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AFRICAN SNAKES-ELAPIDAE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Despite urban and environmental changes, venomous snakes are numerous in most parts of Africa. This management is limited to the Family Elapidae (Cobras {genus Naja and genus Boulengerina}, mambas {genus Dendroaspis}, coral snakes {genus Aspidelaps}, garter snakes {genus Elapsoidea) and (Rinkhals {genus Hemachatus haemachatus}) of most medical importance to this region (Warrell, 1995).
    B) There are over two dozen species of elapids with cobras being considered the most venomous snakes of this region. Elapids can be described as having relatively short (up to about 10 mm long) fixed, front (proteroglyphous) fangs, but the mambas have fangs that are mounted at the very front of the maxilla which can rotate at its articulation with the pre-frontal bone. Fatalities have been reported among 11 species of African/Middle Eastern elapids (Warrell, 1995).
    C) This region includes the whole continent of Africa including Madagascar and "the Arabian Peninsula" bounded to the north by Syria and the northeast by Iraq. Turkey and Iran and other Asian countries are NOT included and can be found in the management titled: ASIAN SNAKES-ELAPIDAE. Some geographic overlap may occur in this management with venomous snakes of the Middle East. Please refer to the SNAKES, MIDDLE EASTERN management as appropriate.

Specific Substances

    A) AFRICAN GARTER SNAKES
    1) Elapsoidea chelazzi
    2) E. guntheri
    3) E. laticincta
    4) E. loveridgei
    5) E. nigra
    6) E. semiannulata
    7) E. sundevallii
    COBRAS
    1) Boulengerina annulata
    2) B. christyi
    3) Naja haje
    4) N. katiensis
    5) N. melanoleuca
    6) N. mossambica
    7) N. nigricollis
    8) N. nivea
    9) N. pallida
    10) Paranaja multifasciata
    11) Pseudohaje goldii
    12) P. nigra
    13) Walterinnesia aegyptia
    CORAL SNAKES
    1) Aspidelaps lubricus
    2) A. scutatus
    MAMBAS
    1) Dendroaspis angusticeps
    2) D. jamesoni
    3) D. polylepis
    4) D. viridis
    RINGHALS
    1) hemachatus haemachatus

Available Forms Sources

    A) SOURCES
    1)
    AFRICAN GARTER SNAKESCOMMON NAME
    Elapsoidea chelazzi(unreported)
    E. guntheri(unreported)
    E. laticincta(unreported)
    E. loverdgeiLoveridge's garter snake
    E. nigra(unreported)
    E. semiannulata(unreported)
    E. sundevalliiSundevall's garter snake
    Homoroselaps lacteusSpotted harlequin or dwarf garter snake

    2)
    COBRASCOMMON NAME
    Boulengerina annulataringed water cobra
    B. christyiChristy's water cobra
    Naja hajeEgyptian cobra
    N. katiensiswestern brown spitting cobra
    N. melanoleucablack and white lipped or forest cobra
    N. mossambicaMoscambique spitting cobra, M'Fezi
    N. nigricollisblack-necked spitting cobra
    N. niveaCape cobra
    N. pallidared spitting cobra
    Paranaja multifasciataburrowing cobra
    Pseudohaje goldiiGold's, false or tree cobra
    Walterinnesia aegyptiaWalter Innes's snake or black desert cobra

    3)
    CORAL SNAKESCOMMON NAME
    Aspidelaps lubricusSouth African coral snake
    A. scutatusshield or shield-nose snake

    4)
    MAMBASCOMMON NAME
    Dendroaspis angusticepscommon or eastern green/white-mouthed mamba
    D. jamesoniTraill's, Jameson's or western green mamba
    D. polylepisblack or black-mouthed mamba
    D. viridisHallowell's or western green mamba

    5)
    RINGHALSCOMMON NAME
    hemachatus haemachatusringhals

    6) (Warrell, 1995)

