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A Case of Rodenticide Poisoning

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  • 1. A CASE OF JAUNDICE
    • PROF.DR.K.H.NOORUL AMEEN’S UNIT
    • ( M 4)
    • DR.M.ARIVUMANI
  • 2.
    • 20 yrs old Mr.Dhanasekar was referred from vinayaka missions medical college hospital salem to GSH on 8.10.11
    • On 4.10.11 He was taken to a private hospital near salem with c/o vomiting,abdominal pain,giddiness
    • On the suspicious history given by parents Stomcah wash was given at the primary care hospital and he was referred to VMMCH.
  • 3.
    • At VMMCH patient was managed on conservative lines.On 2 nd day of admission patient developed jaundice with altered liver parameters.
    • On probing the patient came out with h/o ingestion of rodenticide poison ON 1.10.11(4 days prior)
    • (RATOL)
  • 4.
    • He was managed conservatively with
    • N-acetyl cysteine,
    • dextrose,
    • vitamin k etc
  • 5.
    • Since the patients jaundice was progressively increasing he was referred to SMCH for liver transplantation.
  • 6.
    • Patient on 8.10.11 got admitted in our IMCU with c/o yellowish discolouration of eyes
    • h/o abdominal pain
    • h/o vomiting
    • h/o anorexia
    • no h/o fever
    • no h/o pedal edema,
    • no h/o abdominal distension
  • 7.
    • no h/o bleeding manifestation
    • no h/o altered sensorium /seizures
    • Past history
    • no h/o jaundice in the past
    • no h/o blood transfusion
  • 8.
    • On admission patient was
    • conscious,oriented
    • afebrile,not dyspnoeic
    • icteric
    • no cyanosis,no clubbing,no pedal edema
    • Vitals
    • PR-88/min
    • RR-24/min
    • BP-100/60mmhg
  • 9.
    • CVS S1 S2 heard,no murmur
    • RS –NVBS heard,no creps
    • P/A-Right hypochondrial tenderness +
    • no organomegaly
    • CNS- NFND
  • 10. CBC 4.10.11 7.10.11 8.10.11 13.10.11 15.10 Hb 15.5 14.2 14.1 14.0 13.8 TC 6400 7200 6100 6500 5800 PCV 46.5 42.6 42 42 41.4 PLT 219000 75000 68000 120000 150000
  • 11. RFT WITH ELECTROLYTES 4.10 6.10 8.10 18.10 SUGAR 90 110 85 104 UREA 36 25 26 32 CREATININE 0.4 0.8 0.7 0.6 SODIUM 131 133 129 134 POTASSIUM 5.2 6.4 5.2 4.5 CHLORIDE 103 98.6 90 BICORBONATE 18 22 23
  • 12. LFT 4/10 6/10 8/10 (sp 3) 9/10 12/10 18/10 Total bilirubin 18.2 17.2 11.6 20.1 16.9 11.6 direct 9.9 9.3 8.93 8.9 8.3 5.1 indir 8.3 7.9 2.67 11.2 8.6 SGOT 2240 750 480 138 77 164 SGPT 1556 335 910 99 236 161 SAP 239 720 558 GGT 76 64 Total protein 6.5 4.6 5.2 albumin 3.1 3.0 3.1
  • 13. 4/10 7/10 8/10 9/10 12/10 18/10 PT Test Control >2min 13sec 42sec 12.5sec 37sec 13sec 26sec 12sec 20sec 11sec 13.4sec PTT Test Control 53sec 24.7sec 23sec 48sec 45sec 40sec 30sec INR 3.3 2.8 2.2 1.8 1.3
  • 14. ABG-COMPENSATED RESPIRATORY ALKALOSIS
  • 15. URINE Colour Yellow Appearance Cloudy Specific gravity 1.010 PH 7.0 Protein Negative Sugar Nil Ketone Absent Rbc Nil Pus cells 2-5 Epithelial cell 2-3 BS/BP Positive Urobilinogen increased
  • 16.
    • Serum LDH- 383U/L(135-225U/L)
    • Reticulocyte count-2.3 %
    • HBsAg-negative
    • HIV-negative
    • Anti HCV-negative
    • Anti HEV-negative
    • ANA-negative
    • Serum cerruloplasmin 30mg/dl
    • Peripheral smear
    • RBC-erythropenia with predominantly normochromic normocytic RBC
    • WBC-mild leukocytosis +
    • Platelets-mild thrombocytopenia seen.
  • 17.
