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MIDDLE EASTERN SNAKES-ELAPIDAE

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Several of the world's most lethal snakes are found in the Middle East. There are 51 species of snakes in the Middle East, and venomous varieties are divided into 5 families: the Colubridae, Elapidae, Aractaspididae, Hydrophidae and Viperidae. This management is limited to ELAPID snakes of the Middle East.
    B) Viperidae and Atractaspididae are discussed in MIDDLE EAST SNAKES-VIPERIDAE management.
    C) Colubrids are discussed in SNAKES, COLUBRID, OLD WORLD management.
    D) Hydrophidae are discussed in SEA SNAKES management.

Specific Substances

    1) ELAPIDAE
    a) Walterinnesia aegyptia
    1) Black desert cobra
    2) Walter Innes's snake
    b) Naja haje
    1) Egyptian cobra
    2) Banded cobra
    c) Naja naja
    1) Indian cobra
    d) Naja oxiana
    1) Trans-Caspian cobra
    2) Central Asian cobra
    3) Oxus cobra
    2) Middle eastern snakes
    3) SAUDI ARABIAN SNAKES
    4) SNAKE BITE (MIDDLE EASTERN)
    5) SNAKE BITE (SAUDI ARABIAN)
    6) SNAKES, SAUDI ARABIAN

Available Forms Sources

    A) FORMS
    1) ELAPIDAE: The Elapidae elaborates mainly neurotoxins and have a curare-like effect on the neuromuscular junction (Kellaway et al, 1932). Delivery is affected by anteriorly placed, fixed, deeply-grooved fangs which are almost tubular. In Saudi Arabia, there are 2 species.
    a) NAJA HAJE ARABICUS, the Arabian Cobra, is found in the mountainous areas of the southern half of the Kingdom. It is mainly diurnal and the largest snake in the region, with a maximum length of 2.5 meters, accounting for its Arabic name of "hannish thaiban" (snake of snakes). Its color varies from golden yellow to brown or grey.
    b) WALTERINNESIA AEGYPTIA, Innes' Cobra, is widely distributed throughout the arid desert land. Probably mainly subterranean, it tends to be rather docile and reports of bites are very rare. The snake is black and no more than 1.2 meters long.

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: This management is limited to elapids of the Middle East region of most medical importance. Some geographic overlap may occur in this management with venomous snakes of Africa. Please refer to the AFRICAN SNAKES-ELAPIDAE management as appropriate.
    B) TOXICOLOGY: Snake venom varies in composition and quantity depending on the species and size of the snake and the mechanical efficiency in which the bite occurs. Elapid venoms are likely to have neurotoxic activity. The venom is delivered via grooves in the snake's teeth. In general, elapid venom contains alpha-bungarotoxin which targets nicotinic acetylcholine receptors at the neuromuscular junction. Clinically important components of elapid venom in this region include post-synaptic "alpha-toxins"; long (70 to 74 amino acids) and/or short (60 to 62 residues ) neurotoxins have been found in cobras (ie, N haje) and the desert black cobra (W. aegyptia) of this region.
