Steroid-Induced Psychosis in the Pediatric Population: A New Case and Review of the Literature

Abstract

Objectives:

Iatrogenic steroid-induced psychosis is a rare but serious adverse side effect seen largely in the adult population that less commonly affects children and adolescents. Given the significant distress steroid-induced psychosis may cause, recommendations are needed for effective management. Here we conducted a systematic review of the literature and report a new case of steroid-induced psychosis in a 12-year-old patient.

Methods:

We performed a systematic search using Embase, PubMed, Scopus, and PsychInfo. Key terms included (“steroid induced” or “corticosteroid induced” or “glucocorticoid induced”) and (“psychosis” or “hallucinations” or “delusions”) and (“child” or “adolescent” or “pediatric”). A total of 15 articles of steroid-induced psychosis in children and adolescents were found in the scientific literature. This report includes those articles and a novel case of steroid-induced psychosis.

Results:

Children with asthma, autoimmune diseases, and cancer have been reported to experience steroid-induced psychosis. The mean age of children with steroid-induced psychosis was 12 ± 3.6 years. Our team presents a report of steroid-induced psychosis in a 12-year-old patient with discoid-type lupus erythematosus. Within days of treatment with 40 mg prednisone daily, this patient began to drool, became mute, and was responding to internal stimuli. Treatment was difficult secondary to the acute exacerbation of lupus, requiring ongoing therapy. It was initially unclear whether the acute psychosis was a manifestation of lupus, a side effect of medication, or a combination of the two risk factors. Neurology consultation ruled out lupus cerebritis. Psychosis was treated with haloperidol 5 mg. Psychosis did not resolve until the steroid taper was complete and the patient was no longer taking any prednisone.

Conclusions:

Given the common use of glucocorticoid therapy in children, it is important that physicians and parents recognize the signs of steroid-induced psychosis and are aware of the data on treating this complication.

Background

Glucocorticoids have been instrumental in treating certain cancers, asthma, autoimmune disease, and other major medical illnesses in the pediatric and adult populations since the 1950s. Their side effect profile, however, often limits their clinical use. Steroid-induced psychosis is a well-recognized phenomenon in adults and presents in 6% of those treated (Dubovsky et al. 2012). Although pediatric steroid-induced psychosis can occur, the literature is sparse and no incidence has been reported (Bag et al. 2012). The term “steroid psychosis,” however, has been in the literature for decades and is used to refer to a wide range of neuropsyhiatric symptoms that arise with steroid use. This broad definition increases the challenge of determining the true incidence and prevalence of the condition (Dubovsky et al. 2012).

Steroid-induced psychosis in the adult and pediatric populations most commonly presents shortly after onset of high-dose steroid treatment. It is often accompanied by mood and anxiety symptoms and personality changes (Stuart et al. 2005). These psychiatric manifestations secondary to steroid use are often quite alarming. Affective symptoms such as grandiosity, irritability, emotional lability, pressured and rapid speech, and sucidiality, as well as psychotic symptoms including delusions, paranoia, and hallucinations, have all been documented (Stuart et al. 2005).

The literature sheds some light on the mechanism of action of glucocorticoid on the central nervous system that may contribute to mood and behavior changes. First, glucocorticoids have been reported to produce dose-dependent damage to the hippocampus, although this finding has been debated and may require concomitant stress (Maggio and Segal 2007). This is associated with memory and other cognitive deficits (Dubovsky et al. 2012). Second, glucocorticoids evert dose-dependent effects on the hypothalamic-pituitary-adrenal axis and on serotonin (5-HT) systems in the brain. Specficially, they reportedly lower serotonin levels, and although these lower serotonin levels may be part of the therapeutic effect of steroids (particularly with asthma), this may also contribute to neuropsychiatric symtpoms seen in children taking them (Pretorius 2004). By virtue of negative feedback, glucocorticoids inhibit adrenocorticotropic hormone (ACTH) and corticotropin releasing hormone (CRF) release and synthesis in the anterior pituitary gland and hypothalamus, respectively. However, they increase CRF availability in the amygdala, which is associated with anxiety and mood changes.