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) This management is limited to the discussion of Elapidae of Africa and those species of most medical importance to this region.
    2) African elapids possess relatively short (up to about 10 mm long), fixed, front (proteroglyphous) fangs; the exception is the mamba which has the fang mounted at the very front of the maxilla which can rotate at its articulation with the pre-frontal bone. Fatalities have been reported with nearly half of the 27 species in this region.
    a) Sea snakes will not be discussed here. Please refer to the SEA SNAKES management for further information.
    b) Some geographic overlap may occur in this management with venomous snakes of the middle east. Please refer to the SNAKES, MIDDLE EASTERN management as appropriate.
    3) 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.
    4) Clinically, unlike many elapid envenomations that produce neurotoxicity, African elapids are more likely to cause local tissue necrosis following envenomation. Several species, however, can produce severe neurotoxic effects: (Dendroaspis {mambas}, Naja haje {Egyptian cobra} and Naja nivea {Cape cobra}).
    a) 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.
    5) EARLY EFFECTS - Vomiting, "heaviness" of the eyelids, blurred vision, drowsiness, paraesthesia of the mouth, tongue or lips, headache and dizziness can occur. Paralysis may start within 15 minutes following some elapid bites.
    a) The following neurological effects may occur following Elapidae envenomation: drowsiness, paraesthesia, abnormalities of taste and smell, ptosis, external ophthalmoplegia, 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. Some patients may retain the ability to flex fingers or toes in response to questions.
    1) 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.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Inoculation of the eyes with the venom from spitting cobras may cause intense pain, blepharospasm, conjunctivitis and in severe cases blindness.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Hypotension, chest pain, cardiac arrest and circulatory failure have been reported following some elapid envenomations.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Respiratory dysfunction is associated with progressing neurotoxicity.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Severe neurotoxic effects can occur from bites by mambas and some cobras. Mild envenomation symptoms (ie, dizziness, drowsiness) may develop after envenomation by other elapids.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea and vomiting may occur as an early symptom of elapid envenomation. Diarrhea has also been reported.
    0.2.12) FLUID-ELECTROLYTE
    A) WITH POISONING/EXPOSURE
    1) Inappropriate antidiuretic hormone secretion was reported in a child following envenomation by a Aspidelaps lubricus infuscatus.
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Coagulation disturbances are rare following elapid envenomations and have only been reported following N. nigricollis bites.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Similar to viper venom, African elapid species can produce severe local tissue reaction (ie, pain, swelling, blistering). This is a prominent finding for African elapid envenomations.
    2) Excessive sweating can be an early symptom of envenomation.
    0.2.15) MUSCULOSKELETAL
    A) WITH POISONING/EXPOSURE
    1) Generalized muscular weakness and muscle fasciculations have been reported following envenomation.

Laboratory Monitoring

    A) Obtain serum electrolytes and monitor fluid balance as indicated following significant gastrointestinal loss.
    B) Monitor vital signs. Hypotension may occur as a result of cardiotoxicity or from hypovolemia. Monitor neurologic function frequently.
    C) 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.
    D) Culture wound if evidence of secondary infection develops.
    E) Elapids of Africa 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.
    F) Monitor the bite site for edema, discoloration, bleb formation and evidence of tissue necrosis or infection.

Treatment Overview

    0.4.4) EYE EXPOSURE
    A) Some species of African cobras are able to "spit" venom which can injure the eye. All patients sustaining an ocular exposure to venom should be evaluated at a health care facility for possible eye injury.
    B) Spitting cobras (i.e., H. haemachatus, N. nigricollis, N. pallida, N. katiensis, N. mossambica) can produce intense conjunctivitis, corneal erosions, complicated by secondary infections, anterior uveitis, and permanent blindness (Warrell, 1995).
    C) Immediately remove contact lenses and irrigate exposure eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes.
    0.4.7) BITES/STINGS
    A) Following elapid envenomation, neurotoxicity may develop rapidly and appear similar to a curare-like effect. Progressive descending paralysis is a concern with some species of African elapids (notably the mambas {Dendroaspis}, Egyptian cobra {Naja haje} and Cape cobra {Naja nivea}) which can cause severe neurotoxic effects; evaluate respiratory function, immediate intubation and mechanical ventilation may be required.
    B) Antivenoms are available to treat elapid snake bites of this region and are indicated in patients with systemic effects after envenomation (i.e., progressive neurotoxicity). See detailed treatment section for specific antivenoms and doses.
    C) Most antivenoms contain animal proteins; skin testing is recommended. Anaphylaxis can occur.
    D) ALLERGIC REACTION: MILD/MODERATE: Antihistamines with or without inhaled beta agonists, corticosteroids or epinephrine. SEVERE: Oxygen, aggressive airway management, antihistamines, epinephrine, corticosteroids, ECG monitoring, and IV fluids.
    E) Monitor for signs and symptoms of local tissue reaction. Antibiotics may be indicated to treat local infection. Give analgesics as needed. Administer tetanus booster, if applicable.
    F) Localized and superficial necrosis has been reported. Debridement may be required following severe envenomations. Obtain a surgical consult as indicated.
    G) Hypotension has occurred infrequently following envenomation.
    1) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.