    • ECG-normal
    • Chest x ray- noraml
    • USG abdomen-liver normal in size,normal echo texture,ascites +(minimal),splenomegaly+
  • 18.
    • RATOL-Rodenticide poisoning(yellow phosphorus)
    • Acute liver failure-recovering
  • 19. GASTROENTEROLOGIST OPINION
    • Opined as acute fulminant hepatitis (toxic)
    • Conservative management
  • 20. TREATMENT GIVEN
    • Intravenous dextrose
    • Inj vitamin k 10mg iv od
    • Inj ranitidine 50mg iv bd
    • Cap.UDCA 300mg BD
    • Other supportive measures
    • FFP transfusion
  • 21. RODENTICIDE POISONING
    • ORGANIC
    • coumarins
    • warfarins and superwarfarins.
    • indandiones
    • INORGANIC
    • thallium sulphate
    • yellow phosphorus
    • zinc phosphide
    • aluminium phosphide
    • arsenic
  • 22. COUMARINS AND INDANDIONES
    • Coumarins and indandiones depresses the hepatic synthesis of vitamin k dependent clotting factors.
    • They also increase the permeabilty of capillaries predisposing to haemorrhage.
    • Mostly present as epistaxis,bleeding gums,hematuria,echymoses.
    • Continuous Monitoring of PT is necessary.
  • 23.
    • Vitamin k1 phytonadione 12-25mg oral or 10mg parenterally.
    • Intravenous infusion of vtamin k1(aquamephyton) in saline or dextrose is recommended for continuous bleeding.
    • There is no need to begin therapy unless the INR> 2. No data exist to prove that such therapy prevents anticoagulation, although vitamin K therapy is shown to reverse anticoagulation once it develops.
    • With long-acting anticoagulants, treatment may need to be at much higher doses and for a protracted period of time
  • 24. THALLIUM SULFATE
    • Insidious onset
    • Early symptoms include nausea,vomiting,bloody diarrhoea,stomatitis,salivation
    • Liver injury can occur
    • Muscle weakness,paresthesia,tremor,ptosis,ataxia,
    • myoclonic jerks,
    • Hypotension,ventricular arrythmias
    • ARDS
  • 25. PHOSPHORUS POISONING
    • Elemental phosphorus exists in two forms—red and yellow.
    • Red phosphorus is nonvolatile, insoluble, and unabsorbable, and therefore nontoxic when ingested.
    • Yellow phosphorus (also referred to as white phosphorus) is a severe local and systemic toxin causing damage to gastrointestinal, hepatic, cardiovascular, and renal systems
  • 26. YELLOW PHOSPHORUS
    • Yellow phosphorus is used as rodenticides and in fireworks.
    • 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% .
  • 27.
    • Yellow phosphorus emits smoke(Phosphine gas) and has very strong garlicky odour. It can get absorbed 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.
    • Phosphorus is a general protoplasmic poison causing cardiac, hepatic, renal, and multiorgan failure
  • 28.
    • The patient with yellow phosphorus intoxication passes through three stages.
    • FIRST STAGE- occurs during the first 24 hours in which patient is either asymptomatic or has signs and symptoms of local gastrointestinal irritation.
    • SECOND STAGE- occurs between 24 to 72 hours after ingestion. 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
  • 29. 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.
  • 30. THIRD STAGE (ADVANCED) OCCURS AFTER 72 HOURS UNTIL THE RESOLUTION OF SYMPTOMS OR DEATH(CONT….)
    • 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.
  • 31. PATHOLOGY
    • Liver shows extensive hepatocyte periportal necrosis with balloon degeneration.
    • Acute Toxicity: Zone 1 necrosis +/-
    • microvesicular steatosis.
  • 32.  
  • 33. ZINC PHOSPHIDE
    • Patients presents with same systemic toxicities encountered in yellow phosphorus poisoning jaundice,hepatic failure
    • Tetany due to hypocalcemia
    • Renal tubular damage
    • Arrythmias ,cardiomyopathy
  • 34. MANAGEMENT
    • There is no specific antidote for yellow phosphorus. Treatment is directed at removal of the poison and supportive therapy.
    • N-acetyl cysteine can be tried if patient presents early.150mg/kg bolus,50mg/kg over 4 hours,then 100mg/kg over next 16hours.
  • 35. MANAGEMENT
    • 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
    • charcaol can be used
  • 36.
    • vitamin k 10- 20mg iv in repeated dose
    • Intravenous dextrose
    • Fresh frozen plasma to correct coagulopathy.
