Multiple-etiology delirium and catatonia in an alcoholic with tubercular meningoencephalitis

Abstract

Delirium is a clinical entity with a variety of possible etiological conditions. Clinicians must be vigilant for the possibility of additional etiological factors. Secondly, catatonic patients should be carefully looked for general medical conditions. This case report depicts a chronic alcoholic who presented with withdrawal delirium, later on developed catatonia and then was diagnosed to have tubercular meningoencephalitis, a rare clinical sequence.

Delirium is defined as acute onset of fluctuating cognitive impairment and a disturbance of consciousness. Major causes of delirium are central nervous system disease, systemic disease, and substance intoxication or withdrawal.[1] Occasionally, delirium may be due to multiple etiologies. In a study by Webster[2] et al., multiple etiologies (49.3%) constituted the largest cause of delirium. Jebraj P reported a case of tubercular meningitis masked by delirium in an alcoholic.[3]

Catatonia is a disorder characterized by movement abnormalities usually associated with schizophrenia, mood disorders, and less frequently general medical conditions. Barnes et al., found it to be 20% in a neurology ward,[4] while Rosebush et al., reported that two-thirds of catatonics in an adult psychiatric ward had associated medical illness.[5] In developing countries malaria, tuberculosis and typhoid are important though under-recognized causes of catatonia.[6]

Here, we present a case report of a chronic alcoholic who presented with withdrawal delirium, later on developed catatonia and was finally diagnosed to have tubercular meningoencephalitis, a clinical sequence which has never been reported. So our case has two unique findings, first association of alcohol withdrawal delirium with tubercular meningoencephalitis which has been reported only once in the literature[3] and second is presentation of catatonia in meningoencephalitis which has never been reported from India.

CASE REPORT

A 40-year-old male presented to the emergency department with complaints of irrelevant talk, abnormal behavior, and disorientation for four days. He had multiple generalized tonic clonic convulsions two days back. On admission he was afebrile, anxious, restless and confused with doubtful neck rigidity since he kept himself stiff and was non-cooperative during examination. He had tremors in both hands, pulse 106/min, blood pressure 146/96 mm of Hg and respiratory rate of 20/min. His remaining general physical examination was unremarkable. History revealed him to be an alcoholic for 12 years with psychological and physical dependence, with abstinence for five days. His childhood history was unremarkable. He had no past history of any medical or surgical illness except frequent cough and occasional fever for few weeks for which he took cough syrups and antipyretics directly from chemists without any consultation with doctor. He was a salesman in a grocery shop with difficulties in saving his job because of frequent absenteeism. His wife reported him to be a happy type of person during the initial three-four years of starting alcohol with friends. He gradually became alcohol-dependent, irritable, abusive and frequently aggressive to the wife and both children of 10 and 12 years of age. There was no history of any promiscuous behavior or sexually transmitted disease.

On mental status examination (MSE) he had altered sensorium with poor concentration, disorientation to time and place, short-term memory impairment, slurring of speech, increased psychomotor activity and irritable mood.

On the basis of history and MSE a diagnosis of alcohol withdrawal delirium was made and patient admitted. He was started on chlordiazepoxide 25 mg four times a day with adequate fluids and multivitamins. His hemoglobin was 12.5 gm/dl, total leucocyte count 6700/mm³ with 80% polymorphonuclear cells and 20% lymphocytes. Erythrocyte sedimentation rate was 48 mm per h and random blood sugar was 124 mg/dl. Serum bilirubin total was 1.8 mg/dl and direct was 0.9 mg/dl, Alanine amino transferase ALT was 58 and aspartate amino transferase (AST) was 97 IU/L. Renal function test, serum electrolytes, thyroid function test, lipid profile, HIV test, electrocardiogram and computed tomography scan of head were unremarkable. During second and third day of admission his psychomotor activity slightly decreased to normal. Abdominal ultrasound showed fatty liver. On fourth day morning he developed rigidity of limbs, mutism with apathetic look, open eyes and fixed gaze but no emotional responsiveness. His stuporous state was not associated with posturing or waxy flexibility. Injection lorazepam 4 mg twice a day was added to reduced dose of chlordiazepoxide 25 mg twice a day considering his condition as unusual catatonic manifestation of alcohol withdrawal. Reviewing his temperature charts revealed that he had been having an evening rise of temperature during all these days. On reexamination he had neck rigidity. Physician reference was sought and the case was transferred to the medical ward with a clinical diagnosis of alcohol withdrawal with coexistent meningoencephalitis. On further investigation his chest X-ray showed bilateral miliary shadows and cerebrospinal fluid (CSF) examination revealed protein 150 mg%, CSF sugar – 60 mg%, TLC- 60 cells/high power field, differential leucocyte counts- 100% lymphocytes, adenosine deaminase 18 U/L. Diagnosis was then revised to tubercular meningoencephalitis and treatment switched to antituberculous therapy and injection dexamethasone followed by oral steroids. After three days of starting antitubercular treatment he showed significant improvement and was discharged on Category One antitubercular treatment with advice to follow up treatment from his nearby directly observed treatment supervised (DOTS) centre as the patient was from a remote area. He did not agree to take any anticraving drugs because of poor financial status. He kept his commitment of fortnightly counseling sessions up to three months with complete abstinence and then was lost to follow-up.

DISCUSSION

Delirium is commonly encountered by psychiatrists in alcohol withdrawal states, but coexisting medical illness may be contributory to it which should be carefully looked for, specially electrolyte abnormalities, hypoglycemia, change in fluid status (dehydration or volume overload), uncontrolled pain, etc.

As per diagnostic and statistical manual of mental disorders, 4^th edition (DSM-4) criteria a diagnosis of delirium due to multiple etiologies should be made if patient has disturbance of consciousness, change in cognition, disturbance developing in a short period of time with fluctuating course and evidence from history, physical examination or laboratory finding that delirium has more than one etiology i.e. a general medical condition plus substance intoxication or withdrawal.[7]

This case initially presented with alcohol withdrawal delirium and partially responded to conventional treatment but after that he developed catatonic symptoms which are not found in alcohol withdrawal states. Although catatonic states are uncommon in both tubercular meningoencephelitis and alcohol withdrawl, but between these two former has more probability of having an association with catatonia than later. Catatonia due to meningoencephalitis has been observed by Orland et al.,[8] though it is rare. Similar cases showing association of catatonia with meningoencephalitis have been reported by Ito et al.,[9] and by Carroll et al. In a case report by Caroll et al., the patient had delirium with episodes of catatonic excitement alternating with stupor and was diagnosed to have meningoencephalitis.[10]

History of alcohol withdrawal, partial response to chlordiazepoxide, emergence of catatonic symptoms and good response to treatment of meningoencephalitis indicate that meningoencephalitis might have contributed to the delirium which justifies diagnosis of delirium due to multiple etiologies.

Physicians and psychiatrists are advised to be cautious about two things, firstly, the secondary causes of delirium, and secondly, the potentially serious organic illnesses which may underlie the catatonic syndrome.