ALKALI and ACID POISONING

When suspected, Diagnostic Endoscopy (Beyond the first observable Oesophageal/Gastric lesion is mandatory, even if deep penetrating and circumferential burns burns are present) and NG tube insertion under direct visualization can be done to prevent rupture in the acute setting and for feeding later by living it in place for prolonged (3-4 weeks) periods. Should be done within 12-24 hours after ingestion of an alkali.

AVOID GASTRIC LAVAGE, NEUTRALIZATION; CAN ASPIRATE AND WORSEN STRICTURES.

·       If FIRST DEGREE burns, (edema and erythema)….. can be discharged home if taking orally.

·       If SECOND DEGREE burns (erythema, blistering, superficial ulcerations, fibrinous exudate)….. admit, nil, orally, total parenteral nutrition for initial 7 days. Oral fluids on day 7th. Restart solids as tolerated.

·       If THIRD DEGREE burns (erythematous, deep ulceration, friability, eschar formation, perforation) should be managed in ICU setting. TPN/feeding jejunostomy required until GI lesions heal.

If evidence of perforation and peritonitis, or gastric necrosis at endoscopy, or persistently alkaline gastric pH , laparotomy and resection of necrosed tissue should be considered.

 ·       Look for features of third degree burns (erythematous, deep ulceration, fibrinous exudate)….. admit, nil orally, total parenteral nutrition for intial 7 days. Oral fluids on day 7th.Restart solids as tolerated.

·       If THIRD DEGREE burns (erythematous, deep ulceration, friability, eshar formation, perforation) should be managed in ICU setting. TPN/feeding jejunostomy required until GI lesions heal.

If evidence of perforation and peritonitis, or gastric necrosis at endoscopy, or persistently alkaline gastric pH, laparotomy and resection of necrosed tissue should be considered.

 ·       Look for features of third degree burns on endoscopy, full thickness burns with necrotic slough/charred tissue; or GI perforation/peritonitis at initial presentation – proceed with laparotomy.

·       Grade I and II a can be managed in ICU setting. TPN/feeding jejunostomy required until GI lesions heal.

If evidence of perforation and peritonitis, or gastric necrosis at endoscopy, or persistently alkaline gastric pH, laparotomy and resection of necrosed tissue should be considered.

·       Look for features of third degree burns on endoscopy, full thickness burns with necrotic slough/charred tissue; or GI perforation/peritonitis at initial presentation- proceed with laparotomy.

·       Grade I and Grade II a can be managed in wards; II and III needs ICU care, parenteral nutrition.

·       Steroids are contraindicated because they mask the features of peritonitis.

·       Antibiotics only if there is an evidence of infection.

·       Correction of metabolic acidosis or alkalosis.

ACETAMINOPHEN POISONING

 HISTORY:- of an acute overdose (>/= 140 mg/kg) of grug accidenta;/suicidal

PHARMACOKINETICS OF THE DRUG :- T1/2 life = 2-4 hrs; can be prolonged in cases ofhepatotoxicity. Rapidly absorbed from stomach and small bowel.

CLINICAL FEATURES :-

Early featured :- nonspecific of hepatoxicity; within 2-4 hrs. nausea, vomiting, diaphoresis and pallor.

CNS depression is unusual unless depression is unusual unless depressant drugs have been congested. Hepatotoxicity develops within 24-48 hrs. Renal failure may also supervene.

LOOK FOR FEATURES OF HEPATOTOXICITY :-

·       PT is prolonged by twofold.

·       S.BILIRUBIN is > 4mg/dL anytime 3rd to 5th after ingestion of drug drug.

IN PATIENTS WHO RECOVER, LFT RETURNS TO NORMAL WITHIN 1 WEEK;

histological structure returns to normal; within 3 months.

If serum acetaminophen levels are not available, judge the chance of hepatotoxicity based on thefollowing approximation.

Ingested dose

Hepatotoxicity

250mg/kg                                                                            Probable

>140 mg/kg                                                                          Possible

>70 mg/kg                                                                             Possible in high risk cases.

High Risk – patients with Alcoholism, Malnutrition with HIV virus, or patients on therapy withBarbiturates, Phenytoin, and Rifampicin.

Antidote therapy :-

 ·       N-Acetyl cysteine therapy provides protection against Acetaminophen induced hepatotoxicity because of its anti-oxidant action and the improvement it brings about in the microvascular perfusion of the liver in any kind of fulminant hepatitis, only if it is initiated within 24 hours of poisoining.

·       There are some evidences showing that within24-36h also it can be helpful, but the consensus is that it is useful only if administered within 24h of overdose.

·       Protective effect is greatest when the treatment is initiated within 8 hours of poisoning. Thereafter protective effect decreases steadily with time.

·       Both Oral and IV therapy are equally effective.

·       Preparations :- 10% NAC (100 mg/ml), 20% (200mg/ml).

·       ORAL :-

Dilute 10% NAC (1:2) in water/coke/pepsi to make a 5% solution (50 mg/ml). Initial dose 140 mg/kg,maintenance 70mg/kg q4hly for 17 doses. A total of 1330 mg/kg over 72h.

 IV :-

·       Use 20% NAC, 150 mg/kg in 200ml of 5% Dextrose over 15mins. 50mg/kg in 500 ml of 5% Dextrose over 4h; followed by 100mg/kg in 1000ml of 5% Dextrose over 16h. Total dose : 300mg/kg over 20h.

·       Expect and treat dose dependent diarrhoea that occurs 72h after NAC therapy. Self limiting, resolves in 90% of the cases.

TRICYCLIC ANTIDEPRESSANTS (TCAD)

·       ABCDEFG as for all poisons

·       CARDIAC MONITORING FOR ARRHYTHMIAS – Usually occurs within 6 hrs of overdose. (Do not treat if haemodynamically stable) IV Lignocaine 50-100 mg if ventricular tachyarrhythmia sets in. A QRS prolongation of >0.16s correlates best with subsequent seizures and ventricular arrhythmias. Tachycardia is the most sensitive marker of TCAD overdose.

·       GASTRIC LAVAGE – (>250 mg ingested )AND ACTIVATED CHARCOAL.

·       SEIZURE TREATMENT- Usually within 6 hrs. of ingestion.

·       ALKALINIZATION OF BLOOD – to maintain arterial pH at 7.45-7.55. Monitor closely for hypokalemia. This reverses the membrane depressant effects of TCA.

·       LOOK FOR URINARY RETENTION AND CATHETERIZE – Acute urinary retention can occur as a part of anti-cholinergic effect.

·       In case of CO-TOXICITY WITH BARBITURATES……. Caution in using Flumazenil

because it unmasks the seizure potential of TCAD.

·       T1/2=24-30 hours; therefore monitoring should be done till serum levels fall below toxic levels by approximate calculations. DO NOT MEASURE TCAD LEVELS IN BLOOD because itis rapidly metabolized to active metabolites.

OTHER POISONS : START ABCDEFGH as indicated