eMedicine Specialties > Emergency Medicine > Environmental
Snake Envenomation, Brown
Updated: Jun 18, 2009
Introduction
Background
The brown snake, found in Australia, belongs to the family of Elapidae and contains the following species:
- Pseudonaja textilis (common brown snake, also known as eastern brown snake)
Pseudonaja textilis (eastern brown snake).
- Pseudonaja affinis (dugite)
- Pseudonaja nuchalis (western brown snake)
Pseudonaja nuchalis (western brown snake).
- Pseudonaja inframacula (peninsula brown snake)
- Pseudonaja ingrami (Ingram's brown snake)
- Pseudonaja guttata (speckled brown snake)
Pseudonaja guttata (speckled brown snake).
- Pseudonaja affinis tanneri (Tanner's brown snake)
- Pseudonaja modesta (ringed brown snake)
Pseudonaja modesta (ringed brown snake).
Envenomation by P textilis, P nuchalis, P guttata, and P affinis has been documented, but little information is available about the toxic effects of the other species.
All of these snakes occur mainly in inland floodplains with deeply fissured soils. The snakes are active during cooler parts of the day, such as early morning and late afternoon. They exist in 5 different colors, have a highly flexible head, and can squeeze into narrow places. They feed on small animals but also can grip large prey. They may bite humans above the knee by raising their head from the ground and assuming an "S" shape when striking. Unless provoked, they are thought to be reluctant to attack humans.
Most of the literature describing the brown snake consists of case studies of people accidentally bitten and their clinical course. They have less effective dentition than other elapids and may leave little evidence of a puncture wound; however, their venom is readily diffusible and can rapidly enter the circulation.
These snakes are among the most venomous in the world. The common brown snake produces the second most toxic venom known and is the most common cause of snakebite death in Australia. Common to these species' venom are neurotoxins and hemotoxins.
Pathophysiology
Brown snake envenomations are characterized by disseminated intravascular coagulation (DIC), paralysis, and cardiovascular depression. Other, less common, manifestations are conduction defects, thrombocytopenia, renal failure, and intracranial hematomas.
The coagulopathy is characterized by defibrination often accompanied by platelet counts within the reference range. The venom has the ability to convert prothrombin to thrombin and to significantly deplete factors V, VII, protein C, and plasminogen.
Cardiovascular depression may be caused by intravascular coagulation, or the venom may contain a primary myocardial depressant. The potent neurotoxins cause neurological symptoms soon after envenomation. One example is texilotoxin, a multimumeric polypeptide from the common brown snake. These neurotoxins can cause respiratory paralysis by blocking nicotinic acetylcholine receptors at the postsynaptic motor endplate and/or affect neurotransmitter release at presynaptic motor nerve endings. Convulsions may occur. Little or no myotoxicity is present.
Frequency
International
Pseudonaja species live mainly in Australia. About 3000 bites occur per year in Australia from all species of snakes, 500 of which require antivenin. The dugite brown snake may be found in the southwestern corner of Australia, in Western Australia and along the South Australian border. The speckled brown snake can be found from central Queensland to the eastern areas of the Northern Territory. Ingram's snake may be found around Barkly Tableland of the Northern Territory, and the ringed snake may be found in the arid regions of all the mainland states. The western snake may be found throughout Australia and the common brown snake in Queensland, New South Wales, and from Victoria to the southeast of South Australia.
Snakebites tend to occur more often in the warmer months reflecting increased snake activity as well as increased human outdoor activity. The predominance of the bites occur in the lower limb.
Mortality/Morbidity
Of all the cases of snakebites in Australia, only 2-3 fatalities occur per year. As many as 60% of fatalities from snake envenomations may be attributed to the brown snake. Early deaths (within hours) are thought to result from the venom's cardiotoxic effect as well as anaphylaxis to the venom. Delayed deaths appear to result from secondary complications, such as intracranial hemorrhage, from the venom's hemotoxins.
- Approximately 30% of brown snake bites cause systemic envenomation; 60% of bites with systemic involvement produce altered mental status, loss of consciousness, or seizures; and approximately 33% of these present with defibrination syndrome.
