The Journal of Emergency Medicine, Vol. -, No. -, pp. 1–6, 2016
Ó 2016 Elsevier Inc. All rights reserved.
0736-4679/$ - see front matter

http://dx.doi.org/10.1016/j.jemermed.2016.06.016

Selected Topics:
Neurological Emergencies

ISCHEMIC STROKE AFTER WASP STING
Ashish Kulhari, MD, Ashley Rogers, MD, Han Wang, MD, Vishakhadatta Mathur Kumaraswamy, MD,
Wei Xiong, MD, and Michael DeGeorgia, MD
Department of Neurology, University Hospitals Case Medical Center, Cleveland, Ohio
Corresponding Address: Michael DeGeorgia, MD, Director, Neurocritical Care Center, University Hospitals Case Medical Center,
11100 Euclid Avenue, Cleveland, OH 44106

, Abstract—Background: Despite the common occurrence of hymenopteran stings worldwide, primary neurologic manifestations including stroke are rare. We report a
case of a healthy male who developed a right middle cerebral
artery (MCA) territory ischemic stroke after getting stung
by a wasp. Case Report: A 44-year-old man with hypertension presented to the hospital with sudden-onset left hemiparesis, left facial weakness, and dysarthria after being stung
by a wasp. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) scans of the brain revealed a right MCA territory infarct and a lack of flow in
the distal right internal carotid artery and MCA. He was
treated with intravenous tissue plasminogen activator. A
computed tomography angiography scan of the brain performed 24 hours later revealed multiple regions of vasoconstriction in the territory of the bilateral MCA. Evaluations
for causes of stroke, including echocardiography and telemetry, were not revealing. Immunologic testing showed significantly elevated levels of serum wasp immunoglobulin E.
Therapy with aspirin and atorvastatin was started. At
discharge, the patient had a mild left facial droop but
normal strength in his left arm and leg. Why Should
an Emergency Physician Be Aware of This?: Emergency
physicians encounter large numbers of hymenopteran sting
cases each year. These patients typically present with local
reactions, such as itching, pain, and erythema. Systemic
manifestations, such as anaphylaxis causing severe hypotension and bronchospasm, are less common but deadly. Neurologic complications, such as ischemic stroke, are extremely

rare. This manuscript highlights the pathophysiology
and management of stroke after a hymenopteran sting.
There are no guidelines for the management of stroke
after a hymenopteran sting, and therefore we intend to
provide some guidance to physicians for treating stroke
after a hymenopteran sting. Ó 2016 Elsevier Inc. All rights
reserved.
, Keywords—ischemic; stroke; wasp

INTRODUCTION
Hymenopterans—the ‘‘membrane-winged’’ insects that
include ants, sawflies, bees, and wasps—cause nearly
100 million stings worldwide every year (1). Local reactions, such as itching, edema, pain, and erythema, are
common. Systemic manifestations, such as urticaria,
flushing, vomiting, diarrhea, and anaphylaxis causing
severe hypotension and bronchospasm, are less common
but deadly. Neurologic complications, such as ischemic
stroke, are extremely rare; 13 cases of ischemic stroke
after a bee or wasp sting have been published
(Table 1). Previous case reports show that the timing
of stroke ranges from <1 an hour to 24 hours after the
sting. In most of these reported cases, the patient
received multiple stings. There are no specific risk factors for stroke after bee or wasp stings, but all patients
typically experience localized or systemic reactions
before the stroke (2–14).

Reprints are not available from the authors.

RECEIVED: 26 February 2016; FINAL SUBMISSION RECEIVED: 4 May 2016;
ACCEPTED: 4 June 2016
1

Author

Age/Sex

Sting Type and
Location

Onset of Deficits

2

Table 1. Case Reports of Ischemic Stroke after Bee/Wasp Sting
Clinical Findings

MRI/CT Findings

Headache, right
hemiplegia, seizure,
and coma
Right hemiplegia and
global aphasia
Dysarthria and left
hemiparesis within
few hours;
quadriparesis and
obtundation after
24 days

NR; necropsy showed
left hemorrhagic
cortical infarct
Left MCA infarct with
left ICA occlusion
Three small infarcts in
right MCA territory;
24 days later, diffuse
bilateral ischemic
white matter lesions
in left parietal and
insula
Left occipital infarct

36/M

Wasp: multiple; neck,
face, and arms

<1 hour

Riggs et al (3)

38/M

2 days

Riggs et al (4)

