Medical Presentations of Psychosis
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ISSN: 2572-4037 Sulik et al. Int J Psychol Psychoanal 2017, 3:021 DOI: 10.23937/2572-4037.1510021 Volume 3 | Issue 2 International Journal of Open Access Psychology and Psychoanalysis REVIEW ARTICLE Medical Presentations of Psychosis - Mimics and Life-Threat- ening Illnesses Scott Sulik1, Carly Eastin1, Kimberly Nordstrom2,3 and Michael P Wilson1,3* Check for 1University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA updates 2University of Colorado School of Medicine, Aurora, Colorado, USA 3Department of Emergency Medicine Behavioral Emergencies Research lab, Little Rock, Arkansas, USA *Corresponding author: Michael P Wilson, MD, PhD, FAAEM, FACEP, Department of Emergency Medicine Behavioral Emergencies Research lab, Little Rock, Arkansas, USA, E-mail: [email protected] creates a substantial diagnostic challenge, as misdiag- Abstract nosis of delirium is associated with longer lengths of Disordered cognition, commonly but inaccurately referred to stay and higher mortality [1,2]. In addition, treatment as “psychosis”, is a challenging symptom to evaluate and manage in the critical care or emergency department set- for mental status changes due to a medical condition is ting. Although exacerbation of a primary psychiatric disorder often quite different than treatment of a primary psy- may indeed be associated with psychosis, a large number chiatric disorder. of medical illnesses may present similarly. Often, there is no single test to establish a definitive diagnosis. As history This paper will discuss three medical mimics of is usually limited in critically ill patients, a wide differential psychiatric illness that may prove diagnostically chal- diagnosis may be the most important tool utilized by the lenging to the clinician: Alcohol withdrawal syndrome, clinician. In addition, the presence of multiple comorbidi- ties not only makes a medical cause more likely but also anti-NMDA-receptor encephalitis, and serotonin syn- complicates subsequent management. Although the use of drome. Furthermore, this manuscript will discuss meth- antipsychotics may prove successful in addressing symp- ods for diagnosis, clinical pearls, and guidelines for man- toms, failure to treat the underlying medical cause may lead agement of these conditions. to increased morbidity and mortality. Incorporating a wide differential diagnosis, establishing the primary cause, and Alcohol Withdrawal intervening in a goal-oriented manner are the keys to suc- cessful management of critical care psychosis. Epidemiology Alcohol remains a commonly used and abused drug Introduction worldwide, despite its association with over 200 medical Psychiatric complaints are not just limited to the conditions, including liver disease, cancer, and accidental psychiatry ward, but are commonly encountered in the injury. In 2012, 5.9% of global deaths were attributed to emergency department. Psychosis in critical care set- alcohol use [3]. In the United States, as many as 40% of tings is usually not a disease in and of itself, but rather hospitalized patients have alcohol-related medical condi- is usually diagnostic of delirium [1]. The incidence of de- tions [4]. Up to 25% of admitted patients with alcohol use lirium has been reported as high as 80% in critically ill disorder will develop acute withdrawal, often requiring ad- patients [2]. mission due to complications such as respiratory failure, delirium tremens (alcohol withdrawal delirium), infection, Given the high prevalence of delirium, it is important cirrhosis, and gastrointestinal bleeding [5,6]. for the emergency department physician to recognize the numerous medical diseases that may present with Mechanism psychiatric overtones. The presence of psychosis often The central effect of alcohol in the body is mediated Citation: Sulik S, Eastin C, Nordstrom K, Wilson MP (2017) Medical Presentations of Psychosis - Mimics and Life-Threatening Illnesses. Int J Psychol Psychoanal 3:021. doi.org/10.23937/2572-4037.1510021 Received: July 21, 2017: Accepted: December 28, 2017: Published: December 30, 2017 Copyright: © 2017 Sulik S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Sulik et al. Int J Psychol Psychoanal 2017, 3:021 • Page 1 of 7 • DOI: 10.23937/2572-4037.1510021 ISSN: 2572-4037 through two main pathways. Gamma-aminobutyric acid Approximately 5% of patients experiencing alcohol (GABA) is a major inhibitory neurotransmitter that binds withdrawal in the inpatient setting will progress to de- to GABA receptors. Ingestion of alcohol enhances the lirium tremens [13]. Clinical manifestations include de- effect of GABA, although the mechanism is currently