management of common poisoning in ICU

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Management of common poisoning in I.C.U.:

Management of common poisoning in I.C.U. Dr Bikram Gupta MD Anaesthesia PDCC in Critical Care

Agents commonly responsible for acute Poisoning:

Agents commonly responsible for acute Poisoning Pesticides Household chemicals Industrial Chemicals Pharmaceuticals Plant Poisonings & AnimalToxins Organophosphate Carbamates , Organochlorines , Synth . pyrethroids , Rodenticides , Herbicides, Fumigants, Unlabelled powders sold by hawkers Celphos Acids, Bleach, Grain preservatives, Drain cleaners, Naphthalene balls, CuSO 4 , Cosmetics Irritant gases like Chlorine and Ammonia, Acid fumes like Oleum , MethHb forming agents such as Nitrobenzene Sedatives and hypnotics (mostly benzo-diazepines / opioids ) alcohol, antidepressants, antihistaminics , Acetaminophen, salicylates Datura , Argemone (Epidemic dropsy) Plants with digitalis like effect Snake bites , scorpion bites 2

4 situations:

3 4 situations History of ingestion(mostly) History of ingestion History of ingestion ? Poisoning poison is known and treatment is known poison is known but the physician is not very confident about the treatment poison is unknown pt is unconscious does not need any discussion Ask the Poison Center First attend to the patient then poison First attend to the patient then poison Resuscitate the patient without contaminating yourself Resuscitate the patient without contaminating yourself Location and occupation of the patient can be a pointer to the poison Location and occupation of the patient can be a pointer to the poison

General- management:

General- management provision of supportive care prevention of poison absorption enhancement of elimination of poison administration of antidotes

Key steps in the initial m/m of the poisoned patient:

Key steps in the initial m/m of the poisoned patient 1.Secure the ABC Airway – intubate if necessary Breathing- oxygenate/ventilate/monitor Spo 2 Circulation- place IV/fluids or inotropes for decreased BP/ECG 2.Is the patient confused, somnolent, or comatose If yes – A. check blood glucose or give 1 amp D50W IV B. Thiamine 100 mg IV C. Naloxone 0.4-2.0 mg IV If no – A. Brief history and physical examination B. Collect critical labs: - serum electrolytes and glucose - liver and renal profiles - CBC - serum levels- EtOH,acetaminophen,salicylates - urine drug screen with TCA 5

Key steps in the initial m/m of the poisoned patient:

Key steps in the initial m/m of the poisoned patient If specific toxin(s) identified or highly suspected? Yes - give antidote/therapy or contact poison control If patient improving- 1. continue supportive care 2. psychiatry consult No/ or pt not improving – Review available data - Detailed H&P - Consider coingestion (s) - Toxicology consult - Consider nonpoisoning etiology of symptoms 6

History:

History Pill bottles Alcohol Drug history including access Suicide note

What is a Toxidrome?:

What is a Toxidrome ? Several clinically recognizable features, s/s, phenomena or characteristics which often occur together, so that presence of one feature alerts the physician to the others Narrows the differential diagnosis to a specific class of poisons 8

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Toxidrome Features Drugs/Toxins Drug Treatment “DUMBELS ” D - Diarrhoea U - U rinary frequency , M - miosis , B - bradycardia , bronchorrhoea bronchoconstriction , E - emesis, L - lacrimation S – salivation Organophosphates Carbamates Physostigmine Pilocarpine Atropine Oximes for Organophosphates The Cholinergic Toxidrome 9

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The Anticholinergic Toxidrome Toxidrome Features Drug Toxin Drug Treatment Hot as Hare Dry as a bone Red as a beet Mad as a hatter Altered mental status Sedation Mydriasis Tachycardia Fever Dry skin Dry mucous membranes Decreased bowel sounds Flushing Urinary Retention Antihistaminics Atropine Baclofen Benztropine Datura TCA Phenothiazines Scopolamine For life threatening events use Physostigmine * Not indicated for TCA as it may worsen conduction disturbances *not available in India 10

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Sedative Hypnotic Toxidrome Features Drug Toxin Drug Treatment Slurred speech Confusion Stupor Coma Apnoea Anticonvulsants Antipsychotics Barbiturates Benzodiazepines Ethanol Opiates Naloxone Flumazenil Urinary alkalinization for Phenobarbital 11

