|Year : 2015 | Volume
| Issue : 4 | Page : 517-519
Krait envenomation: Strong suspicion and judicious use of anti-snake venom
Lalit Prakash Mali1, Sweta Gupta1, Deepak Sharma2, Mukesh Choudhary3
1 Department of Pediatrics, JLN Medical College, Ajmer, Rajasthan, India
2 Department of Neonatology, Fernandez Hospital, Hyderabad, Telangana, India
3 Department of Medical and Paediatric Oncology, Gujarat Cancer and Research Institute, Ahmedabad, Gujarat, India
|Date of Web Publication||14-Jul-2015|
Department of Medical and Paediatric Oncology, Gujarat Cancer and Research Institute, Ahmedabad, Gujarat
Source of Support: None, Conflict of Interest: None
Snake bite is common in Rajasthan, particularly in rural areas and in the rainy season. In the majority of cases, we usually get compatible history and clinical sign and/or symptoms. However, sometimes, there may be inconsistent history and fang marks may not be appreciable. Here, we report a case wherein snake passed over the body of the patient, no clear history of biting, without any fang marks and patient presented with neuroparalysis within 2-3 h. After ruling out other possible causes, diagnosis of krait envenomation was kept. Anti snake venom was given along with symptomatic and supportive measures, and the patient was discharged home with no residual neurological deficit.
Keywords: Anti-snake venom, envenomation, krait
|How to cite this article:|
Mali LP, Gupta S, Sharma D, Choudhary M. Krait envenomation: Strong suspicion and judicious use of anti-snake venom. Med J DY Patil Univ 2015;8:517-9
|How to cite this URL:|
Mali LP, Gupta S, Sharma D, Choudhary M. Krait envenomation: Strong suspicion and judicious use of anti-snake venom. Med J DY Patil Univ [serial online] 2015 [cited 2022 Oct 7];8:517-9. Available from: https://www.mjdrdypu.org/text.asp?2015/8/4/517/160823
| Introduction|| |
Venomous snakebite is an important, yet neglected public health problem in tropical countries, accounting for significant morbidity and mortality. Presence of many myths and superstitions regarding snake bite management prevail in these areas further complicating management. In India, around 45, 900 deaths are estimated to result annually from snakebites.  The commonly encountered venomous snakes in India include common cobra (Naja naja), common krait (Bungarus caeruleus), Russell's viper (Daboia russelli), and saw-scaled viper (Echis carinatus). Snake venom is broadly categorized as neurotoxins and cytotoxins. Neurotoxic venom produces curare like effects. Neurological manifestations that follow envenoming by elapids (cobras and kraits) include ptosis, external ophthalmoplegia, and paralysis of pharyngeal muscles, followed by respiratory and generalized muscle paralysis. 
| Case Report|| |
A 14-year-old male child was brought in Pediatric emergency. The child was unresponsive, Glasgow Coma Scale score 4 and deeply cyanosed. Blood pressure was 100/70 mm of Hg; Pulse rate was 82/min low volume. Immediately, airway, breathing, and circulation care were started, and the child shifted to intensive care. Upon interrogation parents said that the preceding night while the child was sleeping in the courtyard snake passed over the body of child, but did not bite (as earlier at home told by the child to them). The child became frightened but went back to sleep on assurance by parents. Approximately 2-3 h later in the morning, child developed pooling of secretions in the oral cavity, drooping of eyelids, and respiratory difficulty. Although there were no visible fang marks on the body, considering the critical and deteriorating condition of child polyvalent anti snake venom (ASV) (20 vials) was given, and the child was put on ventilator support. His pupils were bilaterally equal size, reacting to light, meningeal signs were absent, plantar, and deep tendon reflexes were unelicitable. Random blood sugar, complete blood counts, serum electrolytes, liver function test, and renal function test were in normal limits. Bleeding time, clotting time, and prothrombin time were also in normal limits. The child started responding and was extubated on day 3 of admission. On day 5, the patient was discharged with no residual neurological deficit.
