Snake pits

Snake bits Introduced by D. Abdallah Abd El Rahman Ali MohammediaCLASSIFICATION

EPIDEMIOLOGY

MORFOLOGY OF SNAKE

VENOM SYMPTOMS OFB ENVINOMATION

MANEGMENT

SNEKE belong to the fallowing family viperidae elapidae hydrophiidae atractaspididae(most of them are non venomous) colupridae (most of them are nonvenomous)

Bites rate are highest in temperate and tropical Regions where population subsist by manual agriculture Epidemiology

Snake venom apparatus consist of bilateral venom gland situated below and behind the eye and connected by duct to hallow anterior maxillary teeth In viprid teeth are long mobile fang retracted against the roof of the mouthIn elapid and sea snake the fang are smaller and fixed in erect position Snake anatomy

significant envenomation occur in 50% of all venomous snakebitesDifferentiation venomous from non venomous can be difficult Color pattern is notoriously misleading in identifying venomous snake biteFact about snakeAre complex mixture of enzyme ,low molecular weight polypeptide, metal ion haemorrhagins promote vascular bleeding and cause both local and systolic bleeding proteolytic enzymes cause local tissue necrosis myocardial depressant factors reduce cardiac output neurotoxin pre or post synapticaly to inhibit peripheral nerve impulses Most snake venom have multisystem effect on their victims

Venoms most viper and some elapid has necrotizing venoms and present with the fallowing : local manifestation progressive local swelling pain ecchymosis hemorrhagic bullae and serum filed vesicle(over hours or days)Systemic manifestationChange in tasteMouth numbnessMuscle fasciculationTachycardia or bradycardiaHypotension Pulmonary edemaHemorrhage from any anatomical siteRenal dysfunctionClinical manifestation

most elapid have nurotoxic venom that cause neurological dysfunction in the form of fallowing: onset vary from minute to hours early finding include cranial nerve weakness (ptosis ) and altered mental status

sever envenomation result in paralysis include muscle of respiration which lead to death from respiratory failure and aspiration sea snake envenomation usually cause the fallowing : onset delayed for hours local pain MyalgiasRhabdomyolysisneurotoxicity

important point to remember don't attempt to kill the snake after you have bittenDont handle with even killed snake Dont consult traditional healers Avoid incising wound , applying suction to the bite as they are ineffectiveAvoid tourniquet use as it can lead to amputation and loss of function Pressure immobilization should be use only if the offending snake is reliably identified and known to be primarily neurotoxicmanagement

Stabilize airway ,breathing and circulationInstitute monitoring (cardiac and pulse oximeter)Establish two large bore IV line If the pt hypotensive so pollus NS (20-40ML/KG) if hypotension persist then considered 5% albumin (10-20 ml/kg)ivTake rapid history and perfume rapid examination and put the affected limb at the level of the heartMeasure circumferences of bitten extremity every 15 minute until swelling stabilizedIdentify offending reptile if possibleTake blood for (CBC,PT ,INR,PTT,FIBRINOGEN LEVEL,BG,RFT)AND do UG (20 minute whole blood clotting test can be don) repeated 6 hourly after antivenom administration

management

Determine the severity of envenomation Non: fang mark onlyMild: local finding only(pain ,ecchemosis,nonprogressive swelling)Moderet:prgressive swelling systemic sign or symptoms Sever: respiratory distress ,neurological dysfunction and/ or cardiovascular instability)Administer antivenom as indicatedNon or mild: nonModerate :4-6 vialsSever:6vialsMix reconstituted vials in 250ml NS give it iv over 1 hour( be in close attendance)Here you can give prophylactic anti histamine

management

If acute reaction to antivenome occur then:Stop infusionStandard dose epinephrine im ,antihistamine iv and glucocorticoidWhen reaction controlled restart antivenome with further dilutionThen monitor clinical status over 1 hImproved :hospital admissionProgress or not improved :repeat the dose.Pain management: paracetamole or narcotic (avoid aspirin and NSAIDs)Tetanus immunization as needProphylactic antibiotic is no necessary unless prehospital care include incision or mouth suction

managementBlood product and coagulation factor rarely needed if required should be given after anti venom administrationAdmit to hospital (if no evidence of envenoimation monitor for 8 h before discharge)Monitor for evidence of intra compartment pressureWound care (dry dressing )and aseptic debridement of necrotic tissue if coagulation restored Begin physical therapy Warn the pt at discharge about possibility of recurrent caagulopathy and symptoms and sign of delayed serum sickness

managementIf any evidence of neurological deficit it harder to reverse with antivenomGive atropine 0.6 mg iv Fallow by edrophonium 10 mg iv or neostigmine 1.5-2 mg imIf improved at 5 minute continue neostigmine 0.5 mg every 30 min as needed with atropine infusion 0.6 mg over 8 hMonitor for aspiration risk and secure air way with endotracheal intubation as needed

managementRenal failure in mostly is reversible(acute tubular necrosis ) and should be evaluated by nephrologists and refer the pt for peritoneal dialysis or haemodialysis as needed , rarely bilateral cortical necrosis may need renal transplantation

managementIs an IgG molecule isolated from serum of hoarse or sheep when it developed due to injection of venom to the animal blood May be mono specific or poly specific It bind up circulatory venom before they attach to target tissue You should no the species covered by antivenom It must be specific to for offending snake If antivenom does not contain antibody to that snake venom component it will be of no value and may lead to unnecessary complication The efficacy of antivenom in prevention of tissue damage by necrotizing venom is limited

antivenom