Acute opioid toxicity treatment

Clinical Features for acute opioid toxicity treatment is necessary at times.The clinical occurrence of acute opioid toxicity is due to any of the following three main reasons:

• Clinical overdosage: Either iatrogenic or patient-controlled analgesia pumps.

• Accidental overdosage by addicts.

• Attempts at suicide.

Whatever might be the cause, “high degree of suspicion” is the key to diagnosis for acute opioid toxicity treatment .

Stuporous, semicomatose to comatose state: The patient may be arousable with some degree of difficulty to completely not responding to even deep painful stimuli.

The respiratory rate will be at the lowest possible rate (even up to 2—4 breaths per minute), which gradually progresses to respiratory arrest. The cyanosis will be present which will deepen.

Initially the blood pressure may be normal, but as the respiratory failure ensues, hypoxia worsens, the hypotension will immediately follow which requires immediate acute opioid toxicity treatment .

Miosis: Initially pupils will be very small till they become almost “pinpoint”. But as shock and cyanosis worsens, hypoxia sets in, they will slowly dilate and get fixed.

• Urine formation falls, body temperature falls, and diaphoresis sets in. Skin becomes cold and clammy.

• As hypoxia sets in, the skeletal muscle tone is gradually lost and flaccidity sets in, even jaw and tongue fall, worsening airway obstruction.

• The death is due to respiratory failure.

Pathognomonic of acute opioid poisoning is:

a) Pinpoint pupils

b) Coma

c) Respiratory failure

Differential Diagnosis for acute opioid toxicity treatment :

• Organophosphate poisoning

• Pontine haemorrhage

• Sodium vaiproate poisoning

Supportive Management for acute opioid toxicity treatment :

• Airway and ventilatory support.

• Oxygenation to be continued

• Intravenous access

• Monitoring of pulse, non-invasive blood pressure (NIBP), respiratory rate (RR), end-tidal CO2 (Etco2), EC serial arterial blood gas (ABG) for pH monitoring, sensorium, pupillary size, body temperature, etc.

• Inj. Furosemide 10—20 mg IV bolus if required.

Specific requirements for acute opioid toxicity treatment :

1. Inj. Naloxone 0.4mg (400 pg) diluted in 10 cc of distilled water and given slowly while continuously monitoring:

• State of arousal

• Respiratory rate and breathing excursions

• Any occurrences of cardiovascular instability like increased blood pressure/Arrhythmias

Repeat doses of inj. naloxone in increments of 50 j.tg at an interval of 10—15 minutes to maximum total dose of I mg, as part of acute opioid toxicity treatment .

2. Continuous observation for next 24—48 hours.

3. If pulmonary oedema develops then ventilatory support, loop diuretics, need to be initiated.

4. In children, the initial loading may have to be 10—20 pg/ kg, followed by additional doses if required.

Prognosis for acute opioid toxicity treatment :

If the patient is treated in the earlier stages of toxicity, viz, before cerebral hypoxia cardiorespiratory failure has set in, the prognosis is excellent; complete acute opioid toxicity treatment and recovery is possible. Associated complications will invariably increase morbidity and mortality.

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