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Intoxication
Viktória Bertalan M.D.
Diagnosis of poisoning
Diagnosis and treatment often must proceed rapidly!
Toxicology screens
How will the result of the test alter the approach to treatment?
Can the result of the test be returned in time to affect therapy positively?
Limitations:
• panels may look for only 40-100 drugs – more than 10.000 possible drugs or toxins – 6 million chemicals
• a negative result does not always rule out poisoning, negative predictive value is about 70%, positive predictive value 90%
Common drug of abuse panel
History• frequently unreliable or incomplete!
• early signs and symptoms
• drugs taken:– (nonprescription drugs, herbal medicines, vitamins)
patient / family member / friend / paramedics
General findings: autonomic syndromes
1. α-adrenergic:– hypertension with reflex bradycardia, usually with mydriasis (eg,
phenylephrin)
2. ß-adrenergic: – hypotension (ß2-mediated vazodilation) and tachycardia (eg,
caffeine, theophylline)
3. mixed α+ß adrenergic:– hypertension and tachycardia, with mydriasis, sweathening, dry
mucous membranes (eg, cocaine, amphetamines)
4. sympatholytic:– hypotension and bradycardia with miosis (pin point), decreased GI
peristalsis (eg, clonidine, opiates)
General findings: autonomic syndromes
5. Nicotinic cholinergic: – both parasympathetic and sympathetic stimulation,
unpredictable symptoms: cxcessive stimulation frequently causes depolarization blockage.
– Thus• initial tachycardia, may be followed by bradycardia• muscle fasciculations may be followed py paralysis
– eg, nicotin, succinylcholin6. Muscarinic cholinergic:
– bradycardia, miosis, sweathing, hyperperistalsis, bronchorrea, wheezing, excessive salivation, urinary incontinence (eg, bethanechol)
General findings: autonomic syndromes
5. Mixed cholinergic: – both nicotinic and muscarinic receptors are stimulated: mixed effects– usually miotic (pin point) pupils, sweathy skin, increased peristalsis,
fasciculation to paralysis– eg, organophosphate, carbamate insecticides
6. Anticholinergic (antimuscarinic):– Tachycardia, mild hypertension, myosis (widely dilated)– Skin: flushed, hot, dry– Decreased peristalsis, commonly urinary retention– Myoclonic jerking or choreoatetoid movements– Agitation, delirium– Hyperthermia– eg, atropin, antihistamines, antidepressants
Eye findings: • Nystagmus:
– usually horizontal-gaze: eg, barbiturat, etanol, carbamazepine, phenytoin, scorpion envenomation
– PCP (phencyclidine) may cause horizontal, vertical and rotatory
Eye findings:
• Miosis: – Sympatholythic agents:
eg, clonidine, opiates
– Cholinergic agents: eg, carbamate insecticides, nicotine*, organophosphates
Eye findings
• Mydriasis• Sympathomimetics:
– eg, amphetamines, cocaine, LSD (lysergic acid diethylamide), monoamine oxidase inhibitors
• Anticholinergics:– antihistamines, atropine,
tricyclic antidepressants
Skin
• sweating or absence of sweating:– autonomic syndromes
• flushed red: – carbon monoxide
• cherry red
– boric acid
– chemical burns• corrosives or hydrocarbons
– anticholinergic agents
– vasodilatation • eg, phenothiazines
Skin 2
• pale:– with diaphoresis:
sympathomimetic agents
– localised: possible arterial vasospasm (eg, ergot, amphetamines)
• cyanosis:– hypoxia
– sulf- or methemoglobinaemia
Skin
• blisters – insect bites– barbiturates
Abdominal findings: ileus
• paralythic: drugs• mechanical factors
– perforation, peritonitis, mechanical obstruction
• bowel infarction – rare, but catastrophic
– prolonged hypotension
– vasospasm (eg, amphetamines)
Abdominal findings: vomiting
• hematemesis: corrosive substance
Odors
• acetone: acetone, izopropil alcohol
• acrid, pearlike: paraldehyde, chloral hydrate
• bitter almonds: cyanide
• garlic: arsenic, organophosphates
• mothballs: naphtalene
• rotten eggs: hydrogen sulfide
• carrot: water hemlock
Airway
Most common factor contributing to death!
