Version May 2024
INTRODUCTION — This topic will discuss the emergency department evaluation of acute-onset psychosis in children, with an emphasis on detecting emergency medical conditions that require prompt intervention.
The assessment and clinical diagnosis of psychiatric disorders that may present with psychosis in children are discussed separately:
●(See "Pediatric unipolar depression: Epidemiology, clinical features, assessment, and diagnosis".)
●(See "Pediatric bipolar disorder: Clinical manifestations and course of illness" and "Pediatric bipolar disorder: Assessment and diagnosis".)
BACKGROUND — New-onset psychosis in children and adolescents represents an uncommon and complex presenting complaint. Psychosis has been defined as a "disruption in thinking, accompanied by delusions or hallucinations" [1]. Delusions represent false, fixed beliefs that cannot be resolved through logical argument, while hallucinations are false perceptions that have no basis in external stimuli [1].
By contrast, delirium is marked by an altered sensorium, with waxing and waning deficits in attention and concentration. Orientation and concentration are preserved with functional psychosis. However, the distinction between delirium and psychosis in pediatric patients can be difficult to establish, particularly in younger children. Despite these differences, hallucinations may actually represent a symptom of delirium, and separating psychosis and delirium acutely may be impossible.
The onset of psychosis is an important diagnostic element. Acute onset occurs more commonly with an underlying medical cause rather than psychiatric disease. Even patients with symptoms suggestive of a primary psychiatric diagnosis should undergo a medical evaluation to exclude possible reversible etiologies of psychosis.
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of psychosis in children encompasses hypoglycemia, cerebral hypoxia, drug toxicity, medical illness, and psychiatric disease (table 1 and table 2) [2].
Substrate deficiency
●Hypoglycemia – Hypoglycemia is a rare but important cause of psychosis and hallucinations [3,4]. All patients with alterations in mental status require immediate bedside capillary glucose testing. Rapid correction of blood sugar is critical to prevent seizures and persistent neurologic sequelae. Hypoglycemia with abrupt change in behavior may occur in children being treated for type I and type II diabetes; alternatively, hypoglycemia may result from ingestions (eg, ethanol, beta blockers, and sulfonylureas) or from inborn errors of metabolism. (See "Approach to hypoglycemia in infants and children".)
●Cerebral hypoxia – Inadequate brain oxygenation may lead to altered mental status with combative behavior. Thus, any condition that results in hypoxemia (eg, pulmonary insufficiency), insufficient oxygen carrying capacity of the blood (eg, severe anemia), or inadequate brain perfusion (eg, cardiac insufficiency) may result in an encephalopathy with psychotic features. These patients require emergent identification of the underlying cause of cerebral hypoxia and immediate interventions to restore brain oxygenation.
Drug toxicity — Drug exposures are a common cause of delirium, delusions, and/or psychosis, especially in the adolescent population.
Drug overdose or abuse
●Anticholinergic toxicity – Mental status changes from central anticholinergic effects may occur with few, if any, peripheral signs. Anticholinergic toxicity can cause psychosis in both children and adolescents. Common anticholinergic medications include diphenhydramine, atropine, scopolamine, dimenhydrinate, chlorpheniramine, and hyoscyamine, and symptoms may occur even at standard therapeutic doses [5]. Typical and atypical antipsychotic medications also have anticholinergic activity and can produce anticholinergic toxicity in overdose. Recreational use of anticholinergic medications and plants (eg, Datura stramonium [Jimson weed], Datura innoxia [moonflower], Brugmansia species [angel's trumpet]) with severe psychotic symptoms, including paranoia, delusions of persecution, and visual hallucinations, has been reported among adolescents [6]. Other signs of anticholinergic toxicity include mydriasis, dry mucus membranes, lack of diaphoresis, urinary retention, decreased bowel sounds, hypertension, tachycardia, and hyperthermia (table 3). (See "Anticholinergic poisoning".)
●Sympathomimetic toxicity – A wide range of sympathomimetic substances, including pseudoephedrine, dextroamphetamine, "ecstasy" (3,4-methylenedioxymethamphetamine [MDMA]), amphetamine, methamphetamine, and cocaine, have been associated with psychosis in children [7-10]. While these substances exacerbate existing psychosis in patients with psychiatric disease, they may also produce new psychotic symptoms in patients with no prior history of mental illness [7]. Psychosis from sympathomimetic agents is typically accompanied by characteristic findings of hypertension, tachycardia, hyperthermia, mydriasis, and diaphoresis (table 3). (See "Cocaine: Acute intoxication" and "Methamphetamine: Acute intoxication" and "MDMA (ecstasy) intoxication".)
●Hallucinogens – Adolescents may intentionally experiment with these agents to experience hallucinations, while young children may come into contact with them unintentionally. Commonly abused agents include lysergic acid diethylamide (LSD), phencyclidine (PCP), dextromethorphan, ketamine, and Salvia divinorum.
