key: cord-0894441-t9dpmh0h
authors: Zheng, Kenneth I.; Feng, Gong; Liu, Wen‐Yue; Targher, Giovanni; Byrne, Christopher D.; Zheng, Ming‐Hua
title: Extrapulmonary complications of COVID‐19: A multisystem disease?
date: 2020-07-22
journal: J Med Virol
DOI: 10.1002/jmv.26294
sha: 3c97be4e6ead5e7b731f380811eec83b39a23531
doc_id: 894441
cord_uid: t9dpmh0h

The outbreak of coronavirus disease 2019 (COVID‐19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), has been recently declared a pandemic by the World Health Organization. In addition to its acute respiratory manifestations, SARS‐CoV‐2 may also adversely affect other organ systems. To date, however, there is a very limited understanding of the extent and management of COVID‐19‐related conditions outside of the pulmonary system. This narrative review provides an overview of the current literature about the extrapulmonary manifestations of COVID‐19 that may affect the urinary, cardiovascular, gastrointestinal, hematological, hematopoietic, neurological, or reproductive systems. This review also describes the current understanding of the extrapulmonary complications caused by COVID‐19 to improve the management and prognosis of patients with COVID‐19.

The spread of coronavirus disease 2019 , caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has recently become a global pandemic and public health problem in almost all countries. 1-3 SARS-CoV-2 is similar to severe acute respiratory syndrome coronavirus (SARS) and Middle East respiratory syndrome coronavirus in that these coronavirus infections are responsible for severe and potentially life-threatening acute respiratory syndromes in humans. As of 16 June 2020, a total of more than 7 900 000 confirmed cases and approximately 434 796 total deaths for COVID-19 had been reported globally. Unfortunately, there are no targeted drugs for treatment of SARS-CoV-2 infection to date, vaccine development is at an early stage, and the number of infected patients is increasing rapidly worldwide. There is a growing body of evidence suggesting that in addition to the common acute respiratory symptoms (such as fever, cough, and dyspnea), COVID-19 patients may also have signs and symptoms of injury in many other organ systems (as summarized in Figure 1 ), which may further complicate medical management and adversely affect clinical outcomes of these patients.

SARS-CoV-2 is thought to use cell receptor angiotensin-converting enzyme 2 (ACE2) to gain cellular access in humans. 5 The ACE2 receptor is highly expressed in lungs, kidneys, gastrointestinal (GI) tract, liver, vascular endothelial cells, and arterial smooth muscle cells. 6 Thus, all of these organs and systems with high expression of ACE2 receptors might be speculated targets for SARS-CoV-2 infection. 7 The main purpose of this narrative review article is to provide an overview of the current literature on the extrapulmonary Co-first authors: Kenneth I. Zheng and Gong Feng. manifestations and complications of COVID-19 to improve the management and prognosis of these patients.

The diagnosis of SARS-CoV-2 infection is currently established with nucleic acid (RNA) testing of suspected patients using realtime reverse transcriptase-polymerase chain reaction (RT-PCR) techniques by oropharyngeal swabs or, in some cases, by stool samples. 8, 9 Initially, a patient was suspected of SARS-CoV-2 infection if he/she had symptoms of cough, fever and/or dyspnea, and a history of travel to endemic regions affected by the SARS-CoV-2 outbreak; or have had close contact(s) with individuals with an aforementioned travel history. However, due to the everincreasing number of COVID-19 cases, physicians are now recommending RT-PCR testing only in all patients showing any evidence of viral pneumonia on chest X-ray or computed tomography (CT) (eg, ground-glass opacities and exudative lesions). [10] [11] [12] In some cases, absence of fever and typical symptoms in the early stages of viral infection hinders the identification of infection in atrisk individuals. 13 To date, the treatment options are scarce, mostly due to the fact that no targeted therapy for SARS-CoV-2 is available. The mainstay of COVID-19 management is the patient's isolation and supportive medical care, as recommended by National Institutes of Health of the United States and China Center for Disease Control and Prevention, which includes the use of antiviral, antibacterial medications, and oxygenation therapy as appropriate. 14, 15 Initially, corticosteroids were not recommended for routine use as their usage may be associated with delayed viral clearance. 16 The kidneys are one of the most frequently affected extrapulmonary organs in patients infected with SARS-CoV-2; especially, in those patients who are severely ill. [18] [19] [20] 23 Previous studies of patients affected by the 2013 SARS outbreak have shown that kidney damage is mainly characterized by tubular injury (as reflected by abnormal urine test results) and increased serum creatinine and urea nitrogen concentrations. 25, 26 A recent study of 59 patients infected with SARS-CoV-2 (nearly half of whom had a severe illness) showed that mild proteinuria was the commonest kidney abnormality in these patients. In addition, nearly 30% of these patients also had elevated urea nitrogen levels and approximately 20% had increased serum creatinine levels. 27 Currently, the occurrence of acute kidney injury (AKI) among patients with COVID-19 is not consistent across published studies, ranging from 0.1% to 29%. 20 20 In another study, the occurrence of AKI in 58 critically ill COVID-19 patients was as high as 29%, and AKI was also found to be an important risk factor for increased hospital mortality. 28 In a case series of 85 patients with severe SARS-CoV-2 infection, AKI occurred in 23 (27.1%) patients. 29 In this study, a postmortem analysis of six patients revealed the presence of severe acute tubular necrosis with accumulation of SARS-CoV-2 nucleocapsid protein antigens. 24 This finding suggests that the SARS-CoV-2 might directly infect kidney tubules.

