Thought Disorders

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Chapter 110

Thought Disorders

Robert S. Hockberger and John R. Richards

Perspective

In the 1800s, Morel introduced the term dementia praecox to describe a progressive deterioration of mental functioning and behavior with onset in adolescence to early adult life.¹ In 1911, Bleuler detailed the specifics of this disorder, which he termed schizophrenia, or “split-mindedness.”² Early treatments of schizophrenia included ice water immersion, barbiturates or insulin to induce prolonged narcosis or coma, seizure induction with pentylenetetrazol, electroconvulsive therapy, and frontal leukotomy.³ The effectiveness of these treatments was marginal at best, and until recent times, most schizophrenic patients were relegated to lifelong institutionalization.

Modern-era pharmacotherapy for schizophrenia, with chlorpromazine and haloperidol, began in the early 1950s. This treatment proved so successful that by the 1960s, most psychiatrists believed that schizophrenia could be successfully managed in the outpatient setting. In 1965, the Community Mental Health Centers Act initiated the release of medicated schizophrenic patients into the community.⁴ Unfortunately, inadequate family support, unavailability of jobs and low-cost housing, and lack of funding for social services and outpatient psychiatric care left many of these individuals isolated without the tools needed for resocialization. Currently 20 to 40% of homeless people in the United States have a major mental illness.⁵ Emergency departments frequently serve as the primary entry point into the mental health care system for many of these individuals.⁶

Principles of Disease

The etiology of schizophrenia is currently believed to be heterogeneous from interaction of biologic and environmental factors. Studies involving adopted twins whose biologic parents have schizophrenia demonstrate a strong genetic basis for the disorder. Although the overall incidence of schizophrenia in the general population is roughly 1%, it is approximately 10% in first-degree biologic relatives of individuals with the disorder.⁷ With regard to the pathophysiologic mechanism of schizophrenia, dopaminergic, serotonergic, cholinergic, and glutamatergic systems have been implicated.^8–11

Schizophrenia is also postulated to be a neurodevelopmental disorder resulting from the influence of environmental factors on genetically predisposed individuals. Disruptions in fetal brain development, caused by perinatal hypoxia, poor nutrition, infection, and other insults, may set the stage for subsequent development of schizophrenia.1,12 New imaging techniques have documented structural brain abnormalities, most of which appear to be developmental rather than degenerative in nature.⁸ Evidence supports the existence of a progressive continuum of psychotic illness, beginning with unipolar depression and progressing to bipolar illness, schizoaffective psychoses, and finally schizophrenia.^1,13,14

Clinical Features

Overt signs of schizophrenia usually become manifested during adolescence or early adult life. Many patients describe a childhood with few interpersonal relationships and a withdrawn, eccentric personality.

Phases of Schizophrenia

The development of schizophrenia involves three phases.¹⁵ The premorbid phase is characterized by the development of “negative” symptoms with deterioration in personal, social, and intellectual functioning. Patients progressively withdraw from social interactions and neglect personal appearance and hygiene, which negatively affects their work, school, and home life.

The active phase is usually precipitated by a stressful event with development of “positive” symptoms, such as active delusions, hallucinations, and bizarre behavior. Patients may become agitated or exhibit a hypervigilant withdrawal state characterized by rocking or staring. It is during this phase that they are most likely to be brought to the emergency department by family, friends, coworkers, or the police.

In the residual phase, patients are left with impaired social and cognitive ability, marked by bizarre ideation, delusions, peculiar behavior, poor personal hygiene, and social isolation. Most schizophrenic patients require a sheltered environment to function adequately. Despite a wide spectrum of severity, the general course for most patients is one of gradual deterioration with periodic episodes of psychotic decompensation.

Criteria for Schizophrenia

The diagnostic criteria for schizophrenia (Box 110-1) are outlined in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM-IV-TR).¹⁵

BOX 110-1

Summary of DSM-IV-TR Criteria for Schizophrenia

A Presence of two (or more) characteristic symptoms for 1 month (or more) unless treated

1. Delusions

2. Hallucinations

3. Disorganized speech (derailment or incoherence)

4. Grossly disorganized or catatonic behavior

5. Negative symptoms: affect flattening, alogia (poverty of speech), avolition (unable to perform goal-directed activities)

Note: Only one symptom above is required if delusions are bizarre or hallucinations consist of a running commentary.

