Version May 2024
INTRODUCTION — A proportion of patients with coronavirus disease 2019 (COVID-19) can become critically ill due to either the development of acute respiratory distress syndrome (ARDS) or complications of the disease itself.
This topic will discuss the epidemiology, clinical features, and prognosis of adult patients who become critically ill with COVID-19. General clinical features of patients with COVID-19 and management of the critically ill nonintubated and intubated patient with COVID-19 are discussed separately. (See "COVID-19: Clinical features" and "COVID-19: Management of the intubated adult" and "COVID-19: Respiratory care of the nonintubated hypoxemic adult (supplemental oxygen, noninvasive ventilation, and intubation)".) (Related Pathway(s): COVID-19: Anticoagulation in adults with COVID-19.)
EPIDEMIOLOGY — Reports during the initial phase of the pandemic suggest that among those with COVID-19, up to 20 percent develop severe disease requiring hospitalization [1-9]. Among those who are hospitalized, up to one-quarter need intensive care unit (ICU) admission, representing approximately 5 to 8 percent of the total infected population [2,3,8-17]. The spectrum of severity and case fatality rates associated with COVID-19 are discussed separately. (See "COVID-19: Clinical features", section on 'Spectrum of severity and fatality rates'.)
Rates of ICU admission vary. Differences in the rates of ICU admission may relate to local, cultural, and geographic differences in practice and admission criteria for ICU as well as differences in population characteristics within the region served by the ICU. For example, among cohorts from China, rates of ICU admission in hospitalized patients ranged from 7 to 26 percent [2,3,8,10]. Similarly, the proportion of ICU admissions in Italy were between 5 and 12 percent, representing 16 percent of all hospitalized patients [11,12]. In the US and Canada, rates of ICU admission have ranged from 5 to 81 percent [9,13,14,18].
Admission rates to the ICU may be decreasing as the pandemic progresses [15,19,20]. In an analysis of a second surge in Houston, Texas, a smaller proportion of hospitalized patients were admitted to the ICU compared with the first surge (20 versus 38 percent) [15]. The reasons for this are unclear but may include increased adherence to prevention strategies, the development of new therapies, increased comfort with respiratory management outside of the ICU (eg, increased use of noninvasive respiratory support), and altered demographics of infected populations (eg, younger population) [19,20].
Since vaccination is effective at preventing severe disease and death, admission rates to the ICU are likely lower in the United States [21,22]. However, the impact of new viral strains that have the potential for increased virulence is unknown and is under continued investigation. (See "COVID-19: Vaccines" and "COVID-19: Epidemiology, virology, and prevention", section on 'Virology'.)
Males have comprised a disproportionately high number of critical cases in multiple cohorts worldwide (up to three-quarters in early cohorts from China) [10,16,17]; however, some cohort studies have suggested a more even proportion of critically ill men and women [12,13].
Patients in select racial or ethnic minority population may also have a higher risk of severe disease including high rates of hospitalization, ICU admission, and mortality [23,24].
CLINICAL FEATURES IN CRITICALLY ILL PATIENTS — Discussion in this section is limited to clinical features in those who are critically ill. General clinical features of COVID-19 patients are discussed separately. (See "COVID-19: Clinical features".)
Rate and risk of progression to critical illness — Retrospective studies of critically ill patients have suggested that among patients who develop critical illness (ie, acute respiratory distress syndrome [ARDS]), onset of dyspnea is relatively late (median 6.5 days after symptom onset), but progression to ARDS can be swift thereafter (median 2.5 days after onset of dyspnea) [2,3,13,25-27].
Age appears to be the major risk factor that predicts progression to ARDS [5,13,14,27,28]. Others include comorbidities (eg, obesity, hypertension, metabolic syndrome), male sex, socioeconomic background, high fever (≥39°C), blood type, and select laboratory and viral features. These risk factors are discussed in detail separately. (See "COVID-19: Clinical features", section on 'Risk factors for severe illness'.)
