1. According to WHO, there are 3 million cases of acute poisoning annually, with 220,000 deaths, 90% occurring in developing countries. Common poisons in India are insecticides and pesticides. 2. Organophosphorus poisoning inhibits acetylcholinesterase, increasing acetylcholine at receptors. Signs include muscarinic, nicotinic, and CNS effects. Diagnosis involves checking cholinesterase levels. Treatment is with atropine and pralidoxime. 3. Aluminum phosphide poisoning occurs through ingestion of tablets releasing phosphine gas, causing respiratory chain arrest and oxidative stress. Signs include gastrointestinal, hepatic, respiratory, metabolic, and cardiovascular effects

1. GUIDE : DR.A.THAKUR
CANDIDATE: DR.SMIT CHOPRA
MANAGEMENT GUIDELINES OF
COMMON POISIONING

2. GENERAL
MANAGEMENT

3. EPIDEMIOLOGY
According to WHO , there occurs three million acute
poisoning cases with 2,20,000 deaths annually
90% of these fatal poisoning occur in developing countries
Common poisons in india are insecticides and pesticides
such as organophosphorus, aluminium phosphides,
carbamates, rat kill .

4. GENERAL MANAGEMENT
GASTRIC LAVAGE:-
‣ A ryels tube is inserted through patients nose after
locally anaesthetising nose with lignocaine
‣ Ask the patient to swallow the tube and it goes down
through the oesophagus and eventually into the stomach
‣ Dont use force while inserting the tube
‣ Correct placement of the tube is confirmed by pushing
air though a syringe and a gurgling sound is heard by
keeping the stethoscope over epigastric region or gastric
content may be aspirated

5. ‣ Place the patients head down and in left lateral position to
reduce the risk of aspiration while vomiting
‣ Obtain a gastric lavage sample in a syringe for further
identification of poison
‣ At the time of inserting a nasogastric tube patients gag
reflex must be checked, If the gag reflex is absent then
patient needs endotracheal intubation before lavage is
started
▸Gastric lavage is indicated in almost all types of ingested
poisons except corrosive poisonings (as there is risk of
perforation)

7. ORGANOPHOSPH
ORUS POISIONING

8. Absorption- They are absorbed by inhalation, through skin,
mucous membranes and the GI tract
Metabolism- detoxification occurs via cytochrome p450
monooxygenase & excretion occurs through urine
INTRODUCTION

9. MECHANISM OF ACTION
Action- organophosphates inhibit acetylcholinesterases , so
the amount of acetylcholine increases at myoneural junction
which acts mainly on three types of receptors
‣ Muscarinic receptor affecting pupils, bronchial
muscles, salivary and sweat glands, urinary
bladder
‣ Nicotinic receptors which causes twitching of
eyelid, tongue and facial muscles
‣ CNS stimulation causes headache, restlessness
tremor may even lead to convulsions, coma and
death

10. SIGNS AND SYMPTOMS
With massive ingestion or inhalation symptoms might begin
as early as within 5 min
Involuntary muscles and secretory glands are affected first
followed by voluntary muscles followed by vital centres in
brain
Respiratory signs include dyspnoea, bronchoconstriction ,
increased bronchial secretions , pulmonary edema
G.I signs include anorexia, increased salivation, abdominal
cramps, diarrhoea,

11. Miosis, increased lacrimation,blurred vision, urinary
incontinence
Cardiovascular signs include bradycardia (may sometime
cause tachycardia also), conduction blocks, arrhythmia and
hypotension
Muscular weakness ,fasciculation ,cramps may occur as
nicotinic effects
CNS manifestation includes headache, restlessness,
tremors, drowsiness ,confusion ,convulsions may even lead
to coma
Very rarely chromolachryorrhoea (red tears) may occur

13. INTERMEDIATE SYNDROME
In around 20% of cases after 1-4 days, muscle weakness
and paralysis occur.
These occur after the signs and symptoms of acute
cholinergic syndrome is no longer obvious .
The characteristic feature of this syndrome is weakness of
the muscles of respiration and proximal limb muscles and
other features include motor cranial nerve palsies
Diagnosis of intermediate syndrome can be made by 30Hz
rapid nerve stimulation test which shows a decremental
response to stimuli and correlate best with clinical weakness