    C) EPIDEMIOLOGY: Several of the world's most lethal snakes are found in the Middle East. True epidemiologic data on snakebites are difficult to ascertain. Because of the inaccuracies of reporting systems, the estimate of the annual incidence from snakes of the Middle East region is as high as 20,000 bites with 15,000 envenomations and 100 deaths.
    D) DEGREE OF ILLNESS: The degree of illness 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.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: LOCAL TISSUE INJURY: COBRAS (Naja) can produce local envenoming that can include pain, numbness, swelling, blistering and possible necrosis with some species (ie, spitting cobras). PAIN: Usually develops shortly after the bite, but in most cases the pain is localized. Spitting cobras (N katiensis, N mossambica, N nigricollis and N pallida) of Africa can produce immediate severe localized pain; however, other elapids of Africa and the Middle East produce less pain and localized swelling. ONSET: Immediate, severe local pain and swelling is common after envenomations by African spitting cobras. Neurotoxic effects that may occur with some elapid envenomations can begin within 15 minutes of a bite or be delayed up to 10 hours.
    2) SEVERE TOXICITY: SYSTEMIC EFFECTS/EARLY NEUROLOGIC SYMPTOMS: Vomiting, "heaviness" of the eyelids, blurred vision, drowsiness, paraesthesia of the mouth, tongue or lips, headache and dizziness can occur. Paralysis (ptosis and external ophthalmoplegia are early findings) may start within 15 minutes following some elapid bites but can be delayed up to 10 hours or more. The progression of neurotoxic effects following an elapid envenomation include: drowsiness, paraesthesia, abnormalities of taste and smell, paralysis of facial muscles and other muscles innervated by the cranial nerves, aphonia, difficulty in swallowing secretions, respiratory depression/failure (requiring mechanical ventilation) and generalized flaccid paralysis. Patients usually remain conscious and may have the ability to respond by moving their fingers or toes. OUTCOME: Neurotoxic effects from post-synaptic neurotoxins are completely reversible by either response to antivenom or after spontaneous resolution in 1 to 7 days. Effects from pre-synaptic neurotoxins are not readily reversible but will resolve with time. Elapid venom does not appear to have central effects in humans, and patients with generalized neurotoxicity are fully conscious. Patients may require circulatory and/or respiratory supportive care during this period. Deaths have been reported from snakes (N haje, W aegyptia (limited data) originating in this region.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) A low grade fever may develop following an elapid envenomation.

