This document discusses celphos poisoning caused by ingestion of aluminium phosphide. It notes the key identification features are a fishy smell on the breath and vomiting. It then explains the mechanism of toxicity is that phosphine gas is released in the stomach which inhibits enzymes and protein synthesis, particularly cytochrome oxidase. This causes widespread cellular hypoxia. Clinical features that develop within 30 minutes include burning in the chest, vomiting, and diarrhea. Within 6-8 hours, patients can develop cardiovascular issues like hypotension, arrhythmias, and congestive heart failure. Respiratory problems like pulmonary edema may occur later. Management involves gastric lavage, activated charcoal, ventilation, IV fluids, bicarbonate for acidosis

1. Celphos Poisoining
DRx.IMRAN AHMAD
B.SC , BNYS
,D.E.T.C.T(TSM LKO)

2. IDENTIFICATION

3.  Aluminium phosphide (ALP).
 A solid fumigant widely used as a grain preservative.
 Retrostemal burning.
 Epigastric discomfort.
 Recurrent vomiting and diarrhoea.
 There is fishy smell from breath.
INTRODUCTION

4.  After ingestion, phosphine is liberated in the stomach that
is absorbed in to the circulation.
 Phosphine is the protoplasmic poison that inhibit various
enzymes and protein synthesis.
 It is a potant respiratory chain enzyme inhibit produces
widespread cellular hypoxia inhibition of cytochrome
oxidase.
 Inhibition of cytochrome oxides respiration generation of
free oxygen redicals that stimulates super oxides
dismutase.
MECHENISM OF TOXICITY

5.  The fatal dose of an unexposed pellet of ALP is 150-
500 mg.
 Clinical manifestation develop within 30 minutes of
ingestion.
 Next 6-8 hours patients develop systemic features.
i.E CVS/RS.
CLINICAL FEATURES AND FATAL
DOSE

6.  Important:-hypotension shock,tachycardia or
bradycardia and arrhythmias.
 Shock:- because of cardiao toxicity , recurrent
vomiting and vascular injury.
 Congestive heart failure due to myocardial
depression.
 The ECG changes include arrhythmias,blocks,ST
depression and T inversion, ST elevation and various
blocks.
CARDIOVASCULAR FEATURES

7. Cough
Dyspnoea.
Cynosis
Pulmonary oedema and ARDS usually occur after 6-36
hours of ingestion.
RESPIRATORY FEATURES

8. Hypomagnesaemia.
Metabolic acidosis are common.
METABOLIC FEATURES

9. Renal failure (AKI)
Pericarditis
Liver damage indicated by elevated transaminases
and bilirubin .
MISCELLANEOUS

10. Typical features of poisoning.
Fishy smell in the breath and vomitus.
Confirmation can be done by silver nitrate test on
lavage fluid or on breath.
DIAGNOSIS

11. Urine output
ABG
ECG
PT/INR
LFT
KFT
OTHER

12. Gastric lavage :- coconut oil with sodabicarb
(500/50ml).
Activated charcoal .(in sorbitol)
Adequate ventilation and urine output.
Infuse large volumes of saline to maintain the systolic
pressure above 90 mmHg.
Infuse large doses of intravenous bicarbonate to
correct acidosis.
Intrope support:- norepinephrine or dopamine .
Magnesium sulphate
MANAGEMENT

13. IV fluid
Antibiotics
Pantop
Ondensetron
Inj.Analgesics
Inj.NAC
OTHERS

14. Identification
Diagnosis
Lavage
Metabolic acidosis.
POINT TO BE REMEMBER

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