Range Of Toxicity

    A) Fatalities have been reported following envenomations by the genera Naja (N. nivea {cape or yellow cobra} and N. melanoleuca {forest or black and white lipped cobra}) and the species Dendroaspis polylepis {black mamba}.
    B) Severe neurotoxic effects can occur with envenomations by the following species: Dendroaspis (mambas), N. haje (Egyptian cobra) and N. nivea (Cape cobra).
    C) The most common clinical finding following envenomation by African elapids is local tissue necrosis rather than neurotoxicity.
    D) Only the venom of the N. nigricollis is able to produce coagulation disturbances.
    E) Serious eye injury, including blindness, has occurred following envenomation by "spitting" cobras (ringhals {hemachatus haemachatus} and N. nigricollis {black-necked spitting cobra}) species.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) This management is limited to the discussion of Elapidae of Africa and those species of most medical importance to this region.
    2) African elapids possess relatively short (up to about 10 mm long), fixed, front (proteroglyphous) fangs; the exception is the mamba which has the fang mounted at the very front of the maxilla which can rotate at its articulation with the pre-frontal bone. Fatalities have been reported with nearly half of the 27 species in this region.
    a) Sea snakes will not be discussed here. Please refer to the SEA SNAKES management for further information.
    b) Some geographic overlap may occur in this management with venomous snakes of the middle east. Please refer to the SNAKES, MIDDLE EASTERN management as appropriate.
    3) 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.
    4) Clinically, unlike many elapid envenomations that produce neurotoxicity, African elapids are more likely to cause local tissue necrosis following envenomation. Several species, however, can produce severe neurotoxic effects: (Dendroaspis {mambas}, Naja haje {Egyptian cobra} and Naja nivea {Cape cobra}).
    a) 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.
    5) EARLY EFFECTS - Vomiting, "heaviness" of the eyelids, blurred vision, drowsiness, paraesthesia of the mouth, tongue or lips, headache and dizziness can occur. Paralysis may start within 15 minutes following some elapid bites.
    a) The following neurological effects may occur following Elapidae envenomation: drowsiness, paraesthesia, abnormalities of taste and smell, ptosis, external ophthalmoplegia, 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. Some patients may retain the ability to flex fingers or toes in response to questions.
    1) 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.

