Summary Of Exposure |
A) BACKGROUND: This management is limited to the Family Elapidae (Cobras {genus Naja and Ophiophagus hannah}}, kraits {genus Bungarus} and coral snakes {genus Calliophis - Asian coral snakes and genus Maticora - Long-glanded coral snakes) that inhabit this region. Sea snakes are discussed in a separate management - See SEA SNAKES for further information. This management is relevant for the Indian subcontinent, Pakistan, Sri Lanka, Myanmar (Burma), Thailand, China, Taiwan, Laos and Cambodia, Peninsular Malaysia, Philippines, Japan, South Korea, Vietnam, Indonesia, Iran and Nepal. In general, elapids have relatively short (but may be up to 10 millimeters long) fixed, front fangs, that are anchored at the anterior portion of the maxilla. The degree of clinical effects is dependent on several factors: a bite does NOT always result in venom being injected; the quantity of venom injected is variable and depends on the species and size of the snake and the mechanical efficiency in which the bite occurred (eg, both fangs penetrated the skin, repeated strikes). Repeated bites do not result in a depletion of venom stores.
B) EPIDEMIOLOGY: Envenomation is common in indigenous areas of poisonous snakes and can be fatal. Private collectors or zookeepers may be bitten in non-indigenous areas.
C) PHARMACOLOGY/TOXICOLOGY: Elapid venoms are complex, but contain pre- and post-synaptic neurotoxins. Pre-synaptic neurotoxins (phospholipases A(2), beta bungarotoxin) have been found in the venoms of kraits (B. fasciatus and B. multicinctus) and cobras (N. atra). They damage nerve endings, by initial release of an acetylcholine transmitter, then interfere with release. Following krait envenomation, beta-bungarotoxins are associated with the development of neuromuscular paralysis which appears to be poorly reversible by either antivenoms or anticholinesterases. Post-synaptic neurotoxins: These polypeptides produce a curare-like effect, by competing with acetylcholine for receptors in the neuromuscular junction.
D) WITH POISONING/EXPOSURE
1) ONSET: Neurotoxic symptoms can develop within minutes of exposure by the venom of snakes of the Elapidae family; most symptoms develop within 6 hours.
2) ENVENOMATION: NEUROTOXICITY: Initially, the venom causes ptosis, blurring vision, dysconjugate gaze and diplopia due to oculomotor cranial nerve stimulation. Other symptoms of drowsiness or irritability may be present. Secondly, corticobulbar tract dysfunction can occur, causing dysphonia, dysphagia, absent gag reflex, and respiratory dysfunction. Lastly, symptoms progress to cause paralysis of the diaphragmatic muscles resulting in respiratory paralysis; death may result from respiratory failure. Generalized flaccid paralysis is a late finding of envenomation, which occurs with some variability, and presents from 1 to 6 hours after envenomation. LOCAL TISSUE INJURY: The neurotoxic venom produces little or no pain (kraits; genus Bungarus) or swelling immediately after the bite. However, envenomizing by cobras (genus Naja and genus Ophiophagus) can produce almost immediate severe local pain with tissue necrosis possible. OTHER: Renal failure, hypotension, hypokalemia, and hematuria are rare effects. Coagulopathies have NOT been significant clinical effects reported after envenomation by most Asian elapids. However, the O. hannah (King Cobra), and potentially the Naja naja atra (Chinese Cobra) may be able to produce hemorrhagic activity following an envenomation.
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Heent |
3.4.3) EYES
A) WITH POISONING/EXPOSURE 1) Ptosis and paralysis of extraocular muscles have been reported following envenomation, and are consistent with the neurotoxic effects observed in the snakes of the Elapidae family (cobras, mambas, kraits) (Kularatne, 2002; Khandelwal et al, 2007; Agarwal et al, 2006; Sharma et al, 2005; Bawaskar & Bawaskar, 2004; Ronan-Bentle et al, 2004; Kuo & Wu, 1972; Meier & White, 1995; Gold & Pyle, 1998; Anon, 1999). a) CASE SERIES: 5 of 8 patients bitten by B. multicinctus (Chinese Krait) developed ptosis after exposure (Pe et al, 1997).
