CASE SERIES
Year : 2023 | Volume
: 3 | Issue : 1 | Page : 7--12
Neuroparalytic snake bite masquerading as acute abdominal pain in children
Bindu Deopa, Deeksha Kumari Choudhary, Preeti Sehrawat
Department of Pediatrics, GMC, Haldwani, Uttarakhand, India
Correspondence Address:
Dr. Bindu Deopa
Anurjun Nursing Home, Kaladhungi Road, Nainital, Haldwani - 263 139, Uttarakhand
India
Abstract
Background: Neurotoxic snakebite (usually by the krait) presents with abdominal colic and chest pain as a common premonitory sign of envenomation. Being a nocturnal snake, the time of unprovoked painless biting is usually at night and the victims are individuals sleeping on the ground. Thus, history is usually not forthcoming. Snakebite causes morbidity (neuroparalytic, myopathic, vasculopathic, venom-induced consumption coagulopathy, cardiotoxic, nephrotoxic, etc.), and mortality if not given timely treatment with anti-snake venom (ASV), the only specific treatment. Clinical Description: We present four children from a rural background who were admitted successively over a month during the last rainy season. They initially became symptomatic with acute abdominal pain from midnight to early morning time and developed neuroparalytic manifestations within a few hours. On exclusion of other causes by clinical evaluation, we suspected snakebite envenomation though there was no witnessing of the event or evidence of fang bites. Investigations to rule out commonly associated organ dysfunction were ordered. Management: All children were given supportive therapy. Three cases required mechanical ventilation. The first two received ASV relatively late as the suspicion of snakebite was not considered initially. In the third case, the administration of ASV was early and the hospital stay was shorter. The fourth case received ASV at a peripheral health center and was referred in case he required ventilator support. However, his neuroparalysis did not progress to respiratory failure and he was discharged the earliest. Conclusions: Clinicians should consider snakebite in children belonging to rural areas who present with acute abdominal pain during the rainy season, and monitor for signs of neurotoxicity and other clinical manifestations of snake envenomation. A high index of suspicion should be kept, as definitive treatment with ASV results in early recovery without any sequelae, and reduces mortality.
How to cite this article:
Deopa B, Choudhary DK, Sehrawat P. Neuroparalytic snake bite masquerading as acute abdominal pain in children.Indian Pediatr Case Rep 2023;3:7-12
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How to cite this URL:
Deopa B, Choudhary DK, Sehrawat P. Neuroparalytic snake bite masquerading as acute abdominal pain in children. Indian Pediatr Case Rep [serial online] 2023 [cited 2023 Jun 6 ];3:7-12
Available from: http://www.ipcares.org/text.asp?2023/3/1/7/370539 |
Full Text
Acute abdominal pain is a common clinical presentation in any pediatric emergency. These comprise heterogeneous conditions that may be medical (including neuropsychiatric) or surgical in nature. A common but often unrecognized cause of acute abdominal pain is secondary to snakebite envenomation (i.e. the injection of venom into the body usually by a bite or sting). According to the World Health Organization, it is a neglected public health problem. Worldwide, there are 5.4 million estimated number of snakebites annually, out of which 2.5 million cause envenomation, and 81,000–138,000 result in death. The highest number of cases of snakebite envenomation is seen in South Asia, Southeast Asia, and sub-Saharan Africa.[1],[2] The outcome depends on the type of snake, the venom and the amount injected, the general health of the person bitten, and whether the patient receives anti-venom serum (AVS) in time. Children are more severely affected than adults, due to their smaller body mass index.
