Complications – Common complications of COVID-19-related ARDS include acute kidney injury (AKI), elevated liver enzymes, and cardiac injury including cardiomyopathy, pericarditis, pericardial effusion, arrhythmia, and sudden cardiac death. As an example, in a single-center retrospective cohort from China of 52 critically ill patients with COVID-19, complications included AKI (29 percent; half of whom needed renal replacement therapy), liver dysfunction (29 percent), and cardiac injury (23 percent) [
11].
•Cardiac injury appears to be a late complication, developing after the respiratory illness improves. A high rate of cardiomyopathy was noted in a United States cohort (33 percent), and may relate to the older age in that population [
22]. In another United States cohort in New York City, cardiac complications among mechanically ventilated patients included atrial arrhythmias (18 percent), myocardial infarction (8 percent), and heart failure (2 percent) [
30]. One case series reported five patients who developed acute cor pulmonale, most of which occurred in association with hemodynamic instability or cardiac arrest [
35]. All cases were thought to be most likely due to pulmonary embolism (PE), although a definitive diagnosis of PE was confirmed in only one case. Cardiac complications of COVID-19 are discussed in detail elsewhere. (See
"Coronavirus disease 2019 (COVID-19): Myocardial injury" and
"Coronavirus disease 2019 (COVID-19): Arrhythmias and conduction system disease" and
"Coronavirus disease 2019 (COVID-19): Myocardial infarction and other coronary artery disease issues".)
•Sepsis, shock, and multi-organ failure do occur but appear to be less common when compared with non-COVID-19-related ARDS. The need for vasoactive agents is variable, although a significant proportion need vasopressor support for hypotension (often due to sedation medications or cardiac dysfunction). In the cohort study from Wuhan, China, 35 percent of 52 patients received vasoactive agents [
11]. In contrast, in the case series from New York City, 95 percent of the 130 patients who received mechanical ventilation required vasopressor support; the reasons for this were not specified [
30].
•As above, acute kidney injury is common among critically ill patients with COVID-19, and many require renal replacement therapy. This is discussed in detail elsewhere. (See
"Coronavirus disease 2019 (COVID-19): Issues related to kidney disease and hypertension", section on 'Acute kidney injury'.)
•Data on the risk of secondary bacterial pneumonia are limited, but it does not appear to be a major feature of COVID-19. In a cohort of intubated patients from China, hospital-acquired pneumonia, in many cases with resistant pathogens, was reported in 12 percent [
11]. This finding may be related to the high use of glucocorticoids for ARDS management in China. Further data are needed to elucidate the rate of superinfection in other countries.
•Lung compliance is high compared with other etiologies of ARDS and the rate of barotrauma appears to be low with only 2 percent developing pneumothorax, compared with 25 percent of those with severe acute respiratory syndrome coronavirus (SARS-CoV) [
11,36]. There are limited data describing the lung pathology in patients with COVID-19. Case reports from post mortem cases and patients undergoing biopsy for another reason suggest a wide variation from mononuclear inflammation to diffuse alveolar damage, classic of ARDS [
37,38]. (See
"Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults", section on 'Pathologic stages'.)
•Neurologic complications in critically ill patients are common, especially delirium or encephalopathy which manifests with prominent agitation and confusion along with corticospinal tract signs (hyperreflexia). Consistent with this, intensivists have observed that sedation requirements are high in this population, particularly immediately after intubation. In one series of 58 patients with COVID-19-related ARDS, delirium/encephalopathy was present in approximately two-thirds of patients [
39]. In addition, three of 13 patients who had brain MRI had an acute ischemic stroke; eight MRI studies demonstrated leptomeningeal enhancement. Cerebrospinal fluid (CSF) in seven patients was acellular and only one had elevated CSF protein; PCR assays of CSF were negative for the virus. It is unclear whether the neurologic complications noted in this and other reports are due to critical illness, medication effects, or represent more direct effects of cytokines or the SARS-CoV-2 virus [
39-41]. Encephalitis, while reported, is rare [
42]. Similarly, Guillain-Barré-barre syndrome following SARS-CoV-2 virus infection has also been described in a small case series [
43].
•COVID-coagulopathy is common in this population with some patients developing abnormal coagulation profiles and others developing thrombosis. These features are discussed separately. (See
"Coronavirus disease 2019 (COVID-19): Hypercoagulability".)