We present a review of 15 case reports in addition to a report of a 12-year-old female with discoid-type lupus erythematosus to summarize steroid-induced psychosis in the pediatric population. These cases vary in duration, lasting up to 6 months, and resolved after discontinuation of glucocorticoids or with antipsychotic drug medication. We found the more complex the medical management, the more treatment refractory was the psychosis. Understandably, initiation of antipsychotic medication was particularly helpful in situations wherein discontinuation of steroids was not possible.

Unquestionably, steroid-induced psychosis can be distressing for patients, families, and clinicians. By reviewing the literature, we aim to provide potential treatment options and shed light on this condition.

Methods

To obtain all relevant literature reviews, case series, and case reports, multiple systematic searches were performed on various databases. Embase, PubMed, Scopus, and PsychInfo were searched, with searches completed between December 2016 and April 2017. Key terms and key words included (“steroid induced” or “corticosteroid induced” or “glucocorticoid induced”) and (“psychosis” or “hallucinations” or “delusions”) and (“child” or “adolescent” or “pediatric”). From these searches, all articles that had an English language abstract available were screened based on multiple criteria. The criteria included the following:

(1) The article must have clearly demonstrated a steroid-induced psychotic disorder, as per DSM-5 criteria:

(a) Presence of delusions and/or hallucinations

(b) Development of symptomatology during substance intoxication or withdrawal

(d) The disturbance did not occur exclusively during a delirium

(e) There is significant distress or impairment.

(2) The article included dosage information for both the steroid and any treating agents that were used.

(3) The article demonstrated and articulated the correlation and time between administration of steroids and onset of symptoms.

(4) No previous history of psychotic disorder.

The credited sources of all articles that fulfilled these criteria were then searched for any other relevant material. In total, 15 articles found in various case reports, case series, and literature reviews met criteria for inclusion, in addition to the new case presented here (Table 1).

Table 1.