52/M

Wasp: multiple; face
and neck
Wasp: single; location
not recorded

Crawley and
Schon (5)

30/F

Wasp: single; left arm

<1 hour

Vision loss

Bhat et al (6)

35/M

Bee: multiple; all over
body

<1 day

Sciffman
et al (7)

57/F

Honey bee: multiple;
neck, face and arm

2 days

Taurin et al
(8)
Temizoz
et al (9)

36/M

Wasp: location NR

14 days

60/M

Bee: multiple; head
face and limbs

2 hours

Dysarthria, vertigo,
tinnitus, and bilateral
cerebellar signs
Left homonymous
hemianopia and
nausea and vomiting
Nystagmus and nausea
and vomiting
Left hemiplegia and
dysarthria

Dechyapirom
et al (10)

64/M

16 hours

Left hemiplegia and
facial nerve palsy

Rajendiran
et al (11)

25/M

Bee: multiple; face,
neck, chest, and
arms
Bee: multiple; head and
neck

1 day

Left arm weakness and
blurry vision

Viswanathan
et al (12)

59/M

2.5 hours

Bilir et al (13)

35/M

Dysarthria, left
hemiplegia, left facial
weakness, and left
gaze palsy
Right hemiparesis

Left MCA infarct

Wani et al
(14)

40/M

Left hemiplegia, left
gaze preference, and
obtundation

Bilateral thalami and
left parieto-occipital
infarct

Bee: multiple; face,
neck, scalp, and
anterior aspect of
chest
Bee: multiple; NR
Wasp: multiple; face,
head, and neck

A few hours, with
worsening
24 days later

6 hours
1 day

Recovery

Antihistamines,
cortisone, and
phenobarbital
NR

Died

Epinephrine, methylprednisolone, and
diphenhydramine

NR

Epinephrine,
hydrocortisone, and
chlorpheniramine
Dexamethasone,
antihistamines, and
mannitol
Antihistamines and
antiemetics

Full recovery

Left dorsal medulla
infarct
Bilateral frontal lobe
infarcts, right
temporoparietal and
bilateral centrum
semiovale infarct
Right MCA territory
infarct

Methyl-prednisolone

Improved

Epinephrine,
pheniramine,
hydrocortisone,
chlorpheniramine, and
aspirin
Promethazine, methylprednisolone, and t-PA

Mild left-sided
hemiparesis

Right frontoparietooccipital infarct with
hemorrhagic
transformation
Right MCA territory
infarct

Antihistamines and
antiemetics

Full recovery

Antihistamines,
hydrocortisone,
aspirin, atorvastatin,
and heparin
Adrenaline, methylprednisolone, and
ranitidine
Chlorpheniramine and
hydrocortisone

Left strength 4+/5
and resolution of
facial palsy

Bilateral cerebellar
hemorrhagic infarct
Right occipital infarct

NR

Died
Left homonymous
hemianopia

Recovered

Residual right
hemiparesis
Vegetative state

(Continued )

A. Kulhari et al.

Day (2)

Treatment

CT = computed tomography; F = female; ICA = internal carotid artery; M = male; MCA = middle cerebral artery; MRA = magnetic resonance angiography; MRI = magnetic resonance
imaging; NR = not reported; t-PA = tissue plasminogen activator.

t-PA, aspirin and
atorvastatin
Multiple right MCA
territory infarcts,
MRA no signal in
distal right ICA and
MCA
Left hemiplegia and
mild dysarthria
1 hour
Wasp: single; leg
44/M
Current case

Treatment
MRI/CT Findings
Clinical Findings
Onset of Deficits
Sting Type and
Location
Age/Sex
Author

Table 1. Continued

Mild left face droop

3

Recovery

2:

