Chapter 75: The unconscious patient

The state of arousal is determined by the function of the central reticular formation, which extends from the brain stem to the thalamus. Coma occurs when this centre is damaged by a metabolic abnormality or by an invasive lesion that compresses this centre. Coma is also caused by damage to the cerebral cortex.¹

The word ‘coma’ is derived from the Greek koma, which means deep sleep. The deeply unconscious patient is not in a deep sleep. Coma is best defined as ‘lack of self-awareness’.²

The various levels of consciousness are summarised in TABLE 75.1; the levels vary from consciousness, which means awareness of oneself and the surroundings in a state of wakefulness,³ to coma, which is a state of unrousable unresponsiveness. Rather than using these broad terms in clinical practice it is preferable to describe the actual state of the patient in a sentence.

The initial contact with the unconscious patient is invariably sudden and dramatic and demands immediate action, which should take only seconds to minutes. The primary objective is to keep the patient alive until the cause is determined and possible remedial action taken.³

A history can be obtained from relatives, friends, witnesses, ambulance officers or others. The setting in which the patient is found is important. Evidence of discs or cards identifying an illness such as diabetes or epilepsy should be searched for. Is there a known history of hypertension, heart disease, respiratory disease or psychiatric illness?

Questions to be considered⁴

• Is the patient diabetic?

  Does the patient have insulin injections?

  Has the patient had an infection?

  Has the patient been eating properly?

• Is drug overdose possible?

  Has the patient been depressed?

  Has the patient experienced recent stress or personal ‘mishaps’?

  Has the patient been on any medications?

• Is opioid usage possible in this patient?

  Are the presenting circumstances unusual?

• Is epilepsy possible?

  Was twitching in the limbs observed?

  Did the patient pass urine or faeces?

• Is head injury possible?

  Has the patient been in a recent accident?

  Has the patient complained of headache?

• Has a stroke or subarachnoid haemorrhage occurred?

  Has the patient a history of hypertension?

  Did the patient complain of a severe headache?

  Has the patient complained of weakness of the limbs?

• Has the patient bitten the tongue?

General features requiring assessment:

• breathing pattern:

  • – Cheyne–Stokes respiration (periodic respiration) = cerebral dysfunction

  • – ataxic respiration: shallow irregular respiration = brain-stem lesion

  • – Kussmaul respiration: deep rapid hyperventilation = metabolic acidosis

• breath: characteristic odours may be a feature of alcohol, diabetes, uraemia and hepatic coma

• level of consciousness: degree of coma (see TABLE 75.1); the Glasgow coma scale (see TABLE 75.3) is frequently used as a guide to the conscious state

• skin features: look for evidence of injection sites (drug addicts, diabetics) and snake bite marks, colour (cyanosis, purpura, jaundice, rashes, hyperpigmentation) and texture

• circulation

• pulse oximetry

• temperature: consider infection such as meningitis and hyperpyrexia if raised and hypothermia (e.g. hypothyroidism) if low

• hydration: dehydration may signify conditions such as a high fever with infections, uraemia, hyperglycaemic coma

Examination of the head and neck^3,4

The following should be considered:

• facial asymmetry

• the skull and neck: palpate for evidence of trauma and neck rigidity

• eyes, pupils and ocular fundi: look for constricted pupils in opioid overdose

• tongue

• nostrils and ears

• auscultation of the skull

Examination of the limbs

Consider:

• injection marks (drug addicts, diabetics)

• tone of the limbs by lifting and dropping (e.g. flaccid limbs with early hemiplegia)

• reaction of limbs to painful stimuli

• reflexes—tendon reflexes and plantar response

General examination of the body

This should include assessment of the pulses and blood pressure.

Urine examination

Catheterisation of the bladder may be necessary to obtain urine. Check the urine for protein, sugar and ketones.

Diagnosing the hysterical ‘unconscious’ patient

One of the most puzzling problems in emergency medicine is how to diagnose the unconscious patient caused by a conversion reaction (hysteria). These patients really experience their symptoms (as opposed to the pretending patient) and resist most normal stimuli, including painful stimuli.

Method

• Hold the patient’s eye or eyes open with your fingers and note the reaction to light.

• Now hold a mirror over the eye and watch closely for pupillary reaction. The pupil should constrict with accommodation from the patient looking at his or her own image.

Appropriate investigations depend on the clinical assessment. The following is a checklist.

• Blood tests:

  Table Graphic Jump Location

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  – All patients:	blood sugar urea and electrolytes
  – Selected patients:	FBE blood gases liver function tests blood alcohol serum cortisol thyroid function tests serum digoxin

• Pulse oximetry

• Urine tests:

  • – a urine specimen is obtained by catheterisation

  • – test for glucose and albumin

  • – keep the specimen for drug screening

• Stomach contents: aspiration of stomach contents for analysis

• Radiology: CT or MRI scan are the investigations of choice (if available). If unavailable, X-ray of the skull may be helpful.

• Cerebrospinal fluid: lumbar puncture, necessary with neck stiffness, has risks in the comatose patient. A preliminary CT scan is necessary to search for coning of the cerebellum. If clear, the lumbar puncture should be safe and will help to diagnose subarachnoid haemorrhage and meningitis.

• Electroencephalograph

• ECG; look for ↑ QT interval, etc.

Episodic or transient loss of consciousness is a common problem. The important causes of blackout are presented in TABLE 75.4. The history is important to determine whether the patient is describing a true blackout or episodes of dizziness, weakness or some other sensation.

The clinical features of various types of blackouts are summarised in TABLE 75.4.

Epilepsy

Epilepsy is the commonest cause of blackouts. There are various types, the most dramatic being the tonic–clonic seizure in which patients have sudden loss of consciousness without warning. See CHAPTERS 54 and 84.

The typical features (in order) of a tonic–clonic convulsion are:

• aura (sensory or psychological feelings)

• initial rigid tonic phase (up to 60 seconds)

• convulsion (clonic phase) (seconds to minutes)

• mild coma or drowsiness (15 minutes to several hours)—postictal confusion

Associated features:

• cyanosis, then heavy ‘snoring’ breathing

• eyes rolling ‘back into head’

• ± tongue biting

• ± incontinence of urine or faeces

It should be noted that sphincter incontinence is not firmly diagnostic of epilepsy. In less severe episodes the patient may fall without observable twitching of the limbs.⁵

In atonic epilepsy, which occurs in those with tonic–clonic epilepsy, the patient falls to the ground and is unconscious for only a brief period.

Orthostatic intolerance and syncope

In syncope there is a transient loss of consciousness but with warning symptoms and rapid return of alertness following a brief period of unconsciousness (seconds to 3 minutes). The three main syndromes that are outlined in CHAPTER 54 are reflex syncope, postural orthostatic tachycardia syndrome and autonomic failure.

Reflex syncope

Relevant features of reflex syncope or vasovagal or common faint (see TABLE 75.4):

• occurs with standing or, less commonly, sitting

• warning feelings of dizziness, faintness or true vertigo

• nausea, hot and cold skin sensations

• fading hearing or blurred vision

• sliding to ground (rather than heavy full-length fall)

• rapid return of consciousness

• pallor and sweating and bradycardia

• often trigger factors (e.g. emotional upset, pain)

The patient invariably remembers the onset of fainting. Most syncope is of the benign vasomotor type and tends to occur in young people, especially when standing still (e.g. choir boys). It is the main cause of repeated fainting attacks.

The treatment is to avoid precipitating causes (e.g. prolonged standing, especially in the sun) and bend forwards with the head down or lie down with premonitory signs. ‘Smelling salts’ (ammonium carbonate) can be carried and used in these circumstances.

Other forms of syncope

Micturition syncope

This uncommon event may occur after micturition in older men, especially during the night when they leave a warm bed and stand to void. The cause appears to be peripheral vasodilatation associated with reduction of venous return from straining.

Cough syncope

Severe coughing can result in obstruction of venous return with subsequent blackout. This is also the mechanism of blackouts with breath-holding attacks.

Carotid sinus syncope

This problem is caused by pressure on a hypersensitive carotid sinus (e.g. in some elderly patients who lose consciousness when their neck is touched).

Effort syncope

Syncope on exertion is due to obstructive cardiac disorders, such as aortic stenosis and hypertrophic obstructive cardiomyopathy.

Sudden collapse can follow choking. Examples include the so-called ‘cafe coronary’ or ‘barbecue coronary’ when the patient, while eating meat, suddenly becomes cyanosed, is speechless and grasps the throat. This is caused by inhaling a large bolus of meat that obstructs the larynx. To avoid death, immediate relief of obstruction is necessary. An emergency treatment is the Heimlich manoeuvre, whereby the patient is grasped from behind around the abdomen and a forceful squeeze applied to try to eject the food. If this fails, the foreign body may have to be manually removed from the throat.

Drop attacks

Drop attacks are episodes of ‘blackouts’ in which the patient suddenly falls to the ground and then immediately gets up again. They involve sudden attacks of weakness in the legs. Although there is some doubt about whether loss of consciousness has occurred, most patients cannot remember the process of falling. Drop attacks occur typically in middle-aged women and are considered to be brain-stem disturbances producing sudden changes in tone in the lower limbs. Other causes of drop attacks include vertebrobasilar insufficiency, Parkinson disease and epilepsy.⁵

Stokes–Adams attacks (see CHAPTER 70) and cardiac syncope are manifestations of recurrent episodes of loss of consciousness, especially in the elderly, caused by cardiac arrhythmias. These arrhythmias include complete heart block, sick sinus syndrome and ventricular tachycardia. The blackout is sudden with the patient falling straight to the ground without warning and without convulsive movements. The patient goes pale at first and then flushed.

Twenty-four-hour ambulatory cardiac monitoring may be necessary to confirm the diagnosis.

Patients with aortic stenosis are prone to have exercise-induced blackouts. Consider the prolonged QT interval syndrome in all age groups when the person presents with dizziness or blackouts.

Loss of consciousness can occur rarely with vertebrobasilar insufficiency (VBI) transient ischaemic attack. Typical preceding symptoms of VBI include dysphasia, dysarthria, vertigo, vomiting, hemisensory loss, ataxia and transient global amnesia.

Hypoglycaemia

Hypoglycaemia can be difficult to recognise but must be considered as it can vary from a feeling of malaise and lightheadedness to loss of consciousness, sometimes with a convulsion. There are usually preliminary symptoms of hunger, sweating, shaking or altered behaviour. Hypoglycaemic attacks are usually related to diabetes and can occur with oral hypoglycaemics as well as insulin. Causes of hypoglycaemia are presented in TABLE 75.5. Refer to CHAPTER 128.

Some non-life-threatening head injuries are sufficiently serious to cause significant loss of consciousness and retrograde amnesia. The clinical terms used to describe brain injury of concussion, contusion and laceration simply indicate minor to major degrees of a similar injury. Severe individual cases of the above can certainly result in fatal outcomes.

Concussion⁶

Concussion is a transient disturbance of neurological function induced by head injury and resulting in no persistent abnormal neurological signs. There may or may not be brief loss of consciousness. The old definition of loss of consciousness with eventual recovery applies only to more severe forms of concussion. The features of the various grades of concussion are shown in TABLE 75.6.

Take extra care in children who are more sensitive to head injury and need to be kept home for at least 3 days.

Post-concussion syndrome

Occasionally, a person who has an episode of concussion has persistence of headaches and dizziness for a number of weeks. Poor memory and concentration and sluggish decision-making indicate impaired mental capacity. Patients with this problem should be investigated with neuropsychological testing and CT scanning or MRI of the brain.

Links to sports concussion tests⁷

• Pocket Concussion Recognition Tool

• Sports Concussion Assessment Tool 5th edn (SCAT5)

Extradural haematoma

This life-threatening head injury is caused by arterial bleeding between the skull bone and dura mater (see FIG. 75.1). Following injury there may be a short lucid interval followed by loss of consciousness. The patient is restless, confused, irritable (see FIG. 75.2), has severe headaches and develops neurological signs such as seizures, ipsilateral pupil dilatation and facial weakness. A skull X-ray and CT scan should demonstrate the haematoma. Lumbar puncture is contraindicated. Urgent decompression of the haematoma is required.

Subdural haematoma

This is due to a venous bleed between the dura and the arachnoid. It follows injury, which may be seemingly trivial, especially in the elderly, and may be acute, subacute and chronic. Consider it in a person with personality change, slowness and unsteadiness of movement, headache, irritability and fluctuating conscious level. A CT scan or MRI should reveal the haematoma and/or a midline shift. Neurological referral is urgent.

Psychogenic factors leading to blackouts represent a diagnostic dilemma, especially if occurring in patients with tonic–clonic epilepsy. If the attacks are witnessed by the practitioner then the possibility of functional origin can be determined.

Hysterical blackouts or fits are not uncommon and have to be differentiated from hyperventilation. It is unusual for hyperventilation to cause unconsciousness but it is possible to get clouding of consciousness, especially if the patient is administered oxygen.

Other features that suggest psychogenic rather than organic factors are:

• labile affect

• rapidly changing levels of consciousness

• well-articulated speech

• bizarre thought control

Most likely causes to consider

• drug overdose, including alcohol

• head injury

• postictal state (epilepsy or CVA)

• hypoglycaemia or ketoacidosis

• subarachnoid haemorrhage

• respiratory failure

• hypotension, including cardiac arrhythmias or myocardial infarction

• infection, e.g. meningitis

• psychogenic

Basic investigations

• oxygen saturation

• blood glucose

• urine or blood drug profile

• brain CT scan

• lumbar puncture (CT scan permitting)

• routine blood chemistry

• ECG

The first principle of management of a person found unconscious is to keep the patient alive by maintaining the airway and the circulation. The basic management essentials are summarised in TABLE 75.7.

Before embarking on a secondary survey always consider giving the ‘coma cocktail’ (also called TONG²), which refers to the combination of:

The rapid administration of these agents should be considered for any patient^3,8 with an altered level of consciousness because they may lessen or reverse metabolic insult to the brain. Some emergency physicians recommend adding flumazenil to the cocktail.

In the presence of hypoventilation, constricted pupils¹⁰ or circumstantial evidence of opioid use, naloxone (the specific opiate antagonist) should be given intravenously. If there is no response the patient should be intubated before further naloxone is given. Use a nasogastric tube to prevent acute gastric dilatation.

Catheterise to relieve urinary distension, send a urine sample for micro and culture, pregnancy test and drug screen.

Use of flumazenil

Flumazenil is a specific benzodiazepine antagonist and may have an important use in the assessment of the unconscious patient. It can have a dramatic effect on benzodiazepine overdosage. After an initial dose of 0.2 mg IV, 0.3–0.5 mg boluses should be given every 1–2 minutes with caution until a response is observed.⁹

Opioid (heroin) overdose

A known overdose patient should be treated initially with both IV and IM naloxone:

• naloxone 0.4 mg IV (repeat in 3 minutes if necessary)

• naloxone 0.4 mg IM (to maintain cover)