common cause of ALF in southern India

1. RAT KILLER PASTE
POISIONING
Dr. (Maj) Ajay Kandpal
MD MEDICINE, DNB MEDICINE
DM PG (Gastro enterology) STANLEY MEDICAL
COLLEGE
CHENNAI, INDIA
kandykilroy@gmail.com

2. Why This Topic?
 Statistics
 SMC as a centre of liver transplant
 Daily call overs

3. Why So Common..
 Easy availability
 Easy disguise
 Susceptible young population
 Reaction to stress as Potatotes!

5. Scheme Of Presentation
 Historical aspect
 Brief about rodenticides
 Rat killer paste
 Analysis of available articles
 Role of MGE
 Take home messsage

6. Rodenticides
 ORGANIC
 Coumarins
 Warfarins and Superwarfarins
 Indandiones
 • INORGANIC
 Thallium sulphate
 Yellow phosphorus
 Zinc phosphide
 Aluminium phosphide
 Arsenic

7. History
 Glowing element
 Elemental yellow phosphorus was isolated by
the Hamburg merchant Hennig Brandt (or
Brand) in 1669
 Treating Colic,TB asthmatic fevers, tetanus,
apoplexy and gout
 Very low dose was lethal
 Phosphine as war gas

8. Difference
RAT PASTE RAT POWDER/CAKE
BRAND Ratol Mortein
PRINCIPLE
COMPOUND
Yellow Phosphorus Warfarin
MOA Direct toxic, vasculotoxic Coagulation cascade
ANTEDOTE Nil Vit K

9. What Is Rat Killer Paste

10. Phosphorus
 Elemental phosphorus exists in two forms
 Red phosphorus
 Yellow phosphorus

11. Yellow Phosphorus
 Yellow phosphorus is an inorganic substance
used in military ammunition, fire crackers,
fertilizers, and as rodenticide
 The most readily available source of yellow
phosphorus today is rodenticides.
 Rodenticides are available as powders or pastes
containing 2 to 5% of yellow phosphorus.
 Minimum dose 15mg;
 Lethal dose 60mg ( 1mg/kg)
 Mortality rate 27% to 48%

12.  Yellow phosphorus emits smoke(Phosphine
gas) and has very strong garlicky odour. It can
get through skin, mucus membrane,
respiratory and gastrointestinal epithelium.
 Bile salts are important for absorption of
phosphorus. Because of water content and
low oxygen tension, phosphorus remains
stable in gut for longer period.

13. MOA
 Highly corrosive
 The mechanism of toxicity of yellow phosphorus is
by means of an exothermic reaction producing
phosphoric acid that causes direct tissue damage
due to the production of free radicals against
organic molecules. This, in turn, will bring about
changes in ribosomal function and protein
synthesis, failure of regulation of blood glucose,
and fatty degeneration of multiple organs.
 Direct toxic to heart and vessels
 Phosphorus oxide highly toxic to all body organs

14. Manifestations
 Depend on route of delivery
 Time elapsed since exposure

15. Acute Inhalation
 Conjunctivitis
 Mucosal necrosis
 Wheezing
 Chemical pnemonitis
 Non – cardiogenic pulmonary edema

16. Skin Or Eye
 Dermal burns
 Ocular burns

17. Acute Ingestion
 GI symptoms
 Diarrhea with “smoking stools”
 Systemic effects
 Headache, delirium
 Shock
 Seizures
 Arrthymias
 Metabolic
 Hypocalcemia
 Hyperphosphatemia

18. What Happens After Ingestion
 The patient with yellow phosphorus
intoxication passes through three stages.
 First stage
 Second stage
 Third stage

19. First Stage
 Occurs during the first 24 hours
 Asymptomatic
 Signs and symptoms of local gastrointestinal
irritation

20. Second Stage
 Occurs between 24 to 72 hours
 It is an asymptomatic period and the patient
may be discharged prematurely
 There may be mild elevation of liver enzymes
and bilirubin in this stage

21. Third stage (advanced)
 Occurs after 72 hours until the resolution of
symptoms or death.
 Hepatomegaly and jaundice appear-acute
fulminant hepatic failure mandating liver
transplantation.
 Bleeding can occur due to coagulopathy and
thrombocytopenia
 Some patients may develop acute tubular
necrosis and present with acute renal failure.

22. Third stage (advanced)
 Hemolysis can occur due to destruction of
RBC’s by phosphorus
 Central nervous system effects include
changes in mental status like confusion,
psychosis, hallucinations, and coma.
 Cardiac toxicity includes hypotension,
tachycardia, arrhythmias, toxic myocarditis and
cardiogenic shock.

23. Clinical Staging
 Based on the dose
 CAT 1
 >/= 1mg/kg Body weight (LETHAL dose)
 CAT 2
 < 1 Mg/kg body weight (SUBLETHAL dose)
 Based on the time duration

24. Pathology
 Liver shows extensive hepatocyte periportal
necrosis with balloon degeneration.
 Acute Toxicity:
 Zone 1 necrosis +/-
 Microvesicular steatosis.

25. Microscopy

26. HOW TO MANAGE
?

27. General Principles
 No specific antidote
 Treatment is directed at removal of the poison
and supportive therapy.

28. Gastric Lavage
 Gastric lavage with potassium permanganate
is recommended to convert the phosphorus to
relatively harmless oxides.
 0.1 to 0.2 % copper sulphate can be used. it
will precipitate as copper sulphide and coat
over phosphorus particles
 Charcoal can be used

29. NAC
• N-acetyl cysteine can be tried if patient
presents early.
2 ampules contain 400mg

30.  N ACETYL CYSTEINE
 IV continuous infusion
 Acute ingestion (within 8-10 hr after ingestion)
 Administer as 3 doses
 Loading dose: 150 mg/kg IV; mix in 200 mL of
D5W and infuse over 1 hr
 Dose 2: 50 mg/kg IV in 500 mL D5W over 4 hr,
 Dose 3: 100 mg/kg IV in 1000 mL D5W over 16 hr

31.  Intermittent IV administration (total
treatment time 48 hr)
 Late presenting or chronic ingestion (more
than
10 h after ingestion) in patients >40 kg
 Loading dose: 140 mg/kg IV infused over 1 hr
(dilute in 500 mL D5W), THEN
 Maintenance dose: 70 mg/kg IV q4h for at least
12 doses (dilute each dose in 250 mL of D5W and
infuse over minimum 1 hr)

32. King College Criteria For
Transplant
All other causes of fulminant hepatic failure (non-
PCM)
 Prothrombin time >100 seconds (irrespective of the
grade of encephalopathy) or
 Any three of the following variables (irrespective of the
grade of encephalopathy)
 Age <10 years or >40 years
 Etiology: non-A, non-B hepatitis, halothane hepatitis,
idiosyncratic drug reactions
 Duration of jaundice before onset of encephalopathy >7
days
 Prothrombin time >50 seconds
 Serum bilirrubin >18 mg/dl

33. Flowchart MGT
General measures, ABC,
Lavage, Charcoal
NAC
SUPPORTIVE,
TRANSPLANT

34. ARTICLES
 Early use of intravenous N-acetylcysteine in
treatment of acute yellow phosphorus
poisoning
Meban Aibor Kharkongor, Ajay Kumar Mishra, K Fibi
Ninan, Ramya Iyadurai
Department of Internal Medicine, Christian Medical College,
Vellore, Tamil Nadu, India
 Acute yellow phosphorus poisoning causing
fulminant hepatic failure with parenchymal
hemorrhages and contained duodenal
perforation
Reddy Ravikanth, S Sandeep, Babu Philip
Department of Radiology, St. John's Medical College,
Bengaluru, Karnataka, India

35.  “Successful Treatment of Acute Liver Failure due to
Yellow Phosphorus Ingestion in a Rural, Low
Resource Setting” Bassem W Ghali*1,2, Timothy S
Laux 1,2, Gajanan B Phutke1, Reshma D Souza1
and Priyank Jain1,
 Profile of Rat Killer Poisoning Cases in a Tertiary
Care Hospital at Mysore D K Suneetha1 , J
Inbanathan1 , Sowmya Kannoth2 , P K Reshma2 ,
M S Shashank2, Mysore Medical College &
Research Institute, Mysuru, Karnataka, India

36. Take Home
 Late development of complication
 Clinical staging important for triage and
prognostication
 Elevation of prothrombin time can be wrongly
attributed to a warfarin containing rodenticide.

37.  All rodenticide poisoning are not due to
phosphorus derivatives
 Identifying exact component of rodenticide is
mandatory before planning for discharge.
 LFT /PT should be mandatory in all cases.
 All rodenticide poisoning patients should be
reviewed at least once with LFT values in a
week time.

38. THANK YOU