organophosphate poisoning

1. OP POISONING AND ITS
MANAGEMENT

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. 
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. 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. CVS- 1st and 2nd heart sounds heard, no added sounds
 RS- normal vesicular breathe sounds heard
 P/A- soft, non-tender, no organomegaly


6. INVESTIGATIONS
ABGPh- 7.4
Pco2- 34
Po2- 118
ELECTROLYTESNa- 125
K- 6.9
Cl- 108
Ca- 4.35
HCO3-

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. 
Diagnosis???

9. 
Organophosphorus poisoning…

10. COMMON AMONG FARMERS-

11. MECHANISM OF
ACTION
Inactivates
acetylcholinesterase by
phosphorylation, followed
by accumulation of Ach in
the synapses.
 Recovery
 Aging


12. ORGANOPHOSPHORUS COMPOUNDS
NERVE AGENTSG agents- Sarin, tabun, soman
V agents- VX, VE
INSECTICIDESDIMETHYL COMPOUNDS
Dichlorvos
 Fenthion
 malathion

DIETHYL COMPOUNDS
Diazion
 Parathionchlor
 chlorpyrifos


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. 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. 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. 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. 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. 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. iv Diazepam
 Oxygen and ventilatory support


20. INTERMEDIATE SYNDROMEVentilatory support while on sedation
 Parenteral nutrition


21. OPIDNNo specific treatment
 Exercise recommended


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. EXAMINATION:
Patient oriented, dyspnoeic, afebrile
Pulse rate:91/min
Blood pressure= 110/70 mm Hg
Respiratory rate:20/minute
Diffuse abdominal tenderness


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. 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. ODUVANTHALAI POISONING

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. •
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. 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. CLINICAL FEATURES
SYMPTOMS
 Vomiting
 Headache, giddiness
 Palpitations
 Dyspnoea
 Neuromuscular weakness
SIGNS
 Tachypnoea( >30/min)
 Hypotension

31. CHEST X RAY:
may show
infiltrates ( non
cardiogenic
pulmonary
oedema- acute
respiratory
distress
syndrome)

32. ECG

ST segment depression,Prolongation of QT interval,
dysrrhythmias( due to hypokalemia)

33. ARTERIAL BLOOD GAS
Metabolic acidosis
 Lowered HCO3 levels
 Increased anion gap
 Respiratory compensation


34. ELECTROLYTES
Hypokalemia( blood)
 Hyperchloremia

Rise in serum creatinine
 Elevated liver enzymes


35. URINALYSIS
Increased potassium excretion
 Increased urinary pH( distal renal tubular acidosis)
 Decreased urine output( renal failure)


36. CAUSES OF DEATH
Renal failure
 Acute respiratory distress syndrome
 Shock
 Cardiac dysrrythmias


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. OLEANDER POISONING

39. 
Yellow oleander seeds contain highly toxic cardiac
glycosides including thevetins A and B and neriifolin.

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. 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. ECG
 Prolonged
PR interval
FIRST DEGREE HEART BLOCK

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. 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. ACKNOWLEDGEMENT

Dr RAMYA

46. 
Thank you…