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Inoculation of the eyes with the venom from spitting cobras may cause intense pain, blepharospasm, conjunctivitis and in severe cases blindness.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CORTICAL BLINDNESS may occur following some elapid envenomations.
    a) CASE REPORT - Naja Nigricollis (black-necked spitting cobra) - Cortical blindness occurred in a 7-year-old girl after a snakebite presumably by a N. nigricollis. Within the first 24 hours, bilateral optic neuritis was observed. Following a long convalescent period (approximately a month), the patient had residual paralysis, left-sided hemiplegia and was unable to see. Optic atrophy had developed along with partial blindness (Schwersenski & Beatty, 1982).
    b) RINGHALS - The hemachatus haemachatus is highly adapt spitting cobra that can spray a distance of 5 to 7 feet, which is ordinarily aimed at the eyes of the intruder. The venom can produce intense pain and spasm; blindness can occur if the eye is not immediately washed (USDN, 1991).
    c) NAJA NIGRICOLLIS - similar clinical effects as the ringhal and can also produce blindness if the venom is not removed from the eye (USDN, 1991).
    2) PTOSIS has been reported following African elapid envenomations (ie, cobras, coral snakes) (Zaltzman et al 1984; (Blaylock et al, 1985). Effects have been reported, in as little as 30 minutes, after a naja nivea (Cape cobra) bite (Blaylock et al, 1985).
    3) BLEPHAROSPASM/SEVERE CONJUNCTIVITIS
    a) SPITTING COBRAS (the stream of venom ejected forms a fine spray which can be accurate at up to 3 to 4 meters) have produced blepharospasm with severe conjunctivitis after envenomation by naja mossambica (Mozambique spitting cobra) (Tilbury, 1982).
    b) RINGHALS - The hemachatus haemachatus is highly adapt spitting cobra that can spray a distance of 5 to 7 feet; the venom can cause intense pain and spasm (USDN, 1991).
    c) NAJA NIGRICOLIS - similar to the ringhals the venom can be "spit" as far as 9 feet and cause extreme pain and spasm of the eyelids (USDN, 1991).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hypotension, chest pain, cardiac arrest and circulatory failure have been reported following some elapid envenomations.
    3.5.2) CLINICAL EFFECTS
    A) CHEST PAIN
    1) WITH POISONING/EXPOSURE
    a) In a review of case reports, 5 of 15 victims of elapid (genus Dendroaspis) snakebite developed either chest pain or "chest tightness" within the first 30 minutes of exposure. Two other patients had a cardiac arrest within 45 to 140 minutes of envenomation by an unknown elapid species (Blaylock, 1983).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORTS
    1) Dendroaspis polylepis (black mamba) - A 14-month-old female was bitten on the leg by a D. polylepis and was brought to the hospital within 15 minutes of exposure. The patient's condition deteriorated and the child was observed in severe shock (clinical details not described). A first dose of antivenom and hydrocortisone was given within 35 minutes of the bite. Another dose of antivenom was administered and vital signs returned to normal within 80 minutes. No long term sequelae was reported (Hilligan, 1987).
    2) Aspidelaps scutatus (shield-nose snake) - Despite mechanical ventilation and supportive care, which included undiluted polyvalent antivenom, a 4-year-old female died suddenly of cardiac failure approximately 16 hours after receiving a bite to the hand by an Aspidelaps scutatus (van Egmond, 1984).
    C) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Dendroaspis polylepis (black mamba) - Hypotension (BP 100/60) has been reported in an adult following envenomations by D. polylepis. Vital signs improved after the administration of antivenom and supportive care (Hilligan, 1987).
    D) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Dendroaspis polylepis (black mamba) - Envenomation can inhibit a branch of the vagus nerve that controls cardiac conduction resulting in dysrhythmias (USDN, 1991).
    E) MYOCARDIAL INFARCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Dendroaspis polylepis (black mamba) - Myocardial infarction was reported after probable envenomation by a D. polylepis in a 24-year-old male who developed cardiopulmonary arrest approximately 7 hours after exposure. Twenty hours after presentation the patient had a sudden drop in blood pressure (64/44 mmHg) and ST-segment elevation with Q waves (present in the precordial leads). The patient also developed sinus bradycardia which was responsive to atropine along with transient, mild ST-segment elevations which persisted for 5 days. No permanent sequelae occurred (Naidoo et al, 1987).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Respiratory dysfunction is associated with progressing neurotoxicity.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) Dendroaspis polylepis (black mamba) - Envenomation can inhibit respiratory function (USDN, 1991).
    b) Respiratory dysfunction as a result of progression of neurological paralysis has developed following some elapid (genus Dendroaspis {mambas}, genus Naja {N. haje, N. nivea}) envenomations of this region (Warrell, 1995).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Severe neurotoxic effects can occur from bites by mambas and some cobras. Mild envenomation symptoms (ie, dizziness, drowsiness) may develop after envenomation by other elapids.
    3.7.2) CLINICAL EFFECTS
    A) NEUROTOXICITY
    1) WITH POISONING/EXPOSURE
    a) SUMMARY - Neurotoxic effects can be absent or minimal to severe following elapid envenomations in this region. Bites by mambas (genus Dendroaspis), Egyptian cobra (N. haje), and Cape cobra (N. nivea) can produce severe neurotoxicity. The N. mossambica species has also been implicated as a neurotoxic agent in children, but the evidence is not conclusive. Mild neurotoxic symptoms have occurred following H. haemachatus (Ringhals) envenomations and have included drowsiness, vertigo and diplopia (Warrell, 1995).
    b) ONSET - Early symptoms include: vomiting, "heaviness" of the eyelids, blurred vision, paresthesia around the mouth, headache and dizziness. Effects (ie, ptosis and external ophthalmoplegia) can begin within 15 minutes after a bite, but may occur as late as 10 hours after envenomation (Warrell, 1995).
    c) PATHOLOGY - Progression of neurological paralysis includes: the mouth, jaw, tongue vocal cords, airway and eventually the muscles of the respiratory system. Effects generally are reversible (Warrell, 1995).
    B) FLACCID PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) SUMMARY - Neurotoxic effects including paralysis from post-synaptic neurotoxins are completely reversible by either response to antivenom (given soon after envenomation) or after spontaneous resolution in 1 to 7 days. Effects from pre-synaptic neurotoxins are not readily reversible but will resolve with time. It has been suggested that elapid venom does not have a central effect in humans, and the patient remains fully conscious. The focus of care, therefore; is to maintain the patient's respiratory and circulatory function (Harvey, 1985; Warrell, 1995).