In India, there are over 1000,000 estimated snakebites annually causing significant morbidity and 58,000 deaths.[3],[4],[5] The common venomous snakes found in our country include Daboia russelii (Russell's viper), Naja naja (common Indian cobra), Bungarus caeruleus (common krait) [Figure 1], and Echis carinatus (saw-scaled viper).[6] The common krait is a nocturnally active snake that often bites without provocation. It is common in the rural setting and seen in individuals who are habituated to sleeping on the ground. Common reasons for a snakebite by a krait are overlooked because it is painless, and thus, the history is often not forthcoming; fang marks are not visible; the onset of symptoms varies from hours to days; and the clinical presentation is heterogeneous (neurotoxic, myopathic, vasculopathic, venom-induced consumption coagulopathy, cardiotoxic, nephrotoxic, etc.), but not pathognomonic.[7],[8] Hence, unless the event has not been witnessed, it may not be considered a differential diagnosis at all. Thus, the possibility of a snakebite should be considered in children presenting with acute abdominal or chest pain (common initial signs of krait envenomation)[9] followed by neuroparalytic symptoms such as ptosis, exophthalmoplegia, dysphagia, dyspnea, and generalized neuromuscular weakness.[10]{Figure 1}
We present four children who presented to our center during the last rainy season, requiring immediate ventilator support. Each one presented with acute abdominal pain as the initial symptom, developed neuroparalytic manifestations, was considered to be envenomation, managed with AVS, and recovered. The aim of this case series is to sensitize clinicians to this not-so-infrequent presentation (especially in patients from a rural background), so that a high index of suspicion is kept, and appropriate measures can be initiated as early as possible.
Case 1
Clinical description
A 5-year-old girl belonging to a rural area was referred to us from another hospital for providing continuous ventilatory support. The child had developed acute-onset abdominal pain sudden in onset in the early morning, colicky, around umbilical region, nonradiating, and progressively increasing in severity. There was no history of fever, bilious vomiting, loose stools, jaundice, or abdominal distension. The child was given some medication (nature unknown) without significant relief. After 6 h, she became lethargic and was unable to speak. This rapidly progressed to fast irregular breathing followed by labored breathing. There was no history of seizure, altered sensorium, abnormal eye movements, palpitations, bleeding, jaundice, or bleeding from any site. By the time the child reached a peripheral hospital, she was gasping and required emergency intubation. She was transferred to us from there in an ambulance with bag and tube ventilation and intravenous fluid (IVF) support. This was approximately 8 h of becoming symptomatic.
On admission, she was found to be afebrile but hemodynamically compromised with feeble pulses capillary filling time (CFT) >2 s, blood pressure (BP): 60/40 mmHg (<50th percentile, Indian Academy of Pediatrics [IAP] charts), heart rate (HR): 170/min, and oxygen saturation (SPO2): 95% with O2. The weight was 17.8 kg (50–75 percentile, IAP growth charts). She was immediately shifted to ventilator support on pressure control synchronized intermittent mandatory ventilation (SIMV) mode. There was no evidence of jaundice, pallor, rashes, petechiae, or local injury. Her Glasgow Coma Scale (GCS) score was E1VTM1. The pupils were bilaterally equally dilated and sluggishly reacting to light. It was difficult to assess other cranial nerves in the given situation. Patient had power 0/5 in both upper and lower limbs, generalised hypotonia, generalised diminished deep tendon reflexes and bilaterally plantar response were flexor. The respiratory examination was normal with bilateral equal air entry, vesicular sounds, and absence of added sounds. No abnormalities were identified in the cardiovascular system. The abdomen was soft with no organomegaly. Emergency investigations revealed the absence of hypoglycemia (random blood sugar: 102 mg/dl), dyselectrolytemia (sodium: 138 mEq/dl, potassium: 3.7 mEq/dl, and ionized calcium: 1.2 mEq/dl), and metabolic acidosis (pH: 7.26, pCO₂: 32 mmHg, HCO3: 14 mmHg, and lactate: 1.6). The metabolic derangement got corrected after management of shock. Based on the clinical phenotype, we suspected acute encephalopathy syndrome possibly metabolic or poisoning, given the preceding abdominal involvement and rapid progression to altered sensorium. There was no history of witnessed trauma or ingestion of any substance or food from an unknown source. There was no significant past or family history. The child studied in upper kindergarten and was on par with her peers. Her immunization was complete (in fact she had received her booster vaccine a month back).
