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Snake Bite
Background
The brown snake, found in Australia, belongs to the family of Elapidae and
contains the following species: - Pseudonaja guttata (speckled brown snake, shown in
image below)
Pseudonaja guttata (speckled brown snake). - Pseudonaja textilis (common brown snake, also
known as eastern brown snake, shown in image below)
Pseudonaja textilis (eastern brown snake). - Pseudonaja affinis (dugite)
- Pseudonaja nuchalis (western brown snake, shown in
image below)
Pseudonaja nuchalis (western brown snake). - Pseudonaja inframacula (peninsula brown snake)
- Pseudonaja ingrami (Ingram's brown snake)
- Pseudonaja affinis tanneri (Tanner's brown snake)
- Pseudonaja modesta (ringed brown snake, shown in
image below)
Pseudonaja modesta (ringed brown snake).
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.
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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.
Epidemiology
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.
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
Differentials
- CBRNE - Botulism
- Disseminated Intravascular Coagulation
- Snake Envenomations, Cobra
- Snake Envenomations, Coral
- Snake Envenomations, Moccasins
- Snake Envenomations, Mohave Rattle
- Snake Envenomations, Rattle
- Snake Envenomations, Sea
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)
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.
Next Section: Emergency Department Care
Emergency Department Care
*
Stabilization of
airway, breathing, and circulation
*
Oxygen
*
Avoid
nasotracheal intubation to prevent epistaxis.
*
Intravenous
access, cardiac monitoring, and continuous pulse oximetry
*
Tetanus
prophylaxis
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.
In the treatment of venom-induced consumptive coagulopathy,
administration of FFP and/or cryoprecipitate is controversial; it has been
associated with faster resolution of coagulopathy but no change in outcomes.[3]
The most common reasons for antivenom administration were
coagulopathy, neurotoxicity, myotoxicity, and nonspecific systemic effects.[4]
Hypersensitivity reaction to antivenom occurred in 25%
cases, with nearly half the hypersensitivity cases considered to be anaphylaxis
to the antivenom.[4]
Swab the bite for analysis with a CSL Venom Detection Kit,
if available.
Previous
Next Section: Emergency Department Care
Consultations
*
Regional Poison
Control Center
*
Toxicologist or
snake expert
*
Local zoos
Medication
Summary
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
Class
Summary
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.
Antihistamines
Class
Summary
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.
For symptomatic relief of symptoms
caused by release of histamine in allergic reactions.
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.
Competes with histamine or
H1-receptor sites on effector cells in blood vessels and respiratory tract.
Corticosteroids
Class
Summary
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.
Decreases inflammation by
suppressing the migration of polymorphonuclear leukocytes and reversing
increased capillary permeability.
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.
Bronchodilators
Class
Summary
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.
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.
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
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.
Chemically related to atropine. Has
antisecretory properties and, when applied locally, inhibits secretions from
serous and seromucous glands lining the nasal mucosa.
Cholinesterase
inhibitors
Class
Summary
May be useful in reversing
neurological complications of the venom; however, they should not be a
substitute for airway management.
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.
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