Investigations and
management of poisoning
Akshaya SM- 15
Aliya Muhammed-16
Initial approach to the stabilization of the patient who
presents with poisoning:
Goals:
A. Supprot of vital signs
B. Diagnostic testing
C. Reduce absorption of the toxin
D. Enhance of poison elimination
E. Neutralize toxin
Supportive care:
• Maintain physiologic homeostasis: Airway, breathing, circulation
• Prevent and treat secondary complications: like cerebral edema, cardiopulmonary
sepsis, thromboembolic disease, coagulopathy, hypoxia and acute renal failure.
Diagnostic testing:
General tests:
• Complete blood count
• Serum electrolytes, blood urea nitrogen and creatinine
• LFT, ABG, ECG
• Radiographic studies
Specific tests:
• Measurement of drug or toxin concentrations in body fluids (blood, urine, lavage
fluid).
Reduce absorption of the toxin:
• Inhalational exposure: evacuation from toxic environment and provision of
supplemental oxygen.
• Dermal exposure: removal of contaminated clothing and shower or irrigation of
affected site.
• For eye exposure: irrigation of the affected eye by up to 1L of saline.
• Oral exposure: inducing emesis, performing gastric lavage, activated charcoal, whole
bowel irrigation.
• Gastric decontamination.
Enhance of poison elimination:
• Alkalinization of urine using sodium bicarbonate to produce urine with a pH ³ 7.5
(for salicylate, methotrexate, phenobarbital poisoning)
• Extracorporeal removal
– Hemodialysis (for barbiturates, salicylates, valproate, alcohols, glycols)
– Hemoperfusion (for theophylline, digitalis)
Neutralize toxin:
Use antidotes
Neurotoxic plant poisons: Datura poisoning
• Datura stramonium cause anticholinergic syndrome.
• Active agents include atropine and scopolamine.
Clinical features:
• Symptoms often appear within 30 minutes of ingestion and last for 24-48 hrs.
• Tachycardia, anhidrotic hyperthermia, mydriasis, dryness of mouth, urinary
retention, flushing, agitation, delirium, hallucination.
• Death is due to respiratory paralysis or cardiovascular collapse.
Mx:
• Gastric lavage and supportive therapy.
• Control of hyperthermia.
• Activated charcoal adsorbs the alkaloids.
• Benzodizepines to treat agitation
Cardiotoxic plant poisons:
• Oleander, calotropis
• They inhibit sodium –potassium ATPase pump leading to increase in intracellular Na+ and
Ca+
Symptoms:
• Nausea ,vomiting ,dizziness , burning sensation on ingestion
• Sinus bradycardia , heart block , ventricular ectopics and tachycardia.
Treatment:
• Atropine 0.6mg to maintain heart rate around 80/min
• Sodium bicarbonate 50 ml IV 6th hourly if acidosis is present
Opioid poisoning
• Is extracted from poppy seeds (papaver somniferum)
• Opioid agonists: Morphine, heroin, hydromorphone, fentanyl, codeine.
Clinical features:
Respiratory depression, euphoria, pupillary constriction, hypothermia, drying of
secretion, decreased blood pressure
Mx:
• Ensure adequate ventilation.
• Management of complications such as ARDS.
• Antidote: Naloxone, Naltrexone
Naloxone IV 0.4-2 mg every 2-3 minutes as needed.
Corrosives:
Eg:
Acids: hydrochloric, sulphuric, acetic, lactic, oxalic, carbolic acid.
Alkalis: sodium and potassium, soaps, detergents.
Heavy metal salts.
Formalin, iodine tincture.
Note: acids cause coagulative necrosis and alkalis cause liquefactive necrosis
Clinical features:
• Oropharyngeal, epigastric or retrosternal pain associated with dysphagia or
odynophagia
• Hypersalivation, nausea, vomiting, hematemesis
• Severe forms can damage larynx, bronchial necrosis, perforation of stomach.
• Late complication: esophageal strictures and stenosis, gastric stenosis,
esophageal and stomach cancer
Management:
• External decontamination after initial resuscitation; if needed
• Gastric lavage and neutralizing chemicals is contraindicated.