2) Blurred vision has been reported following elapid envenomation (Meier & White, 1995; Pe et al, 1997; Bawaskar & Bawaskar, 2004). a) CASE SERIES: In a review of 8 patients bitten by B. multicinctus (Chinese Krait), 50% (n=4) experienced blurred vision (Pe et al, 1997).
3) Double vision has been reported following B. caeruleus (Common krait) envenomation (Kularatne, 2002). 4) SPITTING VENOM: All species of Asian cobra have the physical ability to "spit" their venom several meters into the face (can include the eyes, nasal and buccal membranes) of a potential aggressor. Immediate intense pain in the eye, blepharospasm, edema, leucorrhea and possible corneal erosion are possible (Buranasin, 1993; Meier & White, 1995). 5) OPTIC NEURITIS: A 50-year-old farmer was bitten by an Indian Black Cobra and received antivenom, but reported diminished vision one day after exposure, which seemed to improve after several days. Six days following the bite, the patient developed a sudden decline in vision with bilaterally sluggish pupils and a normal fundus. Treatment included intravenous dexamethasone and oral ciprofloxacin. Vision improved (Menon et al, 1997). 3.4.6) THROAT
A) WITH POISONING/EXPOSURE 1) Abnormalities of taste and smell may occur after Elapidae exposure (Anon, 1999).
2) Dysphagia has been commonly reported following elapid envenomation and is associated with the venom's neurotoxic effects (Meier & White, 1995; Gold, 1996; Gold & Pyle, 1998). Increased salivation has also been reported (Gold, 1996).
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Cardiovascular |
3.5.2) CLINICAL EFFECTS
A) CONDUCTION DISORDER OF THE HEART 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Cardiovascular effects are generally NOT associated with Elapidae species (Anon, 1999), but cobra venom does have cardiotoxic properties (Britt & Burkhart, 1997).
B) TACHYCARDIA 1) WITH POISONING/EXPOSURE a) CASE SERIES: B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait, severe envenoming was reported in 101 patients. Mild to moderate tachycardia (heart rate to 150 beats/min) was reported in 45 (44%) and 38 (37%) of patients in the severe group, and 46 (52%) and 4 patients in the mild to moderate group, respectively (Kularatne, 2002).
C) VENTRICULAR BIGEMINY 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 23-year-old man was bitten on the finger by a N. kaouthia and developed infrequent ventricular extrasystoles with a left bundle branch pattern approximately 2 hours after envenomation. Heart rate varied from 90 to 147 beats/minute and the extrasystoles progressed to bigeminy. Four hours after being bitten, the patient received 1 vial of monovalent N. kaouthia antivenom and the patient's rhythm changed to ventricular quadrigeminy followed by normal sinus rhythm within 30 minutes of administration. No further ECG changes were observed; no serious dysrhythmias developed (Ismail et al, 2012).
D) HYPERTENSIVE EPISODE 1) WITH POISONING/EXPOSURE a) CASE SERIES: B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait, severe envenoming was reported in 101 patients. Hypertension can develop and is more likely to occur in patients with a severe envenomation (Kularatne, 2002).
b) Transient hypertension occurred in an adult following a bite by a B. multicinctus (Chan et al, 1995).
c) CASE REPORT: An adult developed mild hypertension (169/105) after envenomation by Naja kaouthia (Ronan-Bentle et al, 2004).
d) CASE REPORT: Hypertension was reported in 2 patients following envenomation by B. caeruleus (Bawaskar & Bawaskar, 2004).
e) CASE REPORT: Severe hypertension (240/130 mmHg) was reported in a 19-year-old man who was bitten by a suspected Indian elapid snake. The patient also developed tachycardia, ptosis, areflexia, and weakness in all extremities. Following antivenom administration and intravenous nitroglycerin infusion, the patient recovered without sequelae (Agarwal et al, 2006).
E) HYPOTENSIVE EPISODE 1) WITH POISONING/EXPOSURE a) Hypotension has been reported following envenomation by B. multicinctus, B. caeruleus, and Ophiophagus species (Kuo & Wu, 1972; Myint et al, 1991; Bawaskar & Bawaskar, 2004). b) CASE REPORT: A 30-year-old reptile handler developed severe labile hypotension (systolic BP between 50 and 90 mmHg) approximately 19 hours after envenomation by an Ophiophagus. Dopamine was required to maintain blood pressure. The patient made a complete recovery following the administration of antivenom some 30 hours (the authors reported difficulty obtaining the antivenom) after exposure (Myint et al, 1991). 1) The authors suggested that venom-induced vasodilatation may have been responsible for the persistent hypotension observed. Improvement did not occur until after antivenom was administered.
