Op poisoning and its management

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organophosphate poisoning

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Op poisoning and its management

  1. 1. OP POISONING AND ITS MANAGEMENT
  2. 2. CASE I HISTORY B Raju a 27 yr old unmarried gentleman, was brought to CMC casualty at 3am on 22-04-11 with alleged history of consumption of Phorate (OP compound) mixed with water, at 5pm the previous evening.  He had 4 episodes of non-projectile, non-bilious vomiting. No h/o blood in vomitus.  No h/o of increased salivation, urination or defecation.
  3. 3.  In the casualty, gastric lavage was done and activated charcoal was given. O/Edrowsy, GCS 15/15 febrile Pulse rate- 100/min Blood presssure- 90/70mmHg Respiratory rate- 28/min 
  4. 4. Neck muscle weakness  Bilateral PINPOINT PUPILS, not reacting to light  No focal neurological deficit  Tone of upper limb muscles increased bilaterally, normal tone in lower limb  Power- grade 3 in all 4 limbs  Reflexes- all deep tendon reflexes are preserved, however plantar reflex was unresponsive bilaterally 
  5. 5. CVS- 1st and 2nd heart sounds heard, no added sounds  RS- normal vesicular breathe sounds heard  P/A- soft, non-tender, no organomegaly 
  6. 6. INVESTIGATIONS ABGPh- 7.4 Pco2- 34 Po2- 118 ELECTROLYTESNa- 125 K- 6.9 Cl- 108 Ca- 4.35 HCO3-
  7. 7.      Hb- 16.3 Platelets- 136000 WBC Total- 7500 WBC Diff- N-83, E-6, B-1, L-10 LFTDirect bilirubin- 0.2 Total bilirubin- 1.1 Total protein- 6.7 Albumin- 3.8 SGOT- 54 SGPT- 63 Alkaline phosphatase- 102
  8. 8.  Diagnosis???
  9. 9.  Organophosphorus poisoning…
  10. 10. COMMON AMONG FARMERS-
  11. 11. MECHANISM OF ACTION Inactivates acetylcholinesterase by phosphorylation, followed by accumulation of Ach in the synapses.  Recovery  Aging 
  12. 12. ORGANOPHOSPHORUS COMPOUNDS NERVE AGENTSG agents- Sarin, tabun, soman V agents- VX, VE INSECTICIDESDIMETHYL COMPOUNDS Dichlorvos  Fenthion  malathion  DIETHYL COMPOUNDS Diazion  Parathionchlor  chlorpyrifos 
  13. 13. CLINICAL FEATURESMuscarinic Cardiovascular Bradycardia Hypotension Respiratory Rhinorrhea Bronchorrhea/spasm Cough Gastrointestinal Increased salivation Nausea/vomiting Abdominal pain Diarrhoea Fecal incontinence Genitourinary Urinary incontinence Ocular Blurred vision/miosis Increased lacrimation Nicotinic Cardiovascular Tachycardia Hypertension Musculoskeletal Weakness Fasciculations Cramps Paralysis Central receptors Anxiety Restlessness Ataxia Convulsions Insomnia Dysarthria Tremors Coma Absent reflexes CS respiration Resp. depression Circulatory collapse
  14. 14. TRIPHASIC ILLNESS… ACUTE CHOLINERGIC SYNDROME-Cholinergic symptoms within first 24 hours Due to persistent depolarization of the neuromuscular junction due to blockade of AChE at all the receptors Features include garlic like odour in the breath/vomit/clothes, bradycardia (80%), miosis, fasciculations, twitching, convulsions, flacid paralysis of limbs and extraocular muscles, central depression of respiratory system. Some response to atropine claimed 
  15. 15. INTERMEDIATE SYNDROME 24-96 hours after poisoning after the cholinergic phase settles  Excess Ach an NMJ causes down regulation of nicotinic receptors- muscles affected  Characterized by proximal neck muscle leading to respiratory distress and failure without muscarinic signs  Without intervention, cyanosis, coma and death occurs rapidly  Incidence 8-49%, lasts for few days to about 3 weeks 
  16. 16. OP INDUCED DELAYED POLYNEUROPATHY 1-3 weeks after acute exposure  Due to degeneration of long myelinated nerve fibres.  Pure motor or sensor-motor  Characterized by cramps in the legs, numbness and paraesthesiae in the distal UL & LL, shuffling gait, foot and wrist drop.  Wasting, DTR reduced/absent, pyramidal tract signs  Recovery is incomplete 
  17. 17. MANAGEMENT Airway - ensure clear airway, clear secretions, check for cough/gag  Breathing - check oxygenation, supplemental O2, breathing pattern & adequacy  Circulation - heart rate, rhythm, blood pressure  Decontamination – gut and skin
  18. 18. ACUTE CHOLINERGIC SYNDROMEAtropine- 1.8- 3mg bolus - dose doubled every 5mins until atropinised - then 20-30% dose needed for maintenance, given as infusion/ hour  Oximes- Pralidoxime chloride (1gm bolus in 30mins, then infusion 0.5g/hr) OR - Obidoxime (0.25mg bolus, then infusion 0.75g/24hr) 
  19. 19. iv Diazepam  Oxygen and ventilatory support 
  20. 20. INTERMEDIATE SYNDROMEVentilatory support while on sedation  Parenteral nutrition 
  21. 21. OPIDNNo specific treatment  Exercise recommended 