• Cardiorespiratory monitoring, full blood count, renal function, coagulation and acid-base
status should assessed.
• An erect chest X–ray should be performed if perforation is suspected and may show
features of mediastinitis or gas under the diaphragm.
• CT scan and endoscopy if doubts of perforation.
• Delayed endoscopy may cause perforation.
• Antibiotics, proton pump inhibitors and H2 blockers are routinely recommended.
• Strong analgesics should be administered for pain.
Methanol and Ethylene glycol:
• Ethylene glycol is found in antifreeze, brake fluids and windscreen washes.
• Methanol is present in some antifreeze, industrial solvents and is an adulterant of illicitly
produced alcohol.
Mechanism of toxicity:
Mainly due to its toxic metabolites which are converted via alcohol dehydrogenase such
as formaldehyde and formic acid and glycolic acid, oxalic acid
Clinical features:
Ethylene glycol Methanol
• Ophthalmoplegia, • Headache, delirium and
• cranial nerve palsies vertigo
• Hyporeflexia, myoclonus, • Visual impairment
• Renal pain and acute • Photophobia
tubular necrosis • Optic disc and retinal
• Hypocalcaemia, oedema
• Hypomagnesaemia • Impaired pupil reflexes
• Hyperkalemia
Investigation:
• Urea, electrolytes, glucose, magnesium, bicarbonates, osmolar and anion gaps should
be measured.
• Confirm by measurement of methanol and ethylene glycol.
Treatment:
a) General measures:
• Correction of acidosis by sodium bicarbonate infusion.
• Gastric lavage
• IV fluids
• Convulsions treated by IV benzodiazepines.
b) Specific measures:
• Fomepiazole or ethanol blocks alcohol dehydrogenase and prevent formation of toxic
metabolites.
• Antidote of methanol poisoning is fomepiazole 15 mg IV followed by 10 mg/kg every 12 hrs.
• Cofactor is given folic acid 50 mg IV every 6 hrs as it enhances the degradation of formic acid
to carbon dioxide.
• Hemodialysis is done in severe metabolic acidosis or evidence of end-organ damage or when
methanol is above 50 mg/dl.
ORGANOPHOSPHORUS POISONING
• OP compounds widely used as pesticide in agriculture.
• Intoxication occurs through inhalation , ingestion and dermal absorption .
Clinical features:
3 phases;
1. Acute cholinergic phase
2. Intermediate syndrome
3. Organophosphate induced delayed neuropathy
Acute cholinergic phase:
Diagnosis:
Clinical diagnosis:
Dreisbach’s severity of OP poisoning:
Grade Symptoms
Mild Nausea
Moderate Lacrimation, salivation, miosis, fasciculation
Severe Incontinence, apneic spells, ARDS, seizures,
coma
Laboratory:
• Red cell cholinesterase
• Plasma cholinesterase
• Electrocardiogram: prolonged QT and sinus tachycardia
• Arterial blood gas: Hypoxemia.
Management:
• Assess and record GCS
• Measure PR and BP and auscultate lungs
• Make patient to lie down in the left lateral position
• Start oxygen
• Set up an infusion of 0.9% NS. Aim at systolic BP >80mm Hg and U/P >30 mL/h.
• Remove contaminated clothes and thoroughly wash the skin with soap and water.
• Intubate if in respiratory distress.
• Perform gastric decontamination with gastric lavage once patient is stabilized and
within 2 hours of ingestion.
Drugs used - Atropine
Life saving in severe toxicity patients .
Reverses Ach induced bronchospasm, bronchorrhea, bradycardia, hypotension
As bolus 1.8-3mg IV stat and check pulse , BP, and chest crepitations after 5 min.
Aim for HR> 80 bpm , SBP>80mm of hg , clear chest.