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Respiratory |
3.6.2) CLINICAL EFFECTS
A) RESPIRATORY FAILURE 1) WITH POISONING/EXPOSURE a) RESPIRATORY MUSCLE PARALYSIS 1) SUMMARY: Neurotoxic effects may result in the rapid onset of respiratory weakness and paralysis following exposure; mechanical ventilation may be required (Sharma et al, 2005; Ronan-Bentle et al, 2004; Seneviratne & Dissanayake, 2002; Karalliedde & Sanmuganathan, 1988; Kuo & Wu, 1972; Pe et al, 1995; Gold & Pyle, 1998).
2) In Sri Lanka, kraits can produce a rapid onset of respiratory failure secondary to respiratory muscle weakness following envenomation. Management includes intubation and mechanical ventilation performed in a timely manner (Seneviratne & Dissanayake, 2002).
b) CASE REPORTS 1) OPHIOPHAGUS HANNAH a) A 43-year-old reptile handler developed rapid respiratory paralysis (approximately 90 minutes after envenomation) requiring intubation and ventilatory support following a bite to the thumb from a King Cobra (O. hannah). The patient received Thai Red Cross Society monospecific King Cobra antivenom (15 vials; a total of 150 mL), and neurological effects improved over 7 hours; the patient extubated himself and remained stable (Gold & Pyle, 1998). The patient left the next morning against medical advice and was lost to follow-up.
2) BUNGARUS CEYLONICUS a) A 45-year-old woman developed dyspnea, cyanosis, and tachypnea (respiratory rate: 50 breaths/minute) about 6 hours after envenomation by a B. ceylonicus (Ceylon krait). She was immediately intubated and ventilated. Generalized paresis and areflexia were noted during ventilation. Treatment also included 10 vials of Haffkeine Institute antivenin upon admission and repeated 6 hours later. Some improvement in muscle activity was noted after 48 hours and the patient was successfully extubated at 78 hours. However, ongoing muscle weakness was noted in the distal lower extremities compared to proximal muscles. Normal muscle strength was noted at 4 weeks (Karalliedde & Sanmuganathan, 1988).
3) BUNGARUS FASCIATUS a) A 13-year-old boy was unable to speak, open his mouth, or swallow after being bitten on his finger from B. fasciatus. He also developed ptosis and drowsiness, with the onset of neurologic symptoms occurring within 2 hours of envenomation. No specific antivenom was available; the patient was given Russell's viper antivenom due to prolonged clotting times (15 minutes) without neurologic improvement. Ventilatory support was not available and the patient died of respiratory failure 14 hours post-envenomation (Pe et al, 1997).
4) BUNGARUS MULTICINCTUS a) A 63-year-old man was bitten on the hand by a Taiwan krait and developed localized symptoms and mental confusion. The patient was admitted approximately 2.5 hours after exposure and was given monovalent antivenom (Taiwan krait), but developed limited respiratory movement and increasing cyanosis, which required emergent tracheostomy and artificial ventilation (Kuo & Wu, 1972).
b) A 30-year-old man developed dizziness and perioral numbness within 1 hour of a bite. He sustained a generalized seizure with respiratory arrest 4 hours after envenomation. He remained ventilator dependent for 8 days despite treatment with 20 ml banded krait antivenom (Chan et al, 1995).
5) NAJA KAOUTHIA a) A 23-year-old woman experienced ptosis, upper extremity weakness, dysarthria, and dysphagia, progressing to respiratory failure, 10 hours after being bitten in the left buttock by N. kaouthia (Asiatic Cobra). Following antivenom administration, the patient recovered without sequelae (Khandelwal et al, 2007).
c) CASE SERIES 1) B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait, envenoming was severe in 101 (48%) cases. Of those severe cases, all required mechanical ventilation secondary to neuromuscular (respiratory) paralysis. Most patients (75%) needed ventilation within 10 hours of the bite. Level of consciousness was also a direct correlation to the duration of respiratory paralysis and the need for longer periods of mechanical ventilation. Treatment was needed from 12 hours to 29 days (mode: 2 days) (Kularatne, 2002).
