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CHAPTER 1
Unconsciousness and Coma
Roger Dalton
CASE HISTORY
A 57-year-old man is found in an unconscious state at home. He was in bed when his wife left at 7.00 a.m. that morning to go to work. On her return home at 3.45 p.m., he was still in the same position in bed, unrousable, incontinent of urine, and the cup of tea she had left for him was untouched. He has been unwell recently, and prescribed a course of antibiotics and co-codamol from his General Practitioner for a discharging ear infection. He suffers from hypertension, type 2 diabetes mellitus and longstanding depression. His medication list shows that he has been prescribed gliclazide 80 mg twice daily, atenolol 25 mg once daily, ramipril 5 mg once daily and amitriptyline 25 mg once daily. He has no known allergies. His wife informs you that he has had bad headaches recently, but that no-one else at home has been unwell.
Question: What differential diagnosis would you consider from the history?
This man is in a coma, which is defined as ‘unrousable unresponsiveness’. Using the objective clinical assessment tool, the Glasgow Coma Score (see Table 1.1), coma is defined as a score of 8 or less. Those patients with a score between 14 and 9 are defined as having altered consciousness and those with a top score of 15 are normal, alert and orientated. When considering a differential diagnosis for the cause of a patient’s unresponsiveness it is important to consider those conditions that are easily reversible first.
Hypoglycaemia
The patient is a known diabetic. Hypoglycaemia or, less commonly, hyperglycaemia can result in altered consciousness and must be actively diagnosed and promptly treated. A simple bedside glucose test will identify abnormalities in blood glucose levels and will guide appropriate therapy.
It is essential that any patient with confusion, altered consciousness, coma or focal neurological signs has their blood glucose estimated as part of the initial assessment. Neurological signs resulting from hypoglycaemia usually resolve quickly with treatment, though the failure to recognise and treat hypoglycaemia promptly may lead to permanent neurological damage.
Table 1.1 The Glasgow Coma Score.
| Eye opening |
| Spontaneously | 4 |
| To speech | 3 |
| To pain | 2 |
| None | 1 |
| Verbal response |
| Orientated | 5 |
| Disorientated speech | 4 |
| Inappropriate words | 3 |
| Incomprehensible sounds | 2 |
| None | 1 |
| Motor response |
| Obeys commands | 6 |
| Localises painful stimuli | 5 |
| Withdrawal from pain | 4 |
| Flexion to pain | 3 |
| Extension to pain | 2 |
| None | 1 |
Box 1.1 Drugs that can affect conscious level
- Alcohol
- Opiates
- Benzodiazepines
- Tricyclic antidepressants
- Street drugs, e.g. gamma-hydroxybutyric acid (GHB)
Drugs and alcohol
Excess alcohol with or without other prescription or recreational drugs is the commonest cause of altered consciousness and not quickly reversible. Of all the drugs that affect a patient’s consciousness (see Box 1.1) opiates are the only group that are readily treatable. Opiate excess leads to coma, and life-threatening respiratory depression, but thankfully can be quickly and effectively treated by the antagonist naloxone. The signs of opiate poisoning are seen in Box 1.2. Naloxone should be administered to any patient with any signs compatible with opiate poisoning.
Box 1.2 Signs of opiate ingestion
- Depressed conscious level
- Depressed respiratory rate
- Pin point pupils
- Needlestick trackmarks
Box 1.3 Signs of tricyclic anti-depressant overdose
- Dry skin and mouth
- Urinary retention
- Tachycardia
- Ataxia
- Jerky limb movements
- Divergent squint
- Altered level of consciousness
Opiate excess should be considered in this man who has had access to the simple analgesic co-codamol, which is a combination of paracetamol and the opiate codeine.
Likewise amitriptyline overdose, a common cause of coma, should be considered in the light of his depression and access to the medication. The clinical signs of tricyclic anti-depressant overdose are found in Box 1.3.
Intracranial haemorrhage
Vascular causes of coma are common. This man is known to have hypertension, which puts him at risk of intracranial haemorrhage. The cardinal features of an intracranial haemorrhage are sudden onset of headache, altered consciousness and focal neurological signs. Spontaneous intracranial haemorrhage usually occurs either into the subarachnoid space or into the ventricles and brain substance itself giving rise to either subarachnoid haemorrhage or intra-parenchymal haemorrhage respectively (see Figure 1.1).
Strokes due to cerebral infarction usually present differently to intracranial haemorrhages. The most important difference is that in most strokes consciousness is not impaired. There may be difficulty communicating with the patient, due to expressive or receptive dysphasia, but conscious level itself is not often altered. In brainstem infarctions, which can produce ‘locked in syndromes’ patients are aware of their surroundings, but unable to respond or communicate, so the patient can appear to be comatose.
Infection
Infection can lead to coma, either systemic infection as in a septicaemic illness, or intracranial infection such as meningitis or encephalitis. Patients with meningitis or encephalitis may present in coma especially if there is raised intracranial pressure.
There will often be a preceding phase characterised by symptoms suggestive of meningeal irritation (stiff neck, headache, photophobia), the signs of raised intracranial pressure (irritability, altered level of consciousness, vomiting, fits) and infection (fever, lethargy). If Neisseria meningitidis is the causative organism, the characteristic petechial/purpural rash is seen in approximately 50% of patients (see Figure 1.2); other organisms can cause less well-defined rashes. Other causative organisms can be seen in Table 1.2.
Figure 1.1 Intracranial haemorrhage. ...
