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CASE REPORT
Year : 2023 | Volume
: 14
| Issue : 1 | Page : 50-52
Reversible brain death: A rare manifestation of snake envenomation
Ankusha Patra, Vrinda Goel, Shiva Narang, Amitesh Aggarwal
Department of Medicine, University College of Medical Sciences and GTB Hospital, Delhi, India
Correspondence Address:
Dr. Shiva Narang
A-16/F-1, A-Block, Dilshad Garden, Delhi - 110 095
India
Source of Support: None, Conflict of Interest: None
DOI: 10.4103/injms.injms_125_22
Snakebite is a serious public health problem and one of the priorities in WHO's list of neglected tropical diseases. It significantly increases morbidity and mortality associated with envenomation in India. A neurotoxic snakebite can present in the form of symptoms ranging from asymptomatic presentation, ptosis, and complete external and internal ophthalmoplegia to complete respiratory failure. This is a case report of a 22-year-old male, who presented with bilateral ptosis and impending respiratory failure. He soon became deeply comatose, with absent brain stem reflexes (mute plantar, fixed pupils, and the absence of the doll's eye reflex) which were suggestive of brain death. He was treated with polyvalent anti-snake venom, anticholinesterases, and supportive therapy and recovered completely with an excellent outcome.
Keywords: Anticholinesterase, anti-snake venom, brain death, snakebite
Snakebite is an acute life-threatening medical emergency, and it is a very well-known preventable health hazard faced by tropical countries with heavy rainfall. In June 2017, WHO added snakebite to its priority list of “neglected tropical diseases.” There are more than 2000 species of snakes in the world out of which 52 venomous snakes are found in India, the majority belonging to three families: Elapidae (Cobra and Krait), Viperidae (Vipers), and Hydrophiinae (Sea Snakes). More than 5–6 lakhs bites occur each year although only 30% are venomous. The mortality in published data is reported to be around 35,000–50,000 per year which is believed to be underreported. The clinical spectrum consists of a wide range of signs and symptoms varying from asymptomatic cases to local tissue necrosis to cases with life-threatening neuroparalytic, vasculotoxic, and myotoxic symptoms depending on the type of snake.[1] A rare manifestation of neurotoxic snakebite mimicking brain death can occur, due to severe envenomation with complete internal and external ophthalmoplegia. Here, we discuss one patient with a classical presentation of neurotoxic snakebite who was initially thought to be brain dead but with supportive care and anti-snake venom (ASV) recovered fully with an excellent outcome.
Case ReportA 22-year-old male presented to a tertiary care hospital in the National Capital Area with a history of snakebites around 3:00 am while sleeping on the roof of his house. The patient stated a black-colored snake bit on the right ear lobe of the patient and complained of drooping of both the eyelids and drowsiness 15–30 min after the bite. The patient presented to the emergency within 1 h of the bite. Soon he developed shortness of breath upon arriving at the emergency. On examination, the patient appeared drowsy, and was not able to speak in sentences, his pulse rate was 122 per min, his blood pressure was recorded as 152/92 mm Hg, and respiratory rate was 20 per min, and his saturation of 96% on room air. There was a bite mark present on the right ear lobe without any soft-tissue reaction along with bilateral ptosis. On central nervous system examination, the patient was conscious and oriented to time, place, and person, there was flexor plantar response, and both the pupils were equal and reacting to light. There was no other focal neurological deficit. The chest was clear, air entry bilaterally was equal with no adventitious sounds. The single breath count was <3. An on-the-spot whole blood clotting time test was <20 min. The patient was electively shifted to mechanical ventilation in anticipation of respiratory failure. Hypoxia was not recorded during or after intubation. On assessment, 6 h postintubation, the patient's Glasgow Coma Scale (GCS) was Eyes 1 Vocal T Motor 1, bilateral plantar reflexes were mute, bilateral pupils were fixed and dilated, and corneal reflexes were absent. Doll's eye reflex was also absent. The patient did not have any spontaneous respiration and was on pressure support ventilation mode of assisted ventilation. On tracheal and oral suction, cough reflex was absent further confirming brain stem involvement. Noncontrast computed tomography scan of the head was normal. The laboratory investigations revealed no significant abnormality with hemoglobin of 12.2 g/dL, total leukocyte count of 19,500/μL, and platelet count of 80,000/μL, with urea of 35 mg/dL and, creatinine 1.1 mg/dL. Along with ventilatory support, the patient was also administered polyvalent ASV 100 mL as an initial dose. Furthermore, neostigmine and atropine were given to reverse neuromuscular blockade (5 doses given at 30 min intervals) intravenously and other supportive treatment in the form of intravenous fluids and broad-spectrum antibiotics was given. Over the next 24 h, two more doses of ASV were given amounting to a total of 300 mL of ASV along with neostigmine and atropine. Nearly 30 h postadmission and 24 h after documentation of loss of brainstem reflexes, the patient started to show signs of recovery. He started blinking his eyes and flickering his fingers but showed no effort for spontaneous respiration. His pupils were reacting to light, and his plantar were flexors. The patient was mechanically ventilated for 5 days, during which his limb and truncal power recovered completely, and he was able to lift his head off the bed. Weaning off trial was given on day 5, which failed as there was no recovery of respiratory muscles. The patient was shifted to synchronized intermittent mandatory ventilation mode of ventilation on day 7 of admission following which he was weaned off the ventilatory support on day 8 by transitioning to continuous positive airway pressure and then a simple oxygen mask for another 2 days. By the time of discharge, the total leukocyte count and platelets had normalized.