2) B. multicinctus (Chinese Krait): 3 of 8 patients died from respiratory failure following bites from Chinese krait. The authors speculated that the fatalities were probably due to the lack of use of mechanical ventilation (Pe et al, 1997).
3) In a series of 35 Thai patients with cobra bites, 9 (26%) developed respiratory failure (Buranasin, 1993).
B) DYSPNEA 1) WITH POISONING/EXPOSURE a) Dyspnea may occur as a result of progressing neurotoxic effects (Kuo & Wu, 1972).
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Neurologic |
3.7.2) CLINICAL EFFECTS
A) CENTRAL NERVOUS SYSTEM FINDING 1) WITH POISONING/EXPOSURE a) The following symptoms have been reported following exposure to elapid species: drowsiness, paraesthesia, paralysis of facial muscles and other muscles innervated by the cranial nerves, aphonia, difficulty in swallowing secretions. Of the more serious complications, respiratory and generalized flaccid paralysis can develop (Sharma et al, 2005; Karalliedde & Sanmuganathan, 1988; Gold & Pyle, 1998; Anon, 1999). Although a patient appears unconscious, most are able to follow simple commands as noted by purposeful movement of the fingers or toes (Myint et al, 1991; Meier & White, 1995). b) Other neurological symptoms may include: headache, dizziness, giddiness, and confusion (Sharma et al, 2005; Meier & White, 1995). Disorientation is generally attributable to anoxia (Chanhome et al, 1998). c) Although more commonly reported with viper venoms, some elapid venoms (Asian cobras) can produce severe local reactions along with paralysis. However, paralysis has been reported with minimal or no local envenomizing following bites from krait (Anon, 1999). d) ONSET: Neurotoxic effects may occur within minutes to hours with most symptoms developing by 4 to 6 hours (Meier & White, 1995; Gold & Pyle, 1998). e) CASE REPORTS 1) BUNGARUS CAERULEUS a) Paresthesias, heaviness, and a prickling sensation at the site of the bite have been reported in several patients following envenomation by B. caeruleus (Bawaskar & Bawaskar, 2004).
2) BUNGARUS CEYLONICUS a) A 45-year-old woman developed dyspnea, cyanosis, and tachypnea (respiratory rate: 50 breaths/minute) about 6 hours after envenomation by a B. ceylonicus (Ceylon krait). She required intubation and ventilation for approximately 6 days. Generalized paresis and areflexia were also present during this period. Treatment also included 10 vials of Haffkeine Institute antivenin upon admission and repeated 6 hours later. Some improvement in muscle activity was noted after 48 hours. However, ongoing muscle weakness was noted in the lower extremities compared to the upper extremities. Normal muscle strength was noted at 4 weeks (Karalliedde & Sanmuganathan, 1988).
3) BUNGARUS FASCIATUS a) CASE REPORT: A 13-year-old boy was unable to speak, open his mouth, or swallow after being bitten on his finger from B. fasciatus. He also developed ptosis and drowsiness, with the onset of neurologic symptoms occurring within 2 hours of envenomation. No specific antivenom was available. Due to prolonged clotting times (15 minutes), the patient was given Russell's viper antivenom without neurologic improvement. Ventilatory support was not available and the patient died of respiratory failure 14 hours post-envenomation (Pe et al, 1997).