For patients with COVID-19 who are critically ill and admitted to the ICU, the length of stay is often prolonged (eg, one to four weeks), unless the reason for admission is for an acute issue that is rapidly reversible (eg, rapid atrial fibrillation, heart failure, hypovolemia). (See 'Length of stay' below.)
Clinical features — Patients who later become critically ill with COVID-19 may present with similar initial respiratory symptoms to those with less severe illness (eg, fever, cough, dyspnea) (see "COVID-19: Clinical features"). Specifically, among those who are critically ill:
●Profound acute hypoxemic respiratory failure from ARDS is the dominant finding [1-3,13,16,17,26,28-36].
●Hypercapnia is rare (unless associated with, for example, a chronic obstructive pulmonary disease exacerbation or narcotic overdose).
●Fevers tend to wax and wane during ICU admission, particularly in the first few days to week.
●The need for mechanical ventilation among those who are critically ill and admitted to the ICU ranges from 20 to 100 percent [2,9,13,14,16-18,28,31,36]. The wide range likely reflects differences in practice, criteria for intubation, and populations served by the ICU. A small proportion require extracorporeal membrane oxygenation. Data suggest decreased rates of mechanical ventilation over time [37], which may be due to changes in patient- and/or practice-level factors.
Patients may also present with features associated with complications of COVID-19 (eg, dehydration and hypovolemia, delirium, stroke, venous thromboembolism, arrhythmia, acute myocardial infarction, heart failure, low urine output from acute renal insufficiency). (See 'Complications' below and "COVID-19: Clinical features", section on 'Acute course and complications'.)
COMPLICATIONS — Common complications of COVID-19-related acute respiratory distress syndrome (ARDS) include acute kidney injury (AKI), elevated liver enzymes, delirium/encephalopathy, cardiac injury (eg, cardiomyopathy, arrhythmia, and sudden cardiac death), and thrombosis [38-42]. 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) [2].
Acute kidney injury — AKI is common among critically ill patients with COVID-19, and a proportion of those require renal replacement therapy (eg, 15 to 30 percent) [18,40]. As an example, in one New York cohort of critically ill patients, one-third required renal replacement therapy for AKI [40]. Further details are provided elsewhere. (See "COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension", section on 'Acute kidney injury'.)
Gastrointestinal complications — Gastrointestinal complications also appear to be more common in patients with ARDS from COVID-19 compared with patients who have ARDS for other reasons (74 versus 37 percent) [43]. These include elevated aminotransferases (55 percent), severe ileus (48 percent), and mesenteric ischemia (4 percent). Further details are provided separately. (See "COVID-19: Gastrointestinal symptoms and complications".)
Neurologic complications — Neurologic complications in critically ill patients are common [44-48]. Among critically ill patients, delirium or encephalopathy is the most common complication and 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. Other common complications include acute ischemic stroke, myositis, Guillain-Barré, and focal neuropathy. Encephalitis is rare [47]. The neurologic complications of COVID-19 are described in detail separately. (See "COVID-19: Neurologic complications and management of neurologic conditions".)
Cardiac injury — Among critically ill patients, cardiac injury may be a complication that is concurrent with the respiratory illness, or a late complication, developing after the respiratory illness improves. (See "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")".)
A high rate of cardiomyopathy was noted among critically ill patients with COVID-19 in one United States cohort (33 percent) in Washington state [13]. In another New York City cohort, 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 [49]. Another study reported that 14 percent of critically ill patients with COVID-19 had a cardiac arrest, with age and comorbidities as risk factor s [50]. In a Philadelphia cohort, among 700 patients with COVID-19, there were 9 cardiac arrests, all of which occurred in the ICU [42].
Cardiac complications of COVID-19 are discussed in detail elsewhere. (See "COVID-19: Arrhythmias and conduction system disease" and "COVID-19: Myocardial infarction and other coronary artery disease issues" and "COVID-19: Cardiac manifestations in adults".)
Thrombosis — A hypercoagulable state resulting in arterial and venous thromboses is common in critically ill patients with COVID-19. While some studies suggest an incidence as high as 30 percent, the true incidence is unknown. Further details are provided separately. (See "COVID-19: Hypercoagulability", section on 'ICU'.)