DiscussionSnakebite is a menace in North India accounting for a common cause of abrupt-onset neuroparalysis in medical emergencies. The incidence is found to be twice as higher in men as compared to women. Half of the snakebites are dry bites, but the venomous ones are usually from three families the Elapidae, Viperidae, and Hydropiinae.[1]Elapidae comprises cobra and krait mostly which have short permanently straight fangs, while on the other hand, snakes in the Viperidae family have long fangs which are folded against the upper jaw.[2] Snakebites are usually seen in rainy seasons, at night, or during harvest season. The Elapidae family is known for neuroparalysis. Cobra venom acts on postsynaptic acetylcholine receptors, while krait acts on presynaptic receptors. The clinical manifestations are usually due to postsynaptic competitive or noncompetitive receptor blockage at the motor end plate or the blockage of the presynaptic release of neurotransmitters. The presynaptic blockage is irreversible and hence the recovery is slower.[2] Agarwal et al. described how neuroparalysis progresses in snakebites.[3] The time of onset of symptoms post a snakebite varies from 4 to 12 h in usual circumstances. The paralysis usually starts with external ophthalmoplegia evident by ptosis to involve proximal muscles (palate, jaw, tongue, etc.) and progresses to distal muscles. The diaphragm is one of the most resistant muscles to neurotoxins. Respiratory failure usually resolves in 2 days. The ophthalmic features in neuroparalysis start with ptosis which goes on to involve the sixth cranial nerve and finally complete ophthalmoplegia with fixed dilated pupils.[4] The internal ophthalmoplegia is mostly due to autonomic dysfunction which causes a state simulating “brain death.” Anadure et al. describe how the neurotoxin of cobra and krait manifests symptoms in humans.[5] Krait venom binds to the presynaptic membrane thus inhibiting the release of acetylcholine. This causes more severe symptoms in patients often leading to the need for mechanical ventilation. Paralysis can persist for weeks and is reversed by supportive management. On the other hand, cobra venom binds to the postsynaptic acetylcholine receptors, and anticholinesterases and ASV have a role in the rapid reversal of symptoms in cobra bites.
Akoz et al. in the study analyzed patient management in snakebites through a series of cases.[6] An interesting observation was noted in snakebite patients, patients usually present with thrombocytopenia and leukocytosis. This is because of thrombomodulation and proinflammatory milieu created in the body postsnakebite. A similar observation can be made in our patient. The TLC and platelets normalized over the course of the which were probably reactionary.
Our patient presented with ptosis and impending respiratory failure. The patient was put on ventilatory support and took about 8 days to completely wean off from ventilator support. This is a rare case and one of its kind at our center where a snakebite presented with symptoms mimicking brain death as evidenced by (GCS of three and absent doll's eye reflex) but completely recovered in 8 days. John et al. reported a similar of a 6-year-old girl who presented with left hand swelling in a drowsy state.[2] The patient was shifted to mechanical ventilation because of poor GCS with absent deep tendon reflexes and fixed dilated pupils. The patient regained complete power in 36 h and was weaned off the ventilator. Pushparajan et al. reported a similar case in where a 73-year-old female presented to a medical emergency with a cobra bite on her right hand.[7] The patient had GCS three with absent brain stem reflexes. She started to regain her muscle power after 36 h postadmission. ALfaifi et al. reported a case of a 57-year-old woman who presented with a similar state after a cobra bite.[8] They also discuss that people with severe envenomation may require higher doses of ASV. Kepeng reported a case of a 69-year-old man who presented with brain stem death post a sea snakebite and was weaned off a ventilator after 20 days.[9] Dayal et al. reported a case of a 10-year-old boy who presented in a gasping state and with fixed dilated pupils after a snake bite.[4] The patient received 15 vials of ASV and started to show recovery on day 3 of admission and artificial ventilation. Mehta et al. reported three similar cases in a case series where a patient presented with symptoms masquerading as brain death.[10]
ConclusionPrompt identification and early initiation of advanced life support in the form of mechanical ventilation along with standard therapy goes a long way to save a patient from a snakebite. No time should be wasted in the decision of early initiation of ventilatory support, this avoids the development of hypoxia and facilitates recovery. Treatment decisions once respiratory failure sets in will obviously do more damage than preemptive treatment. Second, higher doses of ASV can also be given if there are no early signs of recovery. We would also like to highlight that even if signs of brain death set in there is still a chance that the patient can completely recover with continued advanced life support and supportive care. Hence, unrelenting efforts should be put in for this potential cause of reversible brain death-like signs, which in itself is unusual and unheard of in clinical practice.
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