A Clinical Profile of Coma

INTRODUCTION: Impaired consciousness is among the most difficult and dramatic of clinical problems. The brain tolerates only limited physical or metabolic injury, so that impaired consciousness is often a sign of impending irreparable damage to the brain. Stupor and coma imply advanced brain failure, just as, for example, uremia means renal failure, and the longer such brain failure lasts the narrower the margin between recovery and the development of permanent neurologic injury. The limited time for action and the multiplicity of potential causes of brain failure challenge the physician. The physician must organize available information to anticipate as accurately as possible the likelihood that the patient will either recover or remain permanently disabled. Prospective studies of prognosis in adults and children indicate that within a few hours or days after the onset of coma, neurologic signs and electrophysiologic markers in many patients differentiate, with a high degree of probability, the extremes of no improvement or good recovery. Unfortunately, radiologic and biochemical indicators have generally provided less accurate predictions of outcome, with some exceptions. AIM OF THE STUDY: To determine the incidence, etiology, and outcome of coma, to determine the commonest causes of coma, to recognize unusual presentations and to assess the prognosis in these patients. MATERIALS AND METHODS: A total of 100 consecutive patients admitted in a comatose state to the IMCU/medical ward in Government Stanley Medical College, were enrolled in this study after prior written and informed consent. Period of the Study: February 2010 To April 2010. METHODOLOGY: A detailed case history was taken.Depression of consciousness was assessed by the GCS. A detailed clinical examination was done.Investigations were guided by the clinical presentation. Neurological outcomes were determined as intact(normal or no change from pre-morbid condition), impaired (alteration of tone,power or reflexes,cranial nerve dysfunction, ataxia, seizures, persistent vegetative state) or death. Inclusion Criteria: • Cases with coma &focal signs, • Those without focal signs, • Cases with coma & fever. Exclusion Criteria: • Head injury. • Toxin ingestion. CONCLUSION: The GCS is a valuable tool but it may not account for the localized motor, speech and language deficits associated with a focal lesion and hence its accuracy may be affected which has an impact on its prognostic value. The presence of pupillary /eye signs may not portend a poor prognosis in all cases especially in hypoxic injury. The initial GCS may be deceptively low in alcoholics. Caution is required while interpreting the clinical findings in alcoholics. There may be difficulties in differentiating the more serious injuries from reversible signs. The presence of seizures in a comatose patient may not always signify a poor prognosis in all cases. The limitations of our study are that it is an observational study and the number of patients analyzed may not be significant to apply the results to a larger population. The observed proportion might represent the lower limit of a confidence interval rather than the mean. Also, actual outcome from the illness in many instances could be worse than the best neurologic state because some patients who recovered temporarily (48 hrs) died of complications later. A multimodal work up including brain CT, MRI, EEG, somatosensory evoked potentials and clinical examination might be useful in predicting accurate prognosis than any of them alone