    b) CASE REPORTS
    1) NAJA NIVEA (Cape cobra)
    a) Flaccid paralysis has been reported within 4 hours of envenomation by naja nivea (Cape cobra); the patient later reported that he was able to hear and understand, but could not move. The patient required mechanical ventilation for 4.5 days. Spontaneous movement of the arms and legs occurred on day 6 following supportive care.
    b) In another case, a 26-year-old male was also bitten by a naja nivea and received antivenom (40 mL polyvalent antivenom - the authors noted that the dose was too small to correct neurological effects) within 2 hours of envenomation and still developed paralysis within 2.5 hours of exposure. A dose of antivenom was repeated at 4.5 hours with some evidence of neurological improvement. The patient was treated with ventilatory care and supportive therapies with slow resolution of his muscular weakness over an 8 day period. He walked with assistance on day 9, and made a complete recovery.
    c) As evidence by these two cases, the authors suggested that antivenom is of little or no value once paralysis has developed in victims of Cape cobra envenomation. Prostigmine was given to both patients with no benefit reported in reversing paralysis. It is speculated that the failure of the antivenom is suggestive that the toxin is fixed and that neurological impairment only reverses when it has been naturally degraded (Blaylock et al, 1985).
    2) DENDROASPIS POLYLEPIS (Black mamba)
    a) An adult received a snake bite on the hand by a D. polylepis (black mamba) and almost immediately began to develop symptoms of tingling of the tongue and lips; weakness of the lower extremities occurred within 20 minutes of exposure. The patient was later intubated due to increasing chest tightness. The first dose of antivenom was given approximately 2 hours after the bite and was given 2 more times during the course of illness. The patient made a complete recovery 6 days after envenomation (Warrell, 1995).
    b) A 50-year-old female developed complete paralysis following envenomation by a black mamba (identified by a picture only). Although all the muscle groups were paralyzed the patient had some flexor capability in the hands and feet which became a source of communication. Following supportive care, the patient later relayed that she had been conscious throughout her care. Recovery was complete by the 7th day (Harvey, 1985).
    3) DENDROASPIS ANGUSTICEPS (Eastern green mamba)-
    a) Typical symptoms of neurotoxic elapid envenomation have been reported after snake bites by D. angusticeps (Warrell, 1995).
    C) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Drowsiness has been the only neurological symptom reported following some elapid (Naja mossambica {spitting cobra}) envenomations (Tilbury, 1982).
    D) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness is frequently reported as an early symptom of an elapid envenomation (Blaylock, 1983).
    E) HEMIPLEGIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Persistent flaccid paralysis (approximately one month in duration) occurred in a 7-year-old female following a presumed N. nigricollis (Cape cobra) bite. The child developed a residual left hemiparesis and palsy and upper motor neuron lesion of the left facial nerve with paralysis of the left 6th and right 3rd cranial nerves. The authors suggested that the persistent neurological toxicity could not be solely attributable to the snake bite, but developed as a result of possible hypoxia (ie, respiratory arrest occurred 5 hours after envenomation) (Schwersenski & Beatty, 1982).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea and vomiting may occur as an early symptom of elapid envenomation. Diarrhea has also been reported.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting and diarrhea have been reported after elapid (genus Naja {Mozambique spitting cobra}; genus Dendroaspis {black mamba}) envenomations, and can result in hypovolemia in some cases (Tilbury, 1982; Hilligan, 1987).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Coagulation disturbances are rare following elapid envenomations and have only been reported following N. nigricollis bites.
    3.13.2) CLINICAL EFFECTS
    A) BLOOD COAGULATION PATHWAY FINDING
    1) WITH POISONING/EXPOSURE
    a) At the time of this review, only the venom of the N. nigricollis is believed to be able to produce coagulation disturbances (Warrell, 1995).
    b) LACK OF EFFECT
    1) Naja Nivea (Cape cobra) - Coagulopathy was NOT reported in two adults following N. nivea envenomation (Blaylock et al, 1985).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Similar to viper venom, African elapid species can produce severe local tissue reaction (ie, pain, swelling, blistering). This is a prominent finding for African elapid envenomations.
    2) Excessive sweating can be an early symptom of envenomation.
    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 (African cobras) can produce severe local reactions (eg, moderate to severe local pain, swelling, blistering around the affected area, discoloration (a darkening of the site similar to a port wine stain of the skin)) which may or may not be associated with neurologic effects (Tilbury, 1982; Blaylock, 1983; Hilligan, 1987).
    2) SPITTING COBRAS - the venom contains cytotoxins and digestive enzymes which can produce locally necrotic effects (Warrell, 1999).
    B) SKIN NECROSIS
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - In a review of 17 cases of N. mossambica (spitting cobra), 11 victims developed superficial tissue necrosis (described as only the skin and subcutaneous layer) at the site of envenomation. The limited tissue injury may be related to the physical features of the snake which has short fangs (Tilbury, 1982).
    b) CASE REPORTS - Necrosis at the envenomation site occurred in two patients who were bitten by Naja mossambica (Mozambique Spitting Cobra). The first patient was bitten on the left flank resulting in a necrotic area approximately 4 square inches in size that sloughed out and was removed 12 days later. The second patient was bitten on his right index finger resulting in necrosis and eventual loss of the fingertip. Neither patient developed systemic symptoms (Strover, 1973).
    C) SWELLING
    1) WITH POISONING/EXPOSURE
    a) Swelling occurs frequently after receiving a snakebite by an elapid. It may be limited to the immediate area or extend to the adjacent region (Blaylock, 1983).
    D) ITCHING OF SKIN
    1) WITH POISONING/EXPOSURE
    a) Localized pruritus has been reported following envenomation by a mamba (Hilligan, 1987).
    E) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Profuse sweating may develop as an initial symptom of elapid envenomation (Blaylock, 1983).