LSD remains the prototypical hallucinogen and the most extensively studied of such drugs. LSD users report a wide variety of neuropsychiatric symptoms, including:
•Distortions of time perception
•Visual illusions (eg, unusually vivid or distorted objects and intense colors)
•Euphoria and feelings of expansiveness
•Depersonalization
•Blending of the senses (synesthesia)
While intoxicated, most individuals remain oriented and aware that their experiences are drug induced. Signs of sympathetic stimulation are common but generally mild and may include tachycardia, hypertension, mydriasis, piloerection, and diaphoresis. (See "Intoxication from LSD and other common hallucinogens".)
Dextromethorphan, ketamine, and PCP belong to a class of hallucinogens known as dissociative agents that act as antagonists at the N-methyl-D-aspartate (NMDA) receptor; NMDA receptor hypofunction has been postulated as one neurochemical mechanism of psychosis [11]. (See "Intoxication from LSD and other common hallucinogens".)
Dextromethorphan is the most widely available of the dissociative agents, and its recreational misuse is growing among adolescents. Patients intoxicated with dextromethorphan may display euphoria, tachycardia, diaphoresis, hallucinations, agitation, and hyperthermia. Frank psychosis due to dextromethorphan has also been reported. (See "Dextromethorphan misuse and poisoning: Clinical features and diagnosis".)
Initially developed as a field anesthetic for military purposes, ketamine has been a widely used recreational drug since the 1970s. Ketamine abuse is closely associated worldwide with the use of other "club drugs" including ecstasy (MDMA), gamma-hydroxybutyrate (GHB), and methamphetamine, often in the setting of large dance parties known as raves. Ketamine produces visual and auditory hallucinations. In addition, ketamine may cause nystagmus, hyperthermia, hypertension, and tachycardia. (See "Ketamine poisoning".)
PCP can induce acute schizophrenia in adolescents, including agitation, memory loss, psychosis, audio-visual hallucinations, and paranoid delusions. Acute brain syndrome, characterized by confusion, disorientation, poor judgment, and amnesia, is seen in approximately one-third of patients. Recovery from psychosis can take weeks to months. Other clinical features include horizontal, vertical, or rotatory nystagmus; violent behavior; and decreased pain response. (See "Phencyclidine (PCP) intoxication in children and adolescents".)
Salvia divinorum is a perennial herb of the mint family that is gaining popularity among adolescents and young adults because of its easy availability. Plants, leaves, and extracts are available for purchase over the internet, where it is marketed as a legal and safe hallucinogen on many websites. Unlike many of the other hallucinations, salvinorin A, the psychoactive component of Salvia divinorum, displays no serotonergic activity. Instead, salvinorin A is a potent kappa-opioid receptor agonist, provoking dysphoria, synesthesia, and visual hallucinations. (See "Intoxication from LSD and other common hallucinogens", section on 'Salvia divinorum'.)
●Marijuana – Marijuana exposure has also been reported to cause psychotic symptoms either alone or when adulterated with PCP and smoked. There is also evidence that marijuana alone may precipitate schizophreniform symptoms in patients with preexisting risk factors for psychiatric disease.
Drug-related syndromes
●Serotonin syndrome – Serotonin syndrome is a potentially life-threatening condition associated with increased serotonergic activity in the central nervous system (CNS) that may be mistaken for psychosis. Mental status changes can include anxiety, agitated delirium, restlessness, and disorientation. In addition, patients often exhibit autonomic manifestations (eg, diaphoresis, tachycardia, hyperthermia, hypertension) and neuromuscular hyperactivity (eg, hyperreflexia, clonus, lower extremity rigidity). It is seen with therapeutic medication use, inadvertent interactions between drugs, and intentional self-poisoning. (See "Serotonin syndrome (serotonin toxicity)".)
●Baclofen withdrawal – Baclofen withdrawal may be seen in children with cerebral palsy or spinal cord injury who are receiving intrathecal baclofen to treat spasticity. Pump emptying or malfunction can precipitate signs of baclofen withdrawal, including hallucinations, hyperthermia, tachycardia, hypertension or hypotension, and rigidity [12]. Baclofen withdrawal must be considered in any child with a history of chronic baclofen exposure who presents with symptoms of psychosis. The resulting muscle rigidity and hyperthermia may require emergency treatment with baclofen and/or endotracheal intubation with neuromuscular paralysis. Left untreated, the muscle rigidity accompanying baclofen withdrawal may lead to rhabdomyolysis, hyperthermia, severe lactic acidosis, hepatic injury, renal failure, and death.
●Benzodiazepine (sedative) withdrawal – Withdrawal syndromes are an important and potentially life-threatening cause of psychosis in children receiving benzodiazepines and other sedatives chronically during pediatric intensive care [13]. CNS stimulation with hallucinations and seizures may occur if unrecognized. Tapering of intravenous dose and, when possible, switching to oral administration are therapeutic options to prevent withdrawal in these patients. (See "Benzodiazepine poisoning" and "Benzodiazepine withdrawal".)