Reported Cases of Steroid-Induced Psychosis in the Pediatric Population

Article	Age	Gender	Diagnosis	CS type and dose	Dose equivalency (Prednisone)	Clinical description	Outcome	Onset	End
Hall et al. (1979)	17	F	Asthma	Prednisolone oral 60 mg/day	60 mg/day	Fluctuating insomnia, distractibility, emotional lability, grandiosity, pressured speech, agitation	One dose imipramine was administered and patient appeared to get worse; chlorpromazine 800 mg/day was successful.	Within 1 week
Sullivan and Dickerman (1979)	11	M	SLE	50 mg/day prednisone	50 mg/day	Paranoid delusions, loss of function, mute, catatonia	Began improving at 10 mg/day dose of prednisone; full recovery.	4 months	2 months
Ducore et al. (1983)	15	M	ALL	Prednisolone oral 90 mg/day plus IV hydrocortisone as part of chemotherapy	90 mg/day	Anxiety and fear of dying, followed by frank psychosis with delusions of grandeur and persecution, disinhibited behavior	Steroid taper and chlorpromazine (dose unknown) were successful in treating the psychosis. Psychosis lasted beyond the taper of steroid.	6 days	28 days
Ducore et al. 1983	13	F	ALL	Prednisolone oral 40 mg/day	40 mg/day	Disinhibition, regression, apathy, incontinence, frankly psychotic behavior	Steroid taper and chlorpromazine (25 mg TID) were successful in treating the psychosis. Psychosis lasted beyond the taper of steroid.	7 days	11 days
Turktas et al. (1997)	14	M	Asthma	Beclomethasone inhaled 1500 μg/day	^***	Insomnia, visual and auditory hallucinations, pressured speech, labile affect, decreased attention and memory	The BDP was stopped; symptoms resolved entirely within 1 week, budesonide aerosol 400 μg/day was used to manage asthma.	3 days	7 days
Dawson and Carter (1998)	8	M	Asthma	Prednisolone oral 20 mg BID for 5 days	40 mg/day	Hyperactivity, aggression, insomnia, emotional lability, visual hallucinations, pressured speech, episodic crying spells	Diazepam 5 mg orally was given for agitation; she started acting bizarrely on day 2, resolved without other medication after prednisolone discontinuation.	2 days	Within 7 days
Lee 2010	5	F	Asthma	40 mg IV q6 h methylprednisone	200 mg/day	Psychosis	Resolved within hours of decreasing dose to 20 mg IV q6 h.	3 days	Within 7 days
Hergüner 2006	12	F	Nephrotic syndrome (FSGS)	Prednisone oral 48 mg/day	48 mg/day	Anxiety, sleep disturbance, visual and auditory hallucinations, persecutory delusions	Risperidone 1 mg PO QPM; 4 days later symptoms improved, within 3 weeks back to baseline. Patient could not be tapered, kept on prophylactic risperidone.	After 5th pulse	21 days
Ularntinon 2010	8	M	T-cell ALL	2 mg/(kg·day) prednisone	50 mg/day (assuming 25 kg)	Visual hallucinations and psychotic delusions (wanted to “suffocate himself with a skunk”)	0.25 risperidone BID; prednisone was kept on due to management of T-cell ALL.	12 days	Within 7 days
Ularntinon 2010	16	M	Pre-B-Cell ALL	Dexamethasone 12 mg/day pulse	80 mg/day	Manic symptoms (decreased sleep), religious grandiosity, psychosis	Risperidone .5 mg PO QAM and 1 mg PO QPM.	After 5th pulse	Within 7 days
Kim et al. (2010)	11	M	Toxic epidermal necrolysis	High dose IV dexamethasone	^***	Aggression, bizarre behavior, visual and auditory hallucinations	Treated with steroid taper and olanzapine; three days after initiation of olanzapine he was no longer psychotic.	1 day	3 days
Bag et al. (2012)	12	M	Nephrotic syndrome	Prednisone 2 mg/(kg·day) maximum 60 mg/day	60 mg/day	Decreased speech, persecutory delusions, disorientation, catatonia, flat affect	Risperidone 1 mg/day and prednisone tapered and discontinued. On day 7 of treatment, risperidone was increased to 1.5 mg/day; full improvement in 3 weeks.	21 days	21 days
Demir et al. (2012)	17	M	Mumps orchitis	25 mg/day of prednisolone IV	25 mg/day	Sexually explicit behavior, flat affect, auditory hallucinations	Quetiapine 900 mg/day, resolved in 4 weeks. Steroids were discontinued.	3 days	28 days

***

Dose equivalency unknown/not reported.

CS, corticosteroid; mg, milligram; kg, kilogram; IV, intravenous; SLE, systemic lupus erythematosus; ALL, acute lymphocytic leukemia; FSGS, focal segmental glomerulosclerosis; d, day; PO, by mouth; BID, twice daily; QAM, at morning; QPM, at night.

Case

A 12-year-old Haitian female with no medical or psychiatric history presented to the emergency department on November 15, 2016, with a chief complaint of 16 days of fever, fatigue, anemia, oral thrush, and a rash consisting of round hyperpigmented lesions on the face and arms. She was subsequently admitted for medical evaluation. Workup for blood malignancy, HIV, infectious etiologies, and autoimmune diseases was unremarkable. Renal ultrasonography and chest X-ray revealed no abnormalities. Laboratories were positive for anti-Smith, anti-ribonucleoprotein (RNP), anti-smith/ribonucleoprotein anti-nuclear antibodies (SMRNP), and antiribosomal antibodies. ANA, C3, C4, erythrocyte sedimentation rate (ESR), and beta-2 microglobulin were elevated. Skin biopsy of a hyperpigmented, well-circumscribed, 1 cm lesion showed pathology consistent with lupus erythematosus. The patient was found to have discoid lupus erythematosus and was discharged on hydroxychloroquine 900 mg orally every 4 hours, nystatin swish three times daily, and prednisone 80 mg orally per day.