Laboratory Monitoring

    A) Monitor neurologic (eg, presence or absence of ptosis, generalized paralysis) and respiratory function frequently. Monitor vital signs.
    B) Monitor pulse oximetry and/or blood gases and pulmonary function tests (negative inspiratory force, vital capacity and FEV1) to assess respiratory function and need for intubation.
    C) Culture wound if evidence of secondary infection develops.
    D) Elapids of the MIDDLE EAST are NOT likely to produce coagulopathy; therefore, the following tests should only be obtained if evidence of bleeding is present:
    1) Obtain complete blood count with differential. Monitor clotting factors (PT or INR, PTT) and platelet count if coagulopathy is present; studies should be repeated as indicated.
    E) Monitor the bite site for edema, discoloration, bleb formation and evidence of tissue necrosis or infection.

Treatment Overview

    0.4.7) BITES/STINGS
    A) MANAGEMENT OF MILD TO MODERATE ENVENOMATION
    1) Treatment of mild to moderate toxicity begins with symptomatic and supportive care. Wounds should be cleaned and irrigated, and a tetanus toxoid booster should be given if needed. A limb with mild swelling should be kept in a position of comfort and reevaluated for any progression of swelling or signs and symptoms of developing necrosis. Elevate the affected limb. Antivenom may be warranted if clinical or laboratory markers worsen. Monitor neurologic and respiratory function frequently. Early signs of a neurotoxic envenomation include diplopia, ptosis, and ophthalmoplegia. Oxygen is indicated for anoxia and respiratory support, to be given as needed. Obtain baseline laboratory studies, IV access and begin fluids, vital signs, and cardiac monitoring. Antivenoms play a major role in treatment. Administer pain medication, tetanus prophylaxis, and antibiotics as necessary. EYE EXPOSURE: Treatment for patients with venom ophthalmia due to spitting elapids (more common in the continent of Africa) should receive immediate copious irrigation with water or saline, a single application of local anesthetic eye drops may facilitate opening tightly closed eyelids. Treatment with 0.1% epinephrine or 10% phenylephrine eye drops may rapidly relieve pain. Patients should receive fluorescein staining and a slit lamp exam. Patients without corneal erosions may be treated with antibiotic eye ointment, patching, and follow-up. Patients with corneal erosions should be treated with an antibiotic eye drops/ointment, a mydriatic agent, patching, and follow-up for daily slit lamp examinations until healed. Steroids are contraindicated, and antivenom either topically or systemically is not indicated unless there is a separate systemic envenomation.
    B) MANAGEMENT OF SEVERE ENVENOMATION
    1) Patients with severe local signs or symptoms or symptoms of progressive neurotoxicity (includes bulbar palsy that can result in dysphagia, slurred speech, choking, absence of gag reflex, or respiratory muscle paralysis) should receive antivenom (see antidote section). Patients with progressive neurotoxicity often require intubation and mechanical ventilation in addition to antivenom therapy. Patients with neurotoxic symptoms may benefit from treatment with an acetylcholinesterase; a test dose of edrophonium or neostigmine should be given. Patients who respond favorably may be treated with continued dosing of neostigmine with atropine. Patients who develop severe local toxicity with necrotic tissue may require debridement to decrease the risk of infection causing worsening functional status. Compartment syndrome is uncommon, and symptoms may be improved by treatment with antivenom.
    C) DECONTAMINATION
    1) PREHOSPITAL: Immobilize the affected limb and transport the patient to a medical facility. Pressure immobilization (lymphatic compression dressing) may be considered for envenomation from highly neurotoxic snakes and in patients with severe systemic signs of envenomation. Use an elastic, stretchy, crepe bandage (10 cm wide and at least 4.5 meters) or any long strip of material. Bound the bandage firmly around the entire bitten limb; start distally around the fingers or toes and move proximally to include a rigid splint. The bandage should be wrapped similar to a sprained ankle in which the wrap is snug, but does NOT occlude the peripheral pulses and a finger can be easily slipped between the layers. Arterial tourniquets should be avoided, and pressure immobilization should not be performed for envenomations by species that produce local tissue necrosis (eg, unlikely with snakes of this region, may occur in spitting cobras, N nigricollis of Africa), unless life-threatening systemic toxicity is also present.