B Sharp deterioration from prior level of functioning (i.e., work, self-care, interpersonal relations)

C Continuous signs of disturbance for 6 months (or more)

D Schizoaffective disorder and mood disorder with psychotic features have been ruled out

E Not caused by substance abuse, medication, or a general medical condition

Modified from Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text rev. Washington, DC, American Psychiatric Association, 2000.

• The patient must exhibit two or more of the following symptoms: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, and negative symptoms (such as flattening of affect, poverty of speech, or inability to perform goal-directed activities).

• There must be a sharp deterioration from the patient’s prior level of functioning (work, school, self-care, or interpersonal relations), and there must be continuous signs of disturbance for at least 6 months.

• The diagnoses of schizoaffective and mood disorders with psychotic features must be excluded.

• In evaluating these patients, emergency physicians must exclude myriad medical conditions that can mimic or cause psychotic symptoms.

Diagnostic Strategies

Patients with Known Psychiatric Disorders

Patients with previously diagnosed thought disorders who present with mild to moderate exacerbation of their symptoms do not require extensive laboratory evaluation.¹⁶ Because some of these patients may have coexisting substance abuse or undiagnosed medical disorders, a thorough history, detailed physical examination, and routine toxicology studies are indicated for most patients.^17–19 Patients exhibiting severe exacerbation of symptoms accompanied by marked agitation, violent behavior, or significantly abnormal vital signs should undergo more extensive evaluation.

Patients without Known Psychiatric Disorders

Many toxicologic and medical disorders can mimic schizophrenia. Patients with the apparent new onset of psychosis should receive a medical evaluation to exclude toxicologic and medical disorders.20–23 Both the DSM-IV-TR and review articles on this topic emphasize that most toxicologic and medical causes of altered mental status that simulate acute schizophrenia are best recognized by patterns of presentation combined with focused testing based on one’s index of suspicion for nonpsychiatric disease, rather than the reliance on a broad use of screening tests.

Differential Considerations

Medical Disorders

Certain medications and medical disorders may affect thought processes, causing patients to exhibit abnormal behavior (Boxes 110-2 and 110-3). This behavior may range from mild personality changes to apparent acute psychosis, even in the absence of an underlying psychiatric disorder.¹ Factors that should alert one to a medical disorder include the following: history of substance abuse or a medical disorder requiring medication; patient’s age older than 35 years without previous evidence of psychiatric disease; recent fluctuation in behavioral symptoms; hallucinations that are primarily visual in nature; presence of lethargy; abnormal vital signs; and poor performance on cognitive function testing, particularly orientation to time, place, and person. These and other factors may be helpful in differentiating functional (psychiatric) from organic (medical) causes of abnormal behavior and can be easily recalled with the mnemonic MADFOCS (Table 110-1).²⁴

Table 110-1

Factors in Differentiating Organic and Functional Psychosis: MADFOCS

	ORGANIC	FUNCTIONAL
Memory deficits	Recent impairment	Remote impairment
Activity	Psychomotor retardation	Repetitive activity
	Tremor	Posturing
	Ataxia	Rocking
Distortions	Visual hallucinations	Auditory hallucinations
Feelings	Emotional lability	Flat affect
Orientation	Disoriented	Oriented
Cognition	Islands of lucidity	Continuous scattered thoughts
	Perceives occasionally	Unfiltered perceptions
	Attends occasionally	Unable to attend
	Focuses	Unable to focus
Some other findings	Age > 40 years	Age < 40 years
	Sudden onset	Gradual onset
	Physical examination findings often abnormal	Physical examination findings normal
	Vital signs may be abnormal	Vital signs usually normal
	Social immodesty	Social modesty
	Aphasia	Intelligible speech
	Consciousness impaired	Awake and alert

Modified from Frame DS, Kercher EE: Acute psychosis: Functional vs. organic. Emerg Med Clin North Am 9:123, 1991.

Although the classic textbook differentiation between functional and organic causes of abnormal behavior is straightforward, the evaluation of individual patients may be difficult.²¹ A patient with underlying psychiatric disease may develop a medical disorder, which may worsen the patient’s behavioral symptoms and further cloud the distinction between functional and organic disease. This evaluation is particularly difficult in the emergency department when previous medical or psychiatric history is not available, the patient is uncooperative, and the time frame to make a disposition is brief. When the clinical differentiation between functional and organic disease is unclear on the basis of available information, a patient should be thoroughly evaluated to exclude a toxicologic or medical disorder.