CASE REPORT
A 44-year-old right-handed white man with a history of
mild hypertension was working outside when a wasp
stung him on his leg. He acutely developed a diffuse
rash and urticaria but had no cardiorespiratory symptoms. Approximately 1 hour late, he developed left
hemiplegia, a left facial droop, and dysarthria and
was taken to the emergency department (ED) by ambulance. By the time he reached the ED, his symptoms
were starting to improve. On examination, he had
left hemiparesis (Medical Research Council score of
4+/5), mild left facial weakness (upper motor neuron
pattern), and mild dysarthria with a calculated National
Institutes of Health Stroke Scale score of 4. Initial
vital signs revealed hypertension that was probably
caused by cerebral autoregulation in response to
ischemia. His blood pressure was 146/116 mm Hg,
his heart rate was 85 beats/min, his respiratory rate
was 20 breaths/min, and his oxygen saturation was
100% on room air. Routine laboratory examinations
were normal. His electrocardiogram revealed a normal
sinus rhythm. A noncontrast computed topography
(CT) scan of his head was normal. A magnetic resonance imaging (MRI) scan of the brain, however,
showed multiple areas of diffusion restriction in the territory of the right MCA involving both cortical and
deep structures (Figure 1). An intracranial magnetic
resonance angiography (MRA) scan revealed a lack
of signal in the distal right internal carotid artery
(ICA) and MCA that was suggestive of either an occlusion from a thrombus or a critical stenosis (Figure 2).
An extracranial MRA scan was normal. He was still
within 4.5 hours after the onset of symptoms and was
therefore treated with intravenous tissue plasminogen
activator (t-PA). Because of his low National Institutes
of Health Stroke Scale score, endovascular intervention
was not pursued. He was treated with intravenous
steroids and histamine antagonists for systemic allergic
response. A computed tomography angiography scan of
the head performed 24 hours later showed multiple regions of vasoconstriction in the bilateral proximal
MCA arteries (Figure 3). After the results of the CTA
scan of the head, we considered that the distal right
ICA cut-off seen on the MRA scan was caused by severe vasoconstriction of the proximal right MCA interrupting the laminar flow of blood. Evaluation for causes
of stroke, including echocardiography, telemetry, and a
lipid panel, were not revealing. Aspirin and atorvastatin
were started for secondary stroke prevention. Immunologic testing revealed significantly elevated levels of
serum wasp immunoglobulin E. At discharge, 2 days
after admission, a mild left facial droop remained but
he had normal strength in his left arm and leg.

4

A. Kulhari et al.

Figure 1. Magnetic resonance imaging scan of the brain showing diffusion restriction in the territory of the right middle cerebral
artery involving both the cortical and subcortical structures, which is suggestive of acute infarct.

DISCUSSION
The pathophysiology of wasp sting injury stems from
both direct toxic effects from the wasp venom and severe
allergic reactions (15–18). Allergic reactions are mainly
caused by phospholipase, an enzyme in the venom (18).
Vascular pathologies, such as ischemic stroke, are primarily manifestations of the toxic effects of venom.
Wasp venom contains vasoactive peptides, such as thromboxane, leukotrienes, serotonin, and histamine, which
cause vasoconstriction of cerebral vessels, leading to
ischemic stroke (17). These vasoactive peptides are also
prothrombotic and proinflammatory and can lead to
thrombus formation (18). We believe that the mechanism
of stroke in our patient was cerebral vasoconstriction
caused by the vasoactive peptides. In addition, after

wasp stings, patients can develop paroxysmal atrial fibrillation, which can cause cardioembolic cerebral infarcts
(14). Finally, severe hypotension during anaphylaxis after
a wasp sting can also contribute to ischemic stroke (14).
In addition to stroke, other systemic complications,
including cardiac dysrhythmias, myocardial infarction,
acute tubular necrosis, renal failure, hemolysis, rhabdomyolysis, and disseminated intravascular coagulation
can also occur (10).
Management of bee or wasp stings starts with airway,
breathing, and circulation stabilization. Antihistamines,
steroids, and epinephrine are used to control the allergic
response. There are no guidelines for the management
of ischemic stroke after such stings because of the limited
number of cases. Our patient was young with significant
neurologic deficits, and we therefore treated him with

Figure 2. Intracranial magnetic resonance angiography scan (arrows) showing the lack of signal in the distal right internal carotid
and middle cerebral arteries, which is suggestive of a critical stenosis or occlusion.

2:

5

Figure 3. Computed tomography angiography scan of the head (arrows) showing multiple regions of vasoconstriction in the
bilateral M1 segment of the middle cerebral artery.

intravenous t-PA. He fortunately had a good outcome.
Because these patients can develop severe cerebral vasoconstriction, their intravascular volumes and hemodynamic statuses should be closely monitored. We believe
that aggressive blood pressure augmentation and fluid
resuscitation is important in these patients, especially
if the mechanism of stroke is cerebral vasoconstriction
or anaphylaxis. We also believe that steroids and antihistamines play a pivotal role in preventing cerebral vasoconstriction by reducing the intravascular inflammation
caused by the vasoactive peptides present in the wasp
venom. Therefore, we think it is safe to treat these
patients with intravenous steroids and antihistamines.