14. CHRONIC SEQUALE
Delayed sequelae - delayed peripheral neuropathy can
occur one to 5 weeks after exposure. It begins with
paraesthesias and cramps in the calves, followed by
weakness and foot drop and may progress to a flaccid
paralysis resembling GBS . The disease may progress for 2-
3 months
Cause of death - death is caused by respiratory muscle
paralysis , respiratory arrest due to respiratory centre failure
or intense bronchoconstriction and very rarely due to
arrhythmia

16. DIAGNOSIS
Heparinised blood should be collected for cholinesterase
determination . Serum is separated and both are refrigerated .
RBC cholinesterase level less than 50% of normal indicates
poisoning
Plasma cholinesterase is more sensitive and will fall more
rapidly and before that of red cells. Thus if the plasma
cholinesterase level is low and RBCs cholinesterase levels are
relatively unchanged , indicates that amount of exposure is less
and if both are low indicates high amount of exposure
In treated cases the plasma value approach to normal in 7-10
days.

17. MANAGEMENT
The patient is removed from the source of exposure , the
contaminated clothing removed and the exposed areas are
washed with soap and water. If eye is contaminated
conjunctival recess is irrigated.
As soon as patient reaches health care personnel , gastric
lavage should be started
Endotracheal intubation and mechanical ventilation should
be considered if patient is unconscious , crepitations are
present in b/l lung fields and pao2<60mmhg .

18. Atropine sulphate arrest the muscarine effects of
postganglionic parasympathetic activity and arrests CNS
effects it has no effect on nicotinic actions
A foley catheter should be inserted before starting treatment
with atropine

19. Obtain intravenous access and give 3mg of atropine as
bolus
Record
‣ pulse rate,
‣ blood pressure,
‣ pupil size,
‣ presence of sweat and oral secretions ,
‣ auscultatory findings at the time of first atropine dose

20. Systolic blood pressure should be maintained above 80
mmhg
5 min after giving atropine check these vital signs again . If
no improvement has occurred give double the original dose
of atropine
Continue to review every 5 min; give doubling doses of
atropine if response is still absent, once the parameters
have begun to improve cease dose doubling and similar or
smaller doses can be used

21. Give atropine boluses until
‣ the heart rate is more than 80 beats per minute,
‣ the chest is clear ,
‣ tongue is dry ,
‣ sweating stops and
‣ pupils are dilated.
Tachycardia is not a contraindication to atropine boluses.

22. Once the patient is stable and signs of full atropinizaion has
appeared start an infusion of atropine giving every hour 10%-
20% of the total dose needed to stabilise the patient, this
should be continued for at least 24 hrs maintaining the sings
of atropinisation.
Assess the flexor neck strength regularly in conscious
patients by asking them to lift their head off the bed and hold
it in that position while pressure is applied to their forehead,
any sign of weakness is indicates that patient is at risk of
developing respiratory failure (intermediate syndrome).

23. Pralidoxime iodide or PAM acts by competing for the
phosphate moiety of organophosphorus compound and
release it from cholinesterase enzyme. it acts on muscarinic
as well as nicotinic sites.
PAM is given as 30mg/kg or 2g bolus dose followed by an
infusion dose of 8mg/kg/hr they are given up till the patient is
clinically well and atropine has not been needed for 12-24
hrs
If convulsions occurs it is controlled by diazepam , an
anticonvulsant might be added to the treatment

24. Antibiotics can be added to prevent pulmonary infections
Glycopyrrolate can be considered in patients at risk for
recurrent symptoms (after initial atropinization) but who are
developing central anticholinergic delirium or agitation.

25. 10-20

26. CELPHOS
POISIONING

27. INTRODUCTION
Aluminium phosphide is a well
known highly effective outdoor and
indoor insecticide and rodenticide
AlP is synthesised as dark grey
tablets or powder and marketed as
3gm tablet consisting of AIP(56%)
under the brand name CELPHOS
Each tablet releases 1gm of
phosphene
Fatal dose 0.5g

29. EPIDEMIOLOGY
In an autopsy study of unnatural deaths in northwest india
AIP was found to be the most common suicidal poison
,causing 68.4% of total deaths due to poisoning between
1992 to 2002. Between 1977 to 87,barbiturate was most
common cause of death by poisoning where as between
1987 and 1997 they were replaced by organophosphates,
since 1992 AIP has taken over the lead

