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Scorpion sting is common in some global regions and mostly causes local envenoming of varying severity. Some estimates suggest that perhaps only 10% of those stung by even the most medically important species develop severe systemic envenomation; however, the frequency of severe envenomation is higher in children. With few exceptions, systemic envenomation by medically important species is characterized by relatively similar neurotoxic stimulation syndromes.
Here, we report a 12-y-old girl who developed toxic encephalopathy and lethal brain edema owing to scorpion envenomation (Leiurus abdullahbayrami [Scorpiones: Buthidae]). She was transferred to our pediatric intensive care unit from another center after 2 d of follow-up. Based on the documents provided by the other medical unit, the patient was intubated 1 to 2 h after the scorpion sting owing to confusion and respiratory distress and was given tetanus vaccine, 1 vial of antivenom (polyvalent antiscorpion antivenom, Refik Saydam Hygiene Center, Ankara, Turkey), and doxazosin therapy in the initial treating facility. Because the patient experienced cardiac arrest for 5 min, cardiopulmonary resuscitation was performed. When the ejection fraction of the left ventricle was 30% on echocardiography, she was referred to us with a diagnosis of toxic myocarditis.
Immediately after admission to our unit, she was intubated and had decompensated shock findings. Her Glasgow Coma Scale score was 6 of 15. Blood gas findings showed mild acidosis. Laboratory results showed white blood cell levels were 15.73×103·μL-1, hemoglobin was 11.9 g·dL-1, platelets was 254×103·μL-1, serum creatinine was 0.87 mg·dL-1, blood urea nitrogen was 24 mg·dL-1, aspartate aminotransferase was 244 U·L-1, alanine aminotransferase was 71 U·L-1, creatinine kinase was 8191 U·L-1, troponin T was 1924 pg·mL-1 (normal range: 0–14), N-terminal pro-brain natriuretic peptide was >35 ng·L-1, and CK-MB was 75 ng·mL-1 (normal range: 0–3.6); international normalized ratio was 1.59; activated thromboplastin time was 24.9 s; prothrombin time (PT) was 18.4 s; D-dimer was 3789 ng·mL-1 (normal range: 0–243); and fibrinogen was 5.58 g·L-1 (normal range: 2–3.93).
To stabilize the patient, we continued with maintenance fluid, milrinone, and doxazosin therapies and dobutamin to correct hypotension. On the first day of admission, the patient was given 1 more vial of Refik Saydam Hygiene Center polyvalent antiscorpion antivenom therapy. On echocardiography, the ejection fraction was 45 to 50%. Cranial computed tomography (CT) was performed on the third day of admission, with decreased alertness and a Glasgow Coma Scale score of 4. The CT report revealed existing widespread hypodense areas in both cerebral hemispheres, loss of gray and white matter separation, and deletion in sulcal structures compatible with edema (owing to possible toxicologic effects) (Figure 1). Because the patient had brain edema, 0.1 cm3·kg-1·h-1 3% NaCl was started. The patient’s neurologic condition worsened gradually. On the 10th day of hospitalization, neurologic examination revealed absence of all brainstem activity. CT angiography was performed, and the report was compatible with brain death.
Figure 1On the third day of admission, cranial computed tomography revealed widespread hypodense areas in both cerebral hemispheres, loss of gray and white matter separation, and deletion in sulcal structures compatible with severe edema.
Lethal cerebral edema occurred in a 2-y-old male patient who had diffuse brain edema and ischemic changes on CT after scorpion sting and was later reported to be diagnosed with brain death.
Similarly, our patient had diffuse brain edema (owing to possible toxicologic effects) on CT and was diagnosed with brain death on the 10th day of admission. CNS pathophysiologic effects have been hypothetically assigned to venom penetration through the blood-brain barrier because of possible increased permeability in young children.
Symptoms of systemic envenomation may be caused by the venom (toxins) itself or neurotransmitters (catecholamines) and proinflammatory cytokines released owing to the venom.
In conclusion, we believe that this patient had unusually severe brain damage either owing to venom-related direct CNS toxicity (increased permeability of the blood-brain barrier, affecting the CNS neurons) or the secondary effect of proinflammatory cytokines and neurotransmitters affecting blood vessels, which induced brain ischemia and cytolytic brain edema.
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