4) BUNGARUS MULTICINCTUS a) ONSET: In a case series, neurotoxic effects began with 2.5 to 6 hours of envenomizing by B. multicinctus (Chinese Krait) (Pe et al, 1997).
b) MORTALITY: Death ranged from 12 to 30 hours following exposure; with 3 deaths due to respiratory failure (Pe et al, 1997).
c) CASE REPORT: A 36-year-old man was bitten by B. multicinctus and, 1 hour later, experienced difficulty speaking and swallowing, bilateral ptosis, vomiting, and blurred vision. He presented as comatose and in cardiopulmonary arrest. Following resuscitation and administration of bungarotoxin-specific antivenom, he was discharged. One month later, the patient again developed blurred vision, difficulty swallowing, and weakness in his extremities, subsequently becoming comatose for 8 days. After regaining consciousness, electrodiagnostic studies indicated severe sensory and motor polyneuropathy, with axonal degeneration of motor and sensory fibers, suggesting Guillain-Barre syndrome (GBS). Bilateral facial palsy was present and all deep tendon reflexes were absent. On hospital day 21, 5 sessions of plasmapheresis were performed over a 10-day period, with gradual improvement in the patient's neuropathy. Following 4 weeks of intensive inpatient rehabilitation, he became ambulatory with the use of crutches and independent in all activities of daily living (ADL) (Chuang et al, 1996). Because the patient had no previous viral illness or infection, and the snake envenomation was the only preceding condition known, it is speculated that there may be a correlation between the snake bite and development of GBS; however, antivenom therapy may have been a contributory factor.
5) NAJA KAOUTHIA a) CASE REPORT: A 23-year-old woman experienced ptosis, upper extremity weakness, dysarthria, and dysphagia, progressing to respiratory failure, 10 hours after being bitten in the left buttock by N. kaouthia (Asiatic Cobra). Following antivenom administration, the patient recovered without sequelae. A second patient, a 44-year-old man, developed transient dizziness and numbness of the extremities after being bitten on his left hand by N. kaouthia. The patient also recovered without sequelae following antivenom administration (Khandelwal et al, 2007). With the first patient, it is believed that the location of the bite, with a greater volume of adipose tissue, may have resulted in slower systemic absorption of the venom, thus delaying the onset of neurotoxicity.
6) OPHIOPHAGUS HANNAH a) CASE REPORT: A 43-year-old reptile handler developed neurotoxic effects within 90 minutes of envenomation by a O. hannah (King Cobra). Effects included progressive dysarthria, generalized flaccidity, and confusion along with a decline in respiratory function (decline in oxygen saturation). The patient made a complete recovery following infusion of Thai Red Cross Society monospecific King Cobra antivenom (total dose 150 mL) (Gold & Pyle, 1998).
b) CASE REPORT: A 30-year-old reptile handler was bitten by an O. hannah (King Cobra) and developed similar neurological toxicity. Although the patient appeared unconscious, the patient was able to respond to questions by flexing his fingers. Recovery was complete following antivenom administration (Myint et al, 1991).
B) CRANIAL NERVE DISORDER 1) WITH POISONING/EXPOSURE a) Cranial nerve palsies such as ptosis, ophthalmoplegia, diplopia, and difficulty speaking or swallowing are often early neurologic manifestations of envenomation. Fasciculations of the tongue and lips may also develop (Khandelwal et al, 2007; Agarwal et al, 2006; Sharma et al, 2005; Ronan-Bentle et al, 2004; Bawaskar & Bawaskar, 2004; Seneviratne & Dissanayake, 2002; Pe et al, 1997). These neurologic findings may progress to respiratory failure and generalized paralysis in severe cases.
C) HEADACHE 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Headache is a common early systemic symptom of elapid envenomation (Sharma et al, 2005; Gold, 1996; Meier & White, 1995).
b) INCIDENCE 1) B. multicinctus (Chinese Krait): Headache may occur within 1 to 4 hours (Meier & White, 1995).
2) N. kaouthia (Monocellate Cobra): Headache developed within 3 hours (Gold, 1996).
D) DROWSY 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Drowsiness is NOT uncommon following envenomation (Meier & White, 1995).
b) CASE SERIES 1) B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait, envenoming was severe in 101 (48%) cases. Drowsiness was reported in 91 (43%) patients (Kularatne, 2002).
2) B. multicinctus (Chinese Krait): Three of 8 patients envenomated by B. multicinctus (Chinese Krait) developed drowsiness (Pe et al, 1997).
