What questions are particularly important?

What investigations would you like to organize first?

How would you interpret these results? What would you like to do next?

What are you going to do immediately? Describe and justify what you should look for on examination?

What are the common causes of coma? What are the likely causes in this patient?

What is the likely cause for his confusion?

What should you do now?

What is happening?

A.1 All patients with an overdose need a through history including the timing of ingestion, the amount of drugs and if the drugs were taken with alcohol. A collateral history is also important, as is an overdose history. It is useful to classify episodes of attempted self-harm by lethality and by intent, depending on the method used and the patient’s intentions. A paracetamol overdose may be a low intent but often high lethality overdose, as patients may not realize how dangerous large quantities can be.

A.2

A.3 He is dry and in renal failure. This urgently needs to be corrected with aggressive fluid resuscitation and monitoring of fluid balance. Following a paracetamol overdose, the patient is often grossly dehydrated which contributes to renal failure and lactic acidosis.

His very high ALT signifies significant hepatic necrosis but is not, in itself, a prognostic marker. Most importantly, he has a prolonged PT signifying early hepatic failure.

He has high levels of paracetamol. N-acetylcysteine should be commenced without any delay, as it is the only intervention that can prevent multi-organ failure in these patients.

Figure 43.1 Paracetamol treatment chart.

(Courtesy of the Clinical Services Unit of the Royal Adelaide Hospital.)

All patients with deliberate self-poisoning should be assessed by psychiatric services.

A.4 This is a medical emergency.

A: Check and safeguard his airway

B: Check for spontaneous breathing, apply high-flow oxygen and measure his respiratory rate. Roll the patient on to his side (the ‘coma position’). Markedly abnormal breathing patterns are seen in brainstem damage. Compensatory hyperventilation is seen early in metabolic acidosis (e.g. diabetic ketoacidosis, salicylate, methanol, ethylene glycol and other poisonings). Hypoventilation is common in all cases of generalized CNS depression.

C: Measure blood pressure, pulse and assess him for signs of shock. Insert a large bore intravenous cannula, noting his response to painful stimuli. Take blood for laboratory analysis. Commence intravenous isotonic saline. Monitor cardiac rhythm.

Measure blood glucose immediately. He has taken a paracetamol overdose and may have become hypoglycaemic secondary to acute liver failure.

Hypoglycaemia is easily treated, easily missed, and can be fatal. If there is delay or any doubt, administer 50 mL 50% glucose intravenously. This will not do any harm and, if the patient is hypoglycaemic, may save their life.

Consider an opiate overdose or over-prescription (unlikely in this patient). Naloxone is not harmful and will reverse an opiate coma, but it should be given in small increments (e.g. 200 mg doses) as sudden reversal of an opioid overdose may lead to severe and dangerous withdrawal symptoms and an aggressive, uncooperative and delirious patient.

Call the anaesthetic team if his airway is threatened and he may need intubation.

The degree of unconsciousness should be determined by calculating and recording his Glasgow coma score (GCS), as shown in Table 43.1.

Table 43.1 The Glasgow coma score

Spontaneous movements indicate a lesser degree of unconsciousness. Twitching and jerking might indicate seizure activity or serotonergic toxicity. Decorticate or decerebrate posturing or asymmetric responses to pain may indicate neurological injury or dysfunction.

The eyes should be held open and the pupils, spontaneous eye movements and fundi examined. Large pupils are common in overdose of sympathomimetic (e.g. amphetamines) and anticholinergic (e.g. antihistamines, tricyclic antidepressants) drugs. They also occur with drugs that cause retinal toxicity (e.g. quinine, methanol). Small pupils are common with opioid, anticholinesterase and antipsychotic drug overdose. Both large and small pupils can also occur with midbrain or brainstem damage. A unilateral fixed dilated pupil indicates an ipsilateral third nerve palsy, which occurs when raised intracranial pressure leads to tentorial herniation. This may occur in this patient due to cerebral oedema arising from acute liver failure.

The limbs should be tested for tone, response to painful stimuli and reflexes.

A.5 Causes of coma vary, depending on the initial examination findings. The following list is by no means exhaustive. All unconscious patients should receive the same initial emergency management.

The main causes of death from poisoning out of hospital include:

Many of these respond well to supportive care alone. In hospital the poisons which remain a major concern are those that:

Note that most of these substances are not detected by the average ‘drug screen’.

Patients with a GCS <8 usually need to be intubated and admitted to an intensive care unit. At the very least, they warrant urgent anaesthetic/ITU review.

Overdoses produce various physiological effects which need to be treated, such as tachycardia, seizures or hypotension. Current teaching is to ‘treat the patient, not the poison’. Recent thinking employs the concept of ‘toxidromes’ which are groups of symptoms and signs producing a clinical picture in different overdose settings. Table 43.2 illustrates the different groups of ‘toxidromes’.

This patient has developed hypoglycaemia secondary to liver failure from a paracetamol overdose and he should be given IV glucose promptly.

A.6 He may be hypoglycaemic once more but encephalopathy secondary to acute liver failure is likely and may develop very rapidly indeed

A.7 As before: A B C Check his blood glucose once again. Take blood for renal function, liver enzymes, including PT, arterial gases and lactate. Ask for senior help immediately and call for an anaesthetic assessment.

A.8 He has a massive transaminitis secondary to hepatic necrosis, a rapidly rising prothrombin time due to liver failure and renal failure.

The patient has developed hyperacute fulminant hepatic failure. This is encephalopathy occurring in a patient less than 7 days after the onset of jaundice. In paracetamol overdose, this often occurs much more rapidly, sometimes within 48 hours, and the encephalopathy can precede the onset of clinical jaundice.

If the encephalopathy occurs between 7 and 28 days after the onset of jaundice, the condition is termed acute liver failure. If the intervening period is between 28 days and 8 weeks, the term subacute liver failure is used.

Encephalopathy (Box 43.1) due to fulminant hepatic failure is secondary to brain oedema due to cerebrovascular dilatation and rapid swelling of neurones. Early signs may include hyperreflexia, clonus, extensor posturing, teeth grinding as well as irritability. It is not uncommon for these early signs to be misinterpreted as a lack of cooperation or anxiety in such a patient.

Advanced cerebral oedema may lead to pupillary abnormalities due to midline shift or raised intracranial pressure, sustained arterial hypertension, bradycardia and eventually deep coma and death.

Patients with early signs of brain oedema should be managed in ITU and intubated to reduce agitation and allow the administration of anaesthetic agents such as propofol. This patient is confused and agitated so he is moving from stage II to stage III encephalopathy (see Box 43.1). His hypoglycaemia hours earlier was a warning sign that this was to be the likely outcome. A liver transplant centre should be contacted urgently.