30. MECHANISM OF ACTION
AIP in the presence of moisture releases phosphene gas
which is the active form of pesticide , if it comes in contact
with acid (HCl) phosphene is released more vigorously
After ingestion of tablet gastric HCl releases phosphine -
‣ phosphine mainly binds to cytochrome oxidase and
causes respiratory chain arrest.
‣ It also changes valencies of haem component of
haemoglobin.
‣ It also induces oxidative stress and boosts extra-
mitochondrial release of free oxygen radicals that
results in lipid peroxidation of the cell membrane

31. Lethal dose of AIP is around 0.5g those who took >0.5g and
survived had either taken very small amount, the tablet
expired or phosphene gas evaporated because the tablet has
been exposed to air.

33. Gastrointestinal symptoms include vomiting, and epigastric
pain may also cause hematemesis . It causes corrosive
lesions in oesophagus, stomach and duodenum. Dysphagia
is a late complication
Hepatotoxicity occurs leading to jaundice and elevation of
liver enzymes (SGOT & SGPT). Jaundice can even be a
manifestation of intravascular hemolysis
Respiratory sings include tachypnoea, crepitations and
rhonchi sometimes may lead to respiratory distress
syndrome and pulmonary oedema.
SIGNS & SYMPTOMS

34. Metabolic acidosis ,hypokalemia and acute renal failure have
been reported and these changes were associated with higher
mortality rates
Cardiovascular effects include -
‣ Profound and refractory hypotension,
‣ Subendocardial infarction and pericarditis ,
‣ Congestive heart failure,
‣ There occurs left ventricular hypokinesia and ejection
fraction decreases which causes severe hypotension,
‣ ECG shows sinus tachycardia, ST - T changes and
conduction defects

35. Sinus tachycardia dominates in first three to six hours of poisonin

36. DIAGNOSIS
Detection of phosphine gas in gastric fluid or breath through
the silver nitrate test
Gas chromatography is the most sensitive and specific test
for detecting the presence of phosphine in blood/air
Additional supportive evidences can be obtained by
performing various investigations such as
‣ ABG- which shows metabolic acidosis
‣ ECG- shows ST - T changes
‣ serum magnesium- which is on lower side

37. MANAGEMENT
AIP do not have any specific antidote so the treatment is mostly
supportive
Immediate primary survey should be performed to restore
effective oxygenation , ventilation and circulation.Confirm airway
patency and if required protect the airway with endotracheal tube
and start supplemental oxygen.
Contaminated clothes should be removed and skin and eyes
should be washed with water immediately
Establish an intravenous access ,preferably centralvenous line
Close monitoring of blood pressure and ABG should be done
Repeat ECG should be taken every 1/2 hourly till next 12hours

38. Gastric lavage should be performed with potassiumpermanganet
(1:10000) as it oxidises phosphine to non toxic phosphate .
Alternatively coconut oil can be used for gastric lavage, oil inhibits
phosphene release from AIP.
CVP guided fluid should be started and the aim is to keep CVP between
12-14. Fluid infusion rate may be as fast as 1lit/hr
The aim is to keep systolic blood pressure >90 mmhg . If hypotension is
refractory start noradrenaline and dopamine
The role of advanced measures like use of intra aortic ballon pump
(IABP) to mechanically support the heart has been demonstrated in toxic
myocarditis with refractory shock .
Phosphine excretion can be increased by maintaining adequate
hydration and renal perfusion

40. Hydrocortisone 200-400 mg given every 4-6 hourly combats
shock by potentiating the effects of vasopressor
Bicarbonate level less than 15mEq/l requires acidosis
correction with sodabicarb . Aggressive correction of
acidosis results in significant improvement of the patient.
Dialysis may be required for serve acidosis and acute renal
failure
cyanosis not responding to oxygen therapy may be a sign of
methaehemoglobinemia that requires therapy with
intravenous methylene blue (1% solution) at a dose of
2mg/kg over 5 min