Although the underlying virologic mechanisms are not completely understood, it is plausible to speculate that there is binding by the virus to the ACE2 receptor, which is highly expressed in kidney tubules, causing glomerulopathy, acute tubular necrosis, and protein leakage in the Bowman's capsule. [30] [31] [32] However, it is also possible to speculate that AKI could be an epiphenomenon of both respiratory distress syndrome-induced hypoxia and septic shock caused by the SARS-CoV-2. 33 Other autopsy investigations have reported that the endothelium is affected in the kidneys, and is responsible for the proteinuria. 34 SARS-CoV-2 particles in renal endothelial cells may suggest viremia as a possible cause of renal endothelial damage resulting in AKI. 29 More recently, Sun et al 35 have reported the occurrence of subclinical AKI as reflected by increased urinary levels of β2-microglobulin, α1-microglobulin, N-acetyl-β-D-glucosaminidase, and retinol-binding protein (ie, all biomarkers of kidney tubular damage) in a sample of 32 confirmed COVID-19 cases without prior chronic kidney disease. 35 In addition, the severity of kidney tubular damage was also greater in severe COVID-19 patients than in less severely affected patients. 30 Based on the available evidence, we can draw the following considerations: (a) AKI is not uncommon in patients with COVID-19, especially in those with severe COVID-19; patients can present with proteinuria early or at hospital admission, while AKI often develops in later stages of the viral disease (ie, critically ill patients) and is understood as an early sign of multiple organ dysfunction; (b) AKI could be related to direct effects of the virus, and to other concomitant virus-related complications, such as hypoxia and shock; (c) the precise incidence of AKI in SARS-CoV-2 infected patients is not known; however, it is reasonable to assume that AKI is more common in critically ill patients than in those with mild COVID-19 disease; and (d) COVID-19 patients with a prior history of chronic kidney disease are more likely to develop AKI;

and (e) COVID-19 patients with AKI have a poorer prognosis.

Collectively, therefore, it is recommended that physicians who treat COVID-19 patients should pay special attention to acute changes in patients' kidney function. 36, 37 Volume depletion at hospital admission might be suggestive of subsequent occurrence of AKI, especially when COVID-19 patients are infrequently given prehospital fluid resuscitation. In the absence of targeted treatment strategies for SARS-CoV-2 infection, supportive care is the cornerstone in managing COVID-19, and thus, lung-protective ventilation may be used to reduce the risk of AKI by limiting ventilator-induced hemodynamic effects and the cytokine burden on the kidneys. 38 It is also recommended to follow Kidney Disease Improving Global Outcomes supportive care guidelines in patients at risk for AKI. In patients with early signs of hyperinflammation and "cytokine storm," possible strategies such as dexamethasone treatment or cytokine removal need to be explored further.

However, large clinical trials are needed to test the risks and benefits of rigorous interventions in COVID-19 patients specifically at risk of AKI.

In a retrospective study of SARS-CoV-2 infected patients, who were quarantined at the Tongji Hospital, Wuhan, China, from January to February 2020, including 24 patients who were critically ill and 126 who were severely ill, Chen et al 18 reported that approximately 20% of these patients had signs of myocardial injury as reflected by increases in plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) levels. 11 Also, in a retrospective study of 52 critically ill COVID-19 patients, 15 (29%) of these patients had increased cTnI levels (ie, >28 pg/mL). 23 There is an estimated 12% of COVID-19 patients without pre-existing or known ZHENG ET AL. | 3 ischemic heart disease had elevated troponin levels or cardiac arrest during the hospitalization. 39 Particularly, cTnI levels were shown to be above the 99th centile upper normal limit in 46% of nonsurvivors, as compared to 1% of survivors. 40 The rise in cTnI levels together with proinflammatory markers, such as interleukin-6, lactate dehydrogenase (LDH), and D-dimer, might be indicative of cytokine storm or secondary hemophagocytic lymphohistiocytosis, in addition to isolated myocardial injury. However, based on preliminary data, the probability of fulminant myocarditis and cardiogenic shock is low. In addition to the ACE2-dependent infection within myocardium as demonstrated in mice models, 41 some investigators have also suggested a potential mechanism of myocardial injury due to COVID-19-induced cytokine storm that is mediated by a mixed T helper cell response in combination to hypoxia-induced excess of intracellular calcium causing cardiac myocyte cell death. 39, 40 Although it is uncertain whether SARS-CoV-2 may directly damage myocardial tissue and induce a major cardiovascular event, it is currently recommended that physicians should regularly monitor plasma cTnI and NT-proBNP levels in all COVID-19 patients. However, longer-term follow-up studies of cardiac function parameters of these infected patients (also by using transthoracic echocardiographic examination) are needed.

In addition to myocardial injury, arrhythmia is another facet of the cardiac involvement in COVID-19 that ranges from tachycardia to bradycardia and asystole.

A study of 121 COVID-19 patients showed that most of these patients had some type of arrhythmia, including 87 (71.9%) with sinus tachycardia unrelated to fever, 18 (14.9%) with bradycardia, and one patient with paroxysmal atrial fibrillation. 42 Another study has shown that cardiac arrhythmias occurred in 23 (16.7%) of 138 patients with SARS-CoV-2 infection, especially among those admitted to the ICU. 20 Another interesting observation was made among the vasoplegic population (comprising a syndrome of pathologically low systemic vascular resistance in the Wuhan cohort, where a higher proportion of critically ill COVID-19 patients/nonsurvivors had increased blood pressure values, which might contribute to arrhythmia, potentially explaining the pathological activity of SARS-CoV-2 infection. 19, 43 However, due to the retrospective nature of these data, it is difficult to ascertain whether the cause of this observed hypertension is due to physiological reactions to the viral illness, or it is a consequence of virus-induced derangements in ACE2 expression. Overall, this suggests that arrhythmia may be an important complication among patients with SARS-CoV-2 infection.

However, due to the very limited data available, arrhythmia type and corresponding electrocardiogram changes in patients with SARS-CoV-2 infection remain poorly defined. That said, these findings suggest that especially in patients with severe COVID-19, routine electrocardiogram monitoring is needed to closely monitor patients for paroxysmal tachycardias and pulse accelerations that do not match the patient's condition. 44 

In a study involving 99 SARS-CoV-2 infected patients quarantined at Wuhan Jinyintan Hospital, China, there were 11 (11%) deaths due to sudden cardiac arrest among those patients without a prior history of ischemic heart disease. 20 Jaundice is less common and was observed only in a few SARS-CoV-2 infected patients, who died during hospital admission; however, hypoalbuminemia and a longer PT were also observed amongst patients who subsequently died. Liver failure has also been observed with other organ failures in nonsurvivors of SARS-CoV-2 infection and thus, it is not easy at this time to quantify the excess risk of death attributable to liver failure alone. 23 The current evidence suggests that liver injury occurs more frequently among critically ill patients with COVID-19, who have other coexisting causes of liver damage, such as the use of potentially hepatotoxic therapies and the coexistence of systemic inflammatory response, respiratory distress syndrome-induced hypoxia, and multiple organ dysfunction. 53 Several studies showed that in patients with chronic liver diseases, [54] [55] [56] [57] [58] [59] (Table 1 ).

Currently, there is little information on the effect of SARS-CoV-2 infection on GI functions. A retrospective study from Wuhan, China, showed that GI symptoms were generally uncommon among 1099 SARS-CoV-2 infected patients, that is, approximately 5% had nausea and vomiting, while 3.8% had diarrhea. 21 However, among SARS-CoV-2 infected patients who had developed atypical clinical presentations, a substantial portion of these patients had GI symptoms. 68 with a lymphocyte count ranging from 0.5 to 0.3 × 10 9 /L. In contrast, higher white blood cell (ranging from 4.2 to 15.0 × 10 9 /L) and neutrophil counts from days 5 to 19, were reported in nonsurvivors compared to survivors. 20 

Multiple organ failure due to diffuse microvascular damage is an important cause of death in critically ill SARS-CoV-2 infected patients and is associated with cytokine release syndrome caused by an acute immune response. 18, [71] [72] [73] In a retrospective study of 138 confirmed COVID-19 cases, the risk of septic shock was nearly 30-fold higher among ICU patients (30.6%) than among non-ICU patients (1%). 20 In a multicenter Chinese study of 1099 COVID-19 patients, Guan et al 21 reported that septic shock was observed in one (0.1%) patient who was not severely affected and in 11 patients who were severely ill (6.4% most of whom did not survive); disseminated intravascular coagulation (DIC) was also observed in one nonsurvivor. In another study involving 99 patients with SARS-CoV-2 infection, septic shock occurred in 17% of nonsurvivors and in 4% of survivors, respectively; it is also important to note that the occurrence of septic shock among nonsurvivors often led to multiple organ dysfunction syndrome and death. 19 At present, the occurrence of septic shock, organ dysfunction, or organ failure among SARS-CoV-2 infected patients appears to be higher than that of DIC. However, a retrospective analysis of 21 deaths in SARS-CoV-2 infected patients recently reported that 71% of patients who died had DIC with a median time of 4 days from admission to presentation of DIC; whilst the incidence of DIC in surviving patients was 0.6%. 72 These data suggest that acute coagulation disorders and DIC in severe cases of SARS-CoV-2 infection ZHENG ET AL. n/a n/a n/a n/a n/a 6 (6.6%) Patients

Chen et al 18 Elevations in D-dimer levels may be indicative of thrombosis and can be used as a predictor for VTE (sensitivity: 85%, specificity: 88.5%, negative predictive value: 94.7%). 75 The use of anticoagulants is associated with decreased mortality among severe COVID-19 patients.

In a study of 99 severe COVID-19 patients who used low molecular weight heparin (LMWH) for 7 days or longer, the 28-day mortality of heparin users was significantly lower, compared to nonusers, especially amongst those with sepsis-induced coagulopathy score of ≥4 (40.0% vs 64.2%, P = .029). 77 As per recommendations by the American College of Chest Physicians, in the absence of contraindications, thrombotic prophylaxis is recommended in all moderate and severe COVID-19 patients, while LMWH is preferred over direct oral anticoagulants. 79 In patients requiring ICU admission, therapeutic treatment of LMWH can be effective in reducing in-hospital mortality. There is a mixed recommendation for prolonged use of thromboprophylaxis after hospital discharge, 15 

Several factors may induce psychological disorders during quarantine.

History of psychiatric illness was found to be closely associated with anxiety and anger within 2 to 6 months for patients who were subject to release from quarantine. 91 Interestingly, healthcare workers reported more severe symptoms of post-traumatic stress when compared to controls (nonhealthcare workers) after being quarantined. 92 Unsurprisingly, after quarantine, healthcare workers also felt increased levels of stigmatization, having had more avoidance behaviors, reported higher lost in income, and felt more negatively affected psychologically. Among the various psychological effects include increased worry, anger, fear, frustration, guilt, isolation, loneliness, and nervousness. Although one study showed that a cut-off of 10 days of quarantine duration significantly influenced the outcome of psychological impact, 93 it is generally accepted that longer duration of quarantine is more likely to induce poorer psychological outcomes and mental health conditions. 89, 92, 93 Other factors attributable to adverse psychological effects include fear of infection (directed at self-condition or transmitting to others), 84 115 Whether the COVID-19 may also have similar adverse effects on the male reproductive system remains currently not known.

The prevention and control of the COVID-19 outbreak is well underway around the world and efforts must continue to target this virus. The present review article emphasizes that more careful surveillance and management of extrapulmonary complications of COVID-19 patients are needed. Indeed, this viral infection appears to adversely affect not only the respiratory system but also several other organ systems, including the urinary, cardiovascular, GI, and neurological systems. The COVID-19 pandemic has also caused tremendous anxiety and other psychological effects both in suspected and confirmed cases with SARS-CoV-2 infection, while it remains to be clarified if it also causes negative psychological effects on those who have been released from quarantine. However, further research is needed to better understand the underlying mechanisms linking SARS-CoV-2 with the occurrence of multiple extrapulmonary complications. In the meantime, we believe that the frontline multidisciplinary team should carefully monitor multiorgan functions, which may also be the key to the survival of infected patients. We suggest an improved knowledge of COVID-19 related extrapulmonary complications will help to develop better medical management strategies for these patients. 

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The authors declare that there are no conflict of interests. Ming-Hua Zheng http://orcid.org/0000-0003-4984-2631