    2) HOSPITAL: Caution should be used when removing a compression dressing or tourniquet as patients may experience rapid progression or symptoms along with increased venom circulation. Antivenom should be available (and administered if there is evidence of significant envenomation) before a compression dressing is removed.
    D) WOUND CARE
    1) Local wound care and tetanus prophylaxis should be provided for all bites. The introduction of bacteria may occur at the time of the bite. Treatment should consist of cleaning the wound with an antiseptic followed by a booster dose of tetanus toxoid as appropriate. Antibiotic therapy should be initiated only if signs of infection are present. Antibiotics covering Staphylococcus aureus and Enterobacteriaceae bacteria can be useful in the presence of major swelling that is unresponsive to antivenom or suspicion of a secondary infection. Monitor the wound frequently.
    E) AIRWAY MANAGEMENT
    1) Early intubation and mechanical ventilation is recommended if a patient develops progressive neurotoxicity with signs of respiratory difficulty (eg, weakness, paralysis).
    F) ANTIDOTE
    1) Treat patients with severe or progressive symptoms with antivenom. If the snake species is positively identified, administer a species specific antivenom when available. Regional polyspecific antivenoms are appropriate when the snake species cannot be reliably identified or a species-specific antivenom is not available. Information on exotic antivenoms and their location, cross-indexed by snake species, can be obtained from your local poison control center. Indications for antivenom include neurotoxicity, spontaneous bleeding, coagulopathy, hypotension, shock arrhythmias, local envenomation by a species know to cause severe necrosis (eg, unlikely with snakes of this region, can occur with spitting cobras, N nigricollis of Africa), and extensive and rapidly progressive swelling. Antivenom should be given as soon as systemic toxicity or severe local effects are present, although it may still be of benefit late in the course of symptoms. Antivenom administration often does not prevent progression of neurotoxic effects or reverse already-established effects, however, it may decrease the time course of paralysis and recovery.
    G) ENHANCED ELIMINATION
    1) There is no role for hemodialysis or other methods of enhanced elimination in these patients.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: There is no role for home management of a suspected venomous snake bite.
    2) OBSERVATION CRITERIA: Patients with a Middle East elapid bite should be sent to a medical facility and closely observed for the development of symptoms.
    3) ADMISSION CRITERIA: Patients with evidence of progressive local toxicity should be admitted for antivenom treatment and close monitoring. Patients with systemic toxicity including neurotoxicity should be admitted to an ICU at a location with available antivenom.
    4) CONSULT CRITERIA: Contact your local poison control center, a medical toxicologist or toxinologist for any patient with a suspected Middle East elapid bite. Patients with an ocular venom exposure should be evaluated by an ophthalmologist.
    5) TRANSFER CRITERIA: All patients should be taken to the nearest hospital or clinic that stocks antivenom. If in a non-native geographic area the antivenom is not immediately available or routinely stocked, it will have to be obtained from the nearest zoo source, which may be at a distance and require some time. Thus, the patient should be taken to the nearest hospital capable of managing the patient's existing medical condition. If not already done, splint bitten extremity or area prior to transport. Turn patient on their side to prevent aspiration of vomitus.
    I) PITFALLS
    1) Failure to recognize local tissue injury progression, failure to recognize neurotoxic progression early, failure to treat early respiratory distress with acetylcholinesterase inhibitors and/or intubation, failure to administer antivenom early. The onset of neurotoxic signs and symptoms of elapid envenomation may be delayed. Deaths have been reported within 6 to 16 hours after envenomation by cobras.
    J) DIFFERENTIAL DIAGNOSIS
    1) The differential diagnosis includes envenomation by other elapid species (especially African elapids), botulism, Guillain Barre syndrome (Miller Fisher variant), or tetrodotoxin poisoning.