●Neuroleptic malignant syndrome (NMS) – NMS is a rare syndrome in children receiving typical and atypical neuroleptic agents. It is characterized by fever, rigidity, and altered mental status (eg, agitated delirium, confusion, mutism, or catatonia). While symptoms usually develop during the first two weeks of neuroleptic therapy, the association of NMS with drug use is idiosyncratic. NMS can occur after a single dose. Complications include rhabdomyolysis, renal failure, and death. Treatment of this condition requires rapid recognition, aggressive cooling measures (including intubation and paralysis for extreme hyperthermia), and dopaminergic agents, such as bromocriptine and amantadine. (See "Neuroleptic malignant syndrome".)
Drug-induced psychosis
●Steroid-induced psychosis – Steroid-induced psychosis is a well-known complication of glucocorticoid therapy in adults and has been reported in children [14,15]. In many cases, withdrawal of the steroid is sufficient to reverse psychosis, but some patients may require a brief course of antipsychotic medication, particularly when the steroid cannot be stopped [15]. Response to antipsychotic drug treatment is typically complete and occurs within two weeks of initiation of neuroleptics. Patients with systemic lupus erythematosus (SLE) who are on higher doses of corticosteroids present a particular problem since it is often difficult to differentiate psychosis due to prednisone from neuropsychiatric lupus. (See "Major adverse effects of systemic glucocorticoids", section on 'Neuropsychiatric effects' and "Neurologic and neuropsychiatric manifestations of systemic lupus erythematosus".)
●Isoniazid-induced psychosis – Isoniazid-induced psychosis is a rare complication of antituberculous therapy that has been reported widely in patients who have no prior psychiatric history [16]. Symptoms of psychosis typically begin days to weeks after initiation of isoniazid therapy. The mechanism of isoniazid induced psychosis has not been completely elucidated; however, pyridoxine has not been shown to prevent or treat the psychosis symptoms [17].
●Antibiotic-induced mania – Amoxicillin, clarithromycin, and erythromycin have rarely caused neuropsychiatric symptoms including anxiety and hallucinations. The exact mechanism by which these antibiotics may cause psychosis is unknown [18].
●Anticonvulsants – Anticonvulsants, such as phenytoin and topiramate, have also been associated with psychosis [19].
Central nervous system abnormality
●CNS mass lesion – Psychosis can represent an unusual presentation of mass lesion in the CNS (eg, brain tumor, brain abscess); more typical symptoms include headaches, nausea, seizure, personality change, and aphasia. (See "Clinical manifestations and diagnosis of central nervous system tumors in children".)
●Intracranial injury – Any traumatic insult to the brain, including both extra- and intra-axial bleeding, can rarely cause altered mental status with delirium and visual or auditory hallucinations [20]. However, progressive depression of consciousness is much more common. (See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management" and "Intracranial epidural hematoma in children" and "Severe traumatic brain injury (TBI) in children: Initial evaluation and management".)
●Stroke – Stroke may lead to behavior changes with hallucinations depending on the region of the brain that is rendered ischemic. However, neurologic deficits (eg, aphasia, hemiplegia, visual changes) are almost always present as well. (See "Ischemic stroke in children and young adults: Epidemiology, etiology, and risk factors".)
●CNS infections – In children, any serious CNS infection (eg, meningitis, encephalitis) may cause visual hallucinations with altered mental status. Specific association with psychosis has been described for Chlamydia pneumoniae, Mycoplasma pneumoniae, Epstein-Barr virus ("Alice-in-Wonderland" syndrome), and cerebral malaria [21-23]. A history or suspicion of HIV infection should prompt consideration of less common disease processes including toxoplasmosis and progressive multifocal leukoencephalopathy [20]. (See "Approach to the patient with HIV and central nervous system lesions" and "Malaria: Clinical manifestations and diagnosis in nonpregnant adults and children", section on 'Cerebral malaria' and "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Clinical findings'.)
●Postictal psychosis – Postictal psychosis is a rare complication of epilepsy that may start hours to days after a prolonged seizure. The resulting hallucinations may last more than one week [24-26]. In one case series that included five children younger than 16 years old, religious and persecutory delusions with mood disturbance were common with a significant risk of self-harm or harm to others [26]. The psychosis was responsive to antipsychotic medications.
●Temporal lobe epilepsy – Auditory and visual hallucinations may arise from temporal lobe epilepsy in children [27]. This disorder may present with acute, brief episodes of psychosis despite treatment with anticonvulsant medications. Unlike childhood-onset schizophrenia, these patients may have insight into hallucinations and rapidly respond to antipsychotics [27]. (See "Focal epilepsy: Causes and clinical features", section on 'Clinical features'.)