Musculoskeletal

    3.15.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Generalized muscular weakness and muscle fasciculations have been reported following envenomation.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Generalized muscular weakness has been reported following elapid envenomations (Aspidelaps scutatus {shield-nose snake}) with complete recovery of motor function occurring over several days (Zaltzman et al, 1984).
    B) MUSCLE FASCICULATION
    1) WITH POISONING/EXPOSURE
    a) The venom of Dendroaspis angusticeps (green or white mouthed mamba) and Dendroaspis polylepis (black mamba) can produce muscle fasciculations (Warrell, 1995).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain serum electrolytes and monitor fluid balance as indicated following significant gastrointestinal loss.
    B) Monitor vital signs. Hypotension may occur as a result of cardiotoxicity or from hypovolemia. Monitor neurologic function frequently.
    C) 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.
    D) Culture wound if evidence of secondary infection develops.
    E) Elapids of Africa 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.
    F) 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 African 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.
    2) VITAL SIGNS
    a) Monitor vital signs. Hypotension may occur as a result of direct cardiotoxicity or from hypovolemia.

Methods

    A) CHROMATOGRAPHY
    1) Joubert (1988) described a method to identify the structure of Aspidelaps scutatus (shield-nose snake) by purifying the venom by gel filtration and ion exchange chromatography.
    B) ELISA
    1) Venom-antibody has been detected by the ELISA method in the serum of patients with previous snake bites (Pugh & Theakston, 1980).
    C) OTHER
    1) Commercial immunodiagnostic kits are produced by the Commonwealth Serum Laboratories in Australia to assist in the identification of a species (Warrell, 1999).

Treatment

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) Any patient who has been bitten by a proven or suspected venomous elapid should be admitted to a hospital for a 24 hour observation period.
    6.3.6.2) HOME CRITERIA/BITE-STING
    A) There should be NO home treatment for bites from proven or suspected venomous snakes. The goal of prehospital care is rapid transport to a Healthcare facility.
    6.3.6.3) CONSULT CRITERIA/BITE-STING
    A) Consult local herpetologists for proper identification of the snake if it is available.
    6.3.6.5) OBSERVATION CRITERIA/BITE-STING
    A) Any patient suspected of having been bitten but NOT proven to have been bitten should be closely observed for a period of 24 hours.

Monitoring

    A) Obtain serum electrolytes and monitor fluid balance as indicated following significant gastrointestinal loss.
    B) Monitor vital signs. Hypotension may occur as a result of cardiotoxicity or from hypovolemia. Monitor neurologic function frequently.
    C) 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.
    D) Culture wound if evidence of secondary infection develops.
    E) Elapids of Africa 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.
    F) Monitor the bite site for edema, discoloration, bleb formation and evidence of tissue necrosis or infection.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) OPHTHALMIC EXAMINATION AND EVALUATION
    1) Ophthalmology exam is indicated and should be done as soon as possible after injury.
    B) ANTIBIOTIC
    1) Topical antimicrobial agents should be used to prevent or minimize corneal injury (Warrell, 1995).
    C) PAIN
    1) Instill 1% epinephrine eye drops to relieve severe local pain. Symptoms should improve immediately (Warrell, 1999).
    D) ANTIVENOM
    1) Topical or systemic antivenom is not indicated (Warrell, 1995).