Range Of Toxicity

    A) Not all snakes are venomous, and not all venomous snakes inject the same amount of venom if any (ie, dry bites) with each strike. Treatment therefore has to be based on symptoms rather than number of strikes. FATALITIES: Limited data. Deaths have been reported from snakes (N haje, W aegyptia (limited data)) originating in this region.

Summary Of Exposure

    A) BACKGROUND: This management is limited to elapids of the Middle East region of most medical importance. Some geographic overlap may occur in this management with venomous snakes of Africa. Please refer to the AFRICAN SNAKES-ELAPIDAE management as appropriate.
    B) TOXICOLOGY: Snake venom varies in composition and quantity depending on the species and size of the snake and the mechanical efficiency in which the bite occurs. Elapid venoms are likely to have neurotoxic activity. The venom is delivered via grooves in the snake's teeth. In general, elapid venom contains alpha-bungarotoxin which targets nicotinic acetylcholine receptors at the neuromuscular junction. Clinically important components of elapid venom in this region include post-synaptic "alpha-toxins"; long (70 to 74 amino acids) and/or short (60 to 62 residues ) neurotoxins have been found in cobras (ie, N haje) and the desert black cobra (W. aegyptia) of this region.
    C) EPIDEMIOLOGY: Several of the world's most lethal snakes are found in the Middle East. True epidemiologic data on snakebites are difficult to ascertain. Because of the inaccuracies of reporting systems, the estimate of the annual incidence from snakes of the Middle East region is as high as 20,000 bites with 15,000 envenomations and 100 deaths.
    D) DEGREE OF ILLNESS: The degree of illness 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.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: LOCAL TISSUE INJURY: COBRAS (Naja) can produce local envenoming that can include pain, numbness, swelling, blistering and possible necrosis with some species (ie, spitting cobras). PAIN: Usually develops shortly after the bite, but in most cases the pain is localized. Spitting cobras (N katiensis, N mossambica, N nigricollis and N pallida) of Africa can produce immediate severe localized pain; however, other elapids of Africa and the Middle East produce less pain and localized swelling. ONSET: Immediate, severe local pain and swelling is common after envenomations by African spitting cobras. Neurotoxic effects that may occur with some elapid envenomations can begin within 15 minutes of a bite or be delayed up to 10 hours.
    2) SEVERE TOXICITY: SYSTEMIC EFFECTS/EARLY NEUROLOGIC SYMPTOMS: Vomiting, "heaviness" of the eyelids, blurred vision, drowsiness, paraesthesia of the mouth, tongue or lips, headache and dizziness can occur. Paralysis (ptosis and external ophthalmoplegia are early findings) may start within 15 minutes following some elapid bites but can be delayed up to 10 hours or more. The progression of neurotoxic effects following an elapid envenomation include: drowsiness, paraesthesia, abnormalities of taste and smell, paralysis of facial muscles and other muscles innervated by the cranial nerves, aphonia, difficulty in swallowing secretions, respiratory depression/failure (requiring mechanical ventilation) and generalized flaccid paralysis. Patients usually remain conscious and may have the ability to respond by moving their fingers or toes. OUTCOME: Neurotoxic effects from post-synaptic neurotoxins are completely reversible by either response to antivenom or after spontaneous resolution in 1 to 7 days. Effects from pre-synaptic neurotoxins are not readily reversible but will resolve with time. Elapid venom does not appear to have central effects in humans, and patients with generalized neurotoxicity are fully conscious. Patients may require circulatory and/or respiratory supportive care during this period. Deaths have been reported from snakes (N haje, W aegyptia (limited data) originating in this region.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) A low grade fever may develop following an elapid envenomation.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) WALTERINNESIA AEGYPTIA/CASE REPORT: A patient bitten by a Walterinnesia aegyptia developed a fever and an elevated leukocyte count (Lifshitz et al, 2003).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Blurred vision and ptosis are early findings of neurotoxicity following elapid envenomation (Warrell, 1995).
    2) SPITTING COBRAS (typically found in Africa): Conjunctivitis, pain, photophobia and corneal opacification may result from eye contact with the venom of spitting cobras; however, this has not been reported with other elapids of this region. Transient paralysis of the extraocular muscles and temporary loss of vision may occur due to systemic absorption of venom after some snake bites. Other serious eye effects are less common.
    3) DIRECT EYE CONTACT
    a) SPITTING COBRAS: Direct eye contact with venom believed to be from a spitting cobra has resulted in mild discomfort and injection of the eye (Gilkes, 1959). Conjunctivitis, intense pain, blepharospasm, chemosis, photophobia and/or corneal opacification have also been associated with eye contact with spitting cobra venom (Gilkes, 1959; Sinha, 1972; Grant, 1986). However, this has NOT been reported with other elapids of this region.
    b) The severity of the injury in humans may relate to the amount of venom contacting the eyes or may be influenced by infection and other factors. No systemic poisoning has been noted from eye contact with venom (Grant, 1986). Rarely reported systemic effects from contact with spitting cobra venom may be due to absorption of the venom through facial cuts (Gilkes, 1959).
    4) SYSTEMIC EYE EFFECTS
    a) Eye disturbances may occur as a result of systemic absorption of venom from cobra (Elapidae family) or viper (Viperidae family) bites (Grant, 1986).
    1) Reversible paralysis of the extraocular muscles and transient loss of vision are the most common effects. Antivenom generally resolves the paralytic effects.