| Discussion|| |
Neuroparalytic snake bite is a common emergency situation encountered in tropical countries, and severe envenomation may mimic coma and brain death.  To a large extent, the manifestation of snakebite depends upon the species of snake, and therefore, identification of the type of snake is important. At times, the bite mark might not be visible (e.g., in the case of krait). Neurotoxins bind to acetylcholine receptors at the motor end-plate, where they first cause release of acetylcholine at the nerve endings at the myoneural junction and then damage the endings, preventing further release of transmitter. All this leads to a flaccid paralysis of the victim. Paralysis is heralded by ptosis, followed by ophthalmoplegia. Paralysis of facial, palatal, tongue, and neck muscles follow. Respiratory failure, precipitated by upper airway obstruction and paralysis of intercostal and diaphragm, is the usual cause of death.  Our patient most probably had common krait bite with severe envenomation because clinical symptoms and sign match with krait poisoning. This pattern of early morning onset neuroparalysis has been reported in krait bites. ,,, Krait bites usually occur at night, sometimes producing minimal or no pain and local reaction at the bite site. Fang marks may not be appreciable.  Sleeping outdoor on the ground adds to the strong possibility of snakebite. ,, Unlike in cobra envenomation, local signs are absent, and neostigmine is ineffective in improving neuroparalytic features caused by krait envenomation.  Autonomic disturbances (labile hypertension, resting tachycardia, sweating) though common in krait bite were not documented in our patient. The study conducted by Saravu et al. showed the various symptoms of krait envenomation included abdominal pain, dyspnea, dysphagia, oliguria, respiratory paralysis, hypokalemia, coma, and renal failure.  Law et al. reported a case of krait envenomation that presented with coma and hypertension and was discharged successfully.  In other study conducted by Trinh et al. over 1998 and 2007 showed that sign and symptoms of Krait envenomation included Fang marks and numbness as the local signs, and systemic symptoms included bilateral ptosis, persistently dilated pupils, limb weakness, breathlessness, hypersalivation, dysphonia and dysphagia, hyponatremia, rhabdomyolysis, and alteration in blood pressures. 
Other differential diagnoses  such as myasthenic crisis, botulism, Guillain-Barre syndrome (Miller Fisher variant) were excluded based on history, clinical features, course of illness, and response to treatment.
The treatment involves symptomatic and specific approach. The first aid of the patient includes reassurance, immobilizing the bitten limb and transporting the patient to the nearest health care facility at the earliest where definite treatment can be provided. Control anxiety of the patient as excitement will increase heart rate and lead to spread of venom. The things that are to be avoided includes application of tourniquet;  washing of the bite site with soap or any other solution to remove the venom; making cuts or incisions on or near the bitten area to remove the venom;  use of electrical shock;  freezing or applying the extreme cold to the area of bite; application of any kind of potentially harmful herbal or folk remedy; sucking out venom with mouth;  giving the victim drink, alcohol or other drugs and also do not attempt to capture, handle or kill the snake, and patients should not be taken to quacks. 
National Snakebite Management Protocol and WHO protocol have been formulated giving the standard management of snake bit. , The initial management includes dealing with airway, breathing, and treatment of shock (ABC protocol). Administer tetanus toxoid if skin is breached and antibiotics if there is cellulitis or local necrosis. Pain can be relieved with oral paracetamol or tramadol. Aspirin or nonsteroidal anti-inflammatory drugs should not be administered. ASV forms the mainstay of treatment. In India, polyvalent ASV, which is formed against all the four common species namely Russell's viper, common cobra, common krait, and saw-scaled viper is effective and presently there are no monovalent ASVs are available. ASV is produced both in liquid and lyophilized forms and till date no evidence proves superiority of one over the other. Liquid ASV requires a reliable cold chain and has 2-year shelf life. Lyophilized ASV, in powder form, has 5-year shelf life and requires only to be kept cool. ASV should be administered only when there are definite signs of envenomation which could be either coagulopathy or neurotoxicity. Only unbound, free flowing venom in the bloodstream or tissue fluid, can be neutralized by it. It carries the risk of anaphylactic reaction as it is a form from equine serum and doctors should be prepared to handle such reactions. , There is no role of prophylactic administration of ASV to the patient.  The recommended dosages are as following.
• Mild envenomation (systemic symptoms manifest >3 h after bite) neurotoxic/hemotoxic 8-10 vials.
• Severe envenomation (systemic symptoms manifest <3 h after bite) neurotoxic or hemotoxic 8 vials.
Each vial is 10 mL of reconstituted ASV. Children should receive the same ASV dosage as adults. ASV should be administered over 1 h at a constant speed with regular monitoring of the patient. The repeat dose depends on the response of the patient to the first dose. There is no role of local application of ASV as it may increase pain, swelling, and also results in compartment syndrome. , Neostigmine is an anticholinesterase, which is particularly effective in postsynaptic neurotoxins such as those of the cobra and is not useful against presynaptic neurotoxin, that is, common krait and the Russell's viper.  After discharge from hospital, victim should be followed up and advised to return back for any worsening of symptoms like bleeding, pain or swelling at the site of bite, difficulty in breathing, altered sensorium, etc. The patients should also be explained about serum sickness which may manifest after 5-10 days.
| Conclusion|| |
Krait envenomation when severe can cause coma or brain death. Furthermore, autonomic dysfunction is considered in these patients for effective management and treatment. We wish to re-emphasize the fact that a high index of suspicion is required in endemic areas as timely administration of ASV is critical for a favorable outcome.
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