- The subcutaneous median lethal dose (LD50) for the common brown snake in 18- to 21-gram mice is 0.053 mg/kg. The average yield of a venom milking is 4 mg, and the highest recorded yield is 67 mg. The LD50 for other species of brown snake for 18- to 21-gram mice are as follows: 0.47 mg/kg for P nuchalis, 0.66 mg/kg for P affinis, and 0.36 mg/kg for P guttata.
Sex
Males are bitten more frequently than females, presumably because of the greater popularity among males of owning and handling snakes as well as greater risk of occupational and recreational exposure.
Age
Young children tend to become critically ill sooner than adults because of their smaller body weight and tendency to receive multiple bites.
Clinical
History
The bites of Pseudonaja frequently occur on the extremities, mostly on the fingers and feet, because collectors handle them or people accidentally step on them. Unfortunately, unless the patient gives a history of being bitten by a snake, local clues to the evidence of a bite may be subtle or absent because brown snake bites cause little or no local swelling or pain. After giving a history of being bitten by a brown-colored snake, the patient may complain of neurological symptoms within an hour; the symptomatology within a few hours may manifest with a coagulopathy and signs of diaphragmatic paralysis and cardiovascular compromise. The following symptoms may be present:
- Headache
- Nausea and vomiting
- Weakness
- Photophobia
- Irritability
- Diplopia
- Altered mental status
- Dyspnea
- Epistaxis
- Gingival bleeding
- Hematemesis
- Hematochezia
- Oliguria
- Dysphagia
Physical
- Fang marks
- Little to no local edema or erythema
- Bronchospasm
- Ptosis
- Trismus
- Seizures
- Respiratory muscle weakness to apnea
- Cyanosis
- Paralysis
- Hypotension
- Tachycardia or bradycardia
- Cardiac arrest
- Epistaxis
- Hematemesis
- Hematochezia
- Petechia
- Purpura
Differential Diagnoses
| CBRNE - Botulism | Snake Envenomations, Moccasins |
| Disseminated Intravascular Coagulation | Snake Envenomations, Mohave Rattle |
| Snake Envenomations, Cobra | Snake Envenomations, Rattle |
| Snake Envenomations, Coral | Snake Envenomations, Sea |
Workup
Laboratory Studies
- Complete blood count (CBC)
- Prothrombin time (PT)/activated partial thromboplastin time (aPTT)
- Fibrinogen - Severe envenomation associated with afibrinogenemia (<0.3 g/L)
- Fibrin degradation products
- D-dimer
- Electrolytes
- Blood urea nitrogen (BUN) and creatinine
- Urinalysis
- Arterial blood gas (ABG)
- Type and crossmatch for packed red blood cells (PRBCs), fresh frozen plasma (FFP), and platelets
- CSL commercial snake venom qualitative detection kit
- Enzyme immunoassays (EIAs) for quantifying venom concentration - A small study of 27 brown snake envenomed patients showed the median venom concentration was 20 ng/mL. The EIA test is able to detect down to concentrations of 3 ng/mL.[1 ]
Imaging Studies
- Chest x-ray
- Computed tomography (CT) scan of the head if intracranial hemorrhage is suspected
Other Tests
- Electrocardiogram (ECG)
Treatment
Prehospital Care
The goals of prehospital treatment include implementing basic and advanced life support algorithms and ensuring an adequate airway. Consider immobilization of the cervical spine if trauma to the cervical spine is suspected.
- Assess if breathing is adequate. Consider endotracheal intubation if indicated.
- Provide fluid support for hypotension, as well as cardiopulmonary resuscitation (CPR), and administer chemical adjuncts for cardiovascular compromise if necessary.
- Remove patient from further potential harm and institute local wound care. This includes immobilizing the affected limb and maintaining it at the level of the heart. Do not tamper with the bite and avoid potentially harmful procedures such as mouth suction, local application of electrical shock or ice, or cauterization or incision of the bite. Possible complications of these techniques may result in ischemia, gangrene, damage to nerves, congestion, edema, or increased bleeding.