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).
    B) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) WALTERINNESIA AEGYPTIA/CASE REPORT: A 22-year-old woman was bitten on the finger by a desert black cobra (Walterinnesia aegyptia) and developed ventricular premature beats that resolved within 15 hours (Lifshitz et al, 2003).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) Patients with evidence of neurotoxicity may have symptoms that progress to respiratory paralysis (ie paralysis of intercostal muscles and diaphragm) that can lead to respiratory failure despite treatment with antivenom (Warrell, 1995; Warrell, 1993). Prolonged ventilatory support may be necessary.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) NEUROTOXICITY
    1) Early ptosis, external ophthalmoplegia may occur within 15 minutes of envenomation but symptoms can be delayed up to 10 hours or more. Paralysis of the muscles of the face and tongue may be followed by respiratory paralysis and generalized flaccid paralysis (Warrell, 1995; Warrell, 1993).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Systemic absorption of venom following the bite of some snakes in the Elapidae (cobra) and Viperidae (viper) families can result in transient paralysis of the extraocular muscles and temporary visual impairment. Antivenom generally resolves the paralytic effects (Grant, 1986).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Early systemic effects of elapid envenomation are nausea and vomiting (Warrell, 1995; Ben Abraham et al, 2001; Britt & Burkhart, 1997).
    b) WALTERINNESIA AEGYPTIA
    1) DESERT BLACK COBRA: Minimal information. In several cases from Israel, local pain and swelling developed. Other symptoms included fever, general weakness, headache, nausea and vomiting (Warrell, 1995).
    2) DESERT BLACK COBRA/CASE REPORT: A 22-year-old woman was bitten on the finger by a desert black cobra (Walterinnesia aegyptia) and developed local swelling, irritability, fever, tachycardia, ventricular premature beats, nausea and an elevated blood leukocyte count (Lifshitz et al, 2003).
    c) NAJA HAJE
    1) EGYPTIAN COBRA: Widely found in Africa and the Middle East, but bites are not widely reported. Vomiting can be an early finding following envenomation (Warrell, 1995).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) BITE - WOUND
    1) WITH POISONING/EXPOSURE
    a) SUMMARY
    1) Swelling and pain are early symptoms associated with envenoming of elapids in this region. Pain generally increases during the first several hours, and can be accentuated by swelling. Blistering may develop several hours after a bite; necrosis is less likely to develop compared to viper bites. In most cases, swelling and edema appear early, often within 10 minutes of the bite, although in rare cases swelling may not develop for 8 to 12 hours. Generally, symptoms are more severe in bites by African spitting cobras (N. katiensis, N mossambica, N nigricollis, N pallida) compared to the N haje (pain and mild local swelling) of the Middle East (Warrell, 1995; Britt & Burkhart, 1997).
    b) WALTERINNESIA AEGYPTIA
    1) DESERT BLACK COBRA: Minimal information. In several cases from Israel, local pain and swelling developed. Other symptoms included fever, general weakness, headache, nausea and vomiting. Patients recovered without specific treatment (Warrell, 1995).
    c) NAJA HAJE
    1) EGYPTIAN COBRA: Widely found in Africa and the Middle East, but bites are not widely reported. Envenomation can produce neurotoxic effects and localized pain and swelling without the development of necrosis at the bite site (Warrell, 1995).
    d) NAJA NAJA
    1) NAJA NAJA ENVENOMATION: A 26-year-old man, bitten on the right index finger by a pet Black Pakistani Cobra, presented to the ED with severe pain at the bite site. The man was observed for 10 hours on a cardiac monitor and discharged to home with no further swelling or toxicity. Approximately 8 hours later, the patient developed nausea, abdominal pain, swelling of the right upper arm, and severe right-sided chest pain. Lab values were normal except for a white count of 15,300/microliter. After administration of less than 1 vial of an outdated cobra antivenin, the patient developed itching and a rash, which were treated with diphenhydramine and methylprednisolone. The patient recovered over the next 3 days with no further antivenin (Britt & Burkhart, 1997).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor neurologic (eg, presence or absence of ptosis, generalized paralysis) and respiratory function frequently. Monitor vital signs.
    B) Monitor pulse oximetry and/or blood gases and pulmonary function tests (negative inspiratory force, vital capacity and FEV1) to assess respiratory function and need for intubation.
    C) Culture wound if evidence of secondary infection develops.
    D) Elapids of the MIDDLE EAST are NOT likely to produce coagulopathy; therefore, the following tests should only be obtained if evidence of bleeding is present:
    1) Obtain complete blood count with differential. Monitor clotting factors (PT or INR, PTT) and platelet count if coagulopathy is present; studies should be repeated as indicated.
    E) Monitor the bite site for edema, discoloration, bleb formation and evidence of tissue necrosis or infection.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor serum electrolytes and fluid status as indicated following significant gastrointestinal loss.
    B) HEMATOLOGIC
    1) Coagulopathies have been infrequently associated with MIDDLE EASTERN elapid envenomations; therefore, obtain complete blood count with differential, monitor clotting factors (PT or INR, PTT) and platelet count if clinical evidence of coagulopathy is present; studies should be repeated as indicated.
    4.1.4) OTHER
    A) OTHER
    1) WOUND CULTURE
    a) Obtain wound culture in necrotic wounds with suspected infection.