Psychiatric Disorders

A previously undiagnosed patient who presents with an acute functional psychosis may ultimately be given one of several psychiatric diagnoses.¹⁵ A brief psychotic disorder involves the sudden onset of psychotic symptoms in response to major stress and lasts several days to 1 month. Patients with schizophreniform disorder have similar symptoms that last longer than 1 month but less than 6 months. Whereas one third of individuals initially given the diagnosis of schizophreniform disorder recover within 6 months, the other two thirds retain their symptoms and are diagnosed as having schizophrenia. Patients with mood disorders may develop psychotic symptoms. If these symptoms are present only during periods of mood disturbance, the diagnosis of mood disorder with psychotic features is applied; if they persist longer than 2 weeks in the absence of prominent mood symptoms, the diagnosis of schizoaffective disorder is made. Patients with personality disorders may occasionally develop brief psychotic episodes under stress.

Ganser’s syndrome is a symptom complex considered to be emotional in origin in which the patient may appear to have amnesia, hallucinations, or alterations in consciousness, usually in association with physical complaints. An individual with Ganser’s syndrome may have psychotic symptoms for no apparent gain except to assume the role of the psychiatric patient.

Persons with a delusional disorder experience nonbizarre delusions that may dominate their lives. They may believe that famous people are in love with them (erotomanic type), that they have extraordinary powers with a special relationship to a deity or a famous person (grandiose type), that their sexual partner is unfaithful (jealous type), that they are being malevolently treated in some way (persecutory type), or that they have some physical defect or general medical condition (somatic type). Although patients with somatic delusions may experience tactile or olfactory hallucinations related to the delusional theme (e.g., the sensation of being infested with insects), the other features associated with schizophrenia are not present.

Management

General Approach

Patients with thought disorders may be agitated and hyperactive, may be withdrawn but hypervigilant, or may complain of somatic delusions. In addition, they may have paranoid ideation, may be angry they have been brought to the emergency department against their will, or may be frightened because they have been confronted by the police, restrained, and isolated. These patients may be disconcerting to staff because they are often irrational, erratic, and unpredictable in their behavior. Although emergency personnel should remain calm, empathetic, and reassuring in their interactions with patients exhibiting a thought disorder, they must also take steps to ensure staff safety whenever dealing with patients at risk for sudden violence. Such patients include those who have behaved violently before coming to the emergency department, those who physically or verbally threaten staff, and those who have an escalating level of agitation despite verbal attempts to calm them.

Each patient should have a thorough history and physical examination, including a detailed mental status evaluation, to rule out an organic brain syndrome. Valuable information can be obtained from family members, friends, coworkers, neighbors, prehospital personnel, police, and previous medical records (see Table 110-1).²⁴

The most important step in evaluating a patient with a suspected thought disorder is the assessment of the patient’s thought processes through the initial interview. The goals are to establish a positive physician-patient relationship, to make a correct diagnosis, and to gather enough information for an optimal disposition. The interview should be conducted in a quiet, comfortable room with adequate privacy. The examiner should be sitting, and if possible the interview should proceed to completion without interruption. If the patient is believed to be potentially dangerous but is not in need of immediate restraint, the interview should take place in an open area with security personnel nearby.

The emergency physician should begin with an introduction and should express the desire to be “of help” to the patient. The interview begins with open-ended questions designed to assess the patient’s complaint and understanding of the current circumstances. Good opening questions include the following:

Do you understand why you have been brought here today?

You seem to be upset. Can you tell me why?

Do you have any idea why you might be having these symptoms?

The patient’s appearance, body language, affect, and speech are observed during the responses to these questions.

A brief mental status examination is then performed. It may be initiated in a nonthreatening manner by stating, “I am now going to ask you a few questions to see how well you are concentrating.” The patient is first asked about orientation to time, place, and person as this is the most sensitive test for differentiation of organic from functional disease. Patients who are disoriented require a detailed medical evaluation to exclude the presence of an organic brain syndrome. Patients who are oriented are assessed for attention, memory, intellectual functioning, and judgment in an attempt to determine their specific diagnosis, their potential for danger to themselves or others, and their degree of dysfunction and ability to care for themselves in the outpatient setting.

Rapid Tranquilization

When psychotic patients exhibit behavior that is violent or so disorganized and uncooperative that clinical evaluation is impossible, the temporary use of physical restraints is indicated while rapid tranquilization is initiated (see Chapter 189). The technique of rapid tranquilization involves serial doses of a high-potency antipsychotic agent until target symptoms, such as agitation and excessive psychomotor activity, are improved. The goal is to facilitate cooperation of the patient without causing unnecessary sedation, which inhibits further medical and psychiatric assessment. Oral, intramuscular, or intravenous doses can be given every 30 to 60 minutes until the patient becomes calm and more cooperative. If the patient is willing, an oral concentrate is preferred as it implies consent and takes effect almost as quickly as with intramuscular administration.

Haloperidol (Haldol), a butyrophenone, is widely used for rapid tranquilization in the United States.25–27 The initial dose is 5 to 10 mg intramuscularly or intravenously for young to middle-aged patients and 0.5 to 2.0 mg intramuscularly or intravenously for elderly patients. Although rapid tranquilization with haloperidol quickly reduces tension, anxiety, and hyperactivity, delusions and hallucinations may not resolve for several weeks. In 2007 the U.S. Food and Drug Administration (FDA) released a non–black box warning about sudden death with the use of haloperidol in large doses or through the intravenous route. Droperidol (Inapsine), another butyrophenone, has also been extensively used for this indication in doses of 2.5 to 5.0 mg intramuscularly or intravenously.^28,29 Compared with haloperidol, droperidol has a faster onset and shorter duration of action and causes slightly more sedation. In 2001 the FDA issued a black box warning because of reports of a potential association between droperidol and prolonged QT interval, torsades de pointes, and sudden death.³⁰ Despite subsequent studies supporting both the efficacy and safety of droperidol, the FDA warning has resulted in a significant decrease of its use in clinical practice.^31,32 Neuroleptics should not be used for pregnant or lactating women, phencyclidine overdose, or anticholinergic drug–induced psychosis. In addition, although they may be useful to manage agitation in drug or alcohol intoxication, they should not be used as the sole agent in patients with drug or alcohol withdrawal. Newer atypical antipsychotic agents appear to have a broader spectrum of response with fewer side effects than the typical agents. These medications are available in tablet form and should be considered for patients who consent to oral medication. However, oral administration of a pharmacologic agent during an acute episode of agitation and psychosis is usually impossible. Ziprasidone (Geodon), aripiprazole (Abilify), and olanzapine (Zyprexa) are newer atypical antipsychotics currently approved in the United States for intramuscular injection.³³ For ziprasidone, the initial dose is 20 mg intramuscularly, and it can be repeated every 4 hours. It is more effective than haloperidol for sedation and with fewer extrapyramidal side effects, but it is not yet widely used in the emergency department setting.^34,35

Benzodiazepines are effective in managing agitation in patients who have alcohol or sedative-hypnotic withdrawal, cocaine intoxication, or a contraindication to neuroleptic use. Benzodiazepines are helpful adjuncts to neuroleptic medication in providing rapid tranquilization, particularly for combativeness or severe agitation. Lorazepam (Ativan), 1 to 2 mg, is frequently mixed with haloperidol, 5 mg, in the same syringe and administered intramuscularly or intravenously for this purpose.²⁷ Benzodiazepines have also been shown to mitigate catatonic signs in schizophrenic patients.³⁶ Disadvantages of benzodiazepines are the need for repeated dosing and the close monitoring required for potential respiratory depression with large doses.³⁷

Outpatient Management

The outpatient treatment of schizophrenia involves maintenance therapy with neuroleptic agents, family counseling, and social rehabilitation. Emergency physicians rarely prescribe outpatient neuroleptic medications but should be familiar with complications associated with their long-term use.

Box 110-4 lists the most common neuroleptic medications currently used in the United States.^38–44 The mechanism of action is related to the blockade of dopamine receptors in the central nervous system, particularly dopamine D₂ receptors in the basal ganglia and limbic portions of the forebrain. The earlier, less potent drugs, of which chlorpromazine is the prototype, cause more pronounced sedation, orthostatic hypotension, and cardiovascular toxicity from a combination of anticholinergic, antihistaminic, and anti–alpha-adrenergic effects. More potent agents (e.g., haloperidol) are safer, especially in older patients, because of their relative lack of these adverse effects. However, these more potent drugs are associated with a higher incidence of extrapyramidal symptoms, such as dystonias, akathisia, akinesia, and rigidity.