- An elastic bandage placed at the bite site and wrapped proximally to include the entire limb may delay absorption of the neurotoxin into the systemic circulation. Care should be taken not to remove the compression bandage until antivenin therapy is instituted. The bandage should not compromise arterial circulation.
- Attempt to identify the snake, but avoid protracted attempts to locate or capture the snake. If the snake is from a research center or zoo, send specific antivenin with the patient if possible.
Emergency Department Care
- Stabilization of airway, breathing, and circulation
- Oxygen
- Avoid nasotracheal intubation to prevent epistaxis.
- Intravenous access, cardiac monitoring, and continuous pulse oximetry
- Administer antivenin therapy as soon as possible if any signs of systemic involvement are present because the antivenin may reverse coagulopathy. Skin testing before administration of antivenin is not recommended because it delays treatment of this very toxic venom. Furthermore, larger initial doses should be considered if severe envenomation from multiple bites is evident. The dose of antivenom for children should not be reduced since the amount of venom injected by the snake is independent of the victim's size. The improvement of fibrinogen levels, coagulation parameters, and the patient's condition function as surrogate indicators of venom neutralization. A recent study suggests that 5 ampules will adequately treat two thirds of the patients with severe envenomation, but 10 ampules will adequately treat 89% of these patients.[2 ]
- Before the antivenin is given, premedicate the patient with an antihistamine, and continue the antihistamine for 5 days to prevent anaphylaxis.
- Administer corticosteroids if any history of previous serum sickness or allergic reaction to the antivenin is present or for administration of large doses of antivenin.
- Pregnancy is not a contraindication to giving antivenin.
- Edrophonium, neostigmine, and atropine may be given to temporarily reverse respiratory weakness until antivenin is obtained, but it should not delay necessary intubation. Administering FFP, cryoprecipitate, or platelets may be necessary if DIC occurs.
- The most common reasons for antivenom administration were coagulopathy, neurotoxicity, myotoxicity, and nonspecific systemic effects.[3 ]
- Hypersensitivity reaction to antivenom occurred in 25% cases, with nearly half the hypersensitivity cases considered to be anaphylaxis to the antivenom.[3 ]
- Swab the bite for analysis with a CSL Venom Detection Kit, if available.
- Tetanus prophylaxis
Consultations
- Regional Poison Control Center
- Toxicologist or snake expert
- Local zoos
Medication
The antidote for systemic envenomations by the brown snake is the equine-derived antivenin. In a study of 35 patients with severe brown snake envenomation, two thirds of the cases were neutralized with 5 ampules and 89% were neutralized with 10 ampules.[2 ] As with all equine-derived antivenins, anaphylaxis should be anticipated and treated if any allergic reactions occur. Pretreatment with antihistamines and corticosteroids should be included.
Hypotension should be treated with isotonic crystalloid infusions and vasopressors if blood pressure is refractory to fluids alone.
Tetanus toxoid should be given when indicated.
Cholinesterase inhibitors, such as edrophonium and neostigmine, may be given to palliate the neurological sequelae of the venom but should not replace definitive airway control.
Antivenin
Gives passive immunity to the venom and should be administered immediately if any signs of systemic toxicity are present.
Antivenin
According to the Antivenin Index, the monovalent form is not carried in the US but may be found in Australia (Commonwealth Serum Laboratories, Melbourne, Australia). The polyvalent antivenin may be obtained at the Bronx Zoo, but a local zoo may be contacted.
Skin testing before antivenin administration is not recommended because it may sensitize the individual to future antivenin use and will delay the administration of the antivenin. Antihistamines and subcutaneous epinephrine should be administered (if no contraindications are present) before giving the antivenin.
1 U neutralizes 0.01 mg venom in vitro.
Dosing
Adult
Dilute 1000 U in a 1:10 solution IV over 30 min and repeat according to clinical response
Pediatric
Administer as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity; may give in severe envenomation despite hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Because of presence of horse serum, agents for emergency treatment of anaphylaxis should be available
Antihistamines
H1 and H2 blockers should be given to prevent immune mediated responses and may be continued for an additional 5 days or for as long as symptoms persist.
Diphenhydramine (Benadryl)
For symptomatic relief of symptoms caused by release of histamine in allergic reactions.
