its on aluminium phosphide poisoning management

1. Acute Aluminum
poisoning:
Phosphide

2. Acute Aluminum Phosphide
poisoning:
 Acute aluminum Phosphide poisoning is an
extremely lethal poisoning.
 Ingestion is usuallysuicidal in intent, uncommonly
accidental and rarely homicidal.
 Unfortunately the absenceof a specific antidote results
in very high mortalityand the key to treatment lies in
rapid decontamination and institutionof resuscitative
measures

3.  Aluminum Phosphide (AlP) is a solid fumigant which
has been in extensive use since the 1940s. It has rapidly
becomeone of the mostcommonlyused grain
fumigants becauseof its properties which are
considered to be near ideal; it is toxic to all stages of
insects, highly potent, does not affect seed viability, is
free from toxic residues and leaves little residue on
food grains.1

4.  Unfortunately, its widespread use has been associated
with a galloping rise in the incidence of alphos
poisoning
 In a studyconducted by Siwach and Gupta,aluminium
phosphide poisoning was found to be the most
commoncause of acute poisoning in India.

5.  It was also found to be the most common cause of
suicidal death in north India.
 Poisoning shows a distinct male preponderance in the
lowersocio-economic strata and in rural areas,
probably due to the heavy social stress burden
in this group.

6.  Trade names
Celphos,alphos,fumigran,chemfume
 Aluminum Phosphide is available in the form of 3 gm
tabletsor 0.6 gm pellets
 Each 3 gm tablet releases 1 gm and each 0.6 gm pellet
0.2 gm of Phosphine gas on exposure to moisture

7.  Phosphine gas is colourlessand odorless.
Howeveron exposure toair itgives a foul odour
(garlicky ordecaying fish)
 The fatal dose is around 0.5 gm.

8. Mechanism of action
 Mitochondrial respiraratory chain is necessary for
survival and vitalityof normal bodycells.
 Aluminum Phosphide when ingested, liberates a lot of
Phosphine gas in the stomach which has a very
pungent smell.
 Phosphine gas is rapidly absorbed from the stomach
and inhibits the mitochondrial respiratory chain and
hence leads to cell necrosis and death

9.  . It has a very destructiveeffect on myocardial cells i.e.
cells of the heart muscleand leads on to myocarditis.
 The degree of myocarditis can vary from mild to severe
and it can cause heart failure.
 Itcan alsocauseventricular fibrillation and sudden
death.

10. Clinical features
 Nausea, vomiting and abdominal pain are the earliest
symptoms thatappearafter ingestion
 Gastrointestinal symptoms which present in moderate
to severe poisoning are excessive thirst, abdominal
pain and epigastric tenderness

11.  cardiovascular abnormalities seen are
 profound hypotension and shock
 dry pericarditis
 myocarditis,
 acutecongestive heart failure
 Arrhythmias – sinus tachycardia/ bradycardia with
heart blocks/ ventricular fibrillation

12.  Respiratorysystem
 Dyspnoea,
 Type I or II respiratory failure.
 pleural effusion
 ARDS

13.  Nervous system manifestations
 Headache,
 dizziness,
 altered mental status,
 convulsion,
 acute hypoxicencephalopathy
 coma.

14.  Renal and hepatic failures
 bleeding diathesis due tocapillary damage,
 acuteadrenocortical insufficiency
 severe metabolicacidosis.

15. Diagnosis
 A positive historyof ingestion .
 The presence of typical clinical features,
 garlickyodour from the mouth
 highlyvariablearrhythmias in ayoung patientwith
shock and no previous history of cardiac disease .
 Silver Nitrate Test.

16. Laboratory investigations
 Leucopenia - indicates severe toxicity
 Increased SGOT or SGPT
 Raised blood urea/ serum creatinine
 metabolicacidosis
 decreased magnesium
 Measurement of plasma renin - direct relationship
with mortality and is raised in direct proportion to
doseof pesticide
 The serum level of cortisol.
the

17.  Chest X-ray - hilaror perihilar congestion if ARDS
develops / pleural effusion
 ECG - shows various manifestations of cardiac injury
(ST depression orelevation, bundle branch block,
ventriculartachycardia, ventricularfibrillation).
 Echocardiography - Wall motion abnormalities,
generalized hypokinesia of the leftventricle,
decreased ejection fraction and pericardial effusion

18. Management
 The most important factor forsuccess is resuscitation
of shock and institutionof supportive measuresas
soon as possible
 Intravenousaccess should be established and 2-3 litres
of normal salineare administered within the first 8-12
hrguided bycentral venous pressure(CVP) and
pulmonarycapillary wedge pressure(PCWP). The aim
is to keep the CVP ataround 12-14 cm of water.
 Someworkers have recommended rapid infusion of
saline (3-6 litres) in the initial 3 hr.

19.  Low dose dopamine (4-6 μg/kg/min) is given to keep
systolic blood pressure >90 mm Hg

20.  Hydrocortisone 200-400 mg every 4-6 hr is given
intravenously to
 combat shock,
 reduce the doseof dopamine,
 topotentiate the responsivenessof the body to
endogenousand exogenouscatecholamine's.

21.  Oxygen inhalation is given for hypoxia.
 ARDS requires intensive care monitoring and
mechanical ventilation.

22. To reduce the absorption of
phosphine,
 Gastric lavage with potassium permanganate
(1:10,000) is done.
 Permanganate is used as itoxidizes PH3 to form non-toxic
phosphate.
 This is followed by a slurryof activated charcoal
(approximately 100 gm) given through a nasogastric tube.
 A cathartic (liquid paraffin) is given toaccelerate the
excretion of aluminum phosphideand Phosphine.
 Antacids and proton pump blockers are added for
symptomatic relief.

23. Phosphine excretion increased by
 Maintaining adequate hydration and renal perfusion
with
 intravenous fluidsand lowdose (4-6 μg/kg/min)
dopamine.
 Diuretics like frusemidecan be given if systolic blood
pressure is >90 mm Hg to enhance excretion
 as the main routeof elimination of phosphine is renal

24.  All types of ventricular arrhythmias seen
in these patients and the management is the same as
forarrhythmias in othersituations
 Bicarbonate level less than 15 mEq/L requires sodabicarb in
a dose of 50-100 mEq intravenously every 8 hour till the
bicarbonate level rises to 18-20 mEq/L
 Dialysis indicated for severe acidosis and acute renal
failure

25. Poor Prognostic
Developmentof
 refractory shock,
 ARDS,
 Asp pneumonitis,
 metabolicacidosis,
 Coma
 severe hypoxia,
 Gastrointestinal bleeding,
 Pericarditis
markers

26. Mortality
 The mortality rate is highlyvariable, ranging from 37-
100%
 Can reach more than 60% even in experienced and
well equipped centre

27.  The average time interval between intake of poison
and death is three hours with a range of 1-48 hours,
 95% of the patients die within 24 hours and the
commonest cause of death in this group is arrhythmia.
 Death after 24 hours is due to shock, acidosis, ARDS
and arrhythmia