METHYL ALCOHOL AND ALUMINIUM POISONING

1. DR. KALPANA CHETIA
ASSOC . PROF. OF MEDICINE, JMCH,
JORHAT, ASSAM

2. GENERAL CONSIDERATION
 Methyl alcohol is also known as wood alcohol.
 It is a colourless liquid with a characteristic odour and
bitter taste .
 It is found in many industrial and home chemicals.
 It is widely used for duplicating fluids, varnishes ,
stains , paint thinners and dyes .
 It is added to ethanol to render it unfit to drink.
 It is also the main constituent of carburetor fluid.
 Most of the poisoning occur due to consumption of
adulterated ethyl alcohol.

3. MECHANISM OF TOxICITY
 Methanol as such is not a toxic agent .
 Its metabolites formaldehyde and formic acid are
responsible for its toxicity .
 The ocular involvement is due to local production of
formaldehyde.
 The enzyme responsible for conversion of methanol to
formaldehyde is alcohol dehydrogenase while
formaldehyde dehydrogenase and other enzymes
convert formaldehyde to formic acid.

4. Toxic quantity
 Amount 15 -30 ml 40% methanol have produced
deaths whereas some patients may survive 500 ml of
the same.
 It depends upon individuals .

5. CLINICAL FEATURES: CNS
 Toxicity usually seen between 12 -24 hours .
 CNS Toxicity : dizziness, weakness and headache .
Later the patient may develop coma and seizures.
 Methanol has a particular predilection for causing
putamenal damage and survivors may be left with
extra pyramidal movement disorders.

6. CLINICAL FEATURES
 Ocular Toxicity: It is delayed feature of methanol
Toxicity and the patient complains of visual difficulty .
Examination may reveal pupillary dilatation, retinal
edema and hyperemia of the optic disc.
 GIT Toxicity : nausea, abdominal pain

7. Clinical feature
 Toxicity can result following its absorbtion through
skin and respiratory tract apart from oral ingestion.
 Symptoms -within an hour
 Early feature-
Ataxia,
Drowsiness,
Dysarthria and
Nystagmus often associated with vomiting.

8.  Headache ,dizziness,confusion, vertigo.
 Marked muscular weakness, depressed cardiac action and
kypothermia
 Visual impairment and photophobia develop,associated
with optic disc and retinal edema and impaired pupil
reflexes.
 Blindness may be permanent
 Pancreatitis and impaired liver function also have been
reported.
 In fatal cases convulsions and death occurs from
respiratory failure.

9. Management
 Investigations – sr.creat, urea,
electrolyte,chloride,bicarbonate,RBS,magnasium,
calcium,plasma osmolarity and ABG – in all cases
 The osmolal and anion gap should be
calculated[na+k]-[Cl+HCO3]

10. TREATMENT
 Gastric lavage- with 5% bicarbonate solution/ activated
charcoal
 Antidote-
-Ethanol or formepizole in all patients with
suspected significant exposure while awaiting for lab
investigations.
-Block alcohol dehydrogenage and delay the
formation of toxic metabolites until parent drug is
eliminated in urine or by dialysis
-Continued until methanol concentration are
undetectable.

11.  Inj sodium bicarbonate- for correction of metabolic
acidosis(250ml of 1.26% solution,repeated as
necessary)
 I/V benzodiazepine – for convulsions
 Hemodialysis or hemofiltration
-Should be used in severe
poisoning,especially if renal failure is present
or there is visual loss
-Should be continued until acute toxic
features are no longer present and methanol
concentration are no longer detectable.

12. Aluminium phosphide poisoning

13. Aluminium phosphide
 Aluminium phosphide(ALP) is a solid
fumigant,pesticide,insecticide and rodenticide
 On coming in contact with moisure ALP liberate
phosphine which is a systemic poison and affect all
organs of the body
 Has garlicky odour.

14. Clinical feature
Mild intoxication- Nausea ,vomiting,headache and
abdominal pain
Moderate and severe poisoning systemic menifestations
are early and progressive and mostly fatal
GIT – Nausea, vomiting ,diarrhoea, retrosternal pain
CVS- Hypotension,shock,arrhythmias,myocarditis,acute
congestive heart failure
RESP- Cough and breathlessness progressing to ARDS
and respiratory failure
Hepatic – Jaundice
Renal – Renal failure

15. CNS-
Headache
Dizziness
Altered mental state
Restlessness
Tremor
Paraesthesia,
Convulsion
Acute hypoxic encephalopathy and Coma.
Rarely – muscle wasting and bleeding diasthesis
Cardiogenic shock is the M/C cause of death
Mortality is high -35 to 100%.

