Kill Billy; Volume 3

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    Kill Billy; Volume 3

    EMS calls in to the department and states they are en-route w/ an ETA of 5 minutes w/ an 8 yo M w/ no known PMHx in severe distress, no further history provided.

    3 minutes later an 8 yo M is wheeled into the department by EMS, the child is obtunded, diaphoretic, and has bluish discoloration of his extremities.  His face and lips appear swollen.

    Initial Vitals:

    T 98    HR  56     BP 54/34     R 6       O2 Sat 76% (on NRB)

    Patient is immediately moved to resus area, the leading physician assigns critical roles to individual team members including information gathering from EMS and any available family members, anesthesia and ENT consult and prepartion for possible difficult intubation w/ glideoscope and cric tray at bedside, and establishment of IV access.

    Patient continues to deteriorate, initial IV placed however after 2L NS the IV appeared infiltrated so it was removed, patient was given IM dose of Epi and an IO was placed on his RLE after his clothing was removed, anesthesia arrives and intubates the patient using 10mg Ketamine (reduced dose given state of shock) and 6.0 ET tube [4 + (age/4)].  Central line is placed and patient is started on Epinephrine drip, IV fluids, and given dose of Solumedrol.

    Repeat Vitals

    T 99   HR   132     BP 126/78     R 24 (vent)     O2 Sat 99% (100% O2 on vent)

     

    Breathe…

    On secondary survery after removal of clothing patient is noted to have swollen LLE, on further inspection two distinct puncture wounds are noted on his L calf approx 4 cm apart.  EMS reports they heard family members screaming at the park where patient was found that “he was bitten.”  A few minutes later the patient’s mother and family members arrive screaming “he was bit by a snake and he has a history of asthma and allergies.”  They are able to provide a picture of the snake taken by a bystander who witnessed the event and the ED team is able to identify the species.

    C-atrox-1-080710

    There are 4 types of venomous snakes native to the United States, w/ 20 sub-species living in different geographical areas, climates and habitats. The 4 types are: rattlesnake, copperhead, cottonmouth (or water moccasin), and coral snake. Of these, the rattlesnake is the most common and widespread throughout the U.S.  Approximately 8000 people every year are bitten by poisonous snakes which results in 5-20 deaths.

    The rattlesnake, cottonmouth or water moccasin, and copperhead belong to the Crotalinae sub-family and are also known as “pit vipers.”  They have similar triangular shaped heads and characteristic eliptical, cat-like pupils in their eyes. Pit vipers derive their name from small pits between their eyes and snout, which can sense heat and helps them hunt for warm blooded prey (like in the movie “Predator”).

    Coral snakes belong to the Elipad family and are best identified by their colorful banding.  Other non-venomous snakes such as the king snake have similar markings which led to the following rhyme for identification; “Red and yellow, [will] kill a fellow; red and black, venom lacks.”  Coral snakes discharge venom through grooves on two small, fixed anterior fangs.  The small size of these fangs makes it difficult but not impossible to seriously envenomate humans.  When biting, coral snakes tend to hold and chew in order to pass venom.

    In general, the toxins of coral snakes are more potent than pit vipers, however the apparatus for envenomation by coral snakes is less effective.  Copperheads are the least venomous of the pit vipers, while rattlesnakes are the most venomous.  In the U.S., Eastern and Western Diamondback Rattlesnakes (Crotalus atrax) account for the most deaths.

    Venom composition and toxicity are highly variable and depend on many factors including the species, age, and nutritional status of the snake. The toxins affect multiple organ systems including the cardiovascular, hematologic, respiratory, renal, and nervous systems.  Spread of venom from the site of injection is promoted by the enzymatic destruction of connective tissue.  Almost all snake venom contains hyaluronidase, an enzyme that ensures rapid diffusion of the venom.  Capillary permeability is increased by Crotalinae venom and manifests as local erythema and swelling. Capillary endothelium damage and hemolysis of red blood cells can lead to massive accumulation of fluid in the intracellular spaces leading to hypovolemic shock and hemoconcentration.  Significant local edema near the site of the snake bite can raise concerns about compartment pressures.  Non-surgical management versus fasciotomy is controversial in the setting of elevated compartment pressures.  Recent animal studies suggest that more aggressive use of antivenom is superior to fasciotomy to treat compartment syndrome.

