1. 2 Drugs & Chemicals Poisoning Poisoning By Dr. Jamshidi.

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Drugs & Chemicals Drugs & Chemicals

PoisoningPoisoning

By Dr. JamshidiBy Dr. Jamshidi

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Management of Management of overdoseoverdose

and and poisoning poisoning

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General- evaluationGeneral- evaluation

Rcognition of poisoningRcognition of poisoning

Identification of agents involved Identification of agents involved

Assessment of severity Assessment of severity

Prediction of toxicity Prediction of toxicity

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General- managementGeneral- management

provision of supportive careprovision of supportive care

prevention of poison absorptionprevention of poison absorption

Enhancement of elimination of Enhancement of elimination of

poisonpoison

Administration of antidotes Administration of antidotes

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Supportive careSupportive care

A: A: First, the airway should be cleared First, the airway should be cleared of vomitus or any other obstruction and of vomitus or any other obstruction and an oral airway or endotracheal tube an oral airway or endotracheal tube inserted if needed.inserted if needed.

B: B: Breathing should be assessed by Breathing should be assessed by observation and oximetry and, if in observation and oximetry and, if in doubt by measuring arterial blood doubt by measuring arterial blood gases patients with respiratory gases patients with respiratory insufficiency should be intubated and insufficiency should be intubated and mechanically ventilatedmechanically ventilated

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• C:C: Circulation should be assessed by continuous Circulation should be assessed by continuous monitoring of:monitoring of:

• - pulse rate- pulse rate• - blood pressure- blood pressure• -urinary output-urinary output

• An An intravenousintravenous line should be placed and blood line should be placed and blood drawn fro serum glucose and other routine drawn fro serum glucose and other routine determinationsdeterminations

• Dextrose to treat hypoglycemia (0.5gm/kg)Dextrose to treat hypoglycemia (0.5gm/kg)

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Vital signs, mental status, and pupil size Vital signs, mental status, and pupil size

Pulse oximetry, cardiac monitoring, ECGPulse oximetry, cardiac monitoring, ECG

Protect airwayProtect airway

Intravenous access Intravenous access

cervical immobilization if suspect traumacervical immobilization if suspect trauma

Rule out hypoglycaemiaRule out hypoglycaemia

Naloxone for suspected opiate poisoningNaloxone for suspected opiate poisoning

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HistoryHistory

Pill bottlesPill bottles AlcoholAlcohol Drug history including accessDrug history including access Remember OTC drugsRemember OTC drugs Suicide noteSuicide note National Poisons Information National Poisons Information

Centre (09694)Centre (09694)

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ExaminationsExaminations Drug Physiologic excitation :Drug Physiologic excitation : anticholinergicanticholinergic sympathomimeticsympathomimetic central hallucinogenic agentscentral hallucinogenic agents drug withdrawaldrug withdrawal

Physiologic depressionPhysiologic depression cholinergic (parasympathomimetic)cholinergic (parasympathomimetic) sympatholyticsympatholytic opiate, or sedative-hypnotic agents, or alcohols opiate, or sedative-hypnotic agents, or alcohols

Mixed state –Mixed state – polydrugs, polydrugs, hypoglycemic agents, tricyclic hypoglycemic agents, tricyclic

antidepressants, salicylates, cyanideantidepressants, salicylates, cyanide

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Drug detectionDrug detection

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Drug levelsDrug levels

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Preventing absorptionPreventing absorption

Gastric lavageGastric lavage Not in unconscious patient unless intubated (risk Not in unconscious patient unless intubated (risk

aspiration)aspiration)

Flexible tube is inserted through the nose into the Flexible tube is inserted through the nose into the

stomach stomach

Stomach contents are then suctioned via the tubeStomach contents are then suctioned via the tube

A solution of saline is injected into the tube A solution of saline is injected into the tube

Recommended for up to 2 hrs in TCA & up to 4hrs in Recommended for up to 2 hrs in TCA & up to 4hrs in

Salicylate ODSalicylate OD

Induced VomitingInduced Vomiting Ipecac - Not routinely recommended Ipecac - Not routinely recommended Risk of aspirationRisk of aspiration

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CONTRAINDICATION CONTRAINDICATION OF EMESISOF EMESIS

Corrosives and volatile poisonsCorrosives and volatile poisons Comatose patientsComatose patients Heart disease patientsHeart disease patients Pregnant womenPregnant women Kerosene : may cause Kerosene : may cause

aspiration pneumoniaaspiration pneumonia Convulsant patientsConvulsant patients

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Activated charcoalActivated charcoal Adsorbs toxic substances or irritants, thus Adsorbs toxic substances or irritants, thus

inhibiting GI absorption inhibiting GI absorption

Addition of sorbitol Addition of sorbitol →→laxative effectlaxative effect

Oral: 25-100 g as a single dose Oral: 25-100 g as a single dose Repetitive doses useful to enhance the Repetitive doses useful to enhance the

elimination of certain drugs:elimination of certain drugs: -theophylline-theophylline -phenobarbital-phenobarbital - carbamazepine- carbamazepine - aspirin- aspirin -sustained-release products-sustained-release products

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not effective for:not effective for:- cyanide- cyanide-mineral acids-mineral acids-caustic alkalis-caustic alkalis- organic solvents- organic solvents-iron, ethanol, methanol poisoning, -iron, ethanol, methanol poisoning, lithium lithium

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Elimination of poisonsElimination of poisons

Renal eliminationRenal elimination Medication to stimulate urination or Medication to stimulate urination or

defecation may be given to try to flush the defecation may be given to try to flush the excess drug out of the body fasterexcess drug out of the body faster

Forced alkaline diuresisForced alkaline diuresis Infusion of large amount of NS+NAHCO3Infusion of large amount of NS+NAHCO3 Used to eliminate acidic drug that mainly Used to eliminate acidic drug that mainly

excreted by the kidney eg salicylatesexcreted by the kidney eg salicylates CAUTIONSCAUTIONS Serious fluid and electrolytes disturbance Serious fluid and electrolytes disturbance

may occurmay occur Need expert monitoringNeed expert monitoring

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Elimination of poisonsElimination of poisons

Hemodialysis or haemoperfusionHemodialysis or haemoperfusion: : Reserved for severe poisoning Reserved for severe poisoning

Drug should be dialyzable i.e. protein Drug should be dialyzable i.e. protein bound with low volume of distributionbound with low volume of distribution

may also be used temporarily or as may also be used temporarily or as long term if the kidneys are damaged long term if the kidneys are damaged due to the overdose. due to the overdose.

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HemoperfusionHemoperfusion

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Antidotes Antidotes

Does an antidote exist?Does an antidote exist?

Does actual or predicted severity Does actual or predicted severity of poisoning warrant its use?of poisoning warrant its use?

Do expected benefits of therapy Do expected benefits of therapy outweigh its associated risk?outweigh its associated risk?

Are there contraindications? Are there contraindications?

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Specific overdosesSpecific overdoses

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OpiatesOpiates

Opiat poisoningOpiat poisoning Antidote – naloxoneAntidote – naloxone MoA: Pure opioid antagonist MoA: Pure opioid antagonist

competes and displaces narcotics competes and displaces narcotics at opioid receptor sites at opioid receptor sites

I.V. (preferred), I.M., I.V. (preferred), I.M., intratracheal, SubQ: 0.4-2 mg intratracheal, SubQ: 0.4-2 mg every 2-3 minutes as needed every 2-3 minutes as needed

Lower doses in opiate dependenceLower doses in opiate dependence

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OpiatesOpiates

Elimination half-life of naloxone is Elimination half-life of naloxone is only 60 to 90 minutes only 60 to 90 minutes

Repeated administration/infusion Repeated administration/infusion may be necessarymay be necessary

Side EffectsSide Effects BP changes; arrhythmias; BP changes; arrhythmias;

seizures; seizures; withdrawal syndromewithdrawal syndrome

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BenzodiazepinesBenzodiazepines

Benzodiazepine poisoning Benzodiazepine poisoning

Antidote – flumazenilAntidote – flumazenil MoA: Benzodiazepine antagonist MoA: Benzodiazepine antagonist IV administration 0.2 mg over 15 sec to max IV administration 0.2 mg over 15 sec to max

3mg3mg S/E : arrhythmias; convulsionsS/E : arrhythmias; convulsions C/I concomitant TCAD; status epilepticusC/I concomitant TCAD; status epilepticus Should not be used for making the diagnosisShould not be used for making the diagnosis Benzodiazepines may be masking/protecting Benzodiazepines may be masking/protecting

against other drug effectsagainst other drug effects

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Tricyclic Tricyclic antidepressantsantidepressants PHARMACOLOGY — PHARMACOLOGY — TCAs have several important cellular effects, including TCAs have several important cellular effects, including

inhibition of:inhibition of:

-Presynaptic neurotransmitter reuptake-Presynaptic neurotransmitter reuptake

-Cardiac fast sodium channels -Cardiac fast sodium channels

-Central and peripheral muscarinic acetylcholine -Central and peripheral muscarinic acetylcholine receptorsreceptors

-Peripheral alpha-1 adrenergic receptors -Peripheral alpha-1 adrenergic receptors

-Histamine (H1) receptors -Histamine (H1) receptors

-CNS GABA-A receptors -CNS GABA-A receptors

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TCAD overdoseTCAD overdoseclinical featuresclinical features

Arrhythmias Arrhythmias

- widening of PR, QRS, and QT intervals; - widening of PR, QRS, and QT intervals;

- heart block- heart block

HypotensionHypotension

Anticholinergic toxicityAnticholinergic toxicity

- - hyperthermiahyperthermia

- flushing- flushing

-dilated pupils-dilated pupils

-intestinal ileus-intestinal ileus

-urinary retention-urinary retention

- sinus tachycardia- sinus tachycardia

Confusion, delirium, hallucinationsConfusion, delirium, hallucinations

Seizures Seizures

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TCAD overdoseTCAD overdose DiagnosisDiagnosis

HistoryHistory

Blood/urine toxicology screenBlood/urine toxicology screen

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TCAD overdose -TreatmentTCAD overdose -Treatment

many require intubationmany require intubation

Consider gastric lavage if taken < 2hrsConsider gastric lavage if taken < 2hrs

Activated charcoalActivated charcoal

Treatment of hypotension with isotonic salineTreatment of hypotension with isotonic saline

Sodium bicarbonate for cardiovascular toxicity for cardiovascular toxicity Alpha adrenergic vasopressors Alpha adrenergic vasopressors ((norepinephrine

) ) Benzodiazepines for seizuresBenzodiazepines for seizures

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Sodium Bicarbonate Sodium Bicarbonate in TCA in TCA overdoseoverdose

Hypertonic sodium bicarbonate Hypertonic sodium bicarbonate

(NaHCO3) (NaHCO3)

- QRS widening >100 msec - QRS widening >100 msec

-ventricular arrhythmias -ventricular arrhythmias

-refractory hypotension -refractory hypotension

↑↑ serum pH promotes protein serum pH promotes protein

binding and binding and ↓↓ free drug free drug

concentrationsconcentrations

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Sodium Bicarbonate Sodium Bicarbonate in TCA in TCA overdoseoverdose

reasonable goal pH is 7.50 to 7.55 reasonable goal pH is 7.50 to 7.55

then taper dosethen taper dose

S/E:S/E:

Volume overload Volume overload

hypernatreamiahypernatreamia

metabolic alkalosis metabolic alkalosis

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Special Cautions in TCAD Special Cautions in TCAD overdoseoverdose

Class IA and IC antiarrhythmic agents are Class IA and IC antiarrhythmic agents are

contraindicated eg:contraindicated eg:

quinidinequinidine

DisopyramideDisopyramide

FlecainideFlecainide

propafenonepropafenone

Class IB Lignocaine, phenytoin usedClass IB Lignocaine, phenytoin used

Phenytoin may precipitate arrhythmiasPhenytoin may precipitate arrhythmias

Magnesium may be usefulMagnesium may be useful

Flumazenil must Flumazenil must notnot be given be given

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Salicylate overdoseSalicylate overdose

Aspirin (Aspirin (acetylsalicylic acid)acetylsalicylic acid) Methyl salicylate (Oil of Methyl salicylate (Oil of

Wintergreen)Wintergreen) 5 ml = 7g salicylic acid5 ml = 7g salicylic acid Herbal remediesHerbal remedies

Fatal intoxication can occur after Fatal intoxication can occur after the ingestion of 10 to 30 g by adults the ingestion of 10 to 30 g by adults and as little as 3 g by childrenand as little as 3 g by children

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Salicylate levelsSalicylate levels

-Rapidly absorbed-Rapidly absorbed

-peak blood levels usually occur within -peak blood levels usually occur within

one hourone hour but delayed in overdose 6-35 but delayed in overdose 6-35

hrs plasma salicylate concentrationhrs plasma salicylate concentration

Measure @ 4 hrs post ingestion & every Measure @ 4 hrs post ingestion & every

2 hrs until they are clearly falling2 hrs until they are clearly falling

Most patients show signs of intoxication Most patients show signs of intoxication

when the plasma level exceeds 40 to 50 when the plasma level exceeds 40 to 50

mg/dL (2.9 to 3.6 mmol/L) mg/dL (2.9 to 3.6 mmol/L)

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Salicylate overdoseSalicylate overdose 1- Inhibition of cyclooxygenase results in decreased 1- Inhibition of cyclooxygenase results in decreased

synthesis of prostaglandins, prostacyclin, and synthesis of prostaglandins, prostacyclin, and

thromboxanesthromboxanes 2- Stimulation of the chemoreceptor trigger zone in the 2- Stimulation of the chemoreceptor trigger zone in the

medulla causes:medulla causes: nausea and vomitingnausea and vomiting 3- Activation of the respiratory center of the medulla 3- Activation of the respiratory center of the medulla

results in:results in: tachypnea, hyperventilation, respiratory alkalosistachypnea, hyperventilation, respiratory alkalosis 4- Uncoupled oxidative phosphorylation in the 4- Uncoupled oxidative phosphorylation in the

mitochondria generates heat and may increase body mitochondria generates heat and may increase body

temperaturetemperature 5- Interference with cellular metabolism leads to 5- Interference with cellular metabolism leads to

metabolic acidosismetabolic acidosis

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Clinical featuresClinical features

Early symptoms of aspirin toxicity includeEarly symptoms of aspirin toxicity include::

tinnitustinnitus

FeverFever

VertigoVertigo

NauseaNausea

HyperventilationHyperventilation

VomitingVomiting

diarrhoeadiarrhoea

More severe intoxication can cause:More severe intoxication can cause:

altered mental status, comaaltered mental status, coma

non-cardiac pulmonary edema and deathnon-cardiac pulmonary edema and death

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Metabolic Metabolic abnormalitiesabnormalities

Stimulate the respiratory center directly, early fall in the Stimulate the respiratory center directly, early fall in the

PCO2 and respiratory alkalosis PCO2 and respiratory alkalosis

An anion-gap metabolic acidosis then follows, due to the An anion-gap metabolic acidosis then follows, due to the

accumulation of organic acids, including lactic acid and accumulation of organic acids, including lactic acid and

ketoacidsketoacids

Mixed Mixed respiratory alkalosis and metabolic acidosis with respiratory alkalosis and metabolic acidosis with ↑ ↑

anion gapanion gap

Arterial Ph variable depending on severityArterial Ph variable depending on severity

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Metabolic Metabolic abnormalitiesabnormalities

Metabolic acidosis Metabolic acidosis increases the increases the plasma concentration of plasma concentration of protonated salicylate protonated salicylate

thus worsening toxicity by thus worsening toxicity by allowing easy diffusion of the drug allowing easy diffusion of the drug across cell membranesacross cell membranes

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Salicylate overdose - Salicylate overdose - treatmenttreatment

directed toward increasing systemic pH directed toward increasing systemic pH by the administration of sodium by the administration of sodium bicarbonate bicarbonate

IV fluids +/- vasopressorsIV fluids +/- vasopressors

Supplemental glucose (100 mL of 50 Supplemental glucose (100 mL of 50 percent dextrose in adults) to patients percent dextrose in adults) to patients with altered mental status regardless of with altered mental status regardless of serum glucose concentration to:serum glucose concentration to:

overcome neuroglycopaeniaovercome neuroglycopaenia HemodialysisHemodialysis

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Alkalinization of plasma and Alkalinization of plasma and

urineurine Alkalemia from a respiratory alkalosis is not a Alkalemia from a respiratory alkalosis is not a

contraindication to sodium bicarbonate therapy contraindication to sodium bicarbonate therapy

A urine pH of 7.5 to 8.0 is desirableA urine pH of 7.5 to 8.0 is desirable

Blood gas analysis every two hours Blood gas analysis every two hours

Avoid severe alkalemia (arterial pH >7.60)Avoid severe alkalemia (arterial pH >7.60)

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Haemodialysis - indicationsHaemodialysis - indications

Altered mental statusAltered mental status

Pulmonary or cerebral edemaPulmonary or cerebral edema

Renal insufficiency that interferes with salicylate Renal insufficiency that interferes with salicylate excretionexcretion

Fluid overload that prevents the administration of Fluid overload that prevents the administration of sodium bicarbonatesodium bicarbonate

A plasma salicylate concentration >100 mg/dLA plasma salicylate concentration >100 mg/dL

Clinical deterioration despite aggressive and Clinical deterioration despite aggressive and appropriate supportive careappropriate supportive care

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ParacetamolParacetamol

Widely availableWidely available

Potential toxicity underestimatedPotential toxicity underestimated

Toxicity unlikely to result from a single dose of less Toxicity unlikely to result from a single dose of less

than 150 mg/kg in child or 7.5 to 10 g for adult than 150 mg/kg in child or 7.5 to 10 g for adult

Toxicity is likely with single ingestions greater than Toxicity is likely with single ingestions greater than

250 mg/kg or those greater than 12 g over a 24-hour 250 mg/kg or those greater than 12 g over a 24-hour

period period

Virtually all patients who ingest doses in excess of Virtually all patients who ingest doses in excess of

350 mg/kg develop severe liver toxicity unless 350 mg/kg develop severe liver toxicity unless

appropriately treatedappropriately treated

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Factors influencing Factors influencing toxicitytoxicity Dose ingestedDose ingested

Excessive cytochrome P450 activity due to Excessive cytochrome P450 activity due to

induction by chronic alcohol or other drug use eg induction by chronic alcohol or other drug use eg

carbamazepine, phenytoin, isoniazid, rifampin carbamazepine, phenytoin, isoniazid, rifampin

Decreased capacity for glucuronidation or sulfationDecreased capacity for glucuronidation or sulfation

Depletion of glutathione stores due to malnutrition Depletion of glutathione stores due to malnutrition

or or chronicchronic alcohol ingestion alcohol ingestion

Acute alcohol ingestion is not a risk factor for Acute alcohol ingestion is not a risk factor for

hepatotoxicity and may even be protective by hepatotoxicity and may even be protective by

competing with acetaminophen for CYP2E1 competing with acetaminophen for CYP2E1

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Clinical featuresClinical features Stage I (0.5 to 24 hours) Stage I (0.5 to 24 hours)

No symptomsNo symptoms

Stage II (24 to 72 hours) Stage II (24 to 72 hours)

Subclinical elevations of hepatic aminotransferases Subclinical elevations of hepatic aminotransferases (AST, ALT) (AST, ALT)

-right upper quadrant pain-right upper quadrant pain

-liver enlargement and tenderness-liver enlargement and tenderness

-Elevations of prothrombin time (PT)-Elevations of prothrombin time (PT)

-oliguria and renal function abnormalities may become -oliguria and renal function abnormalities may become evident evident

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Clinical featuresClinical features

Stage III (72 to 96 hours) Stage III (72 to 96 hours)

-Jaundice-Jaundice

-confusion (hepatic encephalopathy)-confusion (hepatic encephalopathy)

-marked elevation in hepatic enzymes-marked elevation in hepatic enzymes

-hyperammonemia-hyperammonemia

lactic acidosis-lactic acidosis-

- renal failure 25%- renal failure 25%

- death- death Stage IV (4 days to 2 weeks)Stage IV (4 days to 2 weeks)

Recovery phaseRecovery phase that usually begins by day 4 that usually begins by day 4 and is complete by 7 days after overdose and is complete by 7 days after overdose

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Paracetamol overdoseParacetamol overdose

The risk of toxicity is best predicted by relating the The risk of toxicity is best predicted by relating the time of ingestion to the serum time of ingestion to the serum paracetamolparacetamol concentration concentration

Peak serum concentrations reached within 4 hrs Peak serum concentrations reached within 4 hrs following overdose of immediate-release preparationsfollowing overdose of immediate-release preparations

May be delayed with extended releases preparations May be delayed with extended releases preparations or drugs that delay gastric emptying (eg, opiates, or drugs that delay gastric emptying (eg, opiates, anticholinergic agents) are coingestedanticholinergic agents) are coingested

Check level at >= 4 hrsCheck level at >= 4 hrs

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Paracetamol overdose Paracetamol overdose treatmenttreatment

Activated charcoal within four hours of Activated charcoal within four hours of

ingestion ingestion

May reduce absorption by 50 to 90 May reduce absorption by 50 to 90

percent percent

Single oral dose of one gram per Single oral dose of one gram per

kilogram kilogram

Inhibits absorption of oral methionineInhibits absorption of oral methionine

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Activated CharcoalActivated Charcoal

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N-acetylcysteine N-acetylcysteine

Antidote – MOA: Antidote – MOA: a glutathione precursor a glutathione precursor

Limits the formation and accumulation of NAPQI Limits the formation and accumulation of NAPQI

Powerful anti-inflammatory and antioxidant effects Powerful anti-inflammatory and antioxidant effects

IV infusion or oral tablets (also oral methionine)IV infusion or oral tablets (also oral methionine)

150mg/Kg over 15 min; 50mg/Kg over next 4 hrs; 150mg/Kg over 15 min; 50mg/Kg over next 4 hrs;

100mg/kg over next 16 hrs up to 36hrs100mg/kg over next 16 hrs up to 36hrs

Beyond 8 hours, NAC efficacy progressively decreases Beyond 8 hours, NAC efficacy progressively decreases

S/Es nausea, flushing, urticaria, bronchospasm, S/Es nausea, flushing, urticaria, bronchospasm,

angioedema, fever, chills, hypotension, hemolysis and angioedema, fever, chills, hypotension, hemolysis and

rarely, cardiovascular collapse rarely, cardiovascular collapse

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Paracetamol overdose Paracetamol overdose treatmenttreatment

At the end of NAC infusion, a blood sample should be At the end of NAC infusion, a blood sample should be

taken for determination of the INR, plasma creatinine taken for determination of the INR, plasma creatinine

and ALT.and ALT.

If any is abnormal or the patient is symptomatic, If any is abnormal or the patient is symptomatic,

further monitoring is required and advice sought from further monitoring is required and advice sought from

the NPIS the NPIS

Patients with normal INR, plasma creatinine and ALT Patients with normal INR, plasma creatinine and ALT

and who are asymptomatic may be discharged from and who are asymptomatic may be discharged from

medical care. medical care.

They should be advised to return to hospital if vomiting They should be advised to return to hospital if vomiting

or abdominal pain develop or recuror abdominal pain develop or recur

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Indications for liver Indications for liver transplantationtransplantation

Liver transplantation is life-saving for fulminant Liver transplantation is life-saving for fulminant hepatic necrosis hepatic necrosis

The indications for liver transplantation are:The indications for liver transplantation are:

1 - Acidosis (pH < 7.3), or 1 - Acidosis (pH < 7.3), or

2 - PT > 100 sec 2 - PT > 100 sec

3 - Creatinine > 300 mcg/l 3 - Creatinine > 300 mcg/l

4 - Grade 3 encephalopathy (or worse)4 - Grade 3 encephalopathy (or worse) It is better to contact the local liver transplant centre It is better to contact the local liver transplant centre

earlier than this. earlier than this. Grossly abnormal prothrombin times should trigger Grossly abnormal prothrombin times should trigger

referral:referral: PT > 20 sec at 24 hr PT > 20 sec at 24 hr PT > 40 sec at 48 hr PT > 40 sec at 48 hr

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Alcohol poisoningAlcohol poisoning

Clinical features of acute alcohol poisoning include:Clinical features of acute alcohol poisoning include:

Ataxia and anaesthesia leading to accidental injury Ataxia and anaesthesia leading to accidental injury

Dysarthria and nystagmus Dysarthria and nystagmus

Drowsiness which may progress to coma Drowsiness which may progress to coma

Inhalation of vomit which can be fatal & should be Inhalation of vomit which can be fatal & should be

prevented prevented

Hypoglycaemia in children and some adults Hypoglycaemia in children and some adults

Check BG TEST and give 50% glucose i.v. if requiredCheck BG TEST and give 50% glucose i.v. if required

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Coma (alcohol induced)Coma (alcohol induced) In cases of alcohol induced coma exclude:In cases of alcohol induced coma exclude:

1.1. Coincident head injuryCoincident head injury

2.2. Hepatic failure Hepatic failure

3.3. MeningitisMeningitis

4.4. Wernicke’s encephalopathy Wernicke’s encephalopathy

5.5. Other associated drug ingestionOther associated drug ingestion A blood test will confirm substantial levels of A blood test will confirm substantial levels of

alcohol alcohol Rule out alcoholic hypoglycaemiaRule out alcoholic hypoglycaemia The airway and circulation must be maintainedThe airway and circulation must be maintained But glucose- containing fluids may precipitate But glucose- containing fluids may precipitate

Wernicke's encephalopathyWernicke's encephalopathy Thiamine should given to allThiamine should given to all Intravenous naloxone has reversed coma in a Intravenous naloxone has reversed coma in a

proportion of casesproportion of cases

1. 2 Drugs & Chemicals Poisoning Poisoning By Dr. Jamshidi.

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Transcript of 1. 2 Drugs & Chemicals Poisoning Poisoning By Dr. Jamshidi.