OP POISONING AND ITS MANAGEMENT

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.

In the casualty, gastric lavage was done and activated charcoal was given.

O/E-

drowsy, GCS 15/15

febrile

Pulse rate- 100/min

Blood presssure- 90/70mmHg

Respiratory rate- 28/min

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

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

INVESTIGATIONS-

ABG-

Ph- 7.4

Pco2- 34

Po2- 118

ELECTROLYTES-

Na- 125

K- 6.9

Cl- 108

Ca- 4.35

HCO3-

Hb- 16.3 Platelets- 136000 WBC Total- 7500 WBC Diff- N-83, E-6, B-1, L-10 LFT- Direct bilirubin- 0.2 Total bilirubin- 1.1 Total protein- 6.7 Albumin- 3.8 SGOT- 54 SGPT- 63 Alkaline phosphatase- 102

Diagnosis???

Organophosphorus poisoning…

COMMON AMONG FARMERS-

MECHANISM OF ACTION

Inactivates acetylcholinesterase by phosphorylation, followed by accumulation of Ach in the synapses.

Recovery Aging

ORGANOPHOSPHORUS COMPOUNDS

Dichlorvos Fenthion malathion

Diazion Parathionchlor chlorpyrifos

DIMETHYL COMPOUNDS DIETHYL COMPOUNDS

NERVE AGENTS- G agents- Sarin, tabun, somanV agents- VX, VE

INSECTICIDES-

CLINICAL FEATURES-Muscarinic Nicotinic Central receptors

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

Cardiovascular Tachycardia Hypertension

Musculoskeletal Weakness Fasciculations Cramps Paralysis

Anxiety Restlessness Ataxia Convulsions Insomnia Dysarthria Tremors Coma Absent reflexes CS respiration Resp. depression Circulatory collapse

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

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

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

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

ACUTE CHOLINERGIC SYNDROME-

Atropine-

- 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)

iv Diazepam Oxygen and ventilatory support

INTERMEDIATE SYNDROME-

Ventilatory support while on sedation Parenteral nutrition

OPIDN-

No specific treatment Exercise recommended

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

CASE 2

EXAMINATION:

Patient oriented, dyspnoeic, afebrile

Pulse rate:91/min

Blood pressure= 110/70 mm Hg

Respiratory rate:20/minute

Diffuse abdominal tenderness

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

ABG

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

ODUVANTHALAI POISONING

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

• 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

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

SYMPTOMS Vomiting Headache, giddiness Palpitations Dyspnoea Neuromuscular weakness

SIGNS Tachypnoea( >30/min) Hypotension

CLINICAL FEATURES

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

ST segment depression,Prolongation of QT interval, dysrrhythmias( due to hypokalemia)

ECG

Metabolic acidosis Lowered HCO3 levels Increased anion gap Respiratory compensation

ARTERIAL BLOOD GAS

Hypokalemia( blood) Hyperchloremia

Rise in serum creatinine Elevated liver enzymes

ELECTROLYTES

Increased potassium excretion Increased urinary pH( distal renal tubular acidosis) Decreased urine output( renal failure)

URINALYSIS

Renal failure Acute respiratory distress syndrome Shock Cardiac dysrrythmias

CAUSES OF DEATH

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)

TREATMENT

OLEANDER POISONING

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

MECHANISM OF ACTION-

Cardiac 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

CLINICAL FEATURES-

Numbness 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

ECG

Prolonged PR interval

FIRST DEGREE HEART BLOCK

MANAGEMENT AND INITIAL STABILISATION

Initial assessment ABC ECG (to detect heart block) Atropine (block the parasympathetic system)

Supportive care 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.

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 rats- Maneksh 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

REFERENCES

ACKNOWLEDGEMENT

Dr RAMYA

Thank you…