Fever, cough, shortness of breath, anosmia, ageusia, or dysgeusia are the most common symptoms of COVID-19. However, a wide variety of atypical presentations have also been described [1]. Some uncommon presentations are related to the hypercoagulable state, while others are a result of the inflammatory response. These manifestations can occur almost at any organ level. For example, cardiac manifestations include acute MI, myocarditis, arrhythmias, and pericarditis. Atypical heart manifestations are more common in individuals with previous heart conditions, but it seems that the high systemic inflammation and the angiotensin-converting enzyme 2 (ACE2) tropism are involved in this relationship and may cause manifestations in previously healthy individuals [2]. ACE 2 is also expressed in the gastrointestinal tract and up to 48% of patients present with gastrointestinal manifestations. They range from liver abnormalities such as mild to moderate liver injury with aminotransferase elevations and albumin decline, also diarrhea, nausea, and vomiting. Similar to the gastrointestinal tract, the nervous system also expresses ACE 2; thus, neuropsychiatric symptoms of COVID-19 occur in up to 36% of patients and are more frequent among those with severe disease [3]. The spectrum of neurological manifestations includes not only cerebrovascular disease and skeletal muscle injury, but also meningoencephalitis, encephalomyelitis, Guillain Barre, and perfusion abnormalities [4,5,6]. Psychiatric manifestations are wide and could be divided into those driven by the infection itself and those driven by stress and isolation related to the pandemic. Delirium has been suggested as the most common neuropsychiatric manifestation [7], but they also include psychosis, dementia-like symptoms, and affective disorders [8].
Considering these diverse presentations, it is relevant for the emergency department physicians to consider COVID-19 in unexplained manifestations of inflammatory disease or arterial and venous thrombosis at any organ level.
Case 1
A 48-year-old man presented to the gastroenterologist with an episode of hiccups lasting at least 96 h. His past medical history only revealed an L5 surgical repair in 2005, and he denied allergies or recent travel. Aside from the hiccups, the patient recalled no other symptoms and denied abdominal pain, nausea, vomiting, diarrhea, chest pain, cough, dyspnea, or fever. He was started on ambulatory treatment with metoclopramide 10 mg every 8 h; however, the symptoms did not resolve.
He presented to the ER approximately 5 h later with the same complaint. His vitals showed a heart rate of 82 beats/min, respiratory rate 20 respirations/min, blood pressure 133/88 mmHg, oxygen saturation 93%, and temperature 36.7 °C. On the physical exam, the patient was alert and oriented with a normal affect and normal gait. The exam revealed no dermatological lesions and benign head, ear, nose, and throat exam. His chest showed a normal diameter. However, lung auscultation revealed the presence of crackles left lung base. The remainder exam was normal.
Initially, he was treated with IV metoclopramide, omeprazole 40 mg, ondansetron 8 mg, and oral frappe magaldrate/dimeticone (80/10 mg) without symptom improvement. Laboratory analysis revealed hyperglycemia (182 mg/dl), thrombocytopenia (81,000/mcl), leucopenia (4,000/mcl), and lymphopenia (700/mcl absolute count). The remaining results were normal (hemoglobin 16.2 g/l, hematocrit 48.3%, BUN 19.2, urea 41.1, serum creatinine 1.1 mg/dl, sodium 136.8 mEq/L, potassium 3.56 mEq/L). A chest X-ray (Fig. 1) revealed bilateral infiltrates. The thoracic CT scan revealed multiple zones of diffuse alveolar infiltrate across all segments of both lungs (Fig. 2).
SARS-CoV-2 PCR results were positive. The patient refused admission and was lost to follow-up.
Case 2
A 43-year-old man was brought to the emergency department by his mother for altered mental status. She reported her son’s symptoms had started 3 days after his father was diagnosed with COVID-19. The patient presented with tachylalia, disorganized ideas, restlessness, delusions of grandeur, emotional lability, hetero-aggression, and aggression towards his mother. His mother revealed a past history of hetero-aggressive episodes which usually resolved during 48 h. Episodes did not affect social or professional functioning and were never medically evaluated.
Aside from his psychiatric symptoms, his vitals were normal, and his physical exam did not reveal any significant findings. Neurology and psychiatry were consulted, and due to known exposure, SARS-CoV-2 PCR was ordered.
While results were pending, we documented hypokalemia K 3.3, elevation of hepatic enzymes (aspartate aminotransferase 53 U/L, alanine aminotransferase 69 U/L), indirect hyperbilirubinemia (total bilirubin 2.07 mg/dl, indirect bilirubin 1.73 mg/dl, direct bilirubin 0.34 mg/dl), and elevated ferritin levels (595 ng/mL). The rest were within normal limits: C-reactive protein 1.8 mg/dL, erythrocyte sedimentation rate 10 mm/h, procalcitonin 0.05 ng/mL, and fibrinogen 297 g/L.
A contrast brain MRI (Fig. 3) and a thoracic CT (Fig. 4) were obtained to investigate for possible COVID-19-related changes such as encephalitis, stroke, or pulmonary changes. However, there were no significant findings.
A spinal tap and cytological testing yielded the following: transparent, with 0 leucocytes, 0 erythrocytes, and 0 crenocytes. Glucose 65.6 mg/dL, proteins 17.5 mg/dL, the Gram stain did not report any organisms, bacterial antigens were negative, and viral PCR did not detect any pathogen. Chinese ink was negative.
The PCR for SARS-CoV-2 was positive, and the patient was diagnosed with manic psychosis and COVID-19. Due to isolation precautions of the hospital, family members decided to take the patient home in a voluntary discharge. He will receive follow-up care by the neurologist and infectious disease specialist. The patient consented to the publishing of his experience.