The high frequency of severe adverse reactions, poor compliance by patients, and the large number of patients with symptoms refractory to traditional antipsychotic agents prompted the development of new alternative agents. These “atypical” neuroleptic agents block serotonin to a greater extent than dopamine does, resulting in a low incidence of extrapyramidal side effects. Clozapine is particularly effective in patients who have not responded to other antipsychotic drugs.⁴¹ However, clozapine is expensive, has a side effect profile similar to that of the low-potency antipsychotic agents, and causes agranulocytosis in approximately 1% of patients.³⁹ It is recommended only for the treatment of patients with refractory psychosis. Olanzapine, quetiapine, and the newest agent, aripiprazole, are similar to clozapine but have fewer side effects and less risk of agranulocytosis.³⁸ Risperidone, another newer neuroleptic agent with improved effects on negative symptoms, has been found to be superior to haloperidol in several short-term trials.^42–45 The most recent FDA-approved drug (2006), paliperidone (Invega), is the active metabolite of risperidone. Unfortunately, the expense and unavailability of these newer antipsychotic agents limit their utility for treatment of acute psychosis in the emergency department. Ziprasidone, risperidone, and quetiapine have been associated with QT interval prolongation similar to that seen with droperidol and haloperidol but have not yet been found to be associated with sudden cardiac death.⁴⁶

Because of the high incidence of extrapyramidal symptoms in patients treated with high-potency neuroleptics, it is common practice to administer antiparkinsonian drugs (e.g., benztropine, procyclidine, trihexyphenidyl) at the same time either to treat the adverse effects or to prevent them. Prophylactic treatment is most useful in patients with a history of extrapyramidal symptoms, those receiving large doses of high-potency antipsychotic agents, and those in whom the occurrence of these symptoms is likely to increase the risk of noncompliance.

Noncompliance with antipsychotic medication remains a leading cause of psychiatric hospitalization. Patients with recurrent psychotic relapses caused by noncompliance are candidates for treatment with long-acting injectable antipsychotic drugs, usually given every 2 weeks. Three such agents available in the United States are fluphenazine, risperidone, and haloperidol decanoate.⁴⁷

Complications of Neuroleptic Drug Therapy

Dystonia

Acute dystonia, the most common adverse effect seen with neuroleptic agents, occurs in 1 to 5% of patients. This reaction is caused by a disruption of the dopaminergic-cholinergic balance in the nigrostriatal pathways of the basal ganglia, resulting in cholinergic dominance.⁴⁸ Dystonic reactions, which can occur at any point during long-term therapy and up to 48 hours after administration of neuroleptics in the emergency department, involve the sudden onset of involuntary contraction of the muscles of the face, neck, or back. The patient may have protrusion of the tongue (buccolingual crisis), deviation of the head to one side (acute torticollis), sustained upward deviation of the eyes (oculogyric crisis), extreme arching of the back (opisthotonos), and rarely laryngospasm. These symptoms tend to fluctuate, decreasing with voluntary activity and increasing under emotional stress, which occasionally misleads emergency physicians to believe they are factitious.

Dystonic reactions should be treated with intramuscular or intravenous benztropine (Cogentin), 1 to 2 mg, or diphenhydramine (Benadryl), 25 to 50 mg, which usually results in immediate reversal of symptoms. Patients should receive oral therapy with the same medication for 48 to 72 hours to prevent recurrent symptoms.⁴⁸

Akathisia

Akathisia is a state of motor restlessness characterized by a physical need to be moving constantly. It occurs most often in middle-aged patients during the first few months of therapy. Patients usually pace the room and express a sense of inner tension that is not relieved by activity. If asked, they do not want to be constantly moving but feel physically compelled to do so. This reaction can easily be mistaken for a decompensating psychosis, leading to a vicious circle in which more medication is given to treat a side effect caused by the same drug. This misdiagnosis can be avoided by carefully evaluating the patient for the exacerbation of positive psychotic symptoms, which are not increased by akathisia. Akathisia is treated with beta-blockers (e.g., propranolol, 30-60 mg/day) and anticholinergic drugs (e.g., benztropine, 1 mg twice to four times daily). A new potential agent for the treatment of akathisia is glycine, a nonessential amino acid that stimulates glutamatergic neurotransmission.⁴⁹ In addition, if possible, the dosage of the antipsychotic agent should be lowered or replaced with another drug.

Pseudoparkinsonism and Akinesia

A clinical picture can occur that may be indistinguishable from Parkinson’s disease, particularly in elderly patients during the first month of therapy. Treatment with anticholinergic agents (e.g., benztropine) or antiparkinsonian drugs is usually effective. Akinesia, which is characterized by immobility, withdrawal, and lack of motivation, may be mistaken for a postpsychotic depression. It is responsive to antiparkinsonian drugs, but symptoms usually resolve gradually over time.

