybee cause anaphylactic allergic reactions and both cerebral infarction and hemorrhage. Diverse pathophysiological mechanisms have been postulated for the occurrence of these strokes. A 50-year-old man developed a focal neurologic deficit 6 h after a bee sting, which was confirmed to be acute cerebral infarction on magnetic resonance imaging scan.
Keywords: Bee sting, magnetic resonance imaging, stroke
|How to cite this article:|
Balagopal K, Muraleedharan A, Koshy AG, Jacob JP. Cerebral infarction following bee sting. Indian J Med Spec 2021;12:95-7
|How to cite this URL:|
Balagopal K, Muraleedharan A, Koshy AG, Jacob JP. Cerebral infarction following bee sting. Indian J Med Spec [serial online] 2021 [cited 2021 Apr 14];12:95-7. Available from: http://www.ijms.in/text.asp?2021/12/2/95/311313
| Introduction|| |
Neurological complications are rare in bee stings. Apart from anaphylactic allergic reactions, the sting venom of honeybee can cause hemorrhagic as well as ischemic strokes. These neurological deficits are produced by the contents of venom toxins directly or through the anaphylactic shock or pain-induced catecholamines surge. The venom contains biologically active enzymes, amines, and proteins. These substances directly or indirectly cause multitude of medical complications due to local, regional, or systemic allergic reactions. The local reactions cause local edema and swelling with symptoms that usually resolve within 24 h. Contrarily, regional and systemic reactions cause significant morbidity and mortality. These reactions have protean manifestations ranging from anaphylaxis, hypotension, rhabdomyolysis, seizures, disseminated intravascular coagulation to intracranial hemorrhages and cerebral infarctions, leading to the causation of stroke through different mechanisms. Only a few cases are reported in the literature with ischaemic stroke as an initial complication. We report here, a case of cerebral infarction occurring within 6 h of bee sting in a middle-age man, who manifested with limb weakness.
| Case Report|| |
We present here a case of a 50-year-old man with no comorbidities who was bitten by a honeybee with a single sting over his neck. He developed pain and swelling over the site of the bite for which he was taken to a nearby hospital, where he was managed with intravenous antihistaminic agents and steroids. After 6 h of sting, he suddenly developed sudden onset of weakness of right upper and lower limb with difficulty in walking. There was no slurred speech, deviation of angle of mouth, headache, or seizures. Clinical examination revealed the predominant weakness of the right lower limb with a power of 1/5 medical research council grade, right upper limb power 3/5 with brisk knee jerk, and extensor plantar on the right side. Pulse rate and blood pressure on admission were within the normal limits. Cranial nerves and sensory examination was normal as was power on the left side. There was no bladder involvement.
A clinical diagnosis of a possible left cerebral infarction with right-sided weakness was considered due to the upper motor neuron signs on the right side and the history of bee sting. The initial computed tomography brain done was within the normal limits. The patient subsequently underwent magnetic resonance imaging (MRI) of the brain which on T1- and T2-weighted images revealed diffuse aymmetric focal lesions with corresponding ischemic changes in the left frontal lobe and the left temporoparietal area. The lesions showed restriction of diffusion on Diffusion-Weighted Imaging/Apparent Diffusion Coefficient sequences suggestive of multiple infarcts with hemorrhagic transformation in the left middle cerebral artery/anterior cerebral artery territories [Figure 1] and [Figure 2]. MR angiogram of the brain and neck did not show any changes and MRI screening whole spine was normal. Blood parameters revealed elevated levels of creatine phospho kinase (CPK) (3300 U/ml), while coagulation parameters, renal parameters, and platelet counts were within the normal limits. He was treated with anti-edema measures, antiplatelet agents, and low-molecular-weight Heparin. He was given intravenous fluid replacement for hydration in view of elevated CPK levels. He was also started on physiotherapy and exercises. He had rapid improvement in motor power in 5 days and CPK levels came back down to normal limits. He was discharged after a week and asked to come for a follow-up after 4 weeks. Motor power at discharge was almost normal in the right upper and lower limbs.
|Figure 1: Diffusion weighted imaging/apparent diffusion coefficient images showing areas of restricted diffusion in left frontal and temporoparietal regions|
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|Figure 2: Diffusion weighted imaging image showing multiple infarcts left frontal region|
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| Discussion|| |
Bee sting envenomation is quite common. Various manifestations after bee sting have been described. Local reactions are common. Systemic involvement such as vomiting, diarrhea, dyspnea, generalized edema, acute renal failure, myocardial infarction, and cerebral infarction are rare manifestations. Several cases of wasp and bee sting associated with cerebral ischemia have been reported in the literature., Reported neurologic complications include seizure, hemiparesis, and aphasia. The pathophysiology explaining the associated cerebral infarction is unknown. Five major causes of cerebral ischemia are vascular thrombosis, cerebral embolism, hypotension, hypertensive hemorrhage, and hypoxia. Similar to acute myocardial infarction after bee stings, it has been suggested that vasoconstriction secondary to mediators released after the sting, aggravated by exogenous adrenaline and platelet aggregation, contribute to cerebral ischemia. Bee venom itself contains histamine, thromboxane, leukotrienes, and other vasoactive and inflammatory mediators. Both thromboxane and leukotrienes have been shown to cause vasoconstriction resulting in cerebral infarction. In addition, a neuropharmacological (sympathetic) mechanism of endothelial permeability involving the cerebral vasculature with a concurrent systemic thrombogenic or immune response has also been postulated.
In our patient, we postulate that the systemic immune-mediated reaction to the bee sting caused vasoconstriction and a prothrombotic state with subsequent ischemia leading to stroke.
| Conclusion|| |
We aim to highlight two important points with this report. One is that cerebral infarction is important though rare complication of bee stings which must be kept in mind in patients presenting with weakness following envenomation. Furthermore, prompt recognition of the problem will help in early diagnosis and treatment which helps the patient make a quick recovery.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]