E) COMA 1) WITH POISONING/EXPOSURE a) Although not common, neurological symptoms can progress to coma following envenomation if left untreated (Gold, 1996). Coma is generally found secondary to anoxia (Chanhome et al, 1998).
b) Patients may appear to be comatose because of generalized paralysis, but may respond to questions by moving fingers or toes.
c) Coma occurred in a 36-year-old man following envenomation from B. multicinctus (Chuang et al, 1996).
d) CASE SERIES: B. Caerules (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait. Alterations in consciousness were observed in each patient and findings were as follows: no alterations in 60 (29%), drowsiness in 91 (43%), semiconscious in 24 (11%) and deep coma in 35 (17%) patients. Deep coma was defined as an absence of brainstem and spinal reflexes; pupils remained fully dilated and light reflexes were absent. More complications (ie, respiratory impairment, pneumonia, ARDS, dysrhythmias) were likely to occur in patients in a deep coma. There was also a direct correlation between level of consciousness and the duration of respiratory paralysis and the need for longer periods of mechanical ventilation (Kularatne, 2002).
F) AMNESIA 1) WITH POISONING/EXPOSURE a) B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait, envenoming was severe in 101 (48%) cases. Anterograde memory loss was reported in 84 (40%) patients (Kularatne, 2002).
G) NEUROPATHY 1) WITH POISONING/EXPOSURE a) B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait. Delayed neuropathy (ie, conduction defects in the nerves) occurred in 38 (22%) patients. Sensory loss (n=34) at the bite site was also reported and lasted from weeks to months (Kularatne, 2002).
H) SEIZURE 1) WITH POISONING/EXPOSURE a) Generalized seizures were reported in an adult approximately 5 hours after receiving a bite on the forearm by a B. multicinctus (Chinese or Many-banded Krait) (Chan et al, 1995). Seizure activity was likely secondary to hypoxia in this patient.
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Gastrointestinal |
3.8.2) CLINICAL EFFECTS
A) NAUSEA AND VOMITING 1) WITH POISONING/EXPOSURE a) Nausea and vomiting have been reported following bites by various species of cobras (O. hannah and Naja kaouthia) (Gold, 1996; Gold & Pyle, 1998). Severe vomiting was reported in an adult following a bite by a Thailand Spitting Cobra, the patient, however, did NOT develop neurological complications (Stell, 1997).
B) ABDOMINAL PAIN 1) WITH POISONING/EXPOSURE a) Abdominal pain may occur after envenomation by some species of kraits (genus Bungarus) and cobras (genus Naja) (Meier & White, 1995; Gold, 1996; Bawaskar & Bawaskar, 2004).
b) CASE SERIES: B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait. Abdominal pain was the most common early symptom of evenomation. Symptoms usually began within minutes to a few hours (Kularatne, 2002).
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Hepatic |
3.9.2) CLINICAL EFFECTS
A) INFLAMMATORY DISEASE OF LIVER 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 54-year-old man presented with pruritus and yellowish sclera 6 days after eating approximately 20 dried, non-emptied gallbladders of Naja naja atra. Laboratory data revealed elevated liver enzyme concentrations and a liver biopsy confirmed the presence of acute hepatitis, with scattered focal parenchymal necrosis and cholestasis of the bile canaliculi. Following supportive therapy, the patient's liver enzyme levels gradually normalized (Chao et al, 2006).
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Genitourinary |
3.10.2) CLINICAL EFFECTS
A) ACUTE RENAL FAILURE SYNDROME 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 19-year-old man was bitten on the dorsum of the foot by an O. hannah (King Cobra) and developed reddish urine 24 hours after envenomation. The patient went on to develop acute renal dysfunction as a result of intravascular hemolysis, despite antivenom administration. At 3 month follow-up the patient was stable with a normal renal function (Karnchanachetanee, 1994).
b) CASE REPORT: A 54-year-old man developed nonoliguric acute renal failure approximately 37 days after eating 20 dried, unemptied gallbladders of Naja naja atra. Laboratory data revealed elevated BUN and serum creatinine levels that peaked at 119 mg/dL and 10.9 mg/dL. After 6 sessions of plasma exchange and hemodialysis, performed every 2 days over a 9-day period, his serum creatinine level decreased to 2.6 mg/dL, gradually normalizing approximately 3 months postingestion (Chao et al, 2006).
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Acid-Base |
3.11.2) CLINICAL EFFECTS
A) METABOLIC ACIDOSIS 1) WITH POISONING/EXPOSURE a) CASE SERIES: B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait. Metabolic acidosis was observed in 105 (50%) patients within the first 24 hours of envenomation (Kularatne, 2002).