Sepsis, shock, multi-organ failure, secondary infections
●Sepsis, shock, multi-organ failure – In critically ill patients with COVID-19, sepsis, shock, and multi-organ failure occur but appear to be less common compared with non-COVID-19-related ARDS. The need for vasoactive agents is variable. In a cohort study from Wuhan, China, 35 percent of patients received vasoactive agents [2]. In contrast, in a case series from New York City, 95 percent of patients who received mechanical ventilation required vasopressor support [30]. In our experience, hypotension is unusual in the absence of a specific cause, and the need for vasoactive agents is typically driven by sedation medications, cardiac dysfunction, or secondary bacterial infection. (See "Evaluation and management of suspected sepsis and septic shock in adults".)
●Secondary infections – Critically ill patients with COVID-19 are at risk of developing secondary infections, although robust data are limited. Secondary infections include pneumonia (eg, bacterial, fungal), vascular catheter infections, urinary tract infections, Epstein Barr and cytomegalovirus reactivation, and rarely strongyloides reactivation [2,51-53].
Rates vary among studies. As an example, in one retrospective Italian study of 774 critically ill patients with COVID-19, 46 percent had hospital acquired infections, of which one third were multidrug-resistant (MDR) bacteria [52]. Half of hospital acquired infections were ventilator-associated pneumonia (mostly Gram-negative bacteria and Staphylococcus aureus) and one-third were bloodstream infections. As expected, such infections prolonged hospitalization and increased mortality. In contrast, in a cohort of intubated patients from China, hospital-acquired pneumonia, in many cases with resistant pathogens, was reported in 12 percent [2]. Whether rates have increased with the more widespread use of dexamethasone and other immunomodulating agents is unknown.
Several reports have described presumptive invasive aspergillosis among immunocompetent patients with ARDS from COVID-19, although the frequency of this complication is uncertain [54-58]. In one prospective study of 108 patients on mechanical ventilation for COVID-19 in Italy, probable aspergillosis was diagnosed in 30 (28 percent) based on elevated serum or bronchoalveolar lavage (BAL) galactomannan levels, growth of Aspergillus on BAL cultures, or a cavitary infiltrate without other cause [57]. Another registry study reported that 2 percent of COVID-19 patients had proven invasive Aspergillus, while 14 percent had probable infection and 3 percent had possible infection [58].
Cases of mucormycosis have also been reported, primarily from India, among critically ill and other hospitalized patients with COVID-19. This is discussed in detail elsewhere. (See "Mucormycosis (zygomycosis)", section on 'Coronavirus disease 2019-associated'.)
Similarly, cases of reactivated strongyloides have also been described, which is discussed in detail separately. (See "Strongyloidiasis".)
Pneumothorax and barotrauma — Pneumothorax can occur in critically ill patients with COVID-19 who are spontaneously breathing or mechanically ventilated [2,59-66]. Patients with COVID-19-related ARDS on mechanical ventilation may be at increased risk of barotrauma compared with other patients with ARDS, although data are variable with rates ranging from 2 to 40 percent. Rates may be higher in patients receiving invasive ventilation compared with noninvasive ventilation, and those on invasive ventilation are at an increased risk of death compared with non-COVID-19 patients with barotrauma [62,65,66]. (See "Pneumothorax in adults: Epidemiology and etiology", section on 'Necrotizing lung infections' and "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)
LABORATORY FINDINGS — Laboratory findings in critically ill patients with COVID-19 include leukopenia or leukocytosis, lymphopenia, and elevated D-dimer, aminotransferases, lactate dehydrogenase, and ferritin levels. Although these can also be seen with less severe COVID-19, the abnormalities are typically more profound in critically ill patients [1,3,29]. Critically ill patients with COVID-19 may also have an elevated procalcitonin level. (See "Procalcitonin use in lower respiratory tract infections" and "COVID-19: Clinical features", section on 'Laboratory findings'.)
Some patients with severe COVID-19 have laboratory evidence of an exuberant inflammatory response, similar to cytokine release syndrome (CRS), with persistent fevers, elevated inflammatory markers (eg, D-dimer, ferritin, interleukin-6 [IL-6]), and elevated proinflammatory cytokines (eg, IL-6 and tumor necrosis factor [TNF]); these laboratory abnormalities have been associated with poor prognosis [67]. However, some studies suggest that the elevated levels of proinflammatory cytokines associated with critical COVID-19 are lower than those in patients with septic shock [68]. Rare cases of hemophagocytic lymphohistiocytosis (HLH) have also been described [69]. Further details regarding CRS and HLH are provided separately. (See "Cytokine release syndrome (CRS)" and "Clinical features and diagnosis of hemophagocytic lymphohistiocytosis".)
The presence of antiphospholipid antibodies has also been described; however, they are mostly of the IgA subclass, and the clinical significance is unclear [70]. Abnormal coagulation parameters which are commonly seen in COVID-19 patients (eg, elevated D-dimer, prolonged prothrombin time) are also discussed separately. (See "COVID-19: Hypercoagulability", section on 'Evaluation of atypical laboratory findings' and "Diagnosis of antiphospholipid syndrome".)
Data suggest that measuring procalcitonin (PCT) or C-reactive protein (CRP) upon admission to identify bacterial superinfection is not useful [71].
IMAGING — Typical imaging findings do not appear to be different in mild or severe cases of COVID-19 (eg, ground-glass opacification with or without consolidative abnormalities, consistent with viral pneumonia, minimal or no pleural effusions) [2,72-79]. Chest radiography, computed tomography, and lung ultrasonography findings are described separately. (See "COVID-19: Clinical features", section on 'Imaging findings'.)
Our approach to bedside ultrasonography is similar to that of other critically ill patients [80]. (See "Indications for bedside ultrasonography in the critically ill adult patient".)
PATHOLOGY — The lung pathology of COVID-19 pneumonia in critically ill patients remains under study. The pathology in most patients appears consistent with that of acute respiratory distress syndrome (ARDS).
Most autopsy reports describe hyaline membrane changes and microvessel thrombosis suggestive of early ARDS (ie, exudative and proliferative phases of diffuse alveolar damage [DAD]) [81-92]. Other findings include bacterial pneumonia (isolated or superimposed on DAD) and viral pneumonitis [84,88]. Less common findings include acute fibrinous organizing pneumonia (AFOP; in the late stages) [93], amyloid deposition in the heart and lung, and rarely alveolar hemorrhage and vasculitis [88]. (See "Interpretation of lung biopsy results in interstitial lung disease", section on 'Diffuse alveolar damage' and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Pathologic diagnosis and stages'.)
Evidence of pulmonary thrombosis and thromboembolism has also been reported in autopsy series [84,88,89,94]. (See "COVID-19: Hypercoagulability".)
Distant organ involvement has also been seen with the demonstration of virus in organs other than the lung and, in some cases, acute tubular necrosis and a generalized thrombotic microangiopathy in the kidney [84,88]. (See "COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension".)
PROGNOSIS
Mortality — Several retrospective studies have reported variable mortality from COVID-19-related acute respiratory distress syndrome (ARDS) [1-3,15-18,26,28,29,32,33,35-37,95-102]. Mortality appears lower than that in patients with severe acute respiratory syndrome (SARS-CoV-1) or Middle East respiratory syndrome (MERS). The mortality from COVID-19 appears driven by the presence of severe ARDS, and ranges widely, from 12 to 78 percent with an average of 25 to 50 percent. However, death can occur from several other conditions including cardiac arrythmia, cardiac arrest, and pulmonary embolism. Limited data suggest that among those with ARDS, there is no difference in mortality between those who have COVID-19-related ARDS and those with non-COVID-19-related ARDS [102].
In resource-limited settings, mortality may be on the higher end of this range. One study of nearly 4000 patients from 64 intensive care units (ICUs) in 10 African countries reported a 30-day mortality of 48 percent [101]. Mortality ranged from 43 percent for patients referred from the emergency department to 51 percent in patients transferred from another facility.
Mortality may be changing as the pandemic progresses [15,19,37,99,103-106]. In an analysis of patients during a resurgence of COVID-19 in Houston, Texas, in-hospital mortality was lower during the second surge compared with the first surge (5 versus 12 percent) but the difference in ICU mortality was not significant (23 versus 28 percent) [15]. In another French cohort of over 4000 critically ill patients, mortality decreased from 42 to 25 percent over a four-month period during the pandemic [99]. In a United States analysis of 468 patients with COVID-19-related critical illness from March 1, 2020 to May 11, 2020, the mortality decreased from 44 to 19 percent [37]. Another US single-center analysis of three consecutive surges reported between March 2020 and December 2020 a similar reduction between surge 1 and surge 2 (29 percent versus 25 percent) [106]. However, mortality was highest in the third surge (35 percent). Changes in mortality may be reflective of different patient populations, altered comorbidity burdens, staffing burdens of institutions, and/or growing expertise with COVID-19 care. However, reported rates may not accurately reflect differences in practice patterns over the course of the pandemic (eg, early versus late timing of intubation, increasing use of noninvasive modalities).
Risk factors for death — Globally, the consistent major risk factor associated with death in critically ill patients with COVID-19 is older age (≥64 years) [2,3,11,12,14,17,18,26,28,36,97,99-101,107-109]. In one study of over two thousand critically ill patients, age ≥80 years was associated with and 11-fold increased risk of death [109]. Other risk factors associated with death among critically ill patients include the following [2,3,6,9,11,14,17,26,28,29,33,97,99,109-117]:
●The development of ARDS, particularly severe ARDS, and the need for mechanical ventilation
●Comorbidities (eg, obesity, chronic cardiac and pulmonary conditions, hypertension, diabetes, chronic kidney disease, renal replacement therapy, cancer)
●Markers of inflammation or coagulation (eg, fever, D-dimer level >1 microg/mL admission, elevated fibrin degradation products, prolonged activated partial thromboplastin and prothrombin times)
●Select laboratory studies (eg, worsening lymphopenia, neutrophilia, troponin elevation)
●Male sex
●Severity of organ dysfunction on admission
●Right ventricular dysfunction
In resource-limited settings, risk factors for death were similar but also included HIV infection (odds ratio [OR] 1.9) and delay in admission due to resource limitations (OR 2.0) [101].
The rapidity of symptom progression does not appear to predict a worse outcome [2].
While high fever was associated with a higher likelihood of developing ARDS (hazard ratio [HR] 1.77, 95% CI 1.11-2.84), it appears to be associated with a lower likelihood of death (HR 0.41, 95% CI 0.21-0.82) [2,28], a phenomenon that has been noted previously in non-COVID-19-related critical illness. (See "Fever in the intensive care unit", section on 'Outcomes'.)
It is unclear whether vaccination decreases the risk of death in critically ill intubated patients with conflicting data on this issue [118,119].
Several prognostic models have been proposed but none is clearly superior nor accurately predicts deterioration or mortality to a great degree [120,121]. The preintubation sequential organ assessment score has been shown to perform poorly as a predictor of death in patients with COVID-19 [122].
Length of stay — Length of ICU stay and mechanical ventilation is prolonged for patients with COVID-19-related ARDS compared with non-COVID-19-related ARDS, with many COVID-19 patients remaining intubated for at least one to two weeks or longer [17,123,124]. In one retrospective review of 148 patients with COVID-19 the mean time to discontinuation of mechanical ventilation was 33 days and length of stay 55 days [125]. However, the number of days free of mechanical ventilation and length of ICU stay may have improved since the introduction of effective directed therapies for COVID-19 [126]. However, in resource-limited settings, one study reported a mean length of stay of seven days, which may reflect a difference in practice given the limitations at such facilities. Readmission rates among those who have recovered from COVID-19 are discussed separately. (See "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")".)
Long-term sequelae — Prolonged symptoms are common during recovery from critical illness due to COVID-19, and many patients suffer from post-acute COVID-19 syndrome (PACS). PACS shares overlapping symptoms with post intensive care syndrome (PICS), which is a syndrome that many patients experience after discharge from the ICU. In our experience, the rate of long-term complications in critically ill patients with COVID-19 may be higher than usual due to the prolonged nature of intubation and higher use of neuromuscular blockade and sedatives, with or without concurrent glucocorticoid administration. Long-term sequelae that can be seen in patients with COVID-19, including outcomes in tracheostomized patients, and evaluation for and management of PICS are discussed separately. (See "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")" and "Post-intensive care syndrome (PICS) in adults: Clinical features and diagnostic evaluation".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: COVID-19 – Index of guideline topics".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (See "Patient education: COVID-19 overview (The Basics)" and "Patient education: COVID-19 vaccines (The Basics)".)
SUMMARY AND RECOMMENDATIONS
●Rates of ICU admission – Patients with coronavirus disease 2019 (COVID-19) can become critically ill, typically due to the development of acute respiratory distress syndrome (ARDS) and/or complications of the disease. Among patients hospitalized with COVID-19, up to one-quarter require intensive care unit (ICU) admission representing 5 to 8 percent of the total infected population. However, rates of ICU admission vary, reflecting differences in practice, admission criteria, and population characteristics in the region served by the ICU. Rates may change as the pandemic progresses. (See 'Epidemiology' above.)
●Clinical features – Patients who are critically ill with COVID-19 initially present with similar symptoms to those with mild or moderate illness (eg, fever and cough). Onset of dyspnea is relatively late (median 6.5 days after symptom onset), but progression to ARDS with profound hypoxemic respiratory failure can be swift thereafter. Age appears to be the major risk factor that predicts progression to ARDS. A proportion require mechanical ventilation but the rate varies among ICUs (20 to 100 percent). (See 'Clinical features in critically ill patients' above.)
●Complications – Patients may also present with the features associated with the complications of COVID-19. Common complications include the following:
•Acute kidney injury (AKI; one third or more) (see 'Acute kidney injury' above and "COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension", section on 'Acute kidney injury')
•Elevated liver enzymes and other gastrointestinal complications (two-thirds or more) (see 'Gastrointestinal complications' above and "COVID-19: Gastrointestinal symptoms and complications")
•Delirium/encephalopathy (two-thirds) (see 'Neurologic complications' above and "COVID-19: Neurologic complications and management of neurologic conditions")
•Cardiac injury (one-third) (see 'Cardiac injury' above and "COVID-19: Cardiac manifestations in adults" and "COVID-19: Arrhythmias and conduction system disease" and "COVID-19: Myocardial infarction and other coronary artery disease issues")
•Thrombosis (see 'Thrombosis' above and "COVID-19: Hypercoagulability", section on 'ICU')
Less common complications include the following:
•Sepsis, shock, multi-organ failure, secondary infections (see 'Sepsis, shock, multi-organ failure, secondary infections' above and "Evaluation and management of suspected sepsis and septic shock in adults")
•Pneumothorax or barotrauma (see 'Pneumothorax and barotrauma' above and "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults")
●Laboratory and imaging findings – In critically ill patients with COVID-19, laboratory findings include leukopenia or leukocytosis, lymphopenia, and elevated D-dimer, aminotransferases, lactate dehydrogenase, and ferritin; procalcitonin can be elevated as well. Chest imaging findings (predominantly bilateral peripherally distributed ground-glass opacification with or without consolidation) are similar to those seen in less severe illness. (See 'Laboratory findings' above and 'Imaging' above and "COVID-19: Clinical features", section on 'Laboratory findings' and "COVID-19: Clinical features", section on 'Imaging findings'.)
●Lung pathology – The majority of patients who are critically ill due to COVID-19 have lung pathology consistent with ARDS (ie, diffuse alveolar damage). A small proportion have bacterial pneumonia, acute fibrinous organizing pneumonia, amyloid deposition, hemorrhage, or vasculitis. (See 'Pathology' above and "Interpretation of lung biopsy results in interstitial lung disease", section on 'Diffuse alveolar damage' and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Pathologic diagnosis and stages'.)
●Prognