Cases That Test Your Skills

The confused binge drinker Sangeetha Venkataramanan, MD, and Lauren Swager, MD

Mr. P, age 46, says he ‘feels weird’ and describes confusion, How would you paranoia, and suicidal ideations. He is a binge drinker and uses handle this case? Answer the challenge and . How would you treat him? questions throughout this article

CASE Paranoid and confused to cut his throat once when he was “intoxi- Mr. P, age 46, presents to the emergency de- cated.” She says she does not feel safe around partment (ED) with a chief complaint of feeling him because of his labile mood and history of “very weird.” Although he has seen a number aggression. She confirms that Mr. P does not of psychiatrists in the past, he does not recall drink daily but binge-drinks at times. being given a specific diagnosis. He describes Initial mental status examination of evalu- his feelings as “1 minute I am fine and the next ation reveals hyperverbal, rapid speech. Mr. P minute I am confused.” He endorses feeling is circumstantial and tangential in his thought paranoid for the past 6 to 12 months and re- process. He has poor judgment and insight ports a history of passive suicidal ideations. and exhibits suicidal ideations with a plan. On the day he presents to the ED, however, he Toxicology screening reveals a blood has a specific plan to shoot himself. He does level of 50 mg/dL and is positive for Cannabis not report audiovisual hallucinations, but has and opiates. noticed that he talks to himself often. Mr. P reports feeling worthless at times. He Which condition most likely accounts for Mr. P’s has a history of manic symptoms, including de- presentation? creased need for sleep and hypersexuality. He a) bipolar disorder, currently manic describes verbal and sexual by his foster b) substance-induced parents. Mr. P reports using Cannabis and opi- c) cognitive disorder oids occasionally and to drinking every “now d) delirium and then” but not every day. He denies using benzodiazepines. When he is evaluated, he is not taking any medication and has no signifi- TREATMENT Rapid improvement cant medical problems. Mr. P reports a history From the ED, Mr. P was admitted to an inpa- of several hospitalizations, but he could not de- tient psychiatric unit, where he was found scribe the reasons or timing of past admissions. initially to be disoriented to time, place, and Mr. P has a 10th-grade education. He lives Dr. Venkataramanan is a Resident in , and Dr. Swager is with his fiancée, who reports that he has been Assistant Professor, West Virginia University School of Medicine, behaving oddly for some time. She noticed Morgantown, West Virginia. that he has memory problems and describes Disclosure violent behavior, such as shaking his fist at The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers Current Psychiatry her, breaking the television, and attempting of competing products. Vol. 13, No. 3 49 Cases That Test Your Skills

Table 1 Differential diagnosis of altered mental status Condition Features Course Treatment and comments Wernicke’s Ocular signs, , and Sudden Thiamine encephalopathy altered mental status Korsakoff’s and Progressive Donepezil, rivastigmine syndrome confabulation Ocular signs, ataxia, and altered mental status Alcohol-induced Anterograde or retrograde Progressive Abstinence from alcohol; no persisting amnesia validated medical treatment amnestic disorder At least cognitive disturbance Clinical Point Frontotemporal Insidious onset and slow Slowly Selective serotonin reuptake Mr. P’s fluctuating dementia progression progressive inhibitors and atypical Early loss of personal antipsychotics (use a low dosage mental status, gait awareness and social because these patients can be sensitive to medications) instability, and awareness Early signs of disinhibition, An exercise program, modifying confabulation create mental rigidity and the home environment, increased supervision, physical, a high suspicion inflexibility, hyperorality, stereotyped and occupational, and speech therapy for Wernicke’s perseverative behavior, and behavior modification distractibility, and language, encephalopathy emotional, and neurological disturbances Malingering Marked discrepancy Progressive Educate staff about illness between the claimed distress behavior and objective findings Work collaboratively to reduce Lack of cooperation the clinician’s feelings of anger, during evaluation and not frustration, and helplessness complying with treatment Do not limit the patient’s care to a single provider

person. His thought process remained disor- Thiamine and lorazepam are prescribed as ganized and irrational, with significant memo- needed because of Mr. P’s history of alcohol ry difficulties. He is noted to have an unsteady abuse. However, it’s determined that he does gait. Nursing staff observes that Mr. P has sig- not need lorazepam because his vital signs nificant difficulties with activities of daily liv- are stable and there is no evidence of alcohol ing and requires assistance. He talks in circles withdrawal symptoms. and uses nonsensical words. During the course of his 10-day hospitaliza-

His serum vitamin B12 level, folate lev- tion, Mr. P’s cognitive difficulties resolved. He el, rapid plasma reagin, magnesium lev- regains orientation to time, place, and per- Discuss this article at el, and thiamine level are within normal son. He gains skill in all his activities of daily www.facebook.com/ limits; CT scan of the brain is unremarkable. living, to the point of independence, and is CurrentPsychiatry Neuropsychological testing reveals signifi- discharged with minimal supervision. Vitamin cant and diffuse cognitive deficits suggestive B supplementation is prescribed, with close of dysfunction. He is deemed to follow up in an outpatient day program. MRI/ not have decision-making capacity; because SPECT scan is considered to rule out fronto- he has no family, his fiancée is appointed as temporal dementia as recommended by the Current Psychiatry 50 March 2014 his temporary health care proxy. results of his neurocognitive testing profile. Cases That Test Your Skills

Which condition likely account for Mr. P’s Table 2 presentation during inpatient hospitalization? a) Wernicke’s encephalopathy Symptoms and signs b) Korsakoff’s syndrome of Wernicke’s encephalopathy c) malingering over time d) frontotemporal dementia Common at Abnormal eye movement presentation e) a neurodegenerative disease Ataxia Change in vision Confabulation The authors’ observations Confusion Decreased reflexes Mr. P’s fluctuating mental status, gait in- Gait disturbance stability, and confabulation create high sus- Hallucinations picion for Wernicke’s encephalopathy; his Hypotension Clinical Point dramatic improvement with IV thiamine Hypothermia supports that diagnosis. Mr. P attends the The triad that Inability to form new memories outpatient day program once after his dis- includes ocular signs Loss of memory charge, and is then lost to follow-up. Tachycardia such as nystagmus, During inpatient stay, Mr. P eventually Uncommon Behavioral disturbances cerebellar signs, admits to binge drinking several times a Hearing loss and confusion week, and drinking early in the morning, Hypotension and tachycardia supports Wernicke’s which would continue throughout the day. Seizures His significant cognitive deficits revealed by Stupor encephalopathy neuropsychological testing suggests consid- Late-stage Choreic dyskinesia eration of a differential diagnosis of multi- Coma factorial cognitive dysfunction because of: Hyperthermia • long-term substance use Source: Reference 3 • Korsakoff’s syndrome • frontotemporal dementia • a neurodegenerative disease • malingering (Table 1). Diagnosis. Making the correct diagnosis is challenging because the clinical presen- tation can be variable. No lab or imaging Wernicke’s encephalopathy studies confirm the diagnosis. The triad of Wernicke’s encephalopathy is a life-threaten- signs considered to support the diagnosis ing neurologic disorder caused by thiamine include ocular signs such as nystagmus, deficiency. The disease is rare, catastrophic cerebellar signs, and confusion. These in onset, and clinically complex1; as in Mr. signs occur in only 8% to 10% of patients P’s case, diagnosis often is delayed. In au- in whom the diagnosis likely.1,2 topsy studies, the reported prevalence of Attempts to increase the likelihood of Wernicke’s encephalopathy is 0.4% to 2.8%.1 making an accurate lifetime diagnosis of Wernicke’s encephalopathy was suspected Wernicke’s encephalopathy include ex- before death in 33% of alcohol-dependent pa- panding the focus to 8 clinical domains: tients and 6% of nonalcoholics.1 Other causes • dietary deficiency of Wernicke’s encephalopathy include can- • eye signs cer, gastrointestinal surgery, hyperemesis • cerebellar signs gravidarum, a starvation or malnutrition • seizures state, GI tract disease, AIDS, parenteral nu- • frontal lobe dysfunction Current Psychiatry trition, repetitive , and infection.1 • amnesia Vol. 13, No. 3 51 Cases That Test Your Skills

periaqueductal areas.1,4 Atypical lesions Related Resources commonly are seen in the cerebellum, den- • Lough ME. Wernicke’s encephalopathy: expanding the diagnos- tate nuclei, caudate nucleus, and cerebral tic toolbox. Neuropsychol Rev. 2012;22(2):181-194. cortex.1 • Wijnia JW, van de Wetering BJ, Zwart E, et al. Evolution of Wernicke- in self-neglecting alcoholics: preliminary results of relation with Wernicke-delirium and dia- Treatment. Evidence supports use of betes mellitus. Am J Addict. 2012;21(2):104-110. IV thiamine, 200 mg 3 times a day, when Brand Names the disease is suspected or established.1,2 Donepezil • Aricept Rivastigmine • Exelon Lorazepam • Ativan Thiamine • Thiamilate Thiamine has been associated with spo- radic anaphylactic reactions, and should be administered when resuscitation facili- ties are available. Do not delay treatment Clinical Point • mild memory impairment because resuscitation measures are un- • altered mental status.1 available because you risk causing irre- Neither the optimal The sensitivity of making a correct diag- versible .1 dosage of thiamine nosis increases to 85% if at least 2 of 4 fea- In Mr. P’s case, prompt recognition of the nor the appropriate tures—namely dietary deficiency, eye signs, need for thiamine likely led to a better out- duration of treatment cerebellar signs, memory impairment, and come. Thiamine supplementation can pre- have been determined altered mental status—are present. These vent Wernicke’s encephalopathy in some criteria can be applied to alcoholic and patients. Prophylactic parenteral adminis- by randomized, nonalcoholic patients.1 Table 23 (page 51) tration of thiamine before administration of double-blind studies lists common and uncommon symptoms of glucose in the ED is recommended, as well Wernicke’s encephalopathy. as vitamin B supplementation with thia- Although CT scan of the brain is not a re- mine included upon discharge.1,2 Studies liable test for the disorder, MRI can be pow- support several treatment regimens for pa- erful tool that could support a diagnosis of tients with Wernicke’s encephalopathy and acute Wernicke’s encephalopathy.1 We did those at risk of it.1,3,5 not consider MRI in Mr. P’s case because Neither the optimal dosage of thia- the consulting neurologist thought this was mine nor the appropriate duration of unnecessary because of the quick improve- treatment have been determined by ran- ment in his cognitive status with IV thia- domized, double-blind, controlled studies; mine—although MRI might have helped to empirical clinical practice and recommen- detect the disease earlier. In some studies, dations by Royal College of Physicians, brain MRI revealed lesions in two-thirds London, suggest that a more prolonged of Wernicke’s encephalopathy patients.1 course of thiamine—administered as long Typically, lesions are symmetrical and seen as improvement continues—might be in the thalamus, mammillary body, and beneficial.6

Bottom Line Not all patients who present with aggressive behavior, mania, and psychiatric symptoms have a primary psychiatric diagnosis. It is important to consider nutritional deficiencies caused by chronic in patients presenting with acute onset of confusion or altered mental status. Wernicke’s encephalopathy Current Psychiatry 52 March 2014 might be the result of alcohol abuse and can be treated with IV thiamine. Cases That Test Your Skills

Left untreated, Wernicke’s encephalopa- disorder is substantially underdiagnosed; thy can lead to irreversible brain damage.2 as a consequence, patients are at risk of Mortality has been reported as 17% to 20%; brain damage.2 82% of patients develop Korsakoff’s syn- References drome, a chronic condition characterized 1. Galvin R, Bråthen G, Ivashynka A, et al; EFNS. by short-term memory loss. One-quarter Guidelines for diagnosis, therapy and prevention of Wernicke’s encephalopathy. Eur J Neurol. 2010;17(12): of patients who develop Korsakoff’s syn- 1408-1418. drome require long-term residential care 2. Robinson K. Wernicke’s encephalopathy. Emerg Nurse. 2003; 11(5):30-33. because of permanent brain damage.2 3. Sechi G, Serra A. Wernicke’s encephalopathy: new clinical Making a diagnosis of Wernicke’s en- settings and recent advances in diagnosis and management. Lancet Neurol. 2007;6(5):442-455. cephalopathy is a challenge because no 4. Celik Y, Kaya M. Brain SPECT findings in Wernicke’s specific symptom or diagnostic test can be encephalopathy. Neurol Sci. 2004;25(1):23-26. relied upon to confirm the diagnosis. Also, 5. Thomson AD, Guerrini I, Marshall JE. Wernicke’s encephalopathy: role of thiamine. Practical Gastroenterology. Clinical Point patients might deny that they have an al- 2009;33(6):21-30. cohol problem or give an inaccurate his- 6. Thomson AD, Cook CCH, Guerrini I, et al. Wernicke’s One-quarter of encephalopathy: ‘plus ca change, plus c’est la meme chose’. tory of their alcohol use,2 as Mr. P did. The Alcohol Alcohol. 2008;43:180-186. patients who develop Korsakoff’s syndrome require long-term residential care because of brain damage

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