  22. 22. CASE 2 HISTORY:  35 year old male following consumption of oduvanthalai with alcohol, presented with  breathlessness and palpitations  Vomiting (3-4 episodes/day ) a/w abdominal pain  Giddiness
  23. 23. EXAMINATION: Patient oriented, dyspnoeic, afebrile Pulse rate:91/min Blood pressure= 110/70 mm Hg Respiratory rate:20/minute Diffuse abdominal tenderness 
  24. 24. ABG pH 7.33 (7.35- 7.45)  pCO2 33  pO2 97 ELECTROLYTES  Na 128 K 2.1  Cl 102  HCO3 (24-28)  Ca 4.15  Lac 1.0 mmol/l 
  25. 25. Hb 12.2  Creatinine 1.6( 0.5-1.4)  Urinary pH 7 (<6)  LIVER FUNCTION TESTS Bilirubin(total) 0.7 Direct 0.2 Protein (total) 7.4 Albumin 3.9 SGOT 602 (8-40) SGPT 143 (5-35) ALP 336 
  26. 26. ODUVANTHALAI POISONING
  27. 27. CLEISTANTHUS COLLINUS (ODUVANTHALAI) •Commonly consumed as a leaf decoction. •Fatal dose: 10.5 g/kg body weight/ 200-400 leaves •Fatal Period : 1-3 days
  28. 28. • MECHANISM OF ACTION : Injury to the distal renal tubules, pulmonary epithelium and peripheral blood vessels due to glutathione depletion • ACTIVE PRINCIPLE: aryl-naphthalene lignin lactones: Collinusin, the glycosides Cleistanthin A and B, and their genin Diphyllin
  29. 29. hypokalemia due to kaliuresis  cardiac arrythmias  metabolic acidosis due to distal renal tubular acidosis  hypoxia due to ARDS  hypotension due to vasodilatation  Rhabdomyolysis occurs which leads to myoglobinuria and renal failure 
  30. 30. CLINICAL FEATURES SYMPTOMS  Vomiting  Headache, giddiness  Palpitations  Dyspnoea  Neuromuscular weakness SIGNS  Tachypnoea( >30/min)  Hypotension
  31. 31. CHEST X RAY: may show infiltrates ( non cardiogenic pulmonary oedema- acute respiratory distress syndrome)
  32. 32. ECG  ST segment depression,Prolongation of QT interval, dysrrhythmias( due to hypokalemia)
  33. 33. ARTERIAL BLOOD GAS Metabolic acidosis  Lowered HCO3 levels  Increased anion gap  Respiratory compensation 
  34. 34. ELECTROLYTES Hypokalemia( blood)  Hyperchloremia  Rise in serum creatinine  Elevated liver enzymes 
  35. 35. URINALYSIS Increased potassium excretion  Increased urinary pH( distal renal tubular acidosis)  Decreased urine output( renal failure) 
  36. 36. CAUSES OF DEATH Renal failure  Acute respiratory distress syndrome  Shock  Cardiac dysrrythmias 
  37. 37. TREATMENT Supportive measures: Oxygen supplementation and positive pressure ventilatory support  i.v sodium bicarbonate( to correct acidosis)  Potassium citrate administered enterally by NG tube  I.v KCl (to correct hypokalemia)  N-acetyl cysteine 150mg/kg over 1 hour followed by 50mg/kg over 4 hours then 100mg/kg over 16 hours (for decontamination) 
  38. 38. OLEANDER POISONING
  39. 39.  Yellow oleander seeds contain highly toxic cardiac glycosides including thevetins A and B and neriifolin.
  40. 40. MECHANISM OF ACTIONCardiac glycosides bind to Na-K ATPase and reduce uptake of potassium into the cells which causes intracellular Na and Ca accumulation and also transient Ca release from SR.  A transient inward current is produced which increases the arrhythmogenecity of heart 
  41. 41. CLINICAL FEATURESNumbness and heat in the mouth  Purging  Burning pain in the throat  Dryness  Vomiting, diarrhoea  Headache, giddiness, dilated pupils  Loss of muscle power  Weak, rapid, irregular pulse  BP is low  Heart block 
  42. 42. ECG  Prolonged PR interval FIRST DEGREE HEART BLOCK
  43. 43. MANAGEMENT AND INITIAL STABILISATION  Initial assessment     Supportive care     ABC ECG (to detect heart block) Atropine (block the parasympathetic system) Fluid resuscitation Anti emetic Arrhythmia management (bradyarrhythmias…atropine, tachyarrhythmias…lidocaine) Hyperkalemia is due to extracellular shift of potassium rather than an increase in total body potassium and is best treated with insulin-dextrose infusion.
  44. 44. REFERENCES DAVIDSON  A clinical study of renal tubular dysfunction in Cleistanthus Collinus (Oduvanthalai) poisoning Nampoothiri et al  Cleistanthus collinus poisoning- a case report -Benjamin et al  Efficacy of L-cysteine in countering cleistanthus collinus poisoning: an indigenous phytotoxin. Sarathchandra, G.; Murthy, P. B. K. Indian Veterinary Journal 2000 Vol. 77 No. 3 pp. 209-211 ISSN  INDIAN JOURNAL OF PHARMACOLOGY Cleistanthus collinus induces type I distal renal tubular acidosis and type II respiratory failure in ratsManeksh et al.,  Myasthenic crisis-like syndrome due to Cleistanthus collinus poisoning( a case report)-Damodaram et al  Pathophysiology of organ dysfunction in oduvanthalai poisoning- keshavan et al 
  45. 45. ACKNOWLEDGEMENT  Dr RAMYA
  46. 46.  Thank you…

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