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Hematologic |
3.13.2) CLINICAL EFFECTS
A) PROTHROMBIN TIME ABNORMAL 1) WITH POISONING/EXPOSURE a) SUMMARY 1) The O. hannah (King Cobra), the Naja naja atra (Chinese Cobra), and the Naja kaouthia (Asiatic Cobra) have reportedly produced hemorrhagic disturbances following envenomation (Khandelwal et al, 2007; Li et al, 2000; Gold & Pyle, 1998).
b) CASE REPORTS 1) A 43-year-old reptile trainer was bitten on the hand by an O. hannah (King Cobra) and developed an increased prothrombin (15.1) and INR (1.56). Laboratory values were improving approximately 22 hours after exposure following antivenom administration. The patient was lost to follow-up due to the patient refusing further medical treatment (Gold & Pyle, 1998).
2) Thrombocytopenia (platelet count nadir 52,000/mm(3)), an increased prothrombin time (33.4 s), and an increased INR (1.5) were reported in a 23-year-old woman approximately 22 hours after being bitten by N. kaouthia (Asiatic Cobra); however, there was no evidence of bleeding. Following supportive care including antivenom (10 vials SAIMR) administration, the patient's coagulopathy resolved (Khandelwal et al, 2007).
B) BLEEDING 1) WITH POISONING/EXPOSURE a) Although inconsistently reported in the literature (Meier & White, 1995), disorders of platelet aggregation and the coagulation-fibrinolysis system may occur after envenomation by cobras (e.g., O. hannah and Naja naja atra). A disseminated intravascular coagulation (DIC) or a DIC-like syndrome may be produced after bites by these snakes (Li et al, 2000).
C) LEUKOCYTOSIS 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Leukocytosis may occur following envenomation by cobra species (O. hannah {King Cobra} and Naja naja atra {Taiwan Cobra}) (Kuo & Wu, 1972; Karnchanachetanee, 1994; Gold & Pyle, 1998).
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Dermatologic |
3.14.2) CLINICAL EFFECTS
A) SNAKE BITE - WOUND 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Although more commonly reported with viper venoms, some elapid venoms (Asian cobras) can produce severe local reactions (eg, local pain, swelling, blebs, infection and bleeding, inflammation, and necrosis) along with neurotoxic effects (Meier & White, 1995; Anon, 1999). 2) MECHANISM: Its thought that the resulting tissue necrosis is different for elapid and viper venoms (Meier & White, 1995). a) The necrotic effects may be a result of amino acid polypeptides (ie, cytotoxins or cardiotoxins and phospholipases A(2){myotoxins}). The dose of venom injected may also have a role in the degree of local tissue damage.
3) CASE REPORT: A 55-year-old zoo keeper was bitten on the left index finger by an O. hannah (King Cobra) and developed local swelling which improved. However, tissue necrosis later occurred which required surgical debridement (Myint et al, 1991). B) LOCAL INFECTION OF WOUND 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Proteus vulgaris infection has been reported in O. hannah (King Cobra) bites (Karnchanachetanee, 1994); penicillin and gentamicin were used effectively to treat the infection.
2) INCIDENCE: In a series of victims of cobra bite, 54.2% (n=19) developed wound infections (Buranasin, 1993).
b) CASE REPORT 1) Naja naja atra, Cantor (Taiwan Cobra): A 16-year-old boy was bitten by a cobra on the hand; the wound was debrided on admission. Mild swelling with tenderness was noted on the hand, forearm and upper arm. Laboratory results indicated marked leukocytosis (WBC 23,500/mm(3)). Ten days after the bite, large amounts of greenish yellow pus was found in the wound (cultures remained negative), despite intravenous antibiotic therapy. Extensive debridement was then done on a daily basis; pus formation decreased. At one year follow-up, cicatricial extension contracture and ankylosis of the left wrist joint was present (Kuo & Wu, 1972).