flushing, vomiting, diarrhea, and anaphylaxis causing severe hypotension and bronchospasm, are less common
but deadly. Neurologic complications, such as ischemic
stroke after a wasp sting, are rare but may occur and
can be caused by both allergic and toxic reactions to
wasp venom. While there are no specific guidelines for
the management of ischemic stroke in this setting, treatment with intravenous t-PA is reasonable if there are
no contraindications. Because the pathophysiology also
involves cerebral vasoconstriction, careful attention to
intravascular volume and hemodynamic status is important. Steroids and antihistamines may also play a pivotal
role in preventing cerebral vasoconstriction.

WHY SHOULD AN EMERGENCY PHYSICIAN BE
AWARE OF THIS?

REFERENCES

Emergency physicians encounter large numbers of
hymenopteran stings every year. These patients typically
present with local reactions, such as itching, edema, pain,
and erythema. Systemic manifestations, such as urticaria,

1. Sundaramoorthy K, Vishwanathan S, Arulneyam J. Wasp stingsrelated cerebral infarction in a toddy tapper with multiple previous
stings. Eur J Neurol 2011;18:1–3.
2. Day JM. Death due to cerebral infarction after wasp stings. Arch
Neurol 1962;7:184–6.

6
3. Riggs JE, Kotenen LM, Bodensteiner JB, et al. Wasp sting–
associated cerebral infarction: a role for cerebrovascular sympathetic innervation. Clin Neuropharmacol 1993;16:362–5.
4. Riggs JE, Kotenen LM, Wymer JP, et al. Acute and delayed cerebral
infarction after wasp sting anaphylaxis. Clin Neuropharmacol 1994;
17:384–8.
5. Crawley F, Schon F. Cerebral infarction: a rare complication of
wasp sting. J Neurol Neurosurg Psychiatry 1999;66:550–1.
6. Bhat R, Bhat KR, Shivashankar, et al. Bilateral haemorrhagic cerebellar infarction following honey bee sting. J Assoc Physicians India
2002;50:721–2.
7. Schiffman JS, Tang RA, Ulysses E, et al. Bilateral ischaemic optic
neuropathy and stroke after multiple bee stings. Br J Ophthalmol
2004;88:1596–8.
8. Taurin G, Canneva-Bourel ML, Delafosse JM, et al. Dorsal medulla
oblongata stroke after a wasp sting. Rev Neurol (Paris) 2006;162:
371–3.
9. Temizoz O, Celik Y, Asil T, et al. Stroke due to bee sting. Neurologist 2009;15:42–3.
10. Dechyapirom W, Cihan C, Kenneth N. Concurrent acute coronary
syndrome and ischemic stroke following multiple bee stings. Int J
Cardiol 2011;151:e47–52.

A. Kulhari et al.
11. Rajendiran C, Puvanalingam A, Thangam D, et al. Stroke after multiple bee sting. J Assoc Physicians India 2012;60:122–4.
12. Viswanathan S, Muthu V, Singh AP, et al. Middle cerebral artery
infarct following multiple bee stings. J Stroke Cerebrovasc Dis
2012;21:148–50.
13. Bilir O, Ersunan G, Kalkan A, et al. A different reason for cerebrovascular disease. Am J Emerg Med 2013;31:891.e5–6.
14. Wani M, Saleem S, Verma S, et al. Multiple cerebral infarctions
with severe multiorgan dysfunction following multiple wasp stings.
Ann Indian Acad Neurol 2014;17:125–7.
15. Ewan PW. Venom allergy. BMJ 1998;316:1365–8.
16. McHowat J, Kell PJ, O’Neill HB, et al. Endothelial cell PAF synthesis following thrombin stimulation utilizes Ca (2+)-independent
phospholipase A(2). Biochemistry 2011;40:14921–31.
17. Gok S, Ulker S, Huseyinov A, et al. Role of leucotrienes
on coronary vasoconstriction in isolated hearts of arthritic
rats: effect of in vivo treatment with Cl-986, a dual inhibitor
of cyclooxygenase and lipooxygenase. Pharmacology 2000;
60:41–6.
18. Vidhate M, Sharma P, Verma R, et al. Bilateral cavernous sinus
syndrome and bilateral cerebral infarcts: a rare combination after
wasp sting. J Neurol Sci 2011;301:104–6.