●Landau-Kleffner syndrome – Landau-Kleffner syndrome (also called acquired epileptic aphasia) is an extremely rare syndrome in which deterioration of higher cortical functioning (in this case, language capability) is lost because of frequent epileptiform activity. Mutism and behavioral outbursts may be seen. The presentation may mimic that of childhood psychosis. (See "Epilepsy syndromes in children".)
●Subacute sclerosing panencephalitis (SSPE) – SSPE is a progressive, fatal disease of the CNS. The measles virus has been implicated in the pathogenesis of SSPE. However, symptoms may develop years after the initial measles infection. SSPE is a rare cause of psychosis but should be considered in any patient who has had a primary measles infection [28]. (See "Measles: Clinical manifestations, diagnosis, treatment, and prevention", section on 'Subacute sclerosing panencephalitis'.)
Systemic lupus erythematosus — Psychosis is frequently seen in children and adolescents with SLE and CNS inflammation. Patients with SLE may describe auditory or tactile hallucinations. The use of steroids in many patients with SLE further complicates the diagnosis; however, SLE-induced psychosis is typically accompanied by headache, confusion, and difficulty with concentration. (See "Childhood-onset systemic lupus erythematosus (SLE): Clinical manifestations and diagnosis".)
Metabolic disease — Although a rare cause of psychosis, metabolic disease is an important consideration when evaluating acute psychosis, especially in adolescents. Diagnosis during the stage of early psychiatric manifestations may allow for treatment and prevention of permanent neurologic sequelae [29].
●Urea cycle defects – Patients who have partial urea cycle enzyme deficiencies may have atypical presentations consisting of recurrent episodes of bizarre behavior, hallucinations, or delusions during adolescence and adulthood. These patients also typically complain of headache and vomiting. This delayed presentation is most common with partial ornithine transcarbamylase deficiency, although it also occurs with partial activity of all urea cycle enzymes. These patients tend to prefer vegetarian diets because dietary protein intake often is associated with headache. (See "Urea cycle disorders: Clinical features and diagnosis".)
●Acute intermittent porphyria (AIP) – AIP is both the most common and most severe of the rare inherited porphyrias. It is an autosomal dominant disorder resulting from a partial deficiency of porphobilinogen deaminase activity, the third enzyme in the pathway of heme synthesis. Psychiatric complaints may be prominent in AIP and may represent the sole feature of the disease. These include hysteria, anxiety, apathy, depression, phobias, psychosis, organic disorders, agitation, delirium, and altered consciousness (ranging from somnolence to coma). Some patients with AIP develop a psychosis similar to schizophrenia. Previously asymptomatic patients may develop acute psychosis after precipitating factors such as drugs that induce the P450 microsomal oxidase system (eg, barbiturates), fasting, intercurrent illness, and premenstrual hormonal changes in women. (See "Acute intermittent porphyria: Pathogenesis, clinical features, and diagnosis".)
●Wilson disease – An inherited disorder of copper metabolism, Wilson disease may present during adolescence with subacute psychiatric symptoms ranging from depression to frank psychosis characterized by catatonia and paranoia. Wilson disease is diagnosed by the findings of low ceruloplasmin concentrations and elevated urinary copper excretion. It is a potentially reversible cause of psychosis and must be considered in any child or adolescent with new-onset psychiatric symptoms. (See "Wilson disease: Clinical manifestations, diagnosis, and natural history", section on 'Psychiatric symptoms'.)
●Other defects – Acute or subacute psychosis has also been reported as a prominent presenting feature in patients with homocysteine remethylation defects, homocystinuria, adrenoleukodystrophy, some lysosomal disorders, cerebrotendinous xanthomatosis, and alpha- or beta-mannosidosis [29].
Other conditions
●Postpartum psychosis – Postpartum psychosis is an uncommon condition seen up to 30 days after childbirth. It presents with paranoia, delusions, and hallucinations. Psychosis and lack of insight can lead to real risks to both the neonate and mother. Postpartum psychosis requires hospitalization for initiation of antipsychotics and stabilization [30].
●Electrolyte disturbance – Children with hyponatremia or hypernatremia often exhibit behavior changes and encephalopathy that may be difficult to distinguish from acute psychosis. Hypocalcemia and hypomagnesemia may rarely cause frank psychosis. (See "Manifestations of hyponatremia and hypernatremia in adults" and "Clinical manifestations of hypocalcemia" and "Acute toxic-metabolic encephalopathy in children", section on 'Electrolyte derangements'.)
●Uremia or hepatic encephalopathy – Acute mental status changes with hallucinations commonly accompany uremia and hepatic encephalopathy in children. (See "Acute toxic-metabolic encephalopathy in children", section on 'Organ failure'.)
●Hashimoto encephalopathy (HE) – HE is a syndrome that is rarely seen in children and is associated with Hashimoto thyroiditis. HE is believed to be an immune-mediated disorder rather than representing the direct effect of an altered thyroid state on the CNS. Psychosis, particularly visual hallucinations but also paranoid delusions, have been reported in up to one-third of patients and is responsive to corticosteroid therapy and treatment of a dysthyroid state, if present. (See "Hashimoto encephalopathy".)
●Thyroid storm – Although most commonly seen in adults, children very rarely manifest symptoms of thyroid storm including tachycardia, heart failure, and hyperpyrexia (temperature elevation up to 106°F). Agitation, delirium, psychosis, stupor, or coma is usually associated with the diagnosis. Although thyroid storm can develop in patients with longstanding untreated hyperthyroidism, it is more often precipitated by an acute event such as thyroid or nonthyroidal surgery, trauma, infection, or acute iodine load. Rarely, thyroid storm may be associated with ingestion of levothyroxine in children [31]. (See "Thyroid storm".)
●Antiphospholipid syndrome – Antiphospholipid antibody syndrome is traditionally associated with hypercoagulability, thrombocytopenia, and increased risk of fetal loss. This syndrome has also been described in a nine-year-old child with psychosis without evidence of thrombotic disease [32].
Psychiatric disease — A number of primary psychiatric disease entities including depression, bipolar disorder, childhood-onset schizophrenia, and brief reactive psychosis may lead to psychotic symptoms. A history of mental illness in the family, emotional trauma, subacute to chronic symptoms, and coexistent mood disorder suggests a primary psychiatric disorder. However, a psychiatric diagnosis as a cause of psychosis in a child should be pursued only when the potentially fatal and potentially reversible causes of psychosis have been excluded.
The manifestations and diagnosis of psychiatric conditions that may present with psychosis or psychosis-like symptoms in children and adolescents are discussed separately:
●(See "Pediatric unipolar depression: Epidemiology, clinical features, assessment, and diagnosis".)
●(See "Pediatric bipolar disorder: Clinical manifestations and course of illness" and "Pediatric bipolar disorder: Assessment and diagnosis".)
HISTORY — Clinicians must focus on obtaining an inclusive history in order to differentiate the broad range of conditions that may present with psychosis (table 1 and table 2) (see 'Differential diagnosis' above). Historical information of particular importance includes:
●Setting suggestive of drug overdose (eg, adolescent brought from a rock concert, abrupt change in toddler behavior, and suspected ingestion)
●Drug toxicity suggested by the patient's current medications (eg, corticosteroids, neuroleptic agents, isoniazid)
●Presence and severity of constitutional symptoms (fevers, chills, headache) indicating an infectious etiology (eg, meningitis, encephalitis)
●Known history of systemic lupus erythematosus (SLE) or findings (eg, arthralgias, myalgias, and rashes) suggestive of SLE
●A history of head trauma (intracranial injury)
●New onset of neurologic deficits (stroke, brain abscess, brain tumor)
●Seizure disorder or signs suggestive of seizure disorder (inattentiveness, rhythmic blinking or other stereotyped movements)
●Prior episodes associated with possible precipitating factors (eg, menstruation, medications, stress), vomiting, or headache suggestive of metabolic disease (urea cycle defects, acute intermittent porphyria [AIP])
●A family history of psychiatric disease or longstanding bizarre behaviors supporting a diagnosis of a psychiatric disease (although development of a psychotic disorder before the age of 12 is uncommon [33])
PHYSICAL EXAMINATION — Findings of hypoglycemia (altered mental status, diaphoresis, tachycardia, hypotension) and impaired oxygenation (cyanosis, pallor, shock, respiratory distress) require early identification and treatment in the child with acute psychosis. Once the potential for substrate deficiency is addressed, physical examination should focus on other findings suggestive of a specific etiology.
Mental status examination — The patient with psychiatric illness typically has normal vital signs; normal orientation to person, place, and time; and intact memory with good cognitive functioning. Hallucinations are usually auditory in nature.
In contrast, patients with psychosis caused by other medical illness usually have abnormal vital signs, altered mental status, and impaired orientation with compromised intellectual function. Visual and tactile hallucinations are frequently prominent [34].
Suspected drug toxicity — In patients with possible pharmaceutical or drug toxicity presenting with psychotic features, constellations of physical findings can be interpreted in the context of toxic syndromes, or "toxidromes" (eg, serotonin syndrome, hallucinogen exposure, or anticholinergic or sympathomimetic agent overdose) (table 3). (See "Approach to the child with occult toxic exposure", section on 'Diagnosis of poisoning'.)
Other findings — Attention to vital signs, mental status, eye findings, and neurologic examination provide the greatest help in narrowing the differential diagnosis.
●Fever – Fever may occur with any infection but may also signal intoxication with anticholinergic or sympathomimetic agents or withdrawal syndromes.
●Tachycardia – While mild tachycardia may be seen in the presence of primary psychiatric disease, marked tachycardia should prompt the search for infection, pharmacologic/drug exposure, and withdrawal syndromes. (See 'Drug-related syndromes' above.)
●Eye findings – The presence of dilated pupils suggests anticholinergic or sympathomimetic symptoms. Nystagmus may indicate exposure to dissociative agents, such as ketamine, dextromethorphan, or phencyclidine (PCP). Ocular clonus can be seen in the setting of monoamine oxidase toxicity or serotonin syndrome. Conjunctival injection may suggest marijuana use. (See "Approach to the child with occult toxic exposure", section on 'Diagnosis of poisoning'.)
Kayser-Fleischer rings are brownish or gray-green rings that represent fine pigmented granular deposits of copper in Descemet membrane located in the cornea near the endothelial surface (picture 1). They are seen in 90 percent of patients with neurologic presentation of Wilson disease but may require slit lamp examination for detection. (See "Wilson disease: Clinical manifestations, diagnosis, and natural history".)
●Mouth and mucous membranes – Dry mucous membranes are a nonspecific finding that can indicate anticholinergic toxicity, while sialorrhea may occur in the setting of ketamine use. Bruxism has been reported with a variety of serotonergic agents, especially ecstasy (MDMA).
●Neck – Thyromegaly should prompt serologic evaluation of thyroid function and exclusion of thyrotoxicosis.
●Abdominal and genitourinary examination – The presence or absence of bowel sounds can be supportive in distinguishing anticholinergic toxicity from sympathomimetic symptoms. Classically, anticholinergic toxicity slows peristalsis, resulting in decreased or absent bowel sounds. Urinary retention may also occur in the setting of anticholinergic exposure.
●Skin – Diaphoresis is a nonspecific sign that occurs in the setting of hypoglycemia, hyperthyroidism, sympathomimetic exposure, or fever. Absence of sweating is a characteristic finding in anticholinergic toxicity. A malar rash suggests systemic lupus erythematosus (SLE), while track marks must prompt further questioning and testing regarding illicit drug use.
●Central nervous system (CNS) – The neurologic examination is nonfocal in psychosis due to psychiatric illness. The presence of a focal or lateralizing examination suggests a CNS mass lesion, CNS hemorrhage, severe traumatic brain injury, or stroke.
ANCILLARY STUDIES — A rapid blood glucose is of particular importance in the early assessment of children with acute psychosis, especially those with altered mental status. In addition, pulse oximetry or direct measurement of partial pressure of arterial oxygen (PaO2) by arterial blood gas should be obtained in those patients whose evaluation suggests cerebral hypoxia (respiratory distress, hemodynamic instability, pallor, or cyanosis). Patients with hypoglycemia or cerebral hypoxia require additional studies to determine the underlying cause. (See "Acute respiratory distress in children: Emergency evaluation and initial stabilization", section on 'Ancillary studies' and "Shock in children in resource-abundant settings: Initial management" and "Approach to hypoglycemia in infants and children", section on 'Evaluation for the cause of hypoglycemia'.)
In patients with normal blood glucose and oxygenation, the clinical presentation of psychosis largely dictates the extent of ancillary testing that is needed. For example, the adolescent with normal mental status, auditory hallucinations, and strong family history of schizophrenia requires limited, if any, additional laboratory or diagnostic studies beyond a toxicology screen and, in females, a pregnancy test. However, a school-age child with fever, visual hallucinations, and altered mental status warrants extensive evaluation that will likely include blood studies, brain imaging, and lumbar puncture. The following sections summarize laboratory and diagnostic studies that may assist in establishing the underlying diagnosis in children with acute psychosis.
●Complete blood count – An elevated white blood cell count may indicate infection, particularly meningitis or encephalitis, or stress reaction in children with fever. Severe anemia of any etiology may contribute to cerebral hypoxia, and thrombocytopenia raises the risk of a cerebral hemorrhage. Both thrombocytopenia and thrombocytosis may be signs of an acute phase reaction.
Patients with systemic lupus erythematosus (SLE) may have evidence for a hemolytic anemia with accompanying leukopenia and/or thrombocytopenia. Elevated erythrocyte sedimentation rate and antinuclear antibodies may also be present. (See "Childhood-onset systemic lupus erythematosus (SLE): Clinical manifestations and diagnosis", section on 'Diagnosis'.)
●Neuroimaging – Children with findings of head trauma, increased intracranial pressure, focal neurologic deficits, or a decreased level of consciousness should undergo computed tomography of the brain and/or magnetic resonance imaging. Neuroimaging may also play a role in selected children with fever and findings of central nervous system (CNS) infection or persistent visual hallucinations. By contrast, the likelihood of finding a structural cause for psychosis in children without the above features is low (<1 percent) and emergency neuroimaging is not indicated [35]. (See "Severe traumatic brain injury (TBI) in children: Initial evaluation and management".)
●Lumbar puncture – A lumbar puncture should be performed in children with signs of meningitis as long as findings of focal neurologic deficits are not present. (See "Lumbar puncture in children".)