C) EDEMA 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Swelling and erythema is likely to occur following envenomation by a cobra (Bawaskar & Bawaskar, 2004; Ronan-Bentle et al, 2004; Pe et al, 1995; Gold, 1996; Gold & Pyle, 1998).
b) CASE REPORTS 1) A 43-year-old developed immediate edema and erythema which extended to the wrist area following an O. hannah (King Cobra) bite to the thumb. Sensation and range of motion remained stable (Gold & Pyle, 1998).
2) A reptile handler with a prior history of snake bites (various species) was bitten on the finger by an O. hannah and developed immediate local swelling which extended to the proximal half of the forearm within 24 hours; swelling resolved by day 4. Four weeks prior to the bite, the patient received the last of three immunizations (a mixture of venoms); no neurological symptoms developed after this bite (Pe et al, 1995).
3) A 30-year-old reptile handler was bitten on the forearm and developed tense swelling of the entire arm, which extended into the right pectoral and clavicular regions and into the neck 15 hours after envenomation; radial pulse not palpable. Maximum increase in the circumference of the bitten arm was 47%. Approximately, 30 hours after the bite the patient received antivenom. Ten days after the bite, the swelling had improved and only a slight induration at the site remained after 2 weeks (Myint et al, 1991).
D) PAIN 1) WITH POISONING/EXPOSURE a) SUMMARY: Envenoming by elapids may produce various degrees of pain. In general, the neurotoxic venom produces little or no pain or swelling immediately after the bite (Chen et al, 2000a). Due to the absence or minimal pain reported following bites by the genus Bungarus, a delay in seeking medical treatment may occur (Chanhome et al, 1998). 1) However, cobras (genus Naja, and genus Ophiophagus hannah) can produce almost immediate severe localized pain and tenderness; whereas krait (genus Bungarus) bites are virtually painless (Karnchanachetanee, 1994; Meier & White, 1995; Gold, 1996; Gold & Pyle, 1998).
b) CASE SERIES: In a series of 8 patients bitten by B. multicinctus (Chinese Krait) only 1 patient reported pain and/or swelling at the site of the bite (Pe et al, 1997). |
Musculoskeletal |
3.15.2) CLINICAL EFFECTS
A) MUSCLE WEAKNESS 1) WITH POISONING/EXPOSURE a) BUNGARUS CAERULEUS 1) CASE SERIES: B. Caeruleus (Common Krait): In Sri Lanka, a prospective, clinical study was conducted over 3 years in which 210 farmers were bitten by a Common krait. Weakness of limbs and difficulty standing were early clinical findings of envenomation that progressed rapidly to severe neuromuscular paralysis (Kularatne, 2002).
b) BUNGARUS CEYLONICUS 1) CASE REPORT: A 45-year-old woman developed dyspnea, cyanosis, and tachypnea (respiratory rate: 50 beat/minute) about 6 hours after envenomation by a B. ceylonicus (Ceylon krait). She required intubation and ventilation for approximately 6 days. Generalized paresis and areflexia were also present during this period. Treatment also included 10 vials of Haffkeine Institute antivenin upon admission and repeated 6 hours later. Some improvement in muscle activity was noted after 48 hours. However, ongoing muscle weakness was noted in the lower extremities compared to the upper extremities. Normal muscle strength was noted at 4 weeks (Karalliedde & Sanmuganathan, 1988).
B) PARALYSIS 1) WITH POISONING/EXPOSURE a) Generalized flaccid paralysis can occur secondary to the neurotoxic effects of elapid venom; in most cases patients remain conscious as noted by their ability to understand simple commands by purposeful movement of their fingers or toes (Meier & White, 1995).
C) COMPARTMENT SYNDROME 1) WITH POISONING/EXPOSURE a) Compartment syndrome has been reported following cobra bites (Myint et al, 1991; Buranasin, 1993; Karnchanachetanee, 1994). Its been suggested that early antivenom treatment is the best way to prevent irreversible muscle damage (Chanhome et al, 1998).
b) CASE REPORT: A 19-year-old man was bitten on the dorsum of the foot and developed soft tissue swelling from the foot into the groin area with a large blister formation on the lateral aspect of the ankle; peripheral pulses were absent. By the third day, the patient required a bilateral fasciotomy and debridement of necrotic tissue. Fluid culture from the bite was positive for proteus vulgaris; penicillin and gentamicin were given. The patient made a complete recovery (Karnchanachetanee, 1994).
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