Range Of Toxicity

Summary

    A) Fatalities have been reported following envenomations by the genera Naja (N. nivea {cape or yellow cobra} and N. melanoleuca {forest or black and white lipped cobra}) and the species Dendroaspis polylepis {black mamba}.
    B) Severe neurotoxic effects can occur with envenomations by the following species: Dendroaspis (mambas), N. haje (Egyptian cobra) and N. nivea (Cape cobra).
    C) The most common clinical finding following envenomation by African elapids is local tissue necrosis rather than neurotoxicity.
    D) Only the venom of the N. nigricollis is able to produce coagulation disturbances.
    E) Serious eye injury, including blindness, has occurred following envenomation by "spitting" cobras (ringhals {hemachatus haemachatus} and N. nigricollis {black-necked spitting cobra}) species.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Fatalities have been reported with the following species of African elapids (USDN, 1991; Warrell, 1995):
    a) N. haje (Egyptian cobra) - deaths have been reported 6 to 16 hours after bites by large snakes even when antivenom was used.
    b) N. nivea (Cape or Yellow cobra) - Although unlikely to be aggressive, its venom is the most toxic of the African cobras; fatalities can result if NOT treated quickly.
    c) N. melanoleuca (Forest cobra or black & white lipped) - seldom aggressive, but has a highly toxic venom and fatalities have been reported.
    d) Dendroaspis polylepis (Black mamba) - considered one of the most dangerous snakes; a large mamba can secrete enough venom to kill 5 to 10 men. Few victims survive unless antivenom is given soon after a bite. Cardiac dysrhythmias can occur.
    e) Hemachatus haemachatus (Ringhals) - Death may occur after a bite, but eye injury is more likely.
    B) CASE REPORTS
    1) Aspidelaps scutatus (shield-nose snake) - Despite mechanical ventilation and supportive care, which included undiluted polyvalent antivenom, a 4-year-old female died suddenly of cardiac failure approximately 16 hours after receiving a bite to the hand by an A. scutatus (van Egmond, 1984).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) TISSUE NECROSIS - The most common clinical finding following envenomation by African elapids is mild to moderate local tissue necrosis rather than neurotoxicity. Generally, it has less proteases than vipers which causes severe tissue necrosis (Warrell, 1995).
    2) NEUROTOXICITY - Bites by Dendroaspis (mambas), N. haje (Egyptian cobra), and N. nivea (Cape cobra) can produce severe neurotoxicity (Warrell, 1995).
    a) Neurotoxic effects including paralysis are completely reversible either in response to antivenom (given soon after envenomation) or after spontaneous resolution which generally occurs within 1 to 7 days in most cases (Harvey, 1985; Warrell, 1995).
    3) GASTROINTESTINAL DISTURBANCES - Nausea, vomiting and diarrhea have occurred with some elapid (genera Naja and Dendroaspis) envenomations, and can result in hypovolemia in some victims (Tilbury, 1982; Hilligan, 1987) Warrell, 1995).
    4) OPTICAL INJURY - The hemachatus haemachatus (ringhals) is highly adapt spitting cobra that can spray a distance of 5 to 7 feet which is ordinarily aimed at the eyes of its victim. The venom can produce intense pain and spasm; blindness can occur if the eye is not immediately washed (USDN, 1991).
    5) COAGULOPATHIES - At the time of this review, only the venom of the N. nigricollis is believed to produce coagulation disturbances (Warrell, 1995).
    B) CASE REPORTS
    1) GENERAL
    a) SPITTING COBRA - most common sign of systemic envenoming was the presence of leucocytosis, fever and absence of clot retraction (Warrell, 1995).
    2) PEDIATRIC
    a) N. nigricollis (black-necked spitting cobra) - Cortical blindness occurred in a 7-year-old girl after a snakebite presumably by a N. nigricollis. Within the first 24 hours, bilateral optic neuritis was observed. Following a long convalescent period (approximately 30 days), the patient had residual paralysis, left-sided hemiplegia and was unable to see. Optic atrophy had developed along with partial blindness (Schwersenski & Beatty, 1982).
    3) ADULTS
    a) Dendroaspis polylepis (black mamba) - Hypotension (BP 100/60) has been reported in an adult following envenomations by a D. polylepis (Hilligan, 1987). Myocardial infarction was also reported after probable envenomation by a D. polylepis in a 24-year-old male who developed cardiopulmonary arrest approximately 7 hours after exposure. Both recovered without permanent sequelae (Hilligan, 1987; Naidoo et al, 1987).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 120 mcg/kg (RTECS, 2001)
    B) LD50- (INTRAPERITONEAL)MOUSE:
    1) 2800 mcg/kg (RTECS, 2001)
    C) LD50- (SUBCUTANEOUS)MOUSE:
    1) 3320 mcg/kg (RTECS, 2001)
    D) LD50- (INTRAPERITONEAL)MOUSE:
    1) 260 mcg/kg (RTECS, 2001)
    E) LD50- (SUBCUTANEOUS)MOUSE:
    1) 1020 mcg/kg (RTECS, 2001)
    F) LD50- (INTRAPERITONEAL)MOUSE:
    1) 256 mcg/kg (RTECS, 2001)
    G) LD50- (SUBCUTANEOUS)MOUSE:
    1) 550 mcg/kg (RTECS, 2001)
    H) LD50- (INTRAPERITONEAL)MOUSE:
    1) 330 mcg/kg (RTECS, 2001)
    I) LD50- (SUBCUTANEOUS)MOUSE:
    1) 790 mcg/kg (RTECS, 2001)
    J) LD50- (INTRAPERITONEAL)MOUSE:
    1) 120 mcg/kg (RTECS, 2001)
    K) LD50- (INTRAPERITONEAL)MOUSE:
    1) 324 mcg/kg (RTECS, 2001)
    L) LD50- (SUBCUTANEOUS)MOUSE:
    1) 225 mcg/kg (RTECS, 2001)
    M) LD50- (INTRAPERITONEAL)MOUSE:
    1) 83 mcg/kg (RTECS, 2001)
    N) LD50- (INTRAMUSCULAR)MOUSE:
    1) 440 mcg/kg (RTECS, 2001)
    O) LD50- (INTRAPERITONEAL)MOUSE:
    1) 352 mcg/kg (RTECS, 2001)
    P) LD50- (SUBCUTANEOUS)MOUSE:
    1) 2 mg/kg (RTECS, 2001)
    Q) LD50- (INTRAPERITONEAL)MOUSE:
    1) 334 mcg/kg (RTECS, 2001)
    R) LD50- (SUBCUTANEOUS)MOUSE:
    1) 400 mcg/kg (RTECS, 2001)
    S) LD50- (INTRAPERITONEAL)MOUSE:
    1) 140 mcg/kg (RTECS, 2001)
    T) LD50- (SUBCUTANEOUS)MOUSE:
    1) 400 mcg/kg (RTECS, 2001)