Management and outcome
Mechanical ventilation was continued on volume control SIMV mode. Supportive treatment was administered in the form of IVF and inotropic support. Antibiotics were started empirically in view of suspected sepsis. Baseline investigations revealed hemoglobin: 12.8 g/dl, total leukocyte count: 9800/mm3, normal differential leukocyte count, platelet count: 3.6 lacs/mm3, C-reactive protein: 1.1 mg/dl, urea: 38 mg/dl, creatinine: 0.9 mg/dl, serum glutamic-oxaloacetic transaminase: 28 IU/L, serum glutamic-pyruvic transaminase: 30 IU/L, and prothrombin time (PT): 12 s, and international normalized ratio (INR): 0.8. Their general condition and sensorium remained status quo in the first 48 h of hospitalization. Lumber puncture was done on the 3rd day after hemodynamic stabilization of the patient and was found to be acellular with no abnormalities in biochemistry (protein: 32 mg/dl and sugar: 72 mg/dl). The computerized tomography (CT) head was normal. Magnetic resonance imaging could not be done as he required ventilation with O2, and a bedside electroencephalogram was not available to rule out nonconvulsive status epilepsy. The ultrasound (USG) of the abdomen was also normal.
After 3 days, the family members volunteered that two adults from the same village had presented with a similar illness after being bitten by a snake. We found that the family resided in a kaccha house and that the child slept on the floor with his parents. Careful examination could not identify any fang marks or local skin lesions. Nonetheless, the patient was given 10 vials of anti-snake venom (ASV) with concurrent atropine and neostigmine. The whole blood clotting time was <20 min.
There was symptomatic improvement within 48 h of the ASV administration indicated by decreasing requirement of vasopressors and ventilatory settings. Ten more vials of ASV were given. Gradually, the sensorium started to improve and she could be extubated by the 9th day of admission. There was a gradual improvement in the neuromuscular function as well. The child was discharged after 24 days without any neurological sequelae.
Case 2
Clinical description
A 12-year-old boy presented with a history of sudden-onset acute abdominal pain at 4 am in the morning. It was colicky in nature, diffuse, and nonradiating. Within 3 h, the child developed generalized weakness in the form of not able to move his upper or lower limbs, difficulty in speaking, difficulty in deglutition, and labored breathing with increased chest retractions. There was no history of any seizure, altered sensorium, abnormal eye movements, palpitations, bleeding, jaundice, or bleeding from any site. The patient was admitted in a peripheral hospital where he was immediately started on ventilatory support, IVF, antibiotics, vasopressors, and other supportive care. He was transferred to our hospital after 36 h in an ambulance on bag and tube ventilation.
As this patient presented within 2 days of the diagnosis being made in the first case and had a similar clinical phenotype, we kept a high index of suspicion of snakebite envenomation. The child's father was a farmer and their residence was surrounded by the farming lands where snakes were commonly found, especially during the present rainy season. We elicited of history other clinical manifestations secondary to snakebite which is given in [Table 1]. The patient's HR was 102/min, SPO2: 97% with 40% FiO2, peripheral pulses (PP) palpable, CFT maintained, and BP: 104/60 mmHg (50th percentile, IAP charts) on inotropes. His weight was 36 kg (25–50 percentile, IAP growth charts). Pallor, icterus, rashes, and petechiae were absent, and there was no evidence of fang marks or local injury. The GCS score was E1VTM1. Both pupils were equal and normal in size and reacting to light. Other cranial nerves could not be assessed. All four limbs had a power of 0/5 and flaccid tone. There was generalized absence of DTRs and bilateral plantar flexor response. No abnormalities were identified in the cardiovascular system and respiratory system. The abdomen was soft, nontender, and without any organomegaly.{Table 1}
Management and outcome
The patient was given ventilatory support on volume control SIMV mode, IVF with vasopressors (adrenaline and dopamine), IV antibiotics, and tetanus toxoid vaccination. Twenty vials of ASV were administered along with atropine and neostigmine. Investigation reports [Table 1] revealed the absence of hypoglycemia, dyselectrolytemia, hepatitis, coagulopathy, uremia, or metabolic abnormalities (pH: 7.42, pCO2: 36 mmHg, pO2: 102 mmHg, HCO3: 20). The bedside USG was normal. Gradually, the GCS improved and the child got extubated on the 7th day of admission. Gradually, his muscle power improved, his speech became clear, he was able to walk and feed himself, and he was discharged after 2 weeks of admission.