All poisoned patients should be suspected of having potentially compromised airway!
Airway: assessment
• Awake: – likely intact reflexes– should be monitored (potentially rapid loss of
airway!)
• Lethargic or obtunded: – assess: gag or cough reflex– consider endotracheal intubation
Airway: treatment
Optimize the airway position!
B. sniffing position
C. jaw thrust
D. head down, left sided position
Do not perform neck manipulation
if you suspect neck injury!
Airway: clean it!
Remove any obstruction or secretions!
• Magill forceps
Airway: secure it!
• artificial oropharyngeal or nasopharyngeal devices
• endotracheal intubation: – Nasotracheal:
• disadvantages: stimulation of vomiting, spontaneous breath required
– Orotracheal
Breathing:
1. Ventillatory failure
2. Hypoxia
3. Bronchospasm
Breathing: ventillatory failure
1. muscle paralysis: – eg, botulism, nicotine, organophosphates,
strychnine, neuromuscular blockers
2. CNS depression: – eg, antihistamines, barbiturates, ethanol, opiates,
triciclic antidepressants (TCA)
Breathing: hypoxia
1. Insufficient oxygen in ambient air– inert gases: carbon monoxide, methane, propane,
nitrogen
2. Disruption of oxygen absorption by the lung1. pneumonia or noncardiogenic pulmonary edema:
eg. aspiration of gastric contents or hydrocarbons, chlorine, mercury vapor, opiates, paraquat, salicylates, smoke, sedative-hypnotic drugs
2. cardiogenic pulmonary edema: eg. ß-blockers, procainamid, TCA, verapamil
Breathing: hypoxia
3. Cellular hypoxia: 1. limited oxygen binding:
• carbon monoxide, methemoglobinemia
• dissolved oxygen unchanged (pO2), oxygen content deteriorated
2. cellular oxygen utilization disturbances:• cyanide, hydrogen sulfide
• high venous oxygen saturation (decreased cellular oxygen uptake)
Breathing: bronchospasm
1. direct irritant agents: – smoke, chlorine, hydrocarbon aspiration
2. pharmacologic effect: – organophosphate, insecticides, ß-blockers
3. hypersensitivity or allergy
Circulation
1. Bradycardia and AV block
2. QRS interval prolongation
3. Tachycardia
4. Ventricular arrythmias
5. Hypotension
6. Hypertension
Circulation: bradycardia and AV block• cholinergic vagotonic agents:
– digitalis, organophosphates, neostigmine
• membrane-depressant drugs:– ß-blockers, flecainide, quinidine, procainamid, TCA
• sympatholytic agents: – ß-blockers, clonidine, opiates
• other:– calcium antagonists, carbamazepine, lythium, α-agonists
Do NOT treat unless the patient is symptomatic!Both may be a protective reflex in life-threatening
hypertension!
Circulation: bradycardia and AV block
• Differential diagnosis – hypothermia– myocardial ischaemia– electrolyte abnormality (eg, hyperkalaemia)– metabolic disturbance (eg, hypothyroidism)– Cushing-reflex (severe intracranial hypertension)– physiologic athletes, or vaso-vagal reaction
Circulation: bradycardia and AV block
• Rewarm hypothermic patients!– 40-50/min sinus bradycardia is normal when core
temperature is 32-35 °C• Administer atropine
– 0.01-0.03 mg/kg iv.• Use transcutaneous or transvenous PM!• Use specific antidotes!