Dosing
Adult
Pretreatment: 1 mg/kg IV; not to exceed 100 mg
Serum sickness: 1 mg/kg PO prn or 25-50 mg PO q6-8h prn; not to exceed 400 mg/d
Pediatric
Pretreatment: 1 mg/kg IV; not to exceed 100 mg
Serum sickness: 1 mg/kg PO prn, 12.5-25 mg PO tid/qid, 5 mg/kg/d PO, or 150 mg/m2/d; not to exceed 300 mg/d
Interactions
Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patient taking medications that can cause disulfiramlike reactions
Contraindications
Documented hypersensitivity; MAOIs
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction
Cimetidine (Tagamet)
H2 antagonist that, when combined with an H1 type, may be useful in treating itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis that do not respond to H1 antagonists alone. Use this medication in addition to H1 antihistamines.
Dosing
Adult
300 mg IV initially; followed by administration on an outpatient basis 300 mg PO q6h for 2 d, or for as long as clinically indicated; use in addition to H1 antihistamines
Pediatric
25-30 mg/kg/d IV divided qid or 5-10 mg/kg IV in addition to H1 antihistamines; not to exceed 300 mg/dose q6h prn
Interactions
Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Elderly persons may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur
Chlorpheniramine (Chlor-Trimeton)
Competes with histamine or H1-receptor sites on effector cells in blood vessels and respiratory tract.
Dosing
Adult
4 mg PO q4-6h or 8-12 mg SR q8-12h; not to exceed 24 mg/d
10-20 mg IV/IM/SC initially; not to exceed 40 mg/d
Pediatric
<2 years: Not established
2-6 years: 1 mg PO divided q4-6h; not to exceed 6 mg/d
6-12 years: 2 mg PO q4-6h or 8 mg SR PO hs; not to exceed 12 mg/d
>12 years: Administer as in adults
Interactions
CNS toxicity increases with coadministration of other CNS depressants, tricyclic antidepressants, MAOIs, and phenothiazines
Contraindications
Documented hypersensitivity; asthma attacks; narrow-angle glaucoma; symptomatic prostate hypertrophy, bladder-neck obstruction, stenosing peptic ulcer
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
May cause significant confusional symptoms; not for administration to premature or full-term neonates
Corticosteroids
Should be employed when evidence of an allergy-mediated event is present. However, onset of action is approximately 4-6 h and has limited benefit in the initial acute treatment of the rapidly deteriorating anaphylactic patient. Nonetheless, corticosteroids may benefit patients with persistent bronchospasm or hypotension.
Methylprednisolone (Solu-Medrol)
Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Dosing
Adult
Loading dose: 125-250 mg IV
Maintenance dose: 0.5-1 mg/kg/dose IV q6h for up to 5 d
Pediatric
Loading dose: 2 mg/kg IV
Maintenance dose: 0.5-1 mg/kg/dose IV q6h for up to 5 d
Interactions
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics
Contraindications
Documented hypersensitivity; viral, fungal, or tubercular skin infections
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Prednisone (Deltasone, Orasone, Sterapred)
Used for the treatment of a variety of diseases including serum sickness in the outpatient setting. Prednisone is inactive and must be metabolized to the active metabolite prednisolone. The conversion may be impaired in patients with liver disease.
Dosing
Adult
0.05-2 mg/kg/d PO divided bid/qid; not to exceed 80 mg/d or divided bid/qid; taper over 2 wk as symptoms resolve
Pediatric
4-5 mg/m2/d PO or 1-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve
Interactions
Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Contraindications
Documented hypersensitivity; peptic ulcer disease, hepatic dysfunction, GI disease; viral infection, connective tissue infections, fungal or tubercular skin infections
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Bronchodilators
These agents have combined alpha- and beta-adrenergic agonist action and are the agents of first choice in the treatment of anaphylaxis.
An additional option in the management of persistent bronchospasm may be anticholinergic agents. These agents block the action of acetylcholine at parasympathetic sites in bronchial smooth muscle.