Case 3
Clinical description
A 10-year-old boy, a resident of rural Uttarakhand, presented to the Emergency Department of our hospital at midnight with sudden-onset severe abdominal pain, followed by difficulty in breathing and swallowing and drooping of eyelids within an hour.
The child was gasping and in shock at admission and was immediately intubated. His vitals were HR: 62/min (bradycardia present), PP not palpable, CFT prolonged, and BP: 60/34 mmHg (<50th percentile, IAP charts). His weight was 27 kg (25th percentile, IAP growth charts). The GCS could not be assessed as he was deeply sedated. Bilateral pupils were of normal size and equally reacting. The power was 0/5 in both upper and lower limbs, there was generalized hypotonia, the DTRs were diminished, and both Plantar were bilaterally flexor. Systemic examination revealed no abnormalities. Based on our prior experience of this clinical phenotype, and since no clinical clue indicated any other cause, we kept a provisional diagnosis of snakebite. The details of the clinical phenotype are depicted in [Table 1], but there were no clinical clues suggesting any other complication besides neuromuscular paralysis. Management of shock was initiated as per standard protocol, and he was shifted to the pediatric intensive care unit for further management.
Management and outcome
He was placed on ventilator support (volume control SIMV mode) and administered IVF and intravenous (IV) antibiotics. The patient was given 10 vials of ASV along with atropine and neostigmine. The child had received a TT vaccine a week earlier as routine immunization. The details of the investigation profile are depicted in [Table 1]. There was no hypoglycemia, or dyselectrolytemia, but mixed respiratory and metabolic acidosis was present (pH: 7.20, PCO2: 62 mmHg, PO2: 68 mmHg, and HCO3: 16). The level of consciousness and general condition improved very rapidly, and he was extubated after 60 h of admission. Gradually, the power and movement of all four limbs returned and he was able to swallow. He was discharged on the 7th day of admission completely asymptomatic.
Case 4
Clinical description
A 15-year-old boy was admitted in our hospital with a history of acute pain abdomen at 3 am following which he developed neuroparalytic symptoms after 4 h, the details of which are given in [Table 1]. His parents were manual laborers, and the family resided in a kachcha house, where they slept on the floor. There was a significant history of the mother having being bitten by a snake 15 days back. The mother had not had any symptoms except for local swelling at the site of bite. She had been given ASV at the nearby community health center (CHC) and had remained well. The boy was also taken to the same CHC where despite the absence of suggestive history, a snakebite was suspected and he was given 10 vials of ASV and immediately referred to our hospital for further management. We concurred with this diagnosis as we were unable to elicit any symptom or sign that suggested otherwise. There were no clinical indicators of the other complications of snakebite (as outlined previously in the earlier cases).
Patient's Heart rate was 140/min, respiratory rate was 28/min, the SpO2 was 98% at room air , peripheral pulses were palpable, CFT < 2 secs and BP was 110/64 mmHg (50th percentile, IAP BP charts), His weight was 42 kg (10–25th percentile IAP growth charts). No abnormalities were detected on general physical examination. The child exhibited bilateral ptosis, though both pupils were normal in size and reacting equally to light. The power of both upper limb and lower limb was 2/5, with hypotonia and hyporeflexia. Systemic examination was normal.
Management and outcome
We gave the child another 10 vials of ASV given along with atropine and neostigmine. The TT vaccine had already been given in the CHC. The child was kept under close observation and his vital parameters were monitored. The patient does not require any ventilatory or inotropic support. He was started on IVF initially and then shifted to oral feeds. Gradually, the ptosis and neuromuscular paresis of limbs improved and the patient was discharged on the 5th day with complete recovery.