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Narcotic Toxidrome Features Drug Toxin Drug Treatment Altered Mental Status Slow shallow breaths Miosis Bradycardia Hypotesion Hypothermia Decreased Bowel Sounds Dextromethorphan Opiates Pentazocine Propoxyphene Naloxone 12

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Extrapyramidal Toxidrome Features Drug Toxin Drug Treatment Rigidity Tremor Opisthotonus Trimus Hyperreflexia Choreoathetosis Haloperidol Phenothiazines Risperidone Olanzapine Diphenhydramine Benztropine 13

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Serotonin Toxidrome Features Drug Toxin Drug Treatment Irritability Hyperreflexia Flushing Diarrhea Diaphoresis Fever Trismus Tremor Myclonus Fluoxetine Paroxetine Sertraline Trazodone Clomipramine Benzodiazepines Withdrawal of drug Cyprohepatidine (?) 14

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Solvent Toxidrome Features Drug Toxin Drug Treatment Lethargy Confusion Headache Restlessness Incoordination Depersonalization Hydrocarbons Toluene Acetone Naphthalene Chlorinated Hydrocarbons Withdrawal of toxin Avoid catecholamines 15

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Epileptogenic Features Drug Toxin Drug Treatment Tremors Hyperreflexia Tonic clonic seizures Hyperthermia May mimic stimulant patterns Organochlorine pesticides like Endosulfan , Lindane Isoniazid Camphor Strychnine Phencylidine Cocaine Xanthines Antiseizure medications Pyridoxine for Isoniazid Avoid phenytoin for theophylline Induced seizures 16

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Hallucinogenic Toxidrome Features Drug Toxin Drug Treatment Hallucinations Psychosis Panic Fever Mydriasis Hyperthermia Synesthesia * Amphetamines Cannabinoids Cocaine LSD Phencyclidine (May present with miosis ) Benzodiazepines * Synesthesia :One sensory experience described in terms of another sensory experience. 17

Limitations of diagnosis based on toxidromes :

Limitations of diagnosis based on toxidromes Toxidromes are most clinically useful when the patient has been exposed to a single drug . Many toxidromes have several overlapping features . For example, anticholinergic findings are highly similar to sympathomimetic findings, with one exception being the effects on sweat glands: anticholinergic agents produce warm, flushed dry skin, while sympathomimetic produce diaphoresis. 18

Limitations of diagnosis based on toxidromes:

Limitations of diagnosis based on toxidromes Toxidrome findings may also be affected by individual variability, comorbid conditions, and co-ingestants. For example, tachycardia associated with sympathomimetic or anticholinergic toxidromes may be absent in a patient who is concurrently taking ᵝ blockers. When multiple drugs have been ingested, conflicting clinical effects may negate each other and cloud the clinical picture. 19

Preventing absorption:

Preventing absorption Gastric lavage Not in unconscious patient unless intubated (risk aspiration) Flexible tube is inserted through the nose into the stomach Stomach contents are then suctioned via the tube A solution of saline is injected into the tube Recommended for up to 2 hrs in TCA & up to 4hrs in Salicylate OD Induced Vomiting Ipecac - Not routinely recommended Risk of aspiration

Preventing absorption:

Preventing absorption Activated charcoal Adsorbs toxic substances or irritants, thus inhibiting GI absorption Addition of sorbitol → laxative effect Oral: 25-100 g as a single dose

Enhancement of elimination:

Enhancement of elimination Diuresis and manipulation of Urinary pH The goal of diuresis is a urine flow of 3 to 8 ml per kg per hour and that of alkalinisation is a urine PH of 7.5 or greater. An alkaline diuresis solution can be prepared by adding three amp of sod bicarbonate to dextrose 5% in water such that the final solution is nearly isotonic. 22

Pesticide Poisoning:

Pesticide Poisoning Commonest cause of Self-poisoning or Deliberate self-harm (DSH) Accidental poisoning : may occur in children Occupational poisoning : In farmers during spraying or pesticide formulators Routes of exposure: Most pesticides can be absorbed by all routes including dermal route and inhalation route, though toxicity and mortality are highest when ingested for self-harm as usually persons take a large amount 23