– ß-blockers – glucagon – digitalis – Fab fragments– triciclic antidepressant or membrane-depressant drugs –
sodium bicarbonate – calcium antagonist – calcium
Circulation: QRS interval prolongation
• QRS interval prolongation – > 0.12 s in limb leads– eg, ß-blockers,
chloroquin, digitalis, flecainid, hyperkalemia, phenotiazines, quinidine, procainamide, TCA
• Ventricular escape rhythm– complete heart block– digitalis, calcium
antagonists
Circulation: QRS interval prolongation• differential diagnosis:
– intrinsic conduction system disease
• check an old ECG if available
– hyperkalaemia: • sine wave pattern, with wide QRS,
peaked T waves
– hypothermia • <32 °C
• extra terminal QRS deflection (J or Osborne
wave)
Circulation: QRS interval prolongation
• Treatment:– treat hyperkalemia and hypothermia– treat AV block with atropin or PM– for TCA or other sodium channel-blockers give
sodium bicarbonate 1-2 mEq/kg iv bolus, repeat as needed
– antidotes: • digoxin – Fab antibodies• ß-blockers – glucagon • calcium antagonist – calcium
Circulation: tachycardia
1. sympathomimetic agents– amphetamines, caffeine, cocaine, ephedrine, PCP,
theophylline2. agents causing cellular hypoxia
– carbon monoxide, cyanide, hydrogen sulfide, oxidizing agents (methemoglobinaemia)
3. anticholinergic agents– Amanita muscaria mushrooms, antihistamies, atropin,
phenothiazines, TCA4. other
– ethanol or sedative-hypnotic drug withdrawal, vasodilators (reflex tachycardia) tyroid hormone
Circulation: tachycardia
• sinus or supraventricular tachycardia: – may also be a reflex response to hypotension
• sinus tachycardia + QRS interval prolongation– may have the appearance of VT
Circulation: tachycardia
• Differential diagnosis:– occult blood loss– fluid loss– hypoxia– fever and infection– AMI– anxiety– intrinsic conduction system disease (eg, WPW)
Circulation: tachycardia
• Treatment:– hypotension, chest pain– for sympathomimetic-induced: propranolol– for anticholinergic-induced: neostigmin,
physostigmine
In TCA overdose additive depression of conduction may result in asystole!
Circulation: ventricular arrythmias
• VT or VF– amphetamin or other sympathomimetics, aromatic
hydrocarbons, caffeine, cocaine, digitalis, theophylline, TCA
• QT prolongation or torsades des pointes– amiodarone, arsenic, fluorid, TCA, moxifloxacin,
levofloxacin, erythromycin, organophosphates
Circulation: ventricular arrythmias
• treatment: – CPR– for TCA or other sodium channel-blocking drug:
• administer sodium bicarbonate 1-2 mEq/kg iv in repeated boluses until the QRS interval narrows or the pH exceeds 7.7
– for torsade de pointes:• overdrive pacing• administer iv. magnesium sulfate 1-2 g in adults over
20-30 minutes
Circulation: hypotension
hypotension with relative bradycardia
• Sympatholythic agents– β-blockers, clonidine, hypothermia, opiates
• Membrane-depressant drugs– β-blockers (propranolol), procainamid, TCA
• Others: – barbiturates, calcium antagonists, fluoride,
organophosphates and carbamates
Circulation: hypotension
hypotension with tachycardia
• fluid loss or third spancing– amatoxin containing mushroom, arsenic, sedative-
hypnotic agents
• Peripheral venous or arterial dilation– α-agonists, β2-stimulants, caffeine, calcium
antagonists
Hypotension: therapy
• fluid challenge: 10-20 ml/kg
• vasopressor therapy– dopamine, norepinephrine
• TCA, reserpine, norepinephrine more effective (depleted neuronal CA stores)
Antidotes
• sodium bicarbonate – TCA
• glucagon – beta blocker
• calcium – calcium antagonist
• propranolol – theophylline, caffeine, β-agonist overdose.