un- lirium or altered sensorium coupled with autonomic hy- known [7]. Glutamate is a major excitatory neurotrans- peractivity and often hallucinations [16]. The associated mitter acting primarily through NMDA receptors; the hypertension, tachycardia, and hyperventilation leads presence of alcohol inhibits ion flux through the NMDA to increases in cardiac output and oxygen consump- receptor, suppressing activity [8]. The effect of alcohol tion, and subsequently, decreased cerebral blood flow on these two pathways has a synergistic effect on the [17]. This alteration in physiologic state leads to major central nervous system and is responsible for the clini- complications, including electrolyte abnormalities, ar- cal manifestations of alcohol intoxication, namely, seda- rhythmias, pneumonia, and respiratory failure [12]. The tion and anxiolysis [9]. Long-term use of alcohol leads to significance of this stage is not only due to difficulties in upregulation of NMDA receptors and downregulation patient care; it is also associated with a mortality rate of GABA receptors to maintain equilibrium [10]. These up to 15% [18]. alterations in receptor expression persist after alcohol General approach cessation. Increased NMDA activation and loss of GABA inhibition leads to the autonomic excitation and agita- The treatment of alcohol withdrawal syndrome tion seen in alcohol withdrawal. (AWS) varies widely due to its spectrum of severity. Sup- portive care is usually sufficient to treat mild withdrawal Alcohol withdrawal syndrome (AWS) is defined by symptoms that are typically temporary and self-limited. the Diagnostic and Statistical Manual of Mental Disor- Intravenous fluids and antiemetics can be used to ad- ders (DSM) as a recent decrease in or cessation of heavy dress nausea/vomiting and dehydration. In alcohol with- or prolonged alcohol use and the presence of at least drawal syndromes that are severe enough to prompt two of the following: Autonomic dysfunction, hand admission, benzodiazepines have long been considered tremor, insomnia, nausea or vomiting, hallucinations, the mainstay of therapy. All benzodiazepines have been anxiety, agitation, or seizures [11]. The clinical spectrum shown to improve signs and symptoms of withdrawal of alcohol withdrawal generally includes four stages of [16]. Additionally, use of benzodiazepines contributes increasing severity; autonomic hyperactivity, hallucina- to a lower incidence of seizures and delirium tremens tions, neuronal excitation, and delirium tremens [12]. when compared with chlorpromazine, hydroxyzine, However, the progression of symptoms varies greatly thiamine, or placebo [19]. Longer-acting agents (va- between patients, often skipping milder stages before lium, chlordiazepoxide) may be more effective than the development of severe withdrawal. short-acting agents in preventing alcohol withdrawal Psychiatric fake-outs seizures and delirium tremens, but they may also pose an increased risk of oversedation [20,21]. An early or mild presentation can sometimes man- ifest with autonomic symptoms only, including anxiety, Although there is less evidence, several additional nausea/vomiting, tremor, or diaphoresis. Generally, mild agents have also been studied for use as adjuvant ther- presentations do not involve alterations in sensorium apy for alcohol withdrawal. For benzodiazepine-resis- [9]. Consequently, these symptoms can easily be misin- tant delirium tremens, intubation is often required, and terpreted as anxiety, especially if the patient minimizes continuous propofol infusion been utilized with some their drinking history to clinicians. On the more severe success [22,23]. Anticonvulsants, including carbamaz- end, alcoholic hallucinations may occur with alcohol epine and valproic acid, may raise the seizure thresh- withdrawal. These hallucinations are most often visual old but are ineffective as single agents in management and tactile, including the sensation of insects crawling of alcohol withdrawal [24,25]. Few small studies have on the skin, or formication. Auditory hallucinations are suggested phenobarbital is as effective as lorazepam for less common and may point to an alternate cause [13]. treatment of mild withdrawal; however, systematic re- Seizures associated with withdrawal are typically brief views do not show any additional benefit over benzodi- and tonic-clonic in nature, and they often occur without azepines [26-28]. Phenytoin and the newer antiepilep- autonomic symptoms or hallucinations [14]. Persistent tic oxcarbazepine have not been shown to be useful in alterations in mental status in patients with a heavy al- preventing withdrawal seizures [29,30]. β-blockers and cohol-use history should never be