If aim not achieved double the dose every 5 min. Review patient every 5 min. If
improved atropine infusion can be planned
Infusion: Start hourly infusion at 10-20% of total dose of atropine required. Use three
point checklist (secretions, heart rate, pupils ) to reduce infusion rate by 20% every 4
hours once the patient is stable
Pralidoxime :
• Reactiates AchE by removing the phosphoryl group
• Bolus dose : 30 mg/kg in 100 ml NS over 15-30 min
• Maintenance dose : continue IV infusion at 8-12 mg/kg/h
• A fast infusion can cause vomiting, hypertension, arrhythmia or cardiac
arrest
Benzodiazepines :
• For agitation and seizures
• Diazepam 10mg slow IV push, repeat as necessary upto 30-40 mg diazepam
per 24hr can be given
Supportive measures include mechanical ventilation, vasopressors, antibiotics,
diuretics, early enteral feeding, physiotherapy
Intermediate syndrome:
• Develops 1-4 days after exposure and lasts 2-3 weeks.
• Weakness spreads rapidly from ocular muscles to those of head and neck,
proximal limbs and the muscles of respiration resulting in ventilatory failure.
• Management includes maintenance of airway and ventilation.
Organophosphate induced delayed optic neuropathy:
• Develops 2-3 weeks after exposure.
• Features include muscle cramps followed by numbness and paraesthesia
proceeding to flaccid paralysis of limbs with foot and wrist drop
• A high-stepping gait proceeding to paraplegia
• Tendon reflexes are reduced.
Common drug overdosages:
Paracetamol poisoning
Mechanism:
• Toxicity is due to formation of an intermediate reactive metabolite, which binds
covalently to cellular proteins , leading to cell death.
• This causes hepatic and occasionally renal failure.
• Toxicity is likely with single ingestions >250 mg/kg or those >12g over a 24-hr
period.
Clinical manifestations:
Stage I (0.5-24 hrs)
No symptoms; nausea, vomiting and malaise.
Stage II (24-72 hrs)
• Subclinical elevations of hepatic aminotransferases (AST, ALT)
• Right upper quadrant pain, with liver enlargement and tenderness.
• Elevation of prothrombin time, total bilirubin and oliguria and renal function
abnormalities
Stage III (72-96 hrs)
Fulminant hepatic failure, jaundice, confusion (hepatic encephalopathy), marked
elevation of hepatic enzymes, hyper ammonemia, bleeding diathesis, hypoglycemia, lactic
acidosis, renal failure and death.
Stage IV (4 days to 2 weeks)
Recovery phase
Management:
• Activated charcoal ( may reduce absorption by 50-90%)
• Antidote: N-acetylcysteine (NAC)
IV infusion 150 mg/kg over 15 minutes; 50 mg/kg over next 4 hrs; 100 mg/kg over next 16
hrs up to 36 hrs.
Most effective, if started within 8-10 hours after ingestion.
• Alternate medication: Oral methionine.
• Liver transplantation ( it is life-saving for fulminant hepatic necrosis).
Aspirin toxicity
Mechanism:
• Acetylsalicylic acid is hydrolyzed to salicylic acid, responsible for toxic effects.
• It direct stimulation of respiratory centre leading to respiratory alkalosis
• Renal excretion of bicarbonate, Na and K result in metabolic acidosis.
• Disruption of Kreb’s cycle metabolism and glycolysis result in hyperglycemia and
ketonemia
Clinical features:
• Altered mental status
• Sweating
• Pulmonary edema
• Increased vital signs
• Tinnitus
• Irritable
• Nausea and vomiting
Management:
• Initial supportive therapy
• Specific management
– Decreasing absorption ( activated charcoal, gastric lavage)
– Increasing drug elimination ( urinary alkalinization, Hemodialysis)
Cyanide
Inhibits mitochondrial cytochrome oxidase and is an asphyxiating agent.
Clinical features:
• CNS: anxiety, headache, delirium, convulsions, coma, fixed dilated pupils.
• CVS: dizziness, shock
• Respiratory: dyspnea, cyanosis, initially hyperventilation followed by hypoventilation and
pulmonary oedema.
Investigation:
• Arterial and venous pO2
• High anion gap metabolic acidosis
• Blood cyanide levels
Treatment:
• Activated charcoal
• Supplemental oxygen
• Supportive care
• Sodium nitrite 300 mg IV over 5 min.
• Amyl nitrite 0.3 ml inhaled an be repeated after 3-5 min.
• Sodium thiosulphate 12.4g IV over 10-20 min.
• Hydroxycobalamin 4-5g IV (chelates cyanide)
