The Management of Medical Coma

Journal of Neurology, Neurosurgery, and Psychiatry 1993;56:589-598 589 NEUROLOGICAL EMERGENCY J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.6.589 on 1 June 1993. Downloaded from The management of medical coma David Bates The patient who is brought to the hospital of appropriate therapy. It is therefore essen- casualty department, or seen on the Intensive tial for the physician in charge to adopt a sys- Care Unit, though not having been exposed tematic approach initially to ensure to evident trauma, may be harbouring resuscitation, and then to direct further tests delayed effects of trauma such as a subdural towards producing the most rapid diagnosis haematoma or meningitis arising from a basal and the most appropriate therapy. The devel- skull fracture. The problems of raised intra- opment of such a systematic approach cranial pressure following a parenchymal demands an understanding of the pathophysi- haematoma in a hypertensive patient, the ology of consciousness and the ways in which decompensation of a cerebral tumour or col- it may be deranged. lection of pus, means that all possible causes of loss of consciousness must be considered by the physician when dealing with a patient The causes of coma in coma. Thus in the diagnosis of medical The phenomenon of consciousness depends coma it is not easy to exclude the patient in upon an intact ascending reticular activating coma following head injury. substance in the brainstem to act as the alert- If one excludes patients with a transient ing or awakening element of consciousness loss of consciousness following seizure, syn- together with a functioning cerebral cortex of cope, cardiac dysrhythmia or hypoglycaemia both hemispheres which determines the con- and those unresponsive due to impending tent of that consciousness. The ascending death, and considers patients who have been reticular activating substance is a continuous unconscious for some five to six hours, then isodentritic core extending from the medulla 40% of such patients seen in medical practice through the pons to the mid-brain which is will have taken some form of sedative drugs continuous caudally with the reticular inter- with or without alcohol.' Of the remainder mediate grey lamina of the spinal cord and just over 40% will have suffered hypoxic rostrally with the subthalamus, the hypothala- ischaemic insult as the result of cardiac arrest mus and the thalamus.3 Its functions and http://jnnp.bmj.com/ or anaesthetic accident, a third will be uncon- interconnections are considerable and its role scious as a result of cerebrovascular acci- greater than that of a simple cortical arousal dents, either haemorrhage or infarction, and system. There are named nuclei throughout about a quarter will be unconscious as a the reticular formation and, although it was result of metabolic coma including infection, originally considered that cortical arousal renal failure, hepatic failure and complica- depended upon projections from the reticular tions of diabetes mellitus. If one considers formation via the midline thalamic nuclei to only those cases who are initially regarded as the thalamic reticular nucleus and the cortex, on September 24, 2021 by guest. Protected copyright. "of unknown aetiology" the proportion of it now seems unlikely that the thalamic retic- drug overdoses is about 30%, mass lesions ular nucleus is the final relay and the specific about 34% and diffuse metabolic causes role of the various links from the reticular for- account for 36%.2 mation to the thalamus has yet to be identi- Few problems are more difficult to manage fied. than the unconscious patient because the Similarly the neurotransmitters involved in potential causes of loss of consciousness are this arousal system are not fully determined considerable and because the time for diagno- though it seems likely that, in addition to sis and effective intervention is relatively cholinergic and monoaminergic systems, short. All alterations in arousal should be gamma aminobutyric acid (GABA) may be regarded as acute and potentially life threat- important in controlling consciousness." ening emergencies until vital functions are It follows from recognition of the anatomy stabilised, the underlying cause of the coma is and pharmacology of the ascending reticular diagnosed and reversible causes are corrected. activating substance that structural damage to Delay in instituting treatment for a patient this pathway or chemical derangement of the with raised intracranial pressure may have neurotransmitters involved are mechanisms Department of obvious consequences in terms of pressure whereby consciousness may be impaired. Neurology, University coning but similarly the unnecessary investi- Such conditions will occur with focal lesions