On December 4, 2016, the patient re-presented to the Jackson Memorial Holtz Children's Hospital with an altered mental status. Her grandmother reported the adolescent to be mute and drooling excessively. She was readmitted to the pediatric intensive care unit and treated with prednisone 40 mg intravenous (IV) daily. Within 8 days of admission, a psychologist noted the adolescent to be crying inappropriately, disoriented, restless, and unable to sleep. Full psychiatric evaluation was attempted on December 13, 2016, but the patient was found to be intermittently coherent after a 2 mg dose of lorazepam intravenously. Mental status examination was significant for a cachectic black female who was tearful, drooling, had poor eye contact, mute, and paranoid. She refused oral intake. Based on collateral history obtained from the patient's family and primary providers, psychiatry recommended clonazepam 0.25 mg by mouth twice daily and risperidone 0.5 mg by mouth twice daily for mood stabilization and antipscychotic effects. A baseline lipid panel and hgA1C were ordered.

The patient exhibited hyperlipidemia (total cholesterol 261, LDL 188, and HDL 73) and was subsequently changed from risperidone to aripriprazole 2 mg by mouth daily. This antipsychotic was titrated up to 5 mg by mouth daily on December 16, 2017, because the adolescent was exhibiting sufficient response. On December 19, 2016, she was actively responding to external stimuli and was experiencing visual hallucinations. Aripiprazole was increased to 10 mg by mouth daily.

Throughout this time period, psychiatry stressed to the primary team the likely contribution of steroids to her psychotic symptoms. Rheumatology was concerned the patient may have lupus cerebritis or encephalitis, and a full medical workup was completed. MRI showed fluid-attenuated inversion recovery (FLAIR) hyperintensities. Cerebrospinal fluid findings were normal and EEG had findings consistent with mild encephalopathy. After consultation between neurology, rheumatology, psychiatry, psychology, and pediatrics, a steroid taper began on December 21, 2016. The adolescent continued to be altered and aripiprazole dose was increased to 15 mg daily.

Haloperidol 2 mg orally was added on December 27, 2016, because of her poor response. The patient was still found to be disorganized, speaking nonsensically, and whispering intermittently. The plan was to cross-taper aripiprazole and haloperidol starting on December 28, 2016. That day, the patient was found to be catatonic and standing still inappropriately. Lorazepam 0.5 mg by mouth twice a day was initiated. The aripiprazole taper was completed on December 29, 2016. Haloperidol was continued at 5 mg by mouth daily.

On December 30, 2017, the patient was more verbal and was no longer experiencing hallucinations. At this time, she was receiving 10 mg of prednisone daily. Lorazepam was increased to 1 mg by mouth twice a day as the patient appeared to be improving. The steroid taper was completed on January 3, 2017, with the patient on haloperidol 5 mg by mouth daily and lorazepam 1 mg by mouth twice a day. Upon discontinuation of all steroids, the patient was completely organized, no longer responding to external stimuli, was euthymic, and had returned to her baseline level of functioning.

On January 4, the screen for child-related anxiety disorders (SCARED) was given to the patient as she was back to her baseline mental status. The SCARED was 34 indicating clinically significant anxiety. To treat her anxiety, fluoxetine 5 mg by mouth daily was started, haloperidol decreased to 2.5 mg daily, and lorazepam lowered to 0.5 mg twice daily. The patient was discharged on January 5, 2017, on fluoxetine 5 mg by mouth daily, haloperidol 2.5 mg daily, and lorazepam 0.5 mg twice daily. The patient was instructed to continue lorazepam 0.5 mg twice daily for only 1 week.

She presented as an outpatient to our clinic on January 17, 2017, at which time her father informed her physician that psychotropic medications were all discontinued. The patient's family felt that the adolescent no longer benefited from the medications despite the fact that she found it helpful. She completed a SCARED at that time that was 26. She was again prescribed fluoxetine 10 mg daily to target the persistently significant levels of anxiety.

Results

Overall, we identified only 15 reported pediatric cases of steroid-induced psychosis in the literature (Table 1). (Hall et al. 1979; Sullivan and Dickerman 1979; Ducore et al. 1983; Turktas et al. 1997; Dawson and Carter 1998; French et al. 2003; Fleming and Flood 2005; Kim et al. 2010; Ularntinon et al. 2010; Bag et al. 2012; Demir et al. 2012). All cases exhibited new onset psychotic symptoms upon initiation of steroid treatment and resolution of symptomatology upon their discontinuation.

Asthma is the most common indication requiring steroids in pediatric patients. Therefore, it is not surprising that this was the most common diagnosis in the articles reviewed, representing 5 of the 15 articles. (Hall et al. 1979; Dawson and Carter 1998; French et al. 2003; Kim et al. 2010). No particular medical diagnosis appeared to be more prone to an episode of steroid-induced psychosis; however, with more data collected in the future, findings may emerge.

In adults, the incidence of psychiatric manifestations of glucocorticoid use, including psychosis, is dose dependent. In a study of nearly 718 patients, psychiatric reactions occurred in 1.6% of patients receiving a dose of 40 mg/day compared with 18.4% of patients who received doses >80 mg/day (Anon 1972). The lowest reported dosage of steroid-induced psychosis was 25 mg/day in the pediatric cases reviewed (Demir et al. 2012). This suggests that dosages <25 mg/day in the pediatric population may be less likely to cause psychosis. However, this finding is limited by the fact that body weights and body mass indices of the patients included in this review were not provided in the individual case reports. In addition, pediatric patients have lower bioavailability, faster metabolism, and a smaller volume of distribution for medications that would make the consequences of dose adjustments less predictable than adults (Vitiello 2001).

Among the pediatric cases reviewed, 12 of 15 patients had their glucocorticoid dosage tapered down to diminish psychotic symptoms (Hall et al. 1979; Sullivan and Dickerman 1979; Ducore et al. 1983; Turktas et al. 1997; Dawson and Carter 1998; French et al. 2003; Kimmins et al. 2004; Fleming and Flood 2005; Kim et al. 2010; Bag et al. 2012; Demir et al. 2012). This was a successful treatment for four patients (Sullivan and Dickerman 1979; Turktas et al. 1997; French et al. 2003; Kim et al. 2010). Others were coadministered benzodiazepine during their taper or an antipsychotic medication for management of their acute psychotic symptoms (Hall et al. 1979; Ducore et al. 1983; Dawson and Carter 1998; Kimmins et al. 2004; Ularntinon et al. 2010; Bag et al. 2012; Demir et al. 2012).

Owing to medical necessity, three of the cases were unable to be managed by corticosteroid taper (Hergüner et al. 2006; Ularntinon et al. 2010). In these cases, risperidone (0.5–1.5 mg) was used successfully to treat the steroid-induced psycosis. Rispiridone has certain advantages including its observed tolerability, lower propensity for extrapyramidal symptoms (dystonia, akathisia, and parkinsonism), and liquid formulation that allows for lower doses. Some of the cases reviewed used chlorpromazine, quetiapine, or olanzapine, and these antipsychotics were quite effective (Hall et al. 1979; Ducore et al. 1983; Kimmins et al. 2004; Fleming and Flood 2005; Demir et al. 2012). Understandably, the only agent reported that was unsuccessful was imipramine, a tricyclic antidepressant (Hall et al. 1979).

Discussion

In the case we presented, the patient exhibited comorbid hyperlipidemia, a well-known side effect of second generation antipsychotics, rendering risperidone and most of the other second-generation antipsychotics undesirable. Because aripiprazole is considered one of the second-generation antipsychotics least likely to cause weight gain and metabolic syndrome, it was our first choice of treatment. However, when this strategy proved uneffective, we switched to haloperidol.

In addition to factoring in side effects of therapy for steroid psychosis, the physiological effects of the steroids should also be considered. For example, children are often treated with steroids for asthma, eczema, and other common disorders. Long-term steroid use may have impact on serotonergic systems that could conceivably increase the risk for depression, attention-deficit/hyperactivity disorder, impulsive behaviors, and other psychiactric symptoms (Pretorius 2004).

This case series summarized the entirety of the literature on the treatment of steroid-induced psychosis in the pediatric population. Because this side effect is rare in the child and adolescent population, there are no widely accepted guidelines for management. Discontinuation of steroids is the gold standard for alleviating negative side effects, including psychosis, associated with steroid administration. However, many patients receiving steroids cannot be safely tapered and management must include psychopharmacologic interventions. After discontinuing the glucocorticoid, we would suggest conservative use of atypical antipsychotics to address the psychotic symptoms for a limited period of time.

Furthermore, these children may well require steroids in the future for flare-ups of disease and may be prone to developing recurrent psychosis. Consideration must be taken in how to best prevent future episodes of psychosis in these children. One case included in this series used risperidone prophylactically to prevent psychotic events (Hergüner et al. 2006). More research is needed to determine whether antipsychotics should be used prophylactically for those children with a history of steroid-induced psychosis.

Conclusions

Every reported case of steroid-induced psychosis did eventually resolve, whether or not steroids could be discontinued. Therefore, families, patients, and medical personnel can be reassured that with medical management, the child will likely regain functioning and return to baseline status, typically within 1 month. It must be recognized, however, that this reassurance is limited by reporting bias; if there were cases that were not resolved, physicians may be unlikely to report these cases. Therefore, proper education about this potential side effect is imperative.

Steroid-induced psychosis in the pediatric population is a rare but significant complication that patients and families need to be made aware of. There is likely an under-reporting of psychosis in pediatrics as it can be difficult to recognize due to its heterogeneity and the fluctuating nature of steroid-induced psychiatric manifestations. More randomized control trials will be needed to establish the frequency of this side effect as well as those most at risk of developing psychosis. Finally, more longitudinal studies are clearly required to better predict at-risk pediatric patients as well as more reliable methods for patient management.

Clinical Significance

Steroid-induced psychosis is a rare but serious adverse effect of glucocorticoids in the child and adolescent population. There is likely under-reporting of this complication in the literature due to the difficult nature of diagnosing psychosis in children and adolescents. However, treating physicians must be aware of this potential complication and should educate patients and families appropriately. Here, we presented a systematic review of the literature on steroid-induced psychosis in children and adolescents as well as a novel case. By doing so, we hope to provide some guidance to treating this complex condition, particularly due to the ubiquitous nature of glucocorticoids in treating a variety of conditions. Furthermore, patients, families, and physicians alike should find some reassurance that this condition did indeed resolve in all reported cases.

Footnotes

Disclosures

Gabrielle Hodgins, Samantha Saltz, Eric Gibbs, Rolando Gonzalez, and Judith Regan report no competing financial interests. Charles Nemeroff received research/grants from the National Institutes of Health (NIH), Stanley Medical Research Institute, and consulting fees (last 3 years) from Xhale, Takeda, Taisho Pharmaceutical Inc., Prismic Pharmaceuticals, Bracket (Clintara), Total Pain Solutions (TPS), Gerson Lehrman Group (GLG) Healthcare & Biomedical Council, Fortress Biotech, Sunovion Pharmaceuticals Inc., Sumitomo Dainippon Pharma, and Janssen Research & Development LLC, Magstim, Inc. Charles Nemeroff is stockholder of Xhale, Celgene, Seattle Genetics, Abbvie, OPKO Health, Inc., Bracket Intermediate Holding Corp., Network Life Sciences Inc., and Antares, is on scientific advisory boards of American Foundation for Suicide Prevention (AFSP), Brain and Behavior Research Foundation (BBRF) (formerly named National Alliance for Research on Schizophrenia and Depression [NARSAD]), Xhale, Anxiety Disorders Association of America (ADAA), Skyland Trail, Bracket (Clintara), RiverMend Health LLC, and Laureate Institute for Brain Research, Inc., and board of directors of AFSP, Gratitude America, and ADAA. Charles Nemeroff has income sources or equity of $10,000 or more from American Psychiatric Publishing, Xhale, Bracket (Clintara), CME Outfitters, and Takeda. Charles Nemeroff has the following patents in his name: Method and devices for transdermal delivery of lithium (US 6,375,990B1), and method of assessing antidepressant drug therapy via transport inhibition of monoamine neurotransmitters by ex vivo assay (US 7,148,027B2).

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