Pharmacology Toxicology

Toxicologic Mechanism

    A) SUMMARY - African snakes of the Elapidae genera can possess venom which can produce progressive descending paralysis (without severe local tissue necrosis, bleeding/blood clotting disorders or rhabdomyolysis) (Warrell, 1999).
    1) Initially, the venom causes ptosis, blurred vision, dysconjugate gaze and diplopia due to oculomotor cranial nerve stimulation.
    2) Secondly, corticobulbar tract dysfunction occurs causing dysphonia, dysphagia, hyperacusis, headache, dizziness, vertigo and signs of autonomic nervous stimulation such as hypersalivation, congested conjunctivae and "gooseflesh". Loss of sense of smell and taste may be present and either transient or persistent. Progressive descending paralysis can result in an absent gag reflex, and respiratory dysfunction. Lastly, symptoms progress to cause paralysis of the diaphragmatic muscles resulting in respiratory paralysis which may lead to hypoxia, coma, generalized seizures and death may result from respiratory failure (Warrell, 1999).
    3) Generalized flaccid paralysis is a late finding of envenomation, which occurs with some variability, and presents from 1 to 7 hours after envenomation (Warrell, 1995).
    4) NEUROTOXINS - The following neurotoxins have been identified among African elapids:
    a) ELAPIDS - 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) MAMBAS - The venom contains unique neurotoxins; dendrotoxins acting presynaptically on voltage gated potassium channels, and faciculins inhibiting acetylcholine esterase (Warrell, 1999).
    1) Dendroaspis polylepis (black mamba) - A large black mamba can secrete enough venom to kill 5 to 10 men; few people reportedly survive without antivenin. Envenomation can inhibit respiratory function and a branch of the vagus nerve that controls cardiac rhythm can be affected and result in dysrhythmias (USDN, 1991).
    c) SPITTING COBRAS - Their venom contains cytotoxins and digestive enzymes which can produce locally necrotic effects (Warrell, 1999).
    1) RINGHALS - The hemachatus haemachatus is highly adapt spitting cobra that can spray a distance of 5 to 7 feet which is ordinarily aimed at the eyes of the enemy. The venom can produce intense pain and spasm; blindness can occur if the eye is not immediately washed (USDN, 1991).
    2) NAJA NIGRICOLIS - similar to the ringhals the venom can be "spit" as far as 9 feet and cause extreme pain and spasm of the eyelids. Sprayed venom does NOT affect unbroken skin (USDN, 1991).
    a) Unlike other elapid venoms which lack antihemolytic activity, the venom of the N. nigricollis contains a PLA(2)-like anticoagulant, and defective clot retraction has been reported in vitro (Warrell, 1995).
    d) COBRAS - The venom contains long chain post-synaptic neurotoxins which are rich in enzymes including hyaluronidase phospholipase A(2) (Warrell, 1995).

References

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