Insecticides:

Insecticides Organophosphates e.g.malathion, chlorpyriphos, monocrotophos, dimethoate, phorate, quinalphos, ethion, Fenthion Carbamates: Propoxur, Carbaryl Organochlorines: DDT, BHC, Lindane, Endosulfan Synthetic pyrethroids: Cypermethrin, Deltamethrin, Fenvalerate Neonicotinoids: Imidacloprid 24

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Organophosphorus pesticides inhibit the enzyme acetylcholinesterase in synapses and on RBC membranes, and butyrylcholinesterase in plasma. Although acute butyrylcholinesterase inhibition does not seem to cause clinical features, acetylcholinesterase inhibition results in accumulation of acetylcholine and overstimulation of acetylcholine receptors in synapses of the ANS, CNS, and N-M junctions. 25

Acute Cholinergic Crisis:

Acute Cholinergic Crisis Clinical features depend on the type of receptors stimulated by acetylcholine and their location Muscarinic receptors (parasympathetic) : diarrhoea, urinary frequency, miosis, bradycardia, bronchorrhoea and bronchoconstriction, emesis, lacrimation, salivation (DUMBELS), hypotension & cardiac arrhythmias 26

Acute Cholinergic Crisis:

Nicotinic (sympathetic) Tachycardia Mydriasis Hypertension Sweating Nicotinic (N-M Jn) Muscular weakness Paralysis Fasciculation 27 Acute Cholinergic Crisis Tacchycardia can also be caused by hypovolaemia , hypoxia, previous doses of atropine, and alcohol withdrawal Nicotinic & Muscarinic (CNS) Confusion Agitation Coma Respiratory failure

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Result of centrally or peripherally mediated mechanisms. Occurs during the acute cholinergic crisis (type I paralysis) or during an apparent recovery phase (intermediate syndrome, or type II paralysis). Weakness of neck flexors is an early sign of significant muscle weakness. Respiratory failure in OP poisoning 28

Causes of High Case Fatality:

Causes of High Case Fatality High toxicity Difficulty in transporting patients over long distances from rural areas Lack of treatment facilities at PHC & even district hospitals Lack of training in management of pesticide poisoning 29

Diagnosis :

Diagnosis Ask the relatives. Clinical picture, smell of pesticides or solvents Typical s/s When in doubt quantification of plasma and RBC butyrylcholinesterase or acetylcholinesterase is helpful. Cholinesterase ≤ 80% of the lower reference range is probably indicative. In very severe poisonings, may be zero Source: Eddleston et al;Lancet online August, 2007 30

Diagnosis :

Variable onset : Most patients develop severe toxicity within six hours . Patients remaining asymptomatic for 12 hours after ingestion are unlikely to develop major clinical toxicity Exceptions exist with some highly lipophilic organophosphorus compounds (most importantly fenthion), which produce only subtle cholinergic features initially then progressive muscle weakness, including respiratory failure requiring intubation Source: Managing acute organophosphorus pesticide poisoning. Darren M Roberts, Cynthia K Aaron; BMJ,2007 Diagnosis 31

Diagnosis :

The intermediate syndrome is diagnosed by clinical findings associated with a reproducible EMG-nerve conduction study using repeated submaximal tetanic nerve stimulation and measuring compound muscle action potentials. Diagnosis 32

Principles of Treatment:

Principles of Treatment ABC, Oxygen Muscarinic antagonist (Atropine) Acetylcholinesterase reactivator (Oxime) Gastric decontamination only after patient has been fully resuscitated and stabilized Careful observation for changing atropine needs, respiratory function and recurrence of cholinergic crisis 33

Initial Stabilization:

Initial Stabilization Medical emergency Start two I/V lines. Give I/V saline to keep SBP ≥ 80 mm of Hg Patient should be placed in left lateral position with neck extended Watch out for convulsions and give I/V diazepam Record a baseline GCS 34

Gastric lavage:

Gastric lavage Gastric lavage is useful if done within 1-2 hours First aspirate and then do a lavage with 200-300 ml of tap water Comatosed patients should be intubated prior to lavage with a cuffed endotracheal tube Do not carry out lavage in an unwilling conscious patient 35

Skin Decontamination:

Skin Decontamination If there is suspicion of dermal exposure, remove all clothes and wash the skin thoroughly with soap and plenty of warm water Give special attention to skin folds, hair, nails and areas like axillae and groins Use adequate personal protection like gloves and apron 36

Antimuscarinic agents:

Antimuscarinic agents Atropine Before giving atropine, record pulse rate, BP, pupil size, presence of sweat and auscultatory findings Give 1-3 mg bolus of atropine depending on severity and then loading dose of PAM After 5 minutes of atropine, check all parameters again and if no improvement has taken place double the dose of atropine Continue to review every 5 minutes and doubling doses of atropine Once the patient is stable start an infusion of atropine with 10-20% of the total dose needed to stabilize the patient 37

Antimuscarinic agents:

Antimuscarinic agents Target end-points : Clear chest on auscultation with no wheeze HR ≥ 80 per minute Pupils no longer pinpoint Dry axillae SBP ≥ 80 mm Hg 38

Aim of Atropine Therapy::

Aim of Atropine Therapy: No need to aim for a heart rate of 120-140/min. Tachycardia can be caused by hypoxia, agitation, alcohol withdrawal, pneumonia, hypovolemia and fast oxime administration & are not a C/I for atropine Glycopyrrolate : In patients with atropine toxicity, but it does not counteract CNS effects of OPs 39

Glycopyrrolate:

Glycopyrrolate Similar outcomes using continuous infusion. Ampoules of 7.5 mg can be added to 200 ml of saline and infusion can be titrated to drying of secretions. Atropine can be added as a bolus if heart rate goes below 60/min. It may be used where the secretions are difficult to control. Or when it is difficult to differentiate altered level of consciousness due to atropine toxicity or relapse of OP poisoning 40

Why Oximes have been shown to be ineffective in some studies ?:

Why Oximes have been shown to be ineffective in some studies ? Reasons could be Insufficient dose or duration High dose of poison and rapid reinhibition of reactivated enzyme Ageing of inhibited AChE Poor affinity for the particular OP-AChE complex 41

Dose of Oximes:

Pralidoxime in the blood might required to be higher to antagonise the toxic effects of many pesticides. Thus a bolus-loading infusion followed by a maintenance infusion might be the best regimen . On this basis, the WHO has proposed that patients be given about 30 mg/kg pralidoxime salt as a loading dose, followed by an infusion of at least 8 mg/kg/h (in a 50 kg south Asian patient this is roughly equivalent to 1–2 g bolus followed by 0·5 g/h). Dose of Oximes 42

Oximes:

Oximes Pralidoxime is the only oxime available in India. Dose: Give 2gm I/V over 20-30 minutes and then an infusion of 0.5-1gm/hour till atropine is not needed for 12-24 hours and the patient has been extubated. Under ideal condition, serum samples can be assayed for acetyl cholinesterase reactability and this can be used to guide oxime therapy. Rapid infusion may cause vomiting, tachycardia and diastolic hypertension 43

Benzodiazepines:

Benzodiazepines Patients poisoned with OP frequently develop agitated delirium. Cause: Pesticide itself, atropine toxicity, hypoxia, alcohol, and medical complications. Diazepam is first line of treatment for seizures with OP poisoning though seizures are uncommon in well oxygenated patients 44

Carbamate Pesticides:

Carbamate Pesticides Commonest is Baygon which is used as a household pesticide Clinical picture similar to OP poisoning but CNS toxicity is less Plasma and RBC cholinesterase may be depressed for short time but quickly recover Prognosis good 45

Carbamate Pesticides:

Carbamate Pesticides Atropine, Role of PAM is not clear Complications mostly due to aspiration pneumonitis (while doing gastric lavage). Many carbamate formulations are made in petroleum product base. Pulmonary oedema and poor oxygenation may not respond to Atropine and such cases have to be managed as cases of ARDS Carbamates used for agricultural purpose such as Carbofuran, Aldicarb and Methomyl are highly toxic 46

Organochlorine pesticides:

Organochlorine pesticides Examples are DDT, BHC, Lindane, Endosulfan DDT and BHC already discontinued except for public health programs Endosulfan is one of the most commonly used agricultural pesticides Patient will present with convulsions No lab test available for diagnosis Treat with Diazepam, Phenobarbital or other anticonvulsants 47

Fumigants: Aluminium phosphide (AlP): :

Fumigants: Aluminium phosphide ( AlP ): It is available as 3 gm tablets known as Celphos, Alphos, Quickphos It is used for storage of wheat On coming in contact with moist air or gastric contents, releases Phosphine (PH 3 ) gas It is highly toxic and even ½ tablet can be fatal There is no antidote 48

Mechanism of action:

Mechanism of action After ingestion, AlP releases phosphine gas in the presence of HCl in the stomach, which is rapidly absorbed throughout the gastrointestinal tract, leading to systemic toxic effects involving the heart, lung, kidney, liver with manifestation of serious cardiac arrhythmias, intractable shock, acidosis and pulmonary edema. 49

Aluminium phosphide:

Aluminium phosphide Signs and Symptoms : Epigastric pain, retrosternal burning, vomitus smells of decaying fish Severe hypotension or shock is the cardinal feature & is often unresponsive to vasopressors Cardiac arrhythmias and metabolic acidosis Liver damage, Renal failure and ARDS may develop after 24-48 hours simple silver nitrate-impregnated paper test on gastric content or on breath. 50

management:

management Earliest intervention No delay in transport ABG analysis Elective intubation with controlled ventilation Gastric lavage Arterial line/Central line If hypotension then fluid and vasopressors 2 D echo- dobutamine/levosimendon Arrythmias-antiarrythmic drug Mgso 4 - 1g stat, then 1 g every hour for the next 2 h and then 1–1.5 g every 6 h for 5–7 days, if survive NAC – 6 gram over 24 hours 51

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Poisoning with Sedative /Hypnotic drugs:

Poisoning with Sedative /Hypnotic drugs Can be easily detected by urine drug screens Relatively safe drugs unless ingested with other sedatives like alcohol or TCAs The elderly are more sensitive to the CNS depressant effect and those suffering from COPD are more susceptible to respiratory effects. 53

Treatment of Benzodiazepine Overdose: :

Treatment of Benzodiazepine Overdose: Close observation and supportive care  Secure airway and adequate ventilation Flumazenil is a specific antidote , but is very short acting. Should not be routinely used. Flumazenil may precipitate seizures in case TCA are also taken with BZD Induction of acute withdrawal in those suffering benzodiazepine dependence may also trigger seizures or pulmonary aspiration. 54

Flumazenil:

Flumazenil The initial dose is 0.2 mg, and this can be repeated at 1-6 minutes intervals,if necessary,to a cumulative dose of 1 mg. The initial bolus dose of flumazenil is often followed by a continuous infusion of 0.3-0.4 mg/hr. 55

OPIOIDS OVERDOSE – M/M:

OPIOIDS OVERDOSE – M/M Naloxone For depressed sensorium but no respiratory sensorium- initial bolus dose –0.4 mg IV. This can be repeated in 2 minutes, if necessary. Total dose of 0.8 mg should be effective. 56

OPIOIDS OVERDOSE – M/M:

OPIOIDS OVERDOSE – M/M Naloxone For depressed sensorium but no respiratory sensorium- initial bolus dose –0.4 mg IV. This can be repeated in 2 minutes, if necessary. Total dose of 0.8 mg should be effective. For resp. depression- ( hypercapnia, resp rate < 12 breaths/minute)- bolus dose 2 mg IV, if no response in 2-3 minutes- 4 mg bolus then 10 mg bolus then 15 mg bolus then stop and reassess. 57

Paracetamol (Lethal dose:7.5-10 gm):

Paracetamol (Lethal dose:7.5-10 gm ) Mechanism of toxicity At therapeutic doses, 90% of acetaminophen is converted to non-toxic glucuronide and sulfate conjugates and 5% is excreted in the urine unchanged. The other 5% is oxidized in the liver by P450 enzymes to NAPQI(N-acetyl-p- benzoquinoneimine ). At therapeutic amounts glutathione binds with NAPQI to form a non-toxic conjugate 58

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In overdose, glucuronide and sulfate conjugation becomes saturated and an increased proportion of NAPQI is formed . Glutathione levels are depleted. NAPQI remains in its toxic form in the liver causing hepatocellular damage 59

Four phases:

Four phases PHASE 1 (0.5 to 24 hours): Few s/s : malaise, anorexia, nausea, vomiting, pallor PHASE 2 (24 to 72 hours): Right upper quadrant pain may appear indicating hepatic damage with associated raised hepatic transaminases. INR increases. Renal function may begin to deteriorate PHASE 3 (72 to 96 hours): Continuing hepatic centrilobular necrosis with associated coagulation defects, hypoglycemia, metabolic acidosis, and jaundice. Renal failure and cardiac complications frequently occur. Hepatic encephalopathy and death may ensue. PHASE 4 (4 days to 2 week): If phase 3 is survived complete resolution of hepatic and renal function is usual. 60

Treatment :

Treatment Decontamination with activated charcoal (1g/kg BW) is effective within 4 hours . Rapid measurement of plasma acetaminophen (paracetamol) level is necessary. N-acetylcysteine is a life-saving antidote, and while its efficacy declines after approximately eight hours of the acetaminophen (paracetamol) ingestion, it should be administered to all patients with a potentially toxic overdose, regardless of time 61

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Antidote :

Antidote N-acetylcysteine (20%) Administer: 150 mg/kg in 200 mL diluent IV D5 or NS over 60 minutes Followed by 50 mg/kg in 500 mL diluent IV over 4 hours Followed by 100 mg/kg in 1,000 mL diluent IV over 16 hours Total dose : 300 mg/kg over 21 hrs 63

Antidote Endpoint:

Antidote Endpoint At the end of the infusion regimen the patient’s hepatic transaminases, INR and S.creat. should be determined. If these are normal, or normalizing, further N-acetylcysteine is not required. If not, the infusion must continue at a rate of 100 mg/kg in 1,000 mL diluent over 16 hours, until hepatic transaminase levels and INR decline and renal function improves. Supportive care 64

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Signs/Symptoms and Potential Treatments Cobra Krait Russell Viper Saw Scaled Viper Other Vipers Local Tissue Damage/pain YES NO YES YES YES Ptosis/ Neurotoxicity YES YES YES NO NO Coagulation NO NO YES YES YES Renal Problems NO NO YES NO YES

Local symptoms and signs:

Local symptoms and signs • Fang marks • Local pain • Local bleeding • Bruising • Lymphangitis • Lymph node enlargement • Inflammation (swelling, redness, heat) • Blistering • Local infection, abscess formation • Necrosis

Generalised Symptoms and Signs:

Generalised Symptoms and Signs General Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness, prostration Cardiovascular (Viperidae) Visual disturbances, dizziness, faintness, collapse, shock, hypotension, cardiac arrhythmias, pulmonary oedema, conjunctiva oedema

CONTD…:

Bleeding and clotting disorders (Viperidae) Bleeding from recent wounds (including fang marks ,venepunctures etc) and old partly-healed wounds Spontaneous systemic bleeding – from gums, epistaxis Bleeding into the tears Haemoptysis, haematemesis, rectal bleeding or melaena, Haematuria, vaginal bleeding Bleeding into the skin and mucosae (petechiae,purpura,ecchymoses) Intracranial haemorrhage CONTD…

CONTD…:

Renal (Viperidae, sea snakes) Loin pain, haematuria, haemoglobinuria myoglobinuria, oliguria/anuria Symptoms and signs of uraemia Endocrine (acute pituitary/adrenal insufficiency) (Russell’s viper) CONTD…

CONTD…:

CONTD… Neurological (elapidae, russell’s viper) Drowsiness Paraesthesiae Abnormalities of taste and smell “Heavy” eyelids, ptosis External ophthalmoplegia Paralysis of facial muscles and other muscles innervated by the cranial nerves Aphonia Difficulty in swallowing secretions Respiratory and generalised flaccid paralysis Skeletal muscle breakdown (sea snakes, russell’s viper) Generalised pain Stiffness and Tenderness of Muscles, Trismus Myoglobinuria Hyperkalaemia Cardiac arrest Acute renal failure

Coagulation abnormalities are due directly to snake venom interference with the coagulation cascade:

Coagulation abnormalities are due directly to snake venom interference with the coagulation cascade

20 minute whole blood clotting test (20WBCT) :

20 minute whole blood clotting test (20WBCT) This very useful and informative bedside test requires very little skill and only one piece of apparatus - a new, clean, dry, glass vessel (tube or bottle). • Place a few ml of freshly sampled venous blood in a small glass vessel • Leave undisturbed for 20 minutes at ambient temperature • If the blood is still liquid (unclotted) and runs out, the patient has hypofibrinogenaemia (“incoagulable blood”) as a result of venom-induced consumption coagulopathy • In the South East Asian region, incoagulable blood is diagnostic of a viper bite and rules out an elapid bite • Warning! If the vessel used for the test is not made of ordinary glass, or if it has been used before and cleaned with detergent, its wall may not stimulate clotting of the blood sample in the usual way and test will be invalid

Treatment……..:

Treatment…….. CroFab is a venom-specific fragment of IgG, which binds and neutralizes Venom toxin, helping to remove the toxin from the target tissue and Eliminate it from the body.

Dosing: Adult Crotalid envenomation:

Dosing: Adult Crotalid envenomation Initial dose : 4-6 vials, dependent upon patient response. Treatment should begin within 6 hours of snakebite; monitor for 1 hour following infusion. Repeat with an additional 4-6 vials if control is not achieved with initial dose. Continue to treat with 4-6 vial doses until complete arrest of local manifestations, coagulation tests and systemic signs are normal. Monitor closely.

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Maintenance dose : Once control is achieved, administer 2 vials every 6 hours for up to 18 hours. Optimal dosing past 18 hours has not been established; however, treatment may be continued if deemed necessary based on the patient’s condition.

Reconstitution::

Reconstitution: Reconstitute each vial with 10 mL sterile water for injection and mix by gentle swirling. Further dilute total dose in 250 ml NS: use within 4 hours of reconstitution. Note : Reconstitution with 25 mL sterile water for infusion and hand rolling/inverting may result in shorter dissolution times and allow for more rapid administration.

Administration: I.V.:

Administration: I.V. Administer I.V. over 60 minutes at a rate of 25-50 mL/hour for the first 10 minutes. If no allergic reaction is observed, increase rate to 250 mL/hour. Monitor closely. Epinephrine and diphenhydramine should be available during the infusion. Decreasing the rate of infusion may help control some adverse effects.

Contraindications::

Contraindications: Hypersensitivity to any component of the formulation (including papaya or papain), unless benefits outweigh the risks and appropriate management for anaphylaxis is readily available.

Adverse Reactions::

Adverse Reactions: Cardiovascular: Hypotension Central nervous system: Chills Dermatologic: Pruritus, rash, urticaria Respiratory: Asthma, cough, dyspnea, wheezing Miscellaneous: Anaphylaxis, anaphylactoid reaction, hypersensitivity reactions (5% to 19%), serum sickness (5%)

Disease-related concerns::

Disease-related concerns: CroFab should be used within 4-6 hours of snakebite to prevent clinical deterioration and development of coagulation abnormalities. These are due directly to snake venom interference with the coagulation cascade. Recurrent coagulopathy occurs in approximately 50% of patients and may persist for 1-2 weeks or more. Repeat dosing may be indicated. Patients should be monitored for at least 1 week and evaluated for other pre-existing conditions associated with bleeding disorders. In severe envenomations , a decrease in platelets may occur, lasting hours to several days. Blood products are generally ineffective as they are rapidly consumed by circulating venom.

Monitoring::

Monitoring: Parameters: Vital signs, CBC, platelet count, prothrombin time, aPTT, fibrinogen levels, fibrin split products, clot retraction, bleeding and coagulation times, BUN, electrolytes, bilirubin, size of bite area (repeat every 15-30 minutes); intake and output, signs and symptoms of anaphylaxis/allergy. CBC, platelet counts, and clotting studies are evaluated at 6-hour intervals until patient is stable.

Size of bite area marked every 15 minutes:

Size of bite area marked every 15 minutes

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THANK YOU 84

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