16. Management
 Detection of phosphine in the exhaled air or
stomach aspirate using either silver nitrate-
impregnated strip or specific phosphine detector tube
is diagnostic.
 Gas chromatography – most sensitive indicator

17. Treatment
Supportive
 Gastric lavage
 Activated charcoal
 Antacid –reduces absorbtion of phosphine
 No specific antidote
 Management of shock – NS
Low dose dopamin infusion and
inj hydrocortisone
 supplementary Oxygen
 Metabolic acidosis should be corrected with i.v sodium bicarbonate
 Peritoneal or hemodialysis in renal failue

18. Benzodiazepine poisoning

19. Benzodiazepine
 Benzodiazepines are used mainly as antianxiety and
muscle relaxant agents.
 Commonly used preparations
Diazepam,nitrazepam,oxazepam,alprazolam,
Lorazepam,chlorodiazepoxide etc.
 They are of low toxicity when taken alone in
overdose but can enhance CNS depression when
taken with other sedative agents, including alcohol.

20.  Cause significant toxicity in the elderly and those with
chronic lung and neuromuscular disease.
 Absorbtion from GIT is slow and excretion in the
urine may continue for several days.
 Addiction may occur.

21. Clinical features
Acute poisoning:
 Vertigo,slurred speech,nystagmus,diplopia.
 Dysarthria,ataxia,sedation,somnolence, confusion and
coma.
 Respiratory depression and hypotension may occur
with severe poisoning in susceptible groups,espicially
after intravenous administration of short acting
agents.

22. Chronic poisoning
 High dose,long term therapy(30 to 40mg of diazepam
daily) may produce withdrawal symptoms when stops
suddenly.
 Headache,anxiety,insomnia,muscle spam,tremor,
rarely convulsions and psychiatric disturbance.
 Anorexia,vomiting,respiratory depression

23. Treatment
 Gastric lavage
 Activated charcoal –useful after ingestion in
susceptible patients or after mixed overdose,if given
within one hour.
 Monitor conscious level,respiratory rate and oxygen
saturation for at least 6 hours after substantial
overdose.

24. Antidote –
 Flumazenil- specific benzodiazepine antagonist.
Selectively blocks the central effects of benzodiazepine
by competitive interaction at the benzodiazipine
recognition site.
 Dose- 0.1mg/min IV to a total of 1 mg.if resedation
occurs (in 20 to 120 min) the dose is repeated.
 Contraindicated in patients co-ingesting
proconvulsant agents such as TCAs and in those with a
history of seizures

25. Cocain poisoning

26. Cocain
 Cocain is obtained from the leaves of erythroxylum
coca.
 Available as a water soluble hydrochloride salt
suitable for nasal inhalation(snoring),or as an
insoluble free base (crack cocain), vaporises at high
temperature and can be smoked,giving more rapid and
intense effect.
 Desensitizes the terminal nerves and causes
vasoconstriction at the site of application.
 Stimulates the cortex for a short time followed by
depression.

27. Clinical feature
Effects appear rapidly after inhalation and especially after smoking
When inhaled – 1 to 3 min
Iv or smoked – in seconds
Stage of excitement:
 Dryness of mouth,dysphagia,feeling of wellbeing and loss of
depression and fatigue
 Excitement,restless and talkative
 Tachycardia,hyper/hypotension, tachypnoea,dilated
pupil,headache,pallor of skin,cyanosis,sweating and raised
temperature
 Reflexes are exaggerated,may be tremor and convulsion
 Abdominal pain and diarrhoea

28. Stage of depression:
 Within an hour or even less, respiration become
feeble,profuse perspiration,collapse ,convulsion and
death occurs.
 Serious complications usually occurs within 3 hrs of
use and include coronary artery spasm,which may
results in myocardial ischemia or infarction leading
to hypotension,cyanosis and ventricular arrhythmias.
 Cocain toxicity should be considered in young adults
who present with ischemic chest pain.

29. Management
 If taken by mouth-
-Gastric lavage
 If by nose
-Wash out the mucous membrane with water
 If injected
-Apply a ligature above the part
 Treat convulsion
 Maintain ABC

30. All patients should be observed with ECG monitoring for
a minimum of 4 hrs.
-12 Lead ECG,trop T
-Chest pain or hypertension- use benzodiazepines
and iv nitrates, avoid beta blockers.
-CAG should be considered in patients with MI or
acute coronary syndromes.
Metabolic acidosis – sodium bicarbonate inj.

31. Thanks