Venomous Poisoning from Insect Stings, Spider, or Scorpion Bites: A Medical Emergency

Envenomation from insect stings and spider or scorpion bites constitutes medical emergencies that can lead to severe neurological complications, including status epilepticus. This syndrome, characterized by prolonged or recurrent seizures without complete recovery between episodes, can be triggered by inflammatory mechanisms, direct neurotoxicity, and immunological responses to venom.

Managing these emergencies requires a comprehensive understanding of the venom’s pathophysiology and contributing factors, such as concomitant medication use that might exacerbate neurotoxicity.

Pathophysiology of Venom-Induced Status Epilepticus

Status epilepticus associated with envenomation can occur through various mechanisms:

• Direct neurotoxicity. Some venoms affect neuronal ion channels, altering brain excitability and inducing seizures.¹
• Systemic inflammatory response. Venom can activate pro-inflammatory cytokines, promoting neuroinflammation.²
• Drug interactions. Analgesics, such as non-steroidal anti-inflammatory drugs (NSAID) may influence inflammatory pathways and increase the risk of seizures in this context.³

Adverse Drug Reactions in Envenomation

Drugs used to manage pain and inflammation associated with envenomation (such as ketorolac) have been linked to adverse effects that exacerbate pre-existing or latent neurological conditions.³ On the other hand, antivenoms like Alacramyn can be beneficial but also pose risks due to the possibility of severe anaphylactic reactions.^4,5

Similar Reports of Status Epilepticus Secondary to Envenomation

Other reports informing reactions to envenomation include:

• Insect stings. Cases of status epilepticus following bee and wasp stings have been documented, attributed to venom-induced brain inflammation.^6,7
• Ant and spider bites. Fire ants and spiders such as the black widow have also been associated with seizures, likely due to the neurotoxicity of their venom.^8,9
• Scorpion stings. Studies have reported seizures in 7.1% of patients envenomed by scorpions, underscoring the relevance of early medical intervention.¹⁰

Patient Background

A male patient without chronic degenerative conditions and no history of seizures. Traumatic and surgical history includes knee and hip surgery for fracture repair, requiring intraoperative transfusion of an unknown unit type and volume, reportedly without adverse reactions during or post-surgery. No known allergies, habitual or chronic medication use, or toxicomanias are reported. Alcohol consumption is occasional, without episodes of intoxication.

Current Condition

The condition began on Monday, December 19^th 2023, following an unidentifiable envenomation while the patient slept. Initial symptoms included localized pain and swelling on the radial aspect of the right wrist. By the following day, there was increased discoloration, swelling, induration, and intensified pain at the site.

The patient presented to the emergency department on December 20^th 2023 with unrelieved symptoms, where analgesic treatment with intravenous (IV) ketorolac (30 mg) was administered. Minutes later, the patient experienced agitation and respiratory difficulty, prompting admission to the shock unit and advanced airway management.

During subsequent care, despite mechanical ventilation and sedation, the patient displayed persistent abnormal movements with intervals exceeding 5 minutes, averaging three episodes over 30 minutes. Management included benzodiazepines and phenytoin loading, with adjustments to base sedation using propofol and midazolam infusion.

Therefore, it was decided to admit him to the intensive care unit (ICU), where he was administered 6 mg of IV dexamethasone and two vials of Alacramyn in addition to continuing with the support treatment.

Neurological Assessment

Under sedation (propofol at 44 mcg/kg/min and midazolam at 210 mcg/kg/h), the patient achieved a Richmond agitation sedation scale (RASS) of -5 points. Buprenorphine was administered for 24 hours alongside phenytoin (1 g) for loading. Initial observations included hyperreflexia without nuchal rigidity and isochoric pupils with minimal light reactivity. Tonic abnormal movements were noted in all extremities, accompanied by blood pressure spikes, suggesting potential seizure activity.

Cardiovascular System

Continuous cardiac monitoring revealed no conduction or rhythm abnormalities. The patient maintained a stable blood pressure, although deep sedation induced a drop in mean arterial pressure to 45 mmHg, unresponsive to a rapid 250 cc crystalloid infusion. Heart sounds were robust, without arrhythmias, and capillary refill and coloration were adequate.

Pulmonary System

The lungs showed symmetrical expansion with clear vesicular breath sounds bilaterally. The patient was on mechanical ventilation with the following settings: FiO₂ 40%, tidal volume 470 mL, flow 47 mL, respiratory rate 14 breaths per minute, PEEP 5, ratio 1:2.1, mean airway pressure 8.6, and oxygen saturation at 100%. Arterial pCO₂ was 47 mmHg.

Gastro-Metabolic Status

The patient was fasting with a nasogastric tube and was exhibiting moderate alimentary output. Abdominal examination revealed globally reduced peristalsis without organomegaly. Liver enzymes were elevated, with a gamma-glutamyl transferase (GGT) at 229 Ul/L and aspartate aminotransferase (AST) at 228 Ul/L. Blood glucose was 89 mg/dL, and calcium was mildly low at 8.3 mg/dL.

Renal Function

Urine output was 2.2 mL/kg/h with typical macroscopic characteristics. Urinalysis revealed numerous red blood cells, while azotemia markers were within normal limits, although serum chloride was slightly elevated at 111 mEq/L.

Hemato-infectious Assessment

The patient was afebrile with no systemic inflammatory response syndrome (SIRS) indicators. Complete blood count showed leukocytosis (13,000/mm³), monocytosis (13%), and no coagulation, platelet, or hemoglobin abnormalities.

Laboratory findings corroborated seizure activity, showing significantly elevated muscle enzymes, lactate, and transaminases, with mild leukocytosis.

Intensive Care Unit Admission

The patient was admitted to the ICU for 10 days, where he developed a hyperreactive status epilepticus that proved unresponsive to treatment.

General Ward Course

Upon transfer to the internal medicine ward, the patient received analgesia, maintenance fluids, and a polymeric diet (1800 Kcal/day, in three portions). Despite ongoing status epilepticus, the patient did not respond to treatment. Eight days post-ICU discharge, without additional interventions, there was a change in consciousness with a Glasgow coma scale score of 14.

Laboratory Findings

Hematology

• Red blood cells: 4.6 million/µL
• Hemoglobin: 13.7 g/dL
• Hematocrit: 39.7%
• Mean corpuscular volume: 86.7 fL
• Mean corpuscular hemoglobin: 29.9 pg
• Platelets: 224,000/µL
• Leukocytes: 13,030/µL

Coagulation

• Prothrombin activity: 104%
• Prothrombin time: 12.2 sec
• INR: 1.11
• Partial thromboplastin time: 28.1 sec

Biochemical Analysis

• Elevated GGT: 229 Ul/L
• Elevated AST: 228 Ul/L

Imaging

Computed Tomography Scan (Cranium and Thorax)

• Bilateral posterior-basal consolidations suggesting potential pneumonia
• Global cardiomegaly and pansinusitis
• No cranial or cerebellar abnormalities on simple phase imaging

Magnetic Resonance Imaging (1.5 Tesla)

• No acute inflammatory brain processes
• Findings suggest demyelinating plaques and recommend correlation for possible chronic demyelinating processes