    The combined procoagulant effect of the toxins can also mimic disseminated intravascular coagulopathy.  Coagulation factor and platelet replacement therapy should be reserved for patients experiencing life-threatening bleeding.  It is important to note that transfused platelets and coagulation factors in fresh frozen plasma are quickly inactivated by Crotalinae venom.

    Pit viper venom also attacks several crucial elements of the motor nervous system.  Components of venom inhibit presynaptic acetylcholine release, interfere w/ calcium binding on neuronal membranes, and irreversibly block the acetylcholine receptor at the post-synaptic neuromuscular junction.  Neurotoxicity initially manifests as eyelid ptosis, blurred or double vision, ophthalmoplegia, and facial paralysis.  Respiratory morbidity after snakebite is a result of fluid shift into the lungs as well as paralysis of respiratory muscles.

    Acute kidney injury following a pit viper bite occurs in 24-48 hours and requires dialysis in 1 in every 4 patients hospitalized.  The pathogenesis is related to rhabdomyolysis, renal vasoconstriction, direct tubular cell toxicity, and shock.

    After initial resuscitation and stabilization it is important to make appropriate arrangements to attain antivenom.  Antivenom administration with polyvalent Crotalinae ovine immune Fab (FabAV, Crofab, Protherics) is the mainstay for treatment of significant Crotalinae envenomation.  The clinical severity of the bite and not the presumed species of snake should drive the decision to use antivenom.  Maximum benefit is derived from administering antivenom within 6 hours of the snake bite.  Patients presenting w/ minimal and non-progressing swelling, pain, or ecchymosis frequently fully recover w/out FabAV treatment.  However, these patients warrant observation for 12-24 hours to assess for progression of toxicity.  Patients w/ symptoms of moderate or severe toxicity or w/ bite sites that present a possibility for airway obstruction from tissue swelling (bites to the neck or face), should receive FabAV.

    FabAV is a sheep derived immunoglobulin (IgG) designed to neutralize a broad spectrum of Crotalinae venom antigens. Administration and dosing of FabAV is predicated on the clinical severity of the pit viper bite.  The recommended initial dose of FabAV is 4 to 6 vials infused intravenously over an hour.  This initial dose can be doubled in patients presenting w/ signs of severe toxicity.  Repeat and maintenance dosing should be given dependent on the patient’s response and clinical course.  FabAV dosing is dependent on the amount of venom injected and toxicity of the patient and should NOT be adjusted for patient age or weight.  The limitations of FabAV include risk of immediate and delayed hypersensitivity reactions, coagulapathy refractory to antivenom treatment, and expense (approximately $1000 per vial).

    The vast majority of patients bitten by venomous North American snakes recover fully.  Death resulting from Crotalinae envenomation is unusual (<1%) with mortality associated w/ proximal bites, lack or inadequate antivenom treatment, or inadequate resuscitation of shock.

    It is important to note that there are numerous venomous exotic species in the U.S.  These will usually result in bites in domestic or black market settings.

    The patient was successfully resuscitated and transferred to the PICU, he was weaned off pressors on hospital day 2, he did not require hemodialysis and maintained normal renal function despite an initial CPK of 280,000, his coagulation studies normalized by hospital day 4, he did have a prolonged neurologic recovery and eventually required a tracheostomy however after extensive physical and occupational therapy he had near-total neurologic recovery and 6 months following the bite, the patient’s only sequelae were reduced olfactory acuity, ophthalmoplegia, and mild bulbar dysfunction.

    Special Thanks to Dr. Jenny Sanders for this Pearl.

     

     

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