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.6) DISPOSITION/BITE-STING EXPOSURE
    6.3.6.1) ADMISSION CRITERIA/BITE-STING
    A) Patients with evidence of progressive local toxicity should be admitted for antivenom treatment and close monitoring. Patients with systemic toxicity including neurotoxicity should be admitted to an ICU at a location with available antivenom.
    6.3.6.2) HOME CRITERIA/BITE-STING
    A) There is no role for home management of a suspected venomous snake bite.
    6.3.6.3) CONSULT CRITERIA/BITE-STING
    A) Contact your local poison control center, a medical toxicologist or toxinologist for any patient with a suspected Middle East elapid bite. Patients with an ocular venom exposure should be evaluated by an ophthalmologist.
    6.3.6.4) PATIENT TRANSFER/BITE-STING
    A) All patients should be taken to the nearest hospital or clinic that stocks antivenom. If in a non-native geographic area the antivenom is not immediately available or routinely stocked, it will have to be obtained from the nearest zoo source, which may be at a distance and require some time. Thus, the patient should be taken to the nearest hospital capable of managing the patient's existing medical condition. If not already done, splint bitten extremity or area prior to transport. Turn patient on their side to prevent aspiration of vomitus.
    6.3.6.5) OBSERVATION CRITERIA/BITE-STING
    A) Patients with a Middle East elapid bite should be sent to a medical facility and closely observed for the development of symptoms.

Monitoring

    A) Monitor neurologic (eg, presence or absence of ptosis, generalized paralysis) and respiratory function frequently. Monitor vital signs.
    B) Monitor pulse oximetry and/or blood gases and pulmonary function tests (negative inspiratory force, vital capacity and FEV1) to assess respiratory function and need for intubation.
    C) Culture wound if evidence of secondary infection develops.
    D) Elapids of the MIDDLE EAST are NOT likely to produce coagulopathy; therefore, the following tests should only be obtained if evidence of bleeding is present:
    1) Obtain complete blood count with differential. Monitor clotting factors (PT or INR, PTT) and platelet count if coagulopathy is present; studies should be repeated as indicated.
    E) Monitor the bite site for edema, discoloration, bleb formation and evidence of tissue necrosis or infection.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) FIRST AID
    1) FIELD OR FIRST AID TREATMENT
    a) Put victim at rest and keep warm.
    b) Remove rings and constrictive items. Apply dressing if bleeding.
    c) Immobilize injured part in functional position and keep just below heart level.
    d) Give reassurance.
    e) Rapidly transport the patient to the nearest emergency department; ideally a facility with experience in treating snake bites.
    f) If constriction bands or pressure wraps are placed on the wound at the scene and without vascular compromise, they should be left in place until arrival at a health care facility. Consider placement of a constriction band or pressure wrap (to delay systemic absorption of venom) for prolonged transport times or for patients whose conditions are rapidly deteriorating (McKinney, 2001).
    1) The pressure bandage (ie, Sutherland's compression method) is suggested after bites by neurotoxic species such as mambas (Dendroaspis) and cobras (N. haje, N. melanoleuca, N. nivea) which may be found in this region (Warrell, 1995).
    2) Pressure immobilization is not recommended in patients bitten by Middle Eastern viper and spitting cobras because it is likely to produce an intensification of locally necrotic effects by the venom produced by these snakes. Secondary ischemic effects may result from increased pressure in tight fascial compartments, in particular the anterior tibial compartment (Warrell, 1995).
    g) The following first aid measures are contraindicated: ice, tourniquets, incision of any type, and any type of suction. Electric shock treatment for snakebite is ineffective and is potentially quite dangerous (Russell, 1987; Howe & Meisenheimer, 1988; Dart et al, 1988; Bucknall, 1991; Dart & Gustafson, 1991; McKinney, 2001).