Tardive Dyskinesia

Tardive dyskinesia usually appears after several years of neuroleptic drug treatment and is characterized by involuntary movements, especially of the face and tongue, that are described as writhing, grimacing, and choreoathetoid in nature. The earliest manifestation is often a curling or twisting movement of the tongue. The onset of these symptoms can be falsely attributed to psychological factors because they intensify under emotional stress, fatigue, and voluntary activity and disappear with sleep.

The reported prevalence of tardive dyskinesia ranges from 0.5 to 70%, with a mean of 24%.⁴⁸ The incidence of the disorder appears to be directly related to the duration of treatment, total cumulative dosage, evidence of preexisting brain damage, and age of the patient. It is more common in elderly women and patients with associated mood disorders. For patients with mild symptoms, discontinuation or lowering of the dosage of antipsychotic agents, switching to a newer atypical neuroleptic agent, and cotreatment with benzodiazepines may reverse the symptoms. Patients with moderate to severe symptoms are difficult to treat, but some have variable degrees of improvement when they are treated with reserpine or tetrabenazine along with discontinuation of neuroleptic treatment.⁴⁸

Orthostatic Hypotension

All antipsychotic agents can cause orthostatic hypotension, an effect related to alpha-adrenergic blockade. This complication is less common with the more potent agents (e.g., haloperidol). Typically, episodes are mild in severity and brief in duration. Symptomatic patients should be treated with oxygen, Trendelenburg’s position, and intravenous fluid administration. Pressor agents (e.g., dopamine) should be used only for severe, symptomatic episodes that fail to respond to the previous measures. Agents with beta-agonist activity (e.g., epinephrine, isoproterenol) are contraindicated in these patients.

Neuroleptic Malignant Syndrome

Neuroleptic malignant syndrome (NMS) is a life-threatening complication of neuroleptic drug treatment that affects 0.5 to 1% of patients.⁵⁰ It is seen with both typical and atypical neuroleptic agents and usually occurs in the first few weeks after initiation of treatment, but it can also be seen after a recent increase in drug dosage or after parenteral treatment with large doses of neuroleptic agents. NMS is characterized by high fever, severe muscle rigidity, altered consciousness, autonomic instability, and elevated serum creatine kinase levels and can be confused with serotonin syndrome. Additional complications can include respiratory failure, gastrointestinal hemorrhage, hepatic and renal failure, coagulopathy, and cardiovascular collapse.

The pathophysiologic mechanism of NMS is not well understood, but it is thought to be related to dopamine depletion in the central nervous system leading to defective thermoregulation in the hypothalamus. Predisposing factors include exhaustion, dehydration, and the use of long-acting depot neuroleptics. Treatment consists of recognition and discontinuation of the neuroleptic agent, temperature reduction, rehydration with intravenous fluids, and general supportive measures. Dantrolene, a direct-acting muscle relaxant, should be used in severe cases. It can be administered by continuous rapid intravenous push at a minimum initial dose of 1 mg/kg, repeated until symptoms subside or up to a maximum cumulative dose of 10 mg/kg. For severe symptoms, dopamine agonists, such as bromocriptine, levodopa, and amantadine, have shown encouraging results. Because of early recognition and treatment, mortality rates with NMS have decreased from 30% to less than 10%.⁵¹

Disposition

The ultimate disposition of the acutely psychotic patient depends on the underlying cause of the psychosis, whether the patient is a danger to self or others, and the presence of social support in the community. Hospitalization is indicated for patients experiencing their first psychotic episode, for patients deemed to be a danger to themselves (suicidal) or others (homicidal), for patients who are grossly debilitated, for patients who are moderately debilitated but have no social support system within the community, and for patients with either functional or organic psychosis that does not clear with a brief period of treatment and observation in the emergency department. The decision to hospitalize psychotic patients is complex and imprecise and often must be made in a short period with limited information.

A psychiatric short-procedure unit offers a cost-effective alternative to hospitalization.⁵² After stabilization, patients are moved from the emergency department to a separate treatment area, where they are treated for a period of 12 to 24 hours by a small staff of consultants.

Key Concepts

In patients exhibiting abnormal behavior, an organic cause is suggested by new onset of symptoms in a patient older than 35 years, rapid onset of symptoms in a previously normal person, visual hallucinations, abnormal vital signs, and lethargy or disorientation.