Circulation: hypertension
with tachycardia:– generalized sympathomimetic agents
• amphetamines, cocaine, ephedrine, levodopa, LSD, marihuana, MAO inhibitors
– anticholinergic agents• antihistamines, atropine, TCA
– other:• ethanol and sedative hypnotic drug withdrawal, nicotine
(early stage), organophosphates (early stage)
Circulation hypertension
with bradycardia or atrioventricular block– clonidine, ergot derivates, methoxamine,
norepinephrine
Hypertension: complications
• intracranial hemorrhage• myocardial infarction• congestive heart failure• aortic dissection
Hypertension: therapy
• Rapid lowering is desirable: diastolic 100 mmHg (hypertensive) or 80 mmHg
• do not use propranolol or esmolol alone, beta blockers may paradoxically worsen hypertension if it is caused primarily by alpha adrenergic stimulation
Altered mental status
1. Coma or stupor
2. Seizures
3. Confusion or delirium
4. Agitation or psychosis
Altered mental status: coma or stupor
• Generalized CNS depressants– anticholinergics, antihistamines, barbiturates,
benzodiazepines, ethanol, sedative-hypnotic agents, TCA
• Sympatholytic agents– clonidine, methyldopa, opiates
• Cellular hypoxia:– carbon monoxide, cyanide, hydrogen sulfide,
methemoglobinemia, sedium azide
• Other (unknown mechanism)– bromide, disulfiram, lithium, PCP, salicylates
Altered mental status:seizures
• adrenergic sympathomimetic agents– amphetamines, caffeine, cocaine, ephedrine, PCP
• antidepressants and antipsychotics– haloperidol, TCA, SSRI
• others:– antihistamines, β-blockers, ethylene glycol, lead,
methanol, salicylates, strychnine
Altered mental status
• confusion or delirium:– amantadine, anticholinergic agents, antihistamines,
bromde, carbon monoxide, H2 blockers, lead, levodopa, lidocaine, lithium, salicylates, withdrawal from ethanol or sedative-hypnotic drugs
• agitation or psychosis:– amphetamines, caffeine, cocaine, LSD, marihuana,
PCP, procaine, SSRI, steroids, theophylline
Coma
• antidotes: – naloxone: opiates– flumazenil: (BZD)
• can precipitate seizures in pts addicted to BZD or have co-ingested a convulsant drug or poison
Altered mental status: diff. dg
• head trauma other causes of intracranial bleeding
• abnormal levels of blood glucose, sodium...
• hypoxia
• liver or renal failure
• hypothermia / hyperthermia
• infections (encephalitis, meningitis)
Anion gap metabolic acidosis
• normal anion gap: 8-12 mEq/L
• unmeasured anions – eg. phosphate, sulphate and anionic proteins
Anion gap metabolic acidosis:
• elevated anion gap:– hyperlipidaemia– hemodialysis (low-molecular-weight solutes)– lactic acid– unmeasured acid anions
• formate ( mehtanol poisoning)• oxalate (ethylene glycol poisoning)
• narrow anion gap– elevated serum chloride concentration:
• bromide, nitrate overdose– lowered serum sodium concentration
• lithium, calcium, magnesium
Serum osmolality and osmolar gap
• normally 290 mosm/l
• calculated osmolarity 2[Na] + 2[K] + [urea]+ [glc]
• osmolar gap:– measured – calculated: 0±5 mOsm/l
• causes: – low molecular substances: eg, ethanol, glycol
Osmolar gap + anion gap = methanol / ethylene glycol poisoning
(or severe diabetic ketoacidosis!)
Serum glucose level
• altered by nutritional state, endogenous insulin levels, endocrine and liver function
• Hyperglycemia:– usually mild and transient. – eg, caffein, teophylline– if severe:
• dehydration, electrolit imbalance (osmotic effect in the urine)• shifting of water from brain into plasma: hyperosmolar coma
• Hypoglycaemia– seizures, coma or altered mental status– eg, insulin, ethanol, oral sulfonylurea agents, salicylate,
valproic acid
Renal failure• Direct nephrotoxicity:
– acetaminophen, Amanita phalloides mushrooms, ibuprofen, bromates, chlorates, ethylene glycol (oxalate, glycolate), heavy metals
• Hemolysis: – arsine, naphthalene
• Rhabdomyolysis: – amphetamine, cocaine, PCP, strychnine– coma with prolonged immobility– hyperthermia– status epilepticus
• Hypoperfusion
Liver failure
• direct toxicity: – amanita phalloides mushrooms
• hepatotoxic intermediate metabolits:– acetaminophen
• hepatic vein thrombosis– pyrrolizidine alkaloids
Decontamination
Emesis
• Early prehospital management of selected potentially seious oral poisonings, particularly in the home immediate after ingestion
• contraindications:– obunded, comatose or consulsive– risk of CNS depression or seizures– corrosives– aliphatic hydrocarbones (pneumonitis)
• adverse effects:– delayed administration of activated charcoral or oral antidotes– hemorrhagic gastritis or Mallory weiss tear
Gastric lavage
• more invasive
• occasionally used in ED, little evidence
• indications: massive overdose, or a particularly toxic substance
• within 30-60 minutes of ingestion (after several hours delayed gastric emptying eg, salicylates or anticholinergic drugs)
• preparation for endoscopy
Gastric lavage: contraindications
• altered mental status, cunvulsion– endotracheal intubation
• enteric coated pills– too large to eliminate
• corrosive substance– controversial
Gastric lavage: complications• perforation of the esophagus or stomach• bleeding• inadverent tracheal intubation• aspiration
Activated charcoral
• highly adsorbent, made from a distillation of wood pulp
• poorly adsorbed toxins:– alkali, cyanide, ethylene glycol, fluoride, inorganic
salts, iron, lithium, potassium
• dosage: 1g/kg
Whole bowel irrigation
• surgical bowel-cleansing solution (nonabsorbable polyethylene glycol in a balanced electrolyte solution)
• 2L/h until rectal effluent is clear • indications:
– large ingestions of drugs poorly adsorbed to activated charcoral
– large ingestion of enteric coated tablets containing dangerous drugs (eg. verapamil)
– ingestion of foreign bodies (body stuffers)
Enhanced elimination
Does the patient need enhanced removal?
Is the drug or toxin accessible
to the removal procedure?
Urinary manipulation
• the renal route is the significant contributor to total clearance
• Forced diuresis: – may increase GFR risk of volume overload
• Alkalization and ion trapping: – urinary pH manipulation may enhance elimination
of polar drugs eg, salicylates
Renal replacement or other eliminative therapies
• Haemodialysis
• Hemoperfusion
• Plasm exchange
A B C
Airway:Cough and gag reflexesPatient positionClear airway
Disability/altered mental statusHypoglycaemia?Body tempreture (core)Organic causes?Anticonvulsive therapyAdequate sedation
Breathing:Arterial blood gassesAssist with bag/mask deviceGive oxygen
Coma or stupor?Hypothermia?Hyperthermia?SeizuresAgitation?
CirculationBP and pulseECG monitoringstart 1-2 iv. linesRoutine bloodwork
Endotracheal intubation
Respiratory failure?Hypoxia?Bronchospasm?
Bradycardia /AV blockProlonged QTTachycardiaVentricular arrythmiasHypotensionSevere hypertension
Other complications:Urine myoglobinObtain allergy history
Enhanced removalHemodialysisHemoperfusionRepeat dose charcoral
Clinical diagnosisPhysical findingsEssential labtests
Hazardous material?
DecontaminationSkin and eyesEmesis or gastric lavageCharcoral or cathartic
Dystonia or rigidity?Rhabdomyolysis?Allergy or anaphylaxis?
Osmolar gapAnion gap acidosisHyper/hypoglycaemiaHypo/hypernatremiaHypo/hyperkalemiaRenal failureLiver failureToxicology screeningAbdominal X-ray
DispositionToxicology consultationPsychosocial evaluation
Regional poison center consulatation