Delirium or psychosis? Diagnostic use of the sodium amobarbital interview

Delirium or psychosis? Diagnostic use of the sodium amobarbital interview

CASE REPORT ALBERTO B. SANTOS, JR., M.D. DONALD E. MANNING, M.D. WILLIAM M. WALDROP, M.D. Delirium or psychosis? Diagnostic use of the sodium amobar...

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CASE REPORT

ALBERTO B. SANTOS, JR., M.D. DONALD E. MANNING, M.D. WILLIAM M. WALDROP, M.D.

Delirium or psychosis? Diagnostic use of the sodium amobarbital interview The often difficult diagnostic distinction between psychosis and 'delirium is of primary importance, since a diagnosis of delirium forces an inquiry into the underlying organic factors and their prompt correction.· A protOcol for such an investigation has been outlined by Wells. 2 There are, however, cases in the literature that seem to be clinically indistinguishable from delirium an4 yet are regarded by the authors as psychogenic.· In addition, functional psychosis often presents with an associated cognitive impairment, complicating the differential diagnosis. The use ofsodium amobarbital may be of significant value as a differentiating diagnostic tool that can lead to a definitive diagnosis and appropriate treatment.3.4·7 C8Iltreport A 64-year-Old woman experienced the sudden onset of confusion and exhibited bizarre behavior characterized by rambling, mostly incoherent speech and labile mood, with frequent wild swings involving agitated outbursts and periods of withdrawal. On admission to the psychiatric unit, she was moderately agitated, exhibiting purposeless motor activity, and attentive only to the extent of responding to the calling of her name by looking in the direction of the examiner.

From the Medical University ofSouth Carolina. Dr. Santos is now assistant professor of psychiatry and Dr. Manning is associate professor ofpsychiatry at the University; Dr. Waldrop is in the private practice ofpsychiatry in Newport News, Va. Reprint requests to Dr. Santos, M.U.S.C., Department of Psychiatry, 171 Ashley Avenue, Charleston, SC 29403. OCTOBER 1980· VOL 21 • NO 10

History revealed a lifelong pattern of passivity and lack of assertiveness in dealing with family members. Severe depressive symptoms emerged gradually following the death of her husband nine years earlier. She felt lonely and overwhelmed by new family responsibilities. She subsequently moved in with an older cousin who dominated her. In addition, she had difficulty in refusing requests by her two sons for financial and other types of assistance. These factors led to a psychiatric hospitalization for depression one year prior to her present admission. The two sons had been diagnosed as manic depressive and were being maintained on lithium. The patient responded well to antidepressant and supportive therapy during her earlier hospitalization, but was reported to have discontinued the medication upon discharge. She functioned quite adequately during the year immediately preceding her preseht admission. Early on the day of the present admission she was noted to have filled prescriptions for amitriptyline and a nonnarcotic analgeSic, but took only three pills. On the afternoon of admission, we were informed by a daughter-in-law, the patient received a disturbing, threatening phone call from her son's fiancee, who had previously been verbally abusive to the patient on several occasions while intoxicated. Shortly after this call, she experienced the onset of her symptoms. Medical history was positive for open-angle glaucoma, hypertension, recurring urinary tract infections. and arthritis. History was negative for ingestion of alcohol. Physical examination on admission was remarkable in that the patient's temperature was 100, her blood pressure was 200/120, and she had a sinus tachycardia at 114 beats per minute. Initial laboratory tests revealed a white blood count of 10,800 with a shift to the left, a positive urine culture for Proteus, mild dehydration, and an elevated LDH.