●Rapid drug screening of urine – A urine drug screen positive for cocaine, amphetamines, or phencyclidine (PCP) provides supporting evidence for drug abuse as a cause of psychosis. However, urine screens do not detect other toxic causes of psychosis (eg, lysergic acid diethylamide [LSD], ecstasy [MDMA], ketamine, dextromethorphan). In addition, positive and negative immunoassay screens for drugs do not absolutely confirm or refute poisoning diagnoses and may need confirmation by gas chromatography-mass spectrophotometry. The spectrum of drugs included in the urine screen varies by institution. (See "Approach to the child with occult toxic exposure", section on 'Toxicology screens'.)
●Blood chemistries – Evaluation of serum chemistries can identify hypocalcemia, hypomagnesemia, hypernatremia, hyponatremia, and metabolic acidosis (seen in sepsis, severe sympathomimetic toxicity, baclofen withdrawal, and some inborn errors of metabolism).
Serum electrolytes, calcium, phosphate, magnesium, blood urea nitrogen, creatinine, thyroid function (triiodothyronine [T3], thyroxine [T4], thyroid-stimulating hormone [TSH]), liver enzymes (eg, aspartate transferase, alanine transferase), and liver function tests (total and direct bilirubin, total protein, albumen, prothrombin time) are suggested in children and adolescents whose psychosis is not clearly psychiatric in origin and cannot be explained on the basis of substrate deficiency, drug toxicity, or CNS abnormality. (See 'Other conditions' above.)
●Electrocardiogram – In patients with psychosis of unknown etiology, particularly those with anticholinergic features, an ECG should be obtained. The presence of an R wave in aVR suggests the presence of a tricyclic antidepressant or similar substance (such as diphenhydramine). This ECG finding is seen in both therapeutic and toxic exposures. Toxicity is determined by the duration of the QRS interval. A prolonged QRS indicates a blockade of conduction through fast sodium channels in the myocardium and is associated with ventricular dysrhythmias. (See "Tricyclic antidepressant poisoning".)
●Rapid urine pregnancy test – All postmenarchal girls should have urine pregnancy testing performed to help guide further therapeutic decisions with respect to the safety of both the mother and baby.
●Special metabolic studies – When metabolic disease is suspected, specialized studies of urine and blood are needed to confirm the diagnosis. Consultation with an expert in metabolic disease is of great value to ensure that the proper test is performed and to identify the laboratory that is best prepared to perform the test. (See "Metabolic emergencies in suspected inborn errors of metabolism: Presentation, evaluation, and management", section on 'Initial evaluation' and "Inborn errors of metabolism: Identifying the specific disorder", section on 'Laboratory evaluation' and "Acute intermittent porphyria: Pathogenesis, clinical features, and diagnosis", section on 'Diagnostic evaluation' and "Wilson disease: Clinical manifestations, diagnosis, and natural history", section on 'Diagnostic evaluation'.)
●Electroencephalogram – An electroencephalogram is required in all patients with repeated seizures or suspected nonconvulsive status epilepticus (eg, temporal lobe epilepsy) [36].
APPROACH — The child with new-onset psychosis must undergo rapid evaluation that focuses on identifying and treating substrate deficiency, drug toxicity, and central nervous system (CNS) abnormalities (algorithm 1).
Patient and staff safety — While identification and correction of the underlying etiology is vital to overall patient outcome, early management of agitation or violent behavior can be a critical part of diagnosis and treatment, preventing injury to both the patient and staff:
●Verbal de-escalation and reduction of environmental stimulation – The emergency provider should first try verbal de-escalation of the agitated child or adolescent. Key components involve clear, calm statements of what will happen in the emergency department, reduction of environmental stimulation such as loud noise or bright lights, reassurance that the child's safety is of utmost concern, and involvement of ancillary personnel (eg, social work, psychiatry, security) [37].
●Physical restraint – If the patient cannot be verbally redirected, supine physical restraints should be employed by staff trained in their safe placement and life-threatening hypoglycemia or hypoxia should be excluded. (See "Assessment and emergency management of the acutely agitated or violent adult", section on 'Verbal techniques' and "Assessment and emergency management of the acutely agitated or violent adult", section on 'Physical restraints'.)
●Sedation – If agitation persists with physical restraint, then judicious sedation with an intravenous or intramuscular benzodiazepine (eg, lorazepam 0.05 to 0.1 mg/kg) is an option in children with undifferentiated agitation [37,38]. These agents have the advantages of quick onset, short elimination half-life, and utility in patient withdrawal from alcohol or benzodiazepines. Adverse effects include sedation, CNS depression, and paradoxical reactions that result in excitation of the patient. Paradoxical reactions may be more common in children with developmental delay.
The typical antipsychotic agent haloperidol (dose 0.025 to 0.075 mg/kg per dose, maximum 5 mg) is an alternative to benzodiazepine sedation in the acutely psychotic child or adolescent [37-39]. The onset of antipsychotic activity for most neuroleptic agents is delayed on the order of days. However, the sedating properties of neuroleptics often aid in the management of the agitated patient. Many of the severe adverse effects associated with neuroleptics tend to occur in chronic dosing, including pancreatitis, diabetic ketoacidosis, extrapyramidal symptoms, and agranulocytosis. However, serious side effects may occur acutely, including dystonia, hypotension, and electrocardiographic (EKG) interval prolongation. Children may be at greater risk of developing dystonia than adults. The clinician should also be vigilant for manifestations of neuroleptic malignant syndrome (NMS). (See "Neuroleptic malignant syndrome".)
●There are no controlled trials that compare medications for the acute sedation of children and adolescents [37]. Practice patterns among pediatric emergency clinicians suggest that benzodiazepines are favored, although typical antipsychotics are also used [39].
Substrate deficiency — Rapid recognition of hypoglycemia and cerebral hypoxia is essential; all patients with a change in mental status require bedside glucose testing, or empiric therapy with dextrose-containing solutions, if evaluation of serum glucose is delayed. Empiric treatment with supplemental oxygen is warranted until oxygenation can be assessed by pulse oximetry or arterial blood gas measurement.
Vital sign abnormalities — Mild tachycardia may occur in the setting of primary psychiatric disease; however, marked vital sign abnormalities persisting after sedation suggest another medical etiology for psychosis. Fever and tachycardia mandate the search for an infectious process, such as meningoencephalitis. Hyperthermia, tachycardia, or hypertension may also occur in the setting of sympathomimetic and anticholinergic toxicity, thyroid storm, or withdrawal syndromes, such as baclofen withdrawal.
Neurologic deficit — Focal neurologic findings warrant emergency brain imaging that may show a brain tumor, brain abscess, stroke, or cerebral hemorrhage.
Mental status — Children who have altered mental status without evidence for drug intoxication (eg, phencyclidine [PCP], ketamine, dextromethorphan) (table 2) warrant a diligent evaluation, including laboratory studies, brain imaging, and, rarely, electroencephalogram to identify the underlying etiology. Children with normal mental status and auditory hallucinations should undergo urgent psychiatric evaluation. (See 'Mental status examination' above and 'Ancillary studies' above.)
SUMMARY AND RECOMMENDATIONS
●Approach – The new onset of psychosis in a child or adolescent must prompt consideration of other medical etiologies before attributing behavior to a primary psychiatric diagnosis. Given the extensive range of potential causes for psychosis, stepwise and meticulous attention to history, vital signs, physical examination, and ancillary testing should facilitate exclusion of potentially reversible causes of psychosis. This approach is summarized in the algorithm (algorithm 1); key actions include (see 'Approach' above):
•Safety precautions – Early management of agitation or violent behavior is a critical part of diagnosis and treatment in acutely psychotic patients to prevent injury to the patient and staff. The key actions consist of (see 'Patient and staff safety' above):
-Verbal de-escalation and reduction of environmental stimulation
-Safely applied and monitored supine physical restraint if verbal de-escalation fails
-For persistent agitation, sedation with benzodiazepine such as lorazepam (preferred first-line in children); typical antipsychotic agents (eg, haloperidol) may be used for patients not sufficiently responsive to benzodiazepines and still posing a risk of harm to self or others
•Evaluation for nonpsychiatric illness – Identify findings of a nonpsychiatric condition:
-Substrate deficiency – Perform bedside glucose testing and pulse oximetry in all patients with altered mental status; empiric treatment with supplemental oxygen is warranted until hypoxia is excluded. (See 'Substrate deficiency' above.)
-Vital signs – Marked vital sign abnormalities persisting after sedation suggest another medical etiology for psychosis; fever and tachycardia points to an infectious process and, if accompanied by hypertension, sympathomimetic or anticholinergic toxicity (table 3), thyroid storm, or drug withdrawal. (See 'Vital sign abnormalities' above.)
-Focal neurologic deficit – Once hypoglycemia is excluded, focal neurologic findings warrant stabilization, evaluation and treatment of increased intracranial pressure (algorithm 2), and emergency brain imaging to assess for a brain tumor, brain abscess, stroke, or cerebral hemorrhage. (See 'Central nervous system abnormality' above.)
-Mental status – Mental status is typically normal in patients with psychosis associated with a psychiatric condition. Children who have altered mental status without evidence of drug intoxication (eg, phencyclidine [PCP], ketamine, dextromethorphan) (table 2) warrant a diligent evaluation with ancillary studies based upon clinical presentation. (See 'Ancillary studies' above.)
●Differential diagnosis – The tables summarize drug toxicities and nonpsychiatric medical diagnoses associated with acute psychosis in children, highlighting the most common and the most life-threatening causes (table 1). (See 'Differential diagnosis' above.)
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