Epinephrine (Adrenalin, EpiPen)
DOC for treating anaphylactoid reactions. The alpha-agonist effects of epinephrine increase peripheral vascular resistance and reverse peripheral vasodilatation, vascular permeability, and systemic hypotension. Conversely, the beta-agonist effects produce bronchodilatation, positive inotropic and chronotropic cardiac activity, and result in an increased production of intracellular cAMP.
Dosing
Adult
0.01 mL/kg IM/SC of 1:1000 solution initially; not to exceed 0.5 mL of 1:1000 solution (0.5 mg)
Fraction of total dose (0.1 to 0.2 mL) at site of antigenic exposure, if accessible
Severe anaphylaxis (eg, laryngeal edema, respiratory failure, or shock): 10 mL of 1:100,000 dilution of aqueous epinephrine IV over 10 min; if no improvement, titrate to effect (continuous infusion of 4 mcg/mL starting at 1 mcg/min; increase to 4 mcg/min prn)
Pediatric
0.1 mcg/kg/min SC q15min for 2 doses then q4h with increments of 0.1 mcg/kg/min prn; not to exceed 1.5 mcg/kg/min
Interactions
Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
Contraindications
Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; during labor (may delay second stage of labor)
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in elderly persons, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
Albuterol (Ventolin, Proventil)
Beta-agonist useful in the treatment of bronchospasm that is refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta 2-receptors and has little effect on cardiac muscle contractility
Dosing
Adult
Oral: 2-4 mg PO tid/qid; not to exceed 32 mg/d
Inhaler: 1-2 puffs q4-6h; not to exceed 12 puffs/d
Nebulizer: Dilute 0.5 mL (2.5 mg) of 0.5% inhalation in 2.5 mL of sterile saline or water and nebulize; may repeat q4-6h prn
Pediatric
Oral:
<2 years: Not established
2-6 years: 0.1-0.2 mg/kg/dose PO tid; not to exceed 12 mg/d
6-12 years: 2 mg/dose PO tid/qid; not to exceed 24 mg/d
>12 years: Administer as in adults
Inhaler:
<12 years: 1-2 puffs qid with tube spacer
>12 years: Administer inhalant as in adults
Nebulizer:
<5 years: Dilute 0.25-0.5 mL (1.25-2.5 mg) of 0.5% inhalation solution in 1-2.5 mL NS and administer via nebulizer q4-6h
>5 years: Administer via nebulizer as in adults
Interactions
Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders
Theophylline (Aminophylline, Theo-Dur, Slo-bid)
Potentiates exogenous catecholamines. Stimulates endogenous catecholamine release and diaphragmatic muscular relaxation, which in turn stimulates bronchodilation.
For bronchodilation, near toxic (>20 mg/dL) levels are usually required.
Dosing
Adult
5.6 mg/kg loading dose (based on aminophylline) IV over 20 min followed by maintenance infusion of 0.1-1.1 mg/kg/h
Pediatric
<6 weeks: Not established
6 weeks to 6 months: 0.5 mg/kg/h loading dose IV in first 12 h (based on aminophylline) followed by maintenance infusion of 12 mg/kg/d thereafter; may administer continuous infusion by dividing total daily dose by 24 h
6 months to 1 year: 0.6-0.7 mg/kg/h loading dose IV in first 12 h followed by maintenance infusion of 15 mg/kg/d; may administer as continuous infusion, as above
>1 year: Administer as in adults
Interactions
Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects of theophylline; theophylline effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon
Contraindications
Documented hypersensitivity; uncontrolled arrhythmias; peptic ulcers; hyperthyroidism; uncontrolled seizure disorders
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in peptic ulcer, hypertension, tachyarrhythmias, hyperthyroidism, and compromised cardiac function; do not inject IV solution >25 mg/min; patients diagnosed with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearance
Ipratropium (Atrovent)
Chemically related to atropine. Has antisecretory properties and, when applied locally, inhibits secretions from serous and seromucous glands lining the nasal mucosa.
Dosing
Adult
Nebulizer: 1 U dose vial (500 mcg) tid/qid
MDI: 2 puffs qid; not to exceed 12 puffs/d
Pediatric
Nebulizer: 250 mcg tid
MDI: 1-2 puffs tid; not to exceed 6 puffs/d
Interactions
Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol increases effects of ipratropium
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Not indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder-neck obstruction
Cholinesterase inhibitors
May be useful in reversing neurological complications of the venom; however, they should not be a substitute for airway management.