ofNewcastle Upon Tyne, UK gation of patients in metabolic coma with in the brainstem, mass lesions in the posterior D Bates imaging techniques may delay the initiation fossa impinging directly on the brainstem or 590 Bates mass lesions involving the cerebral hemi- Definitions spheres causing tentorial pressure coning and There is a continuum from the individual in J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.6.589 on 1 June 1993. Downloaded from consequently comproming the ascending full consciousness to the patient in deep reticular activating substance either by direct coma. The terminology which is most usually pressure or by a process of ischaemia. In employed derives from the Brain Injuries addition toxins, most commonly ingested Committee of the MRC7:- drugs, may have a significant depressant A) Confusion-"disturbance of consciousness effect upon the brainstem ascending reticular characterised by impaired capacity to think activating substance and thereby result in loss clearly and with customary repetition and to of consciousness. perceive, respond to and remember current The content of consciousness resides in the stimuli; there is also disorientation". cerebral cortex of both hemispheres. Unlike Confusion involves a generalised disturbance those discrete cortical functions such as lan- of cortical cerebral function which is usually guage or vision which are focally located associated with considerable EEG abnormali- within the cortex, the content of conscious- ties. Some authors describe an intervening ness can best be regarded as the amalgum of state between normal consciousness and con- all cognitive function. Coma arising from dis- fusion, that of clouding of consciousness.2 ruption of this cortical activity requires a dif- B) Delirium-"a state of much disturbed con- fuse pathology such as generalised anoxia or sciousness with motor restlessness, transient ischaemia, commonly seen after cardiac arrest hallucinations, disorientation and perhaps or anaesthetic accidents, or the effects of pre- delusions". sumed cortical vasospasm seen in infective C) Obtundation-"a disorder of alertness meningitis or the chemical meningitis follow- associated with psychomotor retardation". ing subarachnoid haemorrhage where gener- D) Stupor-"a state in which the patient, alised cortical ischaemia is believed to be the though not unconscious, exhibits little or no cause of disruption of function. spontaneous activity". Although the individ- For the physician attempting to diagnose ual appears to be asleep he or she will awaken the cause of coma consideration must be to vigorous stimulation but show limited given to:- motor activities and usually fail to speak. A) Supra or infra tentorial mass lesions. E) Coma-"a state of unarousable psycho- Typically these will provide evidence of logic unresponsiveness in which the subjects raised intracranial pressure and commonly lie with eyes closed and show no psychologi- produce focal signs. Pathologies such as neo- cally understandable response to external plasm or haematoma, infarction with cerebral stimulus or inner need". This may be short- oedema, abscess, focal encephalitis and ened to "a state of unarousable unresponsive- venous sinus thrombosis should be ness" which implies both the defect in arousal considered. and in awareness of self or environment man- B) Subtentorial destructive lesions or the local ifest as an inability to respond. A more useful effect of toxin. These pathologies will directly assessment of coma is derived from the hier- damage the ascending reticular activating archical Glasgow Coma Scale8 in which substance as in brainstem infarction, patients who fail to show eye opening in rhombencephalitis, brainstem demyelination response to voice, perform no better than and the much more common effects of self- weak flexion in response to pain and make, at http://jnnp.bmj.com/ poisoning with sedative drugs. best, only unrecognisable grunting noises in C) Diffuse damage to the cerebral cortex. response to pain, are regarded as being in Bilateral cortical injury is most commonly coma. This allows the patients to have an eye seen in states of hypoxia and ischaemia but opening response of two or less, a motor may be mimicked by hypoglycaemia, keto- response of four or less and verbal response of acidosis, electrolyte abnormalities, bacterial two or less. The sum Glasgow score of eight meningitis, viral encephalitis and diffuse post- should not be regarded as being definitive of on September 24, 2021 by guest. Protected copyright. infectious encephalomyelitis. It is also the coma since the total score can be achieved in likely pathology of coma following subarach- several different ways (table 1). noid haemorrhage. F) Vegetative state.

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