Taiwanese Journal of Psychiatry

LETTER TO THE EDITOR
Year
: 2022  |  Volume : 36  |  Issue : 1  |  Page : 44--46

Post-acute delirium of COVID-19 infection: Report of two cases


Dai- Chun Chi1, Chih- Pang Chu2, Tien Wei Yang1, Hu- Ming Chang1,  
1 Department of Psychiatry, Taipei City Hospital Songde Branch, Taipei, Taiwan
2 Department of Psychosomatic Medicine, Taipei City Hospital Songde Branch, Taipei, Taiwan

Correspondence Address:
Hu- Ming Chang
309 Song-de Road, Taipei 110
Taiwan




How to cite this article:
Chi DC, Chu CP, Yang TW, Chang HM. Post-acute delirium of COVID-19 infection: Report of two cases.Taiwan J Psychiatry 2022;36:44-46


How to cite this URL:
Chi DC, Chu CP, Yang TW, Chang HM. Post-acute delirium of COVID-19 infection: Report of two cases. Taiwan J Psychiatry [serial online] 2022 [cited 2022 Jun 29 ];36:44-46
Available from: http://www.e-tjp.org/text.asp?2022/36/1/44/341038


Full Text

The coronavirus disease 2019 (COVID-19) that is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has contributed to considerable morbidity and mortality. In addition to respiratory symptoms, neuropsychiatric manifestations of COVID-19 infection include anosmia, ageusia, headache, and delirium. The incidence of delirium among patients with COVID-19 infection is ranged from 3.3% to 19.6% in retrospective studies [1],[2]. As expected, delirium is more common in patients with severe infection and having other comorbidities [3],[4]. Delirium is most likely to develop during the acute infection stage, but can also precede respiratory symptoms, especially in the elderly [5]. To our knowledge, few reports exist about delirium after COVID-19 infection. We present two cases of patients with delirium occurring after COVID-19 infection.

 Report of Two Cases



Case 1

Mr. A is a patient of a 78-year-old retired businessman, who had a medical history of atrial fibrillation, hypertension, hearing defect, and obstructive sleep apnea. He has received estazolam 2 mg per day regularly for insomnia for six years. He is overcautious and tends to be anxious but does not have any past psychiatric history. He showed no signs of cognitive deterioration before COVID-19 infection. He visited the emergency department for fever and mild cough for one day. The results of laboratory tests revealed thrombocytopenia, elevated serum level of C-reactive protein, and mild hyponatremia but otherwise normal [Table 1]. The finding of chest X-ray showed scattered infiltration and small opacity at the bilateral lung field. He was diagnosed to have COVID-19 according to the polymerase chain reaction (PCR) results.{Table 1}

After the patient was admitted to an isolation ward, he received empirical antibiotics including ceftriaxone and azithromycin and a 7-day course of intravenous dexamethasone 6 mg/day. His fever and cough were subsided on day 3, and he was discharged home on day 14 with improved symptoms.

After discharge, the patient was anxious and believed that COVID-19 might be transmitted to his family. On day 16, his family noticed that he developed excessive worries, repetitive behaviors (Table-hitting with bare hands), inability to do daily tasks (e.g., using mobile phones), and disturbances of sleep-wake cycle. His symptoms had been worsened for one week, and he was admitted to the psychiatric ward on day 23. Upon admission, he was disoriented to time, place, and person and manifested catatonia with signs of mannerism (keeping in praying gesture), echolalia (repeating the question he was asked), verbigeration (repeating with different colors and numbers), and stereotypical behaviors (banging on the bed rails with his hands). The electroencephalogram was normal in finding. The Bush-Francis Catatonia Rating Scale was 27 points. He received quetiapine 50 mg/day for disrupted sleep–wake cycle. He received lorazepam 1 mg injection once to treat catatonia. He was discharged on day 28. In the three months following the COVID-19 infection, he presented himself with improved cognitive function and anxiety symptoms.

Case 2

Miss B is a 40-year-old nurse patient. She had a medical history of hypertension under amlodipine and valsartan treatment, chronic hepatitis B carrier, and obesity. She had no history of psychiatric illnesses. She visited the emergency department for a two-day course of fever and progressive cough. Results of laboratory tests revealed mild lymphopenia but otherwise normal. Results of chest X-ray showed increased infiltrations over bilateral lungs and consolidation at the right lower lung field. She was diagnosed with COVID-19 infection proven by the PCR test. She was admitted to an isolation ward and received empirical antibiotics with ceftriaxone and dexamethasone for seven days. A simple mask with an oxygen flow rate of 8 L/min was used briefly at the emergency department. She was discharged on day 10 with improved respiratory symptoms.

On day 11, her co-worker found that the patient had difficulty to follow simple instructions (taking a taxi), and she was then admitted to the psychiatric ward. After admission, she presented herself with disorientation, attention deficits, incoherent speech, and paranoid feeling (having fear of stealing her credit card). She could not do an abstract thinking test (explaining the meaning of a proverb in mandarin) and a calculation test (counting backward from 100 by serial 7's). She had stable vital signs. Blood tests showed leukocytosis without other signs of infection, which was suspected to be caused by dexamethasone [Table 1]. The results of brain magnetic resonance imaging (MRI) study, and electroencephalogram were normal. Her symptoms were recovered after simplification of medications. She was discharged on day 16 and was able to return to work on day 38. She experienced physical symptoms such as fatigue, chest tightness, and palpitations afterward, but could go back to work as usual.

 Comment



According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), diagnostic criteria for delirium include disturbances in attention and awareness that develop over a short period of time and fluctuate during the course of a day [6]. We have presented two cases of patients with delirium following COVID-19 infection. Their physical conditions did not suggest a vulnerable physical state susceptible to develop a delirium. During the acute phase of infection, they both showed no evidence of delirium. They both developed delirium after discharge from the isolation ward and required readmission. The laboratory tests of these two patients showed typical manifestations of COVID-19 infection, including thrombocytopenia, prolonged prothrombin time, elevated serum level of lactate dehydrogenase, and inflammatory markers including ferritin, C-reactive protein, and erythrocyte sedimentation rate [Table 1], all of them were gradually normalized over the course of the disease. Neither of their laboratory tests showed known poor prognostic factors including lymphopenia (< 1000/uL), elevated serum level of D-dimer, and evidence of cardiac damage (e.g., increased serum level of creatine kinase).

Two proposed mechanisms exist for COVID-19-associated delirium, a direct viral invasion of the brain and a secondary encephalopathy caused by inflammation or other systemic effects of the virus [5]. Similar to SARS-CoV and MERS-CoV, the SARS-CoV-2 also shows neuroinvasive and neurotropic potentials based on the fact that ACE2 receptors are expressed in glial cells and neurons [7]. Since the mechanism of neuropsychiatric symptoms may involve immune-mediated responses, symptoms may occur late in the course of the disease [5].

Delirium is associated with a wide range of medical conditions and hospital beds without windows for natural light. The patients with hospital beds without windows tend to have more possibility in developing delirium than those with windows [8]. But this is not an issue here in this case report because all hospital beds in Taiwan must have windows as stipulated by the Taiwan Joint Commission on Hospital Accreditation and Quality Improvement.

In this study, we still have three factors that cannot be excluded in addition to COVID-19 infection: ·

Antibiotics have been reported to be associated with delirium, which usually begins within a week of antibiotic administration and resolves after discontinuation of antibiotics. From the timing of the delirium in these two cases, it is unlikely that delirium was caused by antibiotics.Dexamethasone 6 mg/day is associated with a 1% incidence of psychiatric adverse effects [9]. From the timing of the delirium in these two cases, it is unlikely that the delirium was caused by dexamethasone.Mild hyponatremia in one of these patients has been reported as a possible contributor to the development of delirium [10].

Since COVID-19-associated delirium can be fully recovered [11], we emphasized on the need for early recognition of delirium in patients with COVID-19 infection. In less severe cases, we can just observe for spontaneous improvement before giving more aggressive treatment such as steroids or intravenous immunoglobulin. Our case report here highlights the need to be aware of the emerging neuropsychiatric manifestations after COVID-19 infection. (The institutional review board of Taipei City Hospital approved the publication of the case report (IRB protocol number = TCHIRB-11008018-E, and date of approval = September 29, 2021) with the waiver of obtaining signed informed consent from those two patients.)

 Financial Support and Sponsorship



None.

 Conflicts of Interest[/TAG:]

All authors declare no conflicts of interest in writing this letter-to-the editor.

References

1Romero-Sánchez CM, Díaz-Maroto I, Fernández-Díaz E, et al.: Neurologic manifestations in hospitalized patients with COVID-19: the ALBACOVID registry. Neurology 2020; 95: e1060-70.
2Zhao XY, Xu XX, Yin HS, et al.: Clinical characteristics of patients with 2019 coronavirus disease in a non-Wuhan area of Hubei Province, China: a retrospective study. BMC Infect Dis 2020; 20: 311.
3Helms J, Kremer S, Merdji H, et al.: Delirium and encephalopathy in severe COVID-19: A cohort analysis of ICU patients. Crit Care 2020; 24: 491.
4Ticinesi A, Cerundolo N, Parise A, et al.: Delirium in COVID-19: epidemiolgy and clinical correlations in a large group of patients admitted to an academic hospital. Aging Clin Exp Res 2020; 32: 2159-66.
5Beach SR, Praschan NC, Hogan C, et al.: Delirium in COVID-19: A case series and exploration of potential mechanisms for central nervous system involvement. Gen Hosp Psychiatry 2020; 65: 47-53.
6American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Washington DC, USA: American Psychiatric Association, 2013.
7Baig AM, Khaleeq A, Ali U, et al.: Evidence of the COVID-19 virus targeting the CNS: tissue distribution, host-virus interaction, and proposed neurotropic mechanisms. ACS Chem Neurosci 2020; 11: 995-8.
8Lee HJ, Bae E, Lee HY, et al.: Association of natural light exposure and delirium according to the presence or absence of windows in the intensive care unit. Acute Crit Care 2021; 36: 332-41.
9Program BCDS: Acute adverse reactions to prednisone in relation to dosage. Clin Pharmacol Ther 1972; 13: 694-8.
10Zandifar A, Badrfam R: Exacerbation of psychosis accompanied by seizure and catatonia in a patient with COVIDens: a case report. Psychiatry Clin Neurosci 2021; 75: 63-71.
11Mcloughlin BC, Miles A, Webb TE, et al.: Functional and cognitive outcomes after COVID-19 delirium. Eur Geriatr Med 2020; 11: 857-62.