    • Non fatty purgatives like mgso4 to eliminate phosphorus
    • Avoid fatty foods since they promote phosphorus absorption.
    • IV steroids
    • exchange transfusion(for hemolysis)-but it does not prevent the onset of coma or increase survival.
    • PD/HD if renal failure develops.
  • 37.
    • Careful monitoring of hepatic and renal function and management of their failure is required.
    • Liver transplantation has been done in suitable candidates for acute hepatic failure
  • 38. KINGS COLLEGE CRITERIA FOR LIVER TRANSPLANTATION
    • Acetaminophen-induced disease
    • Arterial pH <7.3 (irrespective of the grade of encephalopathy) or
    •  
    • Grade III or IV encephalopathy, and
    • Prothrombin time >100 seconds, and
    • Serum creatinine >3.4mg/dl
  • 39. KINGS COLLEGE CRITERIA FOR LIVER TRANSPLANTATION(CONT…)
    •  
    • All other causes of fulminant hepatic failure
    •  
    • 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
  • 40. HEPATOTOXICITY OF METALS-THE CULPRITS
    • Aluminum Manganese
    • Barium Phosphorus
    • Cadmium Thallium
    • Iron Zinc
    • Arsenic
    • Beryllium
    • Chromium
    • Gold
    • Lead
  • 41. HEPATOTOXICITY OF METALS ALUMINUM
    • Non-caseating granulomas in patients on long
    • term hemodialysis (Kurumay et al, 1989)
    • Contributes to hepatic injury in patients on total
    • parenteral nutrition (Klein et al, 1984)
  • 42. HEPATOTOXICITY OF METALS ARSENIC (1)
    • Acute Toxicity
    • Intrahepatic cholestasis
    • Steatosis
    • Zone 3 necrosis
    • ↑ Mitotic activity
    • Venocclusive disease
  • 43. HEPATOTOXICITY OF METALS ARSENIC (2)
    • Chronic Toxicity
    • Hepatoportal sclerosis
    • Systemic arterial disease
    • Cirrhosis
    • Angiosarcoma
    • Hepatocellular carcinoma
  • 44. HEPATOTOXICITY OF METALS BARIUM
    • Intravasation of BaSO4 enema into portal venous
    • system ->portal pylephlebitis or liver abscess
  • 45. HEPATOTOXICITY OF METALS COPPER (1)
    • Acute Toxicity: Zone 3 necrosis; cholestasis;
    • hypertrophy of Kupffer cells with
    • erythrophagocytosis; copper accumulation in Kupffer cells
  • 46. HEPATOTOXICITY OF METALS COPPER (2)
    • Chronic Toxicity:
    • Epithelioid granulomas
    • Cirrhosis with Mallory bodies resembling Indian childhood cirrhosis
    • Angiosarcoma
  • 47.
    • Indian J Pharmacol. 2011 May-Jun; 43(3): 355–356
    • Acute hepatic failure due to yellow phosphorus ingestion
    • Anupama Mauskar, Kunal Mehta, Leena Nagotkar, and Preeti Shanbag
    • Department of Pediatrics, Lokmanya Tilak Municipal General Hospital, Sion, Mumbai, India
  • 48.
    • J Assoc Physicians India. 2003 Aug;51:816-7.
    • Rodenticide-induced hepatotoxicity.
    • Karanth S, Nayyar V.
    • Source
    • Department of Critical Care Medicine, Airport Road, Bangalore 560 017
  • 49.
    • Fernandez OU, Canizares LL. Acute hepatotoxicity from ingestion of yellow phosphorus-containing fireworks.
    • J Clin Gastroenterol. 1995;21:139–42.
    • Santos O, Restrepo JC, Velasquez L, Castano J, Correa G, Sepulveda E, et al.
    • Acute liver failure due to white phosphorus ingestion.
    • Annals of hepatology. 2009;8:162–5.
  • 50. PURPOSE OF PRESENTATION
    • Hepatotoxicity following acute poisoning with rodenticides has been infrequently reported in literature
    • To emphasize the fact that this form of clinical presentation is not unusua l.
    • All rodenticide poisoning are not due to coumarin derivatives.
    • Yellow phosphorus poisoning is benign in early stage,becomes fulminant in 3 rd stage.
    • 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 atleast once with LFT values in a week time.
  • 51. REFERENCES
    • Forensic medicine and toxicology R.N.Karmakar.
    • Medical toxicology Richard.C.Dart.
    • Annals of hepatology april-june 2009.
    • THANK
    • YOU