Case Reports

    A) ADULT
    1) NAJA NAJA ENVENOMATION: A 26-year-old man, bitten on the right index finger by a pet Black Pakistani Cobra, presented to the ED with severe pain at the bite site. The man was observed for 10 hours on a cardiac monitor and discharged to home with no further swelling or toxicity. Approximately 8 hours later, the patient developed nausea, abdominal pain, swelling of the right upper arm, and severe right-sided chest pain. Lab values were normal except for a white count of 15,300/microliter. After administration of less than 1 vial of an outdated cobra antivenin, the patient developed itching and a rash, which were treated with diphenhydramine and methylprednisolone. The patient recovered over the next 3 days with no further antivenin (Britt & Burkhart, 1997).
    2) WALTERINNESIA AEGYPTIA/CASE REPORT: A 22-year-old woman was bitten on the finger by a desert black cobra (Walterinnesia aegyptia) and developed local swelling, irritability, fever, tachycardia, ventricular premature beats, nausea and an elevated blood leukocyte count (Lifshitz et al, 2003).

Summary

    A) Not all snakes are venomous, and not all venomous snakes inject the same amount of venom if any (ie, dry bites) with each strike. Treatment therefore has to be based on symptoms rather than number of strikes. FATALITIES: Limited data. Deaths have been reported from snakes (N haje, W aegyptia (limited data)) originating in this region.

Minimum Lethal Exposure

    A) Not all snakes are venomous, and not all venomous snakes inject the same amount of venom if any (ie, dry bites) with each strike. Treatment therefore has to be based on symptoms rather than number of strikes.
    B) Limited data. Deaths have been reported from snakes (N haje, W aegyptia (limited data)) originating in this region (Warrell, 1995).

Toxicologic Mechanism

    A) SUMMARY
    1) EARLY NEUROLOGIC SYMPTOMS: Vomiting, "heaviness" of the eyelids, blurred vision, drowsiness, paraesthesia of the mouth, tongue or lips, headache and dizziness can occur. Paralysis (ptosis and external ophthalmoplegia are early findings) may start within 15 minutes following some elapid bites but can be delayed up to 10 hours or more. The progression of neurotoxic symptoms following an elapid envenomation include: drowsiness, paraesthesia, abnormalities of taste and smell, paralysis of facial muscles and other muscles innervated by the cranial nerves, aphonia, difficulty in swallowing secretions, respiratory depression (requiring mechanical ventilation) and generalized flaccid paralysis. Patients usually remain conscious and may have the ability to respond by moving their fingers or toes (Warrell, 1995).
    2) OUTCOME: In general, the neurotoxic effects from post-synaptic neurotoxins are reversible by antivenom therapy or spontaneous resolution (range, 1 to 7 days). Effects from pre-synaptic neurotoxins are not readily reversible but will resolve with time. Elapid venom does not appear to have central nervous system effects; therefore, patients with generalized neurotoxicity remain alert. Circulatory and/or respiratory supportive care may be needed until the patient is clinically improved (Monzavi et al, 2014; Warrell, 1995).
    B) NEUROTOXIC ACTIVITY
    1) SUMMARY
    a) NEUROTOXINS: Elapid venoms are likely to have neurotoxic activity. The venom is delivered via grooves in the snake's teeth. In general, elapid venom contains alpha-bungarotoxin which targets nicotinic acetylcholine receptors at the neuromuscular junction. Clinically important components of elapid venom in this region include post-synaptic "alpha-toxins"; long (70 to 74 amino acids) and/or short (60 to 62 residues ) neurotoxins have been found in cobras (ie, N haje) and the desert black cobra (W. aegyptia) (Warrell, 1995)
    2) MIDDLE EASTERN ELAPIDS
    a) MIDDLE EASTERN ELAPIDS (some overlap may occur with African elapids due to geographic proximity): The venom of most elapids is made up of polypeptide cytotoxins, including long and short chain curaremimetic postsynaptic or a-neurotoxins that bind to the acetylcholine receptor at peripheral neuromuscular junctions (Warrell, 1999). The venom of the genus Naja and Hemachatus contain polypeptide cytotoxins and cardiotoxins along with complement activation (Warrell, 1995).
    b) COBRAS: The venom contains long chain post-synaptic neurotoxins which are rich in enzymes including hyaluronidase phospholipase A(2) (Warrell, 1995).

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