Discussion
Snake venom comprises many substances such as different enzymes (constituting 80%–90% of viperid and 25%–70% of elapid venoms), nonenzymatic polypeptide toxins, carbohydrates and metals, lipids, free amino acids, nucleosides, serotonin, and acetylcholine. It also includes digestive hydrolases, hyaluronidase, and kininogenases.[8],[11] Krait bites are characteristically painless and cause minimal or no local envenomation, as is seen with other snakebites.
In our series, all the patients had abdominal pain as the first symptom occurring at night. This is usually due to submucosal bleeding. [Table 2] gives the clinical details of two patients who presented with acute-onset, severe, rapidly increasing abdominal pain in which there were no other manifestations and envenomation was only suspected after other usual causes of abdominal pain could not be found on the usual investigations undertaken in the workup for an acute abdomen (ultrasonography or computed tomography) apart from submucosal bleeding and hemoperitoneum secondary to a deranged coagulation profile. There was a therapeutic response to ASV and symptomatic treatment.[12],[13]{Table 2}
None of our cases were investigated exclusively on the lines of the acute abdomen (though an abdominal USG was performed in the first two cases), as the neuroparalytic manifestations developed rapidly within a few hours of the abdominal pain and all three of them required ventilator support at admission.
Neurotoxic polypeptides in krait venom cause paralysis by blocking transmission at the neuromuscular junction.[8],[14] α-bungarotoxin and cobrotoxin (postsynaptic α-neurotoxins) bind to acetylcholine receptors at the motor endplate, whereas presynaptic (β) neurotoxins (β-bungarotoxin and taipoxin) release acetylcholine at the neuromuscular junctions, damage the endings, and prevent further release of the neurotransmitter.
In a study of 141 adult patients with snakebite due to common krait by Bawaskar et al., 85% of patients had abdominal colic and 72% had chest pain at night followed by other neuroparalytic symptoms within 8 h of being bitten.[9] The onset of neurological manifestations (bilateral ptosis, external ophthalmoplegia, limb paresis/paralysis, and respiratory muscle paralysis) varies from 30 min to 6 h after the onset of these initial symptoms.[7],[10] In this series, all four cases exhibited neurological manifestations within 6 h of the initial symptoms, severe enough in three to affect the respiratory muscles and warrant ventilatory support. The fourth child's neurological manifestations probably did not progress beyond the ptosis and moderate limb involvement probably because he had already been administered ASV at the CHC.
Management comprises monitoring for all possible complications, ASV, and supportive treatment. The baseline workup includes a monogram (hemoglobin, hematocrit, white blood cell count, platelet count), tests for coagulopathy (PT/activated partial thromboplastin time/INR), liver and kidney function tests, serum electrolytes, and electrocardiogram.[2],[8] AVS should be given as soon as its envenomation is suspected. It may reverse the symptoms even if they have been present for several days or, in the case of hemostatic abnormalities, for even 2 or more weeks.[8],[11] In neurotoxicity ASV prevents post synaptic neurotoxicity and myotoxicity. It is recommended that 10–20 vials of ASV be given for the common krait bite, and a second dose be given after 6 h if there is no improvement.[8] A trial of concurrent IV atropine followed by intramuscular neostigmine can be given and repeated if the ptosis disappears or there is improvement in the ventilatory capacity.[8] Supportive treatment depends on the clinical status and includes ventilatory support, IVF, TT vaccination, and antibiotics. Blood products such as packed red blood cells and fresh frozen plasma transfusions are indicated in case there is evidence of consumptive coagulopathy.
This case series highlights the fact that clinicians should suspect envenomation even in the absence of a snakebite, in children presenting with acute abdominal pain followed by clinical features suggestive of complications (neurotoxicity, myopathy, vasculopathy or coagulopathy, etc.); especially if the patient belongs to a rural area, presentation is during the rainy season, there is a history of sleeping on the floor, and symptoms manifest during the night or early morning. Definitive treatment with ASV could save the life and helps in early recovery and good prognosis without any sequelae.
[INLINE:1]
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the parents have given their consent for images and other clinical information to be reported in the journal. The parents understand that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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