41. Treatment with magnesium sulphate has been reported to reduce
mortality upto 50%. Magnesium stabilises the cell membrane and
acts as an antioxidant.
The dosage of magnesium sulphate were found different in different
studies
A. 3g as infusion over 3hrs f/b 6g per 24 hrs for 3-5 days
B. 1gm stat f/b 1gm/hr for next 2 hrs f/b 1g every 6hrs for
5-7 days
C. 4g stat f/b 2g after one hour f/b 1g every 3 hourly for 5-
7 days
D. 3g bolus f/b 0.5g/hr continuous infusion for 5-7 days
ROLE OF MAGNESIUM SULPHATE

42. NEWER MODALITIES
DIGOXIN - it has been hypothesised that treatment with
digoxin increases myocardial contractility and blood pressure
countering the effects of AIP on cardiac myocytes. Mehrpour et
al. have recently reported about successful treatment of an 18
year old girl who had ingested 3g AIP tablet. On hospital
admission her BP was undetectable and she had severe left
ventricular systolic dysfunction . She received dopamine (10
microgram/kg/min) and DIGOXIN (0.5 mg) every six hourly
during the first day and continued with 0.25mg/day on following
days . The ECG parameters became normal on day 3 and
patient was discharged with full recovery
HYPERBARIC OXYGEN- hyperbaric oxygen improves the
survival time in rats poisoned with AIP.

43. Hyperglycaemia on admission has been found to be a
significant poor prognostic factor. Therefore , there is a
possible role of treatment of hyperglycaemia throughout
management of poisoning , which may improve the outcome
N-acetylcysteine - In rats exposed to AIP, N-acetylcysteine
increases survival time and reduce myocardial oxidative
injury

44. ETHYLENE-
DIBROMIDE

45. INTRODUCTION
EDB is an organic compound
easily available in India and is
widely used for fumigating
grains, vegetables and fruit
It is a nonflammable
colourless liquid available as
3ml vial.
Routes of exposure are
through inhalation, skin/eye
contact, ingestion.

46. SINGS & SYMPTOMS
Ethylene dibromide causes depletion in glutathione levels and
cellular disruption. It mainly affects organs such as liver and
kidney and results in progressive dysfunction
Respiratory symptoms include irritation to nose and throat
,sevre exposure may cause cough, bronchitis, pneumonitis.
Pulmonary edema may occur as late manifestations
CNS - EDB is a mild CNS depressant. Drowsiness occurs
following ingestion and inhalation. Large exposures may lead to
coma and death
Skin manifestations include itching and erythema, prolonged
skin contact causes blistering and skin ulcers

47. Ocular effects include conjunctivitis and temporary loss of
vision
Hepatic- significant liver damage results from inhalation or
ingestion of EDB . Hepatic enzymes rises significantly and
may even rise to 3 times the normal value
Renal- Decreased urine output , sometimes anuria may
occur. Increased levels of serum creatinine and urea occurs
which indicates AKI
GI symptoms include abdominal pain, nausea, vomiting, and
sometimes diarrhoea .

48. Metabolic acidosis can occur after high amount of exposure
of EDB
There is inconclusive evidence that EDB may reduce fertility
in men, anti spermatogenic effect has been demonstrated in
various animal species

49. Serum bromide levels can be measured however bromide
levels do not accurately predict the clinical course
Routine laboratory studies such as CBC, serum electrolyte,
Liver function test and Renal function test should be carried
out.
Deranged RFT & LFT indicates poor prognosis.
ABG should be carried out to look for metabolic acidosis
DIAGNOSIS

50. MANAGEMENT
There is no antidote for EDB. Treatment is mainly supportive
Decontamination should be done as early as possible as EDB
is absorbed through skin, hair, eyes, clothes including
footwear.
Remove the clothes and footwear of the patient ,Flush the
exposed skin and hair with water for atleast 15 min, then wash
with soap. Irrigate exposed eye with tap water for 15min.
Gastric lavage should be carried out after decontamination or
along with it.

51. Administer supplemental oxygen by mask to patients who have
respiratory complains. If the patient have respiratory distress or
patient is comatose plan for endotracheal intubation and
ventilatory support
ANTIDOTE- there is no proven antidote for ethylene dibromide ,
Dimercaprol (BAL) or acetylcysteine (mucomyst) have been
suggested as antidote based on postulated mechanism of
ethylene dibromide toxicity . However no studies have tested the
efficacy of these therapies and they are not recommended for
routine use.
Discharge can be planned if the patient has no neuropsychiatric or
pulmonary effects after observing for 24 hours

52. THANK Y