Edrophonium (Enlon, Reversol, Tensilon)
Short active cholinesterase inhibitor that inhibits the destruction of acetylcholine by acetylcholinesterase and may palliate weakness. Facilitates transmission of impulses across myoneural junction and results in increased cholinergic responses (eg, miosis, increased tonus of intestinal and skeletal muscles, bronchial and ureteral constriction, bradycardia, and increased salivary and sweat gland secretions).
Usually administered IV, but, if this is not possible, IM/SC route may be used.
Dosing
Adult
Test dose: 2 mg IV over 15-30 sec; if no response seen, administer 8 mg, 45 sec later; test dose may be repeated after 30 min or, after treating with atropine, administer 10 mg as slow IV push
10 mg IM initially; if no cholinergic reaction occurs, administer 2 mg 30 min later to rule out false-negative reaction
Pediatric
<35 kg: 0.025 mg/kg/dose IV or, after pretreatment with atropine, 5 mg slow IV push
>35 kg: Administer as in adults
Interactions
Atropine, nondepolarizing muscle relaxants, procainamide, and quinidine may decrease effects of edrophonium; succinylcholine, digoxin, IV acetazolamide, neostigmine, and physostigmine may increase effects
Contraindications
Documented hypersensitivity; GI or GU obstruction
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in bronchial asthma and those receiving a cardiac glycoside; may cause cholinergic crisis, which may be fatal; IV atropine should be readily available for treatment of cholinergic reactions
Neostigmine (Prostigmin)
Longer acting cholinesterase inhibitor that can be used when edrophonium is ineffective. Inhibits destruction of acetylcholine by acetylcholinesterase, which facilitates transmission of impulses across myoneural junction.
Dosing
Adult
0.5 mg slow IV push q20min; not to exceed 5 mg
Pediatric
Not established; suggested dose is 0.025-0.08 mg/kg/dose IV/IM once
Interactions
Atropine antagonizes muscarinic effects of neostigmine; effects of neuromuscular agents are increased
Contraindications
Documented hypersensitivity; GI or GU obstruction
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in epilepsy, asthma, bradycardia, hyperthyroidism, cardiac arrhythmias, or peptic ulcer; anticholinesterase insensitivity can develop for brief or prolonged periods
Immune Globulin
Consists of administration of immunoglobulin pooled from serum of immunized subjects.
Tetanus immune globulin (Hyper-Tet)
Used for passive immunization of any person with a wound that might be contaminated with tetanus spores.
Dosing
Adult
Prophylaxis: 250-500 U IM in different anatomical site than tetanus toxoid administration
Clinical tetanus: 3000-10,000 U IM
Pediatric
Prophylaxis: 250 U IM in different anatomical site than tetanus toxoid administration
Clinical tetanus: Administer as in adults
Interactions
None reported
Contraindications
Since antibodies in globulin preparation may interfere with immune response to vaccination, do not administer within 3 mo of live virus immune globulin administration; may be necessary to revaccinate persons who received immune globulin shortly after live virus vaccination
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Persons with isolated immunoglobulin A (IgA) deficiency have potential for developing antibodies to IgA and could have anaphylactic reactions to subsequent administration of blood products that contain IgA; do not perform skin testing since intradermal injection of concentrated gamma globulin may cause localized area of inflammation and can be misinterpreted, causing the medication to be withheld from a patient not allergic to this material; true allergic responses to human gamma globulin given in prescribed IM manner are extremely rare; do not admix with other medications since usually incompatible
Follow-up
Further Inpatient Care
- Admit any person who has been bitten by a brown snake to an intensive care unit.
- Because of the potential lethality of this toxin and since symptoms may be delayed, observe asymptomatic patients in an ICU setting for at least 24 hours.
- Corticosteroids and antihistamines should be continued for at least 5 days.
Further Outpatient Care
- Warn patient of potential serum sickness.
- Instruct patient to return if serum sickness develops.
