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Case Report

Case Report

ACUTE PSYCHOSIS IN A PATIENT OF TUBERCULOUS MENINGITIS DEVELOPING POLYURIA AND DIABETES INSIPIDUS IN SEQUELAE

Atmesh Kumar*,Kamal Nath**.Giridhari Kar***

Shyamanta Das****,Maheshwar Nath Tripathi*****

 

* Postgraduate Trainee, Department of Psychiatry, Silchar Medical College and Hospital,

** Associate Professor, Department of Psychiatry, Silchar Medical College and Hospital

*** Professor, Department of Psychiatry, Silchar Medical College and Hospital

**** Assistant Professor, Department of Psychiatry, Silchar Medical College and Hospital

***** Senior Resident, Department of Psychiatry, Institute of Medical Sciences, Banaras Hindu University.

 

Abstract

A 30 year old female was brought to the psychiatric clinic with symptoms of acute psychosis. She denied having mental illness and attributed her symptoms to severe headache only. Her routine investigations and computed tomography (CT) scan of brain had shown normal findings. Initial diagnosis of acute psychosis was made and the patient was put on tablets olanzapine 10mg at night, clonazepam 0.5 mg twice daily and parenteral diazepam 10mg prn. Her irritability and restlessness decreased and sleep improved but repeat investigations showed electrolyte imbalance with anemia and increased erythrocyte sedimentation rate which were taken due care of. From fourth day onwards she also started developing fever and signs of meningeal irritation with anisocoria. Medicine consultation was made which resulted in probable diagnosis of tubercular meningitis. Repeat CT scan of brain showed features of diffuse cerebral swelling and compressed ventricles bilaterally. Magnetic resonance imaging of brain suggested collection of debris over the optic tract and pituitary gland. Ophthalmological examination revealed no abnormality in funds.  Patient was immediately put on antitubercular drugs, antibiotics, mannitol and steroids along with basic care of nutrition and electrolyte balance. Meanwhile she developed polyuria which could be finally corrected by giving desmopressin suspecting emergence of cranial diabetes insipidus due to pressure over posterior pituitary. Her thyroid profile, chest x-ray, abdominal sonography, human immunodeficiency virus testing, sputum microscopy, tuberculin test and serum calcium and potassium levels had shown normal findings.

Patient was admitted in the ward for about two months and her symptoms improved. Finally at the time of discharge she was conscious and oriented, had some visual disturbance left but was able to take self care and carry out her daily activities with little assistance.

Keywords: Tuberculous meningitis, Psychosis, Polyuria, Diabetes insipidus.

Introduction

Tuberculous meningitis (TBM) is an infection of the membranes covering the brain and the spinal cord (meninges) caused by the bacilli Mycobacterium tuberculosis. It’s a form of central nervous system (CNS) tuberculosis (TB) and is life threatening if left untreated. The infection usually begins elsewhere in the body, usually in the lungs (through inhalation) or rarely following ingestion of infected milk, and then travels through the blood stream to the meninges and the brain parenchyma. TB bacilli seed to the meninges or the brain parenchyma, resulting in the formation of small subpial or subependymal foci of metastatic caseous lesions, termed rich foci which increase in size until rupture.1 The location of the expanding tubercle (rich focus) determine the type of CNS involvement. Tubercles rupturing into the subarachnoid space cause meningitis. Those deeper in the brain or spinal cord parenchyma cause tuberculoma or abscess.1,2 The combination of unrelenting headache, stiff neck, fatigue, night sweats and fever with a cerebrospinal fluid (CSF) lymphocytic pleocytosis and a mildly decreased glucose concentration is highly suspicious for TBM . Empirical therapy for TBM is often initiated on the basis of a high index of suspicion without adequate laboratory support.2

Psychosis is a symptom or feature of mental illness typically characterized by radical changes in personality, impaired functioning and a distorted or non-existent sense of objective reality. Patients suffering from psychosis have impaired reality testing. They may have delusions, prominent hallucinations, disorganized speech and disorganized or catatonic behaviour.3 It results in impairment that grossly interferes with the capacity to meet ordinary demands in life.

Polyuria is a condition in which urine volume is inappropriately high (>3L/d). It may be because of osmotic/solute or pure water diuresis.2

Diabetes insipidus (DI) is a syndrome characterized by the production of abnormally large volumes of dilute urine. The 24-h urine volume is >50ml/kg body weight and the osmolarity is < 300mosm/L. It may be because of decreased secretion or action of arginine vasopressin (AVP) (<80-85% of normal). It may be pituitary DI, nephrogenic DI or primary polydipsia.2

Case History

A 30 year old female was brought to psychiatric clinic with chief complaints of irrelevant talking, irritability, disorganized behaviour ,poor oral intake and constipation for three days; poor social interaction, withdrawn behaviour and disturbed sleep for two months; off and on headache for nine years which had become more severe and frequent during the last two months.

At the time of first interview the patient was uncooperative. She was restless and irritable and was showing hallucinatory behaviour at times. Though she could answer few questions properly but her answers were very brief and occasionally out of track. Most of the time, she insisted to lie down on bed without any disturbances. She attributed her irritability, poor social interaction and loss of interest in talking to others to her severe headache. In between she was also found to scold her two sons by name and respond to them in irritable tone. She was repeatedly rebuking them and urging them not to create noise and trouble. Occasional gestures of trying to catch hold of them along with some searching and picking behaviour was also present. But in reality they were never present in the room, and in fact they had not accompanied her to the hospital from home. She was not passing stool for three days, and prior to this she had constipation for 18 days which was finally relieved by giving enema in a health subcentre. She was also reported to have disturbed sleep at night. She had problems both during initiation and maintenance of sleep. She kept waking, and for last 15 days had become more restless, tried to go out of the house and kept calling to invisible people. She was always preoccupied with her headache, which was generalized, occasionally associated with nausea and had become more severe and frequent during the last two months. This was the first episode of hospital admission though history of over the counter prescription for various complaints was present.

Her routine blood/urine investigations and computed tomography (CT) scan of brain done 15 days earlier showed normal findings. There was no history of head injury, high grade fever, substance abuse, hypertension, diabetes mellitus (DM), TB, ear, nose and throat (ENT) problem or any psychiatric illness.

Initial diagnosis of acute psychosis was made and the patient was put on oral olanzapine 10mg at night and clonazepam 0.5mg twice daily and parenteral diazepam 10mg prn. Routine investigations were done which showed  anaemia (Hb 9.0gm%), leucocytosis (11,940/cmm) with neutrophilia (83.6%), hyponatremia (Na+ 123meq/L), hypokalemia (K+ 2.9meq/L), random blood sugar (RBS) 167mg% and erythrocyte sedimentation rate (ESR) 45mm at the end of first hour, others within normal limits.

Correction of electrolyte imbalance was started along with antibiotics, multivitamins, proton pump inhibitor and intravenous fluid. Her irritability and restlessness decreased and sleep improved. But from fourth day onwards she started developing fever which rose on next day to 102şf. Signs of meningeal irritation were present and the patient became very drowsy. Blood pressure had risen to 150/100 mm Hg. Anisocoria was found with decreased light reactivity bilaterally. Neurological examination found rigidity, plantar indeterminate bilaterally and Glasgow coma scale (GCS) score 6/15. Medicine consultation was made which resulted in probable diagnosis TBM. Antipsychotic and anxiolytic were stopped and antitubercular treatment (ATT) was immediately started with four drugs (rifampicin, isoniazid, pyrazinamide, and ethambutol) with steroid coverage. Meanwhile lumbar puncture was done and CSF showed decreased glucose (40 mg %), increased protein (115 mg %) and increased cell count (40 cells/cmm, mostly lymphocytes, occasional red blood cells [rbcs]) but Ziehl-Neelsen staining did not find any acid fast bacilli (afbs). Antinuclear antibody (latex method) for tuberculosis was negative. Electrolyte imbalance showed some correction (Na+ 124meq/L, K+ 3.4meq/L), and RBS was 209 mg%. CT scan brain (repeat) showed features of diffuse cerebral swelling and compressed ventricles bilaterally. Magnetic resonance imaging (MRI) brain reported collection of debris over the optic tract/chiasma and pituitary gland. Testing for the human immunodeficiency virus (HIV) 1 and 2 were found negative. Sputum for AFB was negative and tuberculin test was also negative. 20% mannitol and oral hypoglycaemic agent (glimeperide) were added to the treatment regime considering presence of cerebral swelling and hyperglycemia.

Patient’s condition remained indifferent for the next three days, during which close monitoring of vitals, blood parameters and input-output charting was done. Febrile episodes started subsiding then onwards and from fifth day of starting ATT fever was absent. But a new problem started surfacing, which was appearance of polyuria. Patient’s urine output was consistently in excess of 3L (range 3-7.5L/day). Water deprivation did not produce much difference. Serum calcium (Ca+) was slightly low (7.5 mg %), K+ had risen to 3.4meq/L following correction, blood glucose was controlled, chest x-ray (CXR) showed normal study, abdominal ultrasonography (USG) showed normal findings except cervical nabothian cyst and suspected dermoid cyst of right ovary. Thyroid profile was done but it did not show any abnormality. Plasma osmolarity was low (273 mmol/L) with low sodium (128 meq/L). It was suspected that polyuria could be the result of cranial DI because of the tubercular infection of the brain and mass/debris over the pituitary gland leading to AVP dysfunction. DDAVP (desmopressin) spray 10 µg twice daily was added to the treatment regime. After some initial erratic response finally urine output got stabilized between 1300-2200 ml/day.

Patient’s drowsy state and meningeal signs at the initiation of ATT had responded very slowly. Fever had subsided after five days but altered consciousness and impaired orientation had remained for about ten to 12 days. Even when she was able to answer few questions properly, her visual disturbance persisted and she was occasionally found to indulge in hallucinatory behaviour, talked in air frequently and called out names of the family members who were actually not present there. Pupils were unequal but reacted to light.

Patient was admitted in the ward for about two months and her symptoms improved. Finally at the time of discharge she was conscious and oriented, had some visual disturbances left, but was able to take self care and carry out her daily activities with little assistance. Blood glucose was controlled and electrolyte levels had touched the baseline levels. She was advised to continue with her ATT, desmopressin and other supportive measures and come for regular scheduled follow-up.

Discussion

About 2000 million people in the world today are infected with TB (i.e. One third of world’s population) but only ten per cent develop clinical disease. Why some people develop clinical disease remains unclear. The reasons are likely to be multifactorial; inherent not just to the individual person, but to their population and environment.4

Investigations that may help in the diagnosis of TBM include full blood count and ESR, which may typically show leukopenia and/or normal white blood cell (WBC) count, but leukocytes and neutrophilia have been reported in some patients with TBM. There may be anaemia with elevated ESR. Electrolytes may show hyponatraemia due to development of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or hyponatremic natriuretic syndrome (role of atrial natriuretic peptide). In about ten per cent of patients the urinalysis may show wbcs without significant bacteriuria i.e. Sterile pyuria.5 CSF may be clear, turbid or xanthochromic and classically cell count may range from 10-500 cells/mm3, predominantly lymphocytic pleocytosis but often with a predominance of neutrophils in the early stages. CSF glucose is usually lower than normal in most of the cases (20-40 mg/dl), while CSF protein may be elevated, ranging from 100-800 mg/dl. Positive smears are typically reported in only 10-40% of cases of TBM in adults but CSF culture remains the ‘gold standard’ to make the diagnosis of TBM. Polymerase chain reaction for the detection of M. Tuberculosis deoxyribonucleic acid has a sensitivity of 70-80% but at the present time is limited by a high rate of false positive results.2 The tuberculin skin test may be negative in some patients with comorbid immunosuppressive illness, but immunocompetent patients usually produce positive reactions to the tuberculin test. Electroencephalographic (EEG) studies often show diffuse slowing, but in cases of cerebral infarction there may be focal slowing. Neuroimaging studies (CT and MRI) may show hydrocephalus and abnormal enhancement of basal cisterns and ependyma. They may also show the presence of intracerebral tuberculoma. CXR may show pneumonic process, adenopathy, fibronodular changes, cavitations and pleural effusion if there is associated tuberculous involvement of the lungs. The patient should also be screened for immunodeficiency states such as retroviral illness, DM and so on.

The World Health Organization (WHO) and the International Union Against Tuberculosis and Lung Disease (IUATLD) recommend diagnosis and classification of cases and assessment of response based on sputum AFB smears.6 But empirical therapy of TBM is often initiated on the basis of a high index of suspicion without adequate laboratory support. Initial therapy is a combination of isoniazid (300mg/d), rifampicin (10mg/kg/d), pyrazinamide (30mg/kg/d in divided doses), ethambutol (15-25mg/kg/d in divided doses) and pyridoxine (50mg/d). If the clinical response is good, pyrazinamide and ethambutol can be discontinued after eight weeks and isoniazid and rifampicin continued alone for next six to 12 months. Six months therapy is acceptable but should be prolonged for nine to 12 months in patients who have an inadequate resolution of symptoms of meningitis or who have positive mycobacterial cultures of CSF during the course of therapy.2,6 Adjunctive treatment with dexamethasone improves survival in patients over 14 years of age but probably does not prevent severe disability.7 Although hyponatremia can be a serious condition, appropriate measures for the management of at risk and affected patients will lead to full recovery in most cases.8

If unrecognized, TBM is uniformly fatal. This disease responds to chemotherapy; however neurological sequelae are documented in 25% of treated cases, in most of which the diagnosis has been delayed.2 The clinical stage at the time of presentation is the single most important predictor of clinical outcome, and two recent studies have shown that age, stage of disease, presence of cranial nerve deficit, presence of SIADH, abnormality of (EEG), abnormality of motor-evoked potentials and low GCS were associated with poor clinical outcome.9

The challenge for the clinician is in determining whether treatment with an antipsychotic is or is not indicated and, if so, the duration of treatment that is required. For patients with an acute onset of symptoms that is consistent with an acute and transient psychosis, antipsychotic medication may or may not be required depending on the severity of symptoms. In some individuals, the use of oral or short-acting parenteral antipsychotic medications on an acute or “as needed” basis is sufficient to control psychotic symptoms without need for ongoing antipsychotic therapy. Treatment with benzodiazepines may be useful in several situations when treating individuals with psychotic disorders. For patients who experience agitation or severe anxiety, benzodiazepines can be used on a short term basis while the patient’s diagnosis and need for antipsychotic treatment are being clarified.10

Polyuria is a condition in which urine volume is inappropriately high (>3L/d). It may be because of osmotic/solute or pure water diuresis . If the urine osmolality is >300 mosm/L, then a solute diuresis is clearly present and a search for the responsible solute(s) is mandatory. If the urine is dilute (<250 mosm/L), then total mosmol excretion is normal and a water diuresis is present.2

DI is a syndrome characterized by the production of abnormally large volumes of dilute urine. The 24-h urine volume is >50ml/kg body weight and the osmolarity is < 300mosm/L. It may be because of decreased secretion or action of AVP (<80-85% of normal). It may be pituitary DI, nephrogenic DI or primary polydipsia . The best way to differentiate these three conditions is to measure plasma or urine AVP (antidiuretic hormone) before and during the fluid deprivation test and analyze the result in relation to the concurrent plasma or urine osmolarity.  The signs and symptoms of uncomplicated pituitary DI can be eliminated completely by treatment with DDAVP which is synthetic analogue of AVP.  The doses required to completely control pituitary DI vary widely, depending on the patient and the route of administration. However they usually range from 1-2µg qd or bid by injection, 10-20µg bid or tid by nasal spray, or 100-400µg bid or tid orally.2

References

1.        Emedicine Specialties > Neurology > Neurological Infections Tuberculous Meningitis, Author: Tarakad S Ramachandran.

2.        Harrison’s Principles of Internal Medicine. 16th Edition. P. 251-2, 953-66, 2483-4, 2098-2100.

3.        Diagnostic and Statistical Manual of Mental Disorders. Fourth edition, text revision (DSM-IV-TR). P. 297.

4.        Thwaites G, Chau TTH, Mai NTH, Drobniewski F, mcadam K, Farrare J. Neurological aspects of tropical disease, tuberculous meningitis. J Neurol Neurosurg Psychiatry 2000; 68:289-99.

5.        Merritt HH, Fremont-Smith F. Cerebrospinal fluid in tuberculous meningitis. Arch Neurol Psychiatry 1933; 33:516–36.

6.        Treatment of tuberculosis in low income countries: Recommendations and Guidelines of the WHO and the IUATLD, Centres for Disease Control and Prevention. Treatment of Tuberculosis, American Thoracic Society, CDC, and Infectious Diseases Society of America. MMWR 2003; 52 (No. RR-11): [p.72-3].

7.        Thwaites GE, Bang ND, Dung NH, Quy HT et al. Dexamethasone for the Treatment of Tuberculous Meningitis in Adolescents and Adults. N Engl J Med 2004; 351:1741-1751.

8.        Palmer BF, Gates JR, Lader M. Causes and management of hyponatremia. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-8856, USA. Ann Pharmacother. 2003 Nov; 37(11):1694-702.

9.        Misra UK, Kalita J, Roy AK, Mandal SK, et al. Role of clinical, radiological and neurophysiological changes in predicting the outcome of tuberculous meningitis; a multivariate analysis. J Neurol Neurosurg Psychiatry. 2000; 68:300–316.

10.     Kaplan & Sadock’s comprehensive textbook of psychiatry. 8th ed. p. 1545-7.