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A chest film showed a small area of atelectasis in the base of her right lung. Serum glucose, calcium, magnesium, ammonia, creatinine, VORL, thyroid profile, and toxic screens were normal. The patient was treated for her dehydration and urinary tract infection and was given vitamin supplements. Her clinical course was one of fluctuating levels of global cognitive impairment, definitely worsening at night. When lucid she confirmed the history as mentioned above. During the day there were intermi«ent periods of somnolence and sleep. Her thought content, when not incoherent, evidenced paranoid morbid delusions, and she reported visual hallucinations. The working diagnosis was delirium and thus the etiologic search continued. EEGs on two occasions were normal, both showing a background low amplitude of diffuse fast rhythm mixed with some posterior alpha rhythm at 12 to 14 cycles per second. Lumbar puncture and skull x-ray films were negative, and a CT scan showed mild to moderate enlargement of the lateral and third ventricles and moderate enlargement of cortical sulci in all areas without midline shift. Serum B12 levels were normal as were folate, lead, urine porphyrins, and sedimentation rates. Antinuclear antibody were positive at 1: 160, but lupus erythematosus preparation was normal, as were rheumatoid factor, C3, C4, and serum anti-DNA. SCreening tests for heavy metals were negative. Since no clear organic etiology was demonstrable, we decided to conduct a sodium amobarbital interview during a relatively lucid period. Immediately prior to infusion the patient was oriented to person and place, but not to time. She performed poor serial threes but could recall five digits forward and four backwards, and had good short-term memory. The patient th'en tolerated 400 mg of intravenous sodium amobarbital given atan average of 5ml/min before sedation became apparent. Following this, the assessment of her sensorium was essentially the same as before sedation, with the exception that she experienced some mild Im'provement in her forward digit span. During the interview she expressed persecutory delusional ideation, describing a fear of "nitwits," which she described as small people "out to rape and murder" her, and associated visual hallucinations. She also expressed much concern over the safety of her family members. Her affect was flat and blunted. Because of the high sedation tolerance, the mild improvement in her sensorium, and the content of the amobarbital interview, we diagnosed the patient as having a functional psychosis. We prescribed treatment with neuroleptics. Within a few days, she manifested clinical improvement, and by the third week of hospitalization she had returned to her premorbid level of functioning.

Discussion This case demonstrates the extreme difficulty there can be in attempting to differentiate functional psychosis

from delirium. The patient's clinical picture was highly suggestive of delirium. She presented with an acute onset, global cognitive impairment that fluctuated over time, with the most severe changes occurring at night. There was a disturbance of sleep pattern and visual hallucinations. Her actions seemed purposeless. Slowing of the EEG provides strong support for the diagnosis of delirium when the clinical picture is uncertain, but in this case two serial EEGs were interpreted as normal. A single EEG that is within normal limits does not rule out the presence of delirium.s In cases ofanxiety, hysteria; and catatonia, the effects of amobarbital are observable chiefly as a general relaxation with a sense of well being, a decrease in inhibitions, and a willingness to discuss intimate topics. 3 On the other hand, in organic conditions, mild neurologic symptoms can become markedly worse, and symptoms such as confabulation, denial of illness, and disorientation may also increase in severity.6 In addition, patients with significant organic disease have less tolerance for barbiturate sedation. The last two points may be of critical importance in differentiating delirium from psychosis. In this patient, the amobarbital interview was the definitive diagnostic procedure. Its use led to the institution of appropriate and efficacious treatment. The patient's cognitive impairment improved during the interview rather than worsening as would be expected if the impairment had been on an organic basis. The patient demonstrated a marked tolerance to barbiturate sedation, which indicated a functional rather than organic etiology. We recommended the amobarbital interview be considered for its diagnostic value when the distinction between delirium and psychosis is a difficult one. 0 The authors wish to thank Dr. Z. J. Lipowskifor his assistance in the management ofthis case. REFERENCES 1. Lipowski ZJ: Delirium, clouding of consciousness and confusion. J NeN Ment Dis 145:227-255, 1967. 2. Wells CE: Chronic brain disease: An overview. Am J Psychiatry 135:1-12, 1978. 3. Ripley, HS: Psychiatric interview, in Freedman AM, Kaplan HI, Sadock BJ (ads): Comprehensive Textbook of Psychiatry II. Baltimore, Williams & Wilkins, 1975, vol I, P 721. 4. Ward NG, Rowlett DB, Burke P: Sodium amylobarbitone in the differential diagnosis of confusion. Am J Psychiatry 135:75-78, 1978. 5. Pro JD, Wells CE: The use of the electroencephalogram in the diagnosis ot delirium. Dis Nerv 5yst 38:804-808, 1977. 6. Cole JO, Davis JM: Narcotherapy, in Freedman AM, Kaplan HI, Sadock BJ (ads): Comprehensive Textbook of Psychiatry II. Baltimore, Williams & Wilkins, 1975, vOl 2, pl969. 7. Lipowski ZJ: Delirium updated. Compr Psychiatr 21: 190-196, 1980.

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