- Follow up patient closely.
Transfer
- Transfer patient to facility capable of intensive care monitoring; and, in case patient develops renal failure and hemodialysis, arrange for transportation to facility with dialysis capabilities.
Deterrence/Prevention
- Professional snake keepers should wear protective gloves when handling all brown snakes.
- The appropriate antivenin must be readily available.
- Wear long pants and covered shoes when traveling to areas inhabited by venomous snakes.
- Avoid approaching or handling snakes, even dead snakes.
- Travel with a companion in case any disability from a snakebite occurs, and be aware of the locations of the nearest medical facilities.
Complications
- Seizures
- Intracranial hemorrhage
- Respiratory compromise
- Weakness
- Bleeding diathesis
- Secondary infections
- Anaphylactoid and serum sickness reactions
Prognosis
- If no systemic symptoms are present, recovery is expected.
- Since the development of antivenin and the use of compression bandages, fatalities from brown snake bites have become rare. However, in spite of prompt medical care and antivenin administration, the potency of the venom has produced fatalities.
Patient Education
- The public should be aware of the danger of being bitten by a brown snake so vigilance may be exercised when traveling or when owning such a snake.
- Because of the potency of the snake venom, the public should not delay seeking medical care.
- For excellent patient education resources, visit eMedicine's Bites and Stings Center. Also, see eMedicine's patient education article Snakebite.
Miscellaneous
Medicolegal Pitfalls
- Measuring the severity of the envenomation by the appearance of the bite is problematic. Brown snakes tend to leave little damage to the skin at the site of penetration.
- Know when to transfer a patient. If admitting facilities do not have the necessary capabilities, such as ICU monitoring or hemodialysis (when needed), then transfer the patient to a facility that can accommodate the patient's needs.
- Patients who have been bitten by a brown snake and are asymptomatic should not be discharged; they should be admitted to an ICU for monitoring and observation because of the potential lethality of this envenomation.
- If possible, consent should be obtained before antivenin administration because of the risks of anaphylaxis.
Multimedia
Media file 1: Pseudonaja guttata (speckled brown snake).
Media file 2: Pseudonaja textilis (eastern brown snake).
Media file 3: Pseudonaja modesta (ringed brown snake).
Media file 4: Pseudonaja nuchalis (western brown snake).
References
O'Leary MA, Isbister GK, Schneider JJ, Brown SG, Currie BJ. Enzyme immunoassays in brown snake (Pseudonaja spp.) envenoming: detecting venom, antivenom and venom-antivenom complexes. Toxicon. Jul 2006;48(1):4-11. [Medline].
Yeung JM, Little M, Murray LM, Jelinek GA, Daly FF. Antivenom dosing in 35 patients with severe brown snake (Pseudonaja) envenoming in Western Australia over 10 years. Med J Aust. Dec 6-20 2004;181(11-12):703-5. [Medline].
Isbister GK, Brown SG, MacDonald E, White J, Currie BJ. Current use of Australian snake antivenoms and frequency of immediate-type hypersensitivity reactions and anaphylaxis. Med J Aust. Apr 21 2008;188(8):473-6. [Medline].
Brimacombe J, Murray A. Envenomation by Ingram's Brown snake (Pseudonaja ingrami). Anaesth Intensive Care. Apr 1995;23(2):231-3. [Medline].
Broad AJ, Sutherland SK, Coulter AR. The lethality in mice of dangerous Australian and other snake venom. Toxicon. 1979;17(6):661-4. [Medline].
Buckley N, Dawson AH. Unusual results of brown snake envenomation. Med J Aust. Jun 21 1993;158(12):866-8. [Medline].
Currie BJ. Snakebite in tropical Australia: a prospective study in the "Top End" of the Northern Territory. Med J Aust. Dec 6-20 2004;181(11-12):693-7. [Medline].
Henderson A, Baldwin LN, May C. Fatal brown snake (Pseudonaja textilis) envenomation despite the use of antivenom. Med J Aust. May 17 1993;158(10):709-10. [Medline].
Hodgson WC. Pharmacological action of Australian animal venoms. Clin Exp Pharmacol Physiol. Jan 1997;24(1):10-7. [Medline].
Isbister GK, O'Leary MA, Schneider JJ, Brown SG, Currie BJ; ASP Investigators. Efficacy of antivenom against the procoagulant effect of Australian brown snake (Pseudonaja sp.) venom: in vivo and in vitro studies. Toxicon. Jan 2007;49(1):57-67. [Medline].
Masci PP, Mirtschin PJ, Nias TN, et al. Brown snakes (Pseudonaja genus): venom yields, prothrombin activator neutralization and implications affecting antivenom usage. Anaesth Intensive Care. Jun 1998;26(3):276-81. [Medline].
Munro JG, Pearn JH. Snake bite in children: a five year population study from South-East Queensland. Aust Paediatr J. Dec 1978;14(4):248-53. [Medline].
Pantanowitz L, Guidozzi F. Management of snake and spider bite in pregnancy. Obstet Gynecol Surv. Oct 1996;51(10):615-20. [Medline].
Ripamonti C, De Conno F, Boffi R, et al. Can somatostatin be administered in association with morphine in advanced cancer patients with pain?. Ann Oncol. Aug 1998;9(8):921-3. [Medline].
Schapel GJ, Utley D, Wilson GC. Envenomation by the Australian common brown snake--Pseudonaja (Demansia) textilis textilis. Med J Aust. Jan 16 1971;1(3):142-4. [Medline].
Sprivulis P, Jelinek GA. Fatal intracranial haematomas in two patients with Brown snake envenomation. Med J Aust. Feb 20 1995;162(4):215-6. [Medline].
Sutherland SK. Concern over the choice of antivenom for "false king brown snake" bites and a plea for a name change. Med J Aust. Feb 15 1999;170(4):187. [Medline].
Sutherland SK. Venomous Creatures of Australia. Oxford University Press; 1981.
Sutherland SK, Leonard RL. Snakebite deaths in Australia 1992-1994 and a management update. Med J Aust. Dec 4-18 1995;163(11-12):616-8. [Medline].
Tibballs J, Sutherland S, Kerr S. Studies on Australian snake venoms. Part 1: The haemodynamic effects of brown snake (Pseudonaja) species in the dog. Anaesth Intensive Care. Nov 1989;17(4):466-9. [Medline].
Tibballs J, Sutherland SK, Kerr S. Studies on Australian snake venoms, Part II: The haematological effects of brown snake (Pseudonaja) species in the dog. Anaesth Intensive Care. Aug 1991;19(3):338-42. [Medline].
Walter FG, Bilden EF, Gibly RL. Envenomations. Crit Care Clin. Apr 1999;15(2):353-86, ix. [Medline].
White J. Envenoming and antivenom use in Australia. Toxicon. Nov 1998;36(11):1483-92. [Medline].
Keywords
snake envenomation, brown snake, snake bite, snakebite, snake venom, antivenin, equine-derived antivenin, neurotoxin, hemotoxin, Pseudonaja textilis, common brown snake, Pseudonaja affinis, dugite, Pseudonaja nuchalis, western brown snake, Pseudonaja inframacula, peninsula brown snake, Pseudonaja ingrami, Ingram's brown snake, Pseudonaja guttata, speckled brown snake, Pseudonaja affinis tanneri, Tanner's brown snake, Pseudonaja modesta, ringed brown snake
Contributor Information and Disclosures
Author
David Cheng, MD, Assistant Professor of Emergency Medicine, Associate Emergency Medicine Residency Director, Associate Medical Director of Emergency Services, University of Arkansas Medical Sciences
David Cheng, MD is a member of the following medical societies: American College of Emergency Physicians, American Heart Association, Council of Emergency Medicine Residency Directors, International Society for Mountain Medicine, National Association of EMS Physicians, Society for Academic Emergency Medicine, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.
Medical Editor
Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Associate Professor, Department of Emergency Medicine, University of Texas-Houston
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.
Pharmacy Editor
John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.
Managing Editor
David Eitel, MD, MBA, Associate Professor, Department of Emergency Medicine, York Hospital
David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
CME Editor
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Chief Editor
Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting