The central reticular formation, which extends from thebrain stem to the thalamus, influences the state of arousal. This complex process involves interactions between the reticular formation, the cortex and brain stem, and all sensory pathways.
CONSCIOUSNESS means awareness of oneself and he surroundings in a state of wakefulness.
CLOUDING OF CONSCIOUSNESS is reduced wakefulness or awareness.
SLEEP is a state of mental and physical inactivity from which the subject can be roused.
STUPOR is an abnormal, sleepy state from which the patient can be aroused by stimuli that may need to be repeated or vigorously applied.
CONFUSION is the state of altered consciousness in which patients are bewildered and misinterpret the world around them.
DELIRIUM is a state of high arousal (seen typically in delirium tremens) in which there is confusion and often hallucinations.
COMA is a state of unrousable unresponsiveness. A grading system for coma used particularly in patients with head injury. An alternative grading system
Causes of coma
Altered consciousness is produced by three types of process affecting the brain stem, reticular formation and the cerebral cortex.
1 Diffuse brain dysfunction. Generalized metabolic (e.g. uraemia) or toxic (e.g. septicaemia) disorders can depress brain function. 2 Direct effect on the brain stem. Lesions of the brain stem itself damage the reticular activating system. 3 Indirect effect on the brain stem. Mass lesions above the reticular activating system in the brain stem. . It is important to understand that single focal brain lesions of the cerebral hemispheres do not produce coma unless they compress the brain stem. Oedema frequently surrounds hemisphere lesions, contributing greatly to their effects.
Other coma-like states include the ‘locked-in syndrome’, a state of unresponsiveness due to massive brain stem infarction. The patient is unable to communicate or move (except sometimes the eyes) but has a functioning cerebral cortex. The ‘chronic vegetative state’, a sequel of head injury for example, implies loss of sentient behaviour, i.e. the patient perceives little or nothing but lies awake, breathing spontaneously: widespread cerebral damage is present.
Unresponsiveness of psychological origin may cause difficulty in the differential diagnosis of apparent coma. The principal causes of coma and stupor are shown in Table 18.23. A common cause of coma is self-poisoning but in malarial zones cerebral malaria is frequently seen
Diffuse brain dysfunction
Drug overdose, alcohol
CO poisoning, anaesthetic gases
Hypoxidischaemic brain injury
Respiratory failure with CO, retention
Hypoadrenalism, hypopituitarism and hypothyroidism
Trauma-following closed head injury
Epilepsy-following a generalized seizure
Encephalitis, cerebral malaria
Metabolic rarities, e.g. porphyria
Direct effect on brain stem
Brain stem haemorrhage or infarction
Brain stem neoplasm
Brain stem demyelination
Indirect effect on brain stem
Hemisphere tumour, infarction, abscess,haematoma,
encephalitis or trauma
THE UNCONSCIOUS PATIENT
Immediate action, which takes only seconds, is essential.
A history should then be obtained from accompanying relatives, friends, ambulance drivers or the police. Many patients with diabetes mellitus, epilepsy or hypoadrenalism, and those who take corticosteroids, wear or carry identifying discs or cards; these should be looked for.
1 The depth of coma should be recorded.
2 A full general and neurological examination should then be carried out.
This is raised in infection and hyperpyrexia and low in hypothermia
The following should be noted:
COLOUR (cyanosis, jaundice, purpura, rashes, pigmentation)
TEXTURE (coarse and dry in hypothyroidism)
PRESENCE OF INJECTION SITES (diabetics, drug addicts)
Alcohol or ketones may be smelt. In hepatic failure and uraemia a distinct fetor is present.
Depressed but regular respiration occurs in most states of stupor and coma. The presence of particular types of respiration may point to the diagnosis:
CHEYNE-STOKES RESPIRATION (periodic respiration) is alternating hyperpnoea and apnoea. In neurological disease it implies bilateral cerebral dysfunction, usually deep in the hemispheres or in the upper brain stem, and may be a sign of incipient ‘coning’. It may occur in metabolic comas, particularly if there is CO2 retention from pulmonary disease.
KUSSMAUL (ACIDOTIC) RESPIRATION is deep-sighing hyperventilation that occurs principally in diabetic ketoacidosis and uraemia.
CENTRAL NEUROGENIC (PONTINE) HYPERVENTILAT10N describes the sustained, rapid, deep breathing seen in patients with pontine lesions.
ATAXIC RESPIRATION is the shallow, halting respiration that occurs when the medullary respiratory centre is damaged. It is frequently a preterminal event.
VOMITING, HICCUP AND EXCESSIVE YAWNING may indicate a lesion in the lower brain stem in a stuporose patient.
Head and neck
The patient should be examined for evidence of trauma and neck stiffness.
The size of the pupils and their reaction to light shouldbe recorded. The following patterns may be seen:
DILATATION OF ONE PUPIL, which becomes fixed to light, indicates herniation of the uncus of the temporal lobe (‘coning’) and compression of the third nerve. This is a potential neurosurgical emergency. ‘PIN-POINT’ LIGHT-FIXED PUPILS occur with pontine lesions (e.g. a pontine haemorrhage) that interrupt the sympathetic pathways.
MID-POSITION OR SLIGHTLY DILATED PUPILS (4- 6 mm) fixed to light and sometimes irregular are seen when damage to the midbrain interrupts the pupillary light reflex.
HORNER’S SYNDROME (ipsilateral pupillary constriction and ptosis,) occurs with lesions of the hypothalamus and also in ‘coning’. FIXED, DILATED PUPILS are a cardinal sign of brain death. They also occur in deep coma of any cause, but particularly coma due to barbiturate intoxication or hypothermia.
MID-POINT PUPILS that react to light are characteristic in coma of metabolic origin and coma due to most CNS-depressant drugs.
Other pupillary changes due to drugs are described on p. 75l.
NB No mydriatic drugs should be given to the unconscious patient.
Papilloedema or retinal haemorrhage should be recorded. Ocular movements In most cases of coma the eyes are slightly divergent. Slow, roving eye movements, usually horizontal, are seen in light coma.
VESTIBULO-OCULAR REFLEXES. Passive head rotation causes conjugate ocular deviation in the direction opposite to the induced head movement (doll’s head reflex). This reflex is lost in very deep coma and is absent in brain stem lesions. It is absent in brain death. A slow tonic deviation of the eyes towards the irrigated ear is seen when ice-cold water is run into the external auditory meatus; this is known as the caloric or vestibuloocular reflex and indicates that the brain stem is intact. In coma, this test is used mainly in the diagnosis of brain death.
ABNORMALITIES OF CONJUGATE GAZE. Sustained conjugate lateral gaze occurs towards the side of a destructive hemisphere lesion (‘the eyes look towards the normal limbs’) because damage to supranuclear pathways prevents contralateral gaze. In a pontine brain stem lesion, sustained conjugate lateral gaze occurs away from
the side of the lesion, ‘towards the paralysed limbs’. Rarely, an irritative lesion in the frontal region (e.g. an epileptic focus) may drive the eyes away from the affected hemisphere, i.e. conjugate deviation may occur away from the side of the lesion. Skew deviation (where one eye is deviated upwards and the other down) is a rare sign. It indicates a brain stem lesion.
SPONTANEOUS EYE MOVEMENTS. Spontaneous eye movements (other than roving eye movements) are distinctly unusual in coma of any cause. The sudden, brisk, downward-‘diving’ eye movement seen in pontine (or cerebellar) haemorrhage is known as
Impairment of consciousness makes it difficult to recognize focal neurological signs. The following should be looked for:
RESPONSE TO VISUAL THREAT IN A STUPOROSE PATIENT-asymmetry indicates hemianopia. TONE -the only evidence of a hemiparesis may be abnormal flaccidity on the affected side.
RESPONSE TO PAINFUL STIMULI -this may be asymmetrical. THE FACIAL APPEARANCE-drooping of one side of
the face, unilateral dribbling, or blowing in and out of the paralysed cheek may occur.
ASYMMETRY OF THE TENDON REFLEXES. ASYMMETRY OF THE PLANTAR RESPONSES. Both are, however, frequently extensor in coma of any cause.
ASYMMETRY OF DECEREBRATE AND DECORTICATE POSTURING.
In many instances the cause of coma will be evident from the history and examination (e.g. head injury, cerebral haemorrhage, self-poisoning), and appropriate investigations should be carried out. If the cause is still unclear, further investigations will be necessary.
Blood and urine
DRUGS SCREEN, e.g. salicylates, diazepam
ROUTINE BIOCHEMISTRY, e.g. urea, electrolytes, glucose, calcium, liver biochemistry
METABOLIC AND ENDOCRINE STUDIES, e.g. thyroid function tests, serum cortisol
Rarities such as cerebral malaria or porphyria should also be considered.
CT head scan
This may indicate an otherwise unsuspected mass lesion or intracranial haemorrhage.
Lumbar puncture should only be performed in coma after careful assessment of the case. It is contraindicated if an intracranial mass lesion is a possibility. A CT scan is often necessary to exclude this. CSF examination is likely to alter therapy only if undiagnosed meningoencephalitis is present
The unconscious patient needs careful nursing, meticulous attention to the airway and frequent observation to detect any change in vital function. Longer-term management requirements are:
SKIN: turning, skin care, avoidance of pressure sores, removal of rings .
ORAL HYGIENE: mouth washes, suction EYE CARE: taping of lids, prevention of corneal damage, irrigation
FLUIDS: intragastric or i.v. fluids
CALORIES: liquid diet through a fine intragastric tube, 3000 kcal (1255 kJ) daily
SPHINCTERS: catheterization only if necessary (Paul’s tubing if possible); avoidance of constipation (evacuate rectum manually if necessary)
The outlook depends upon the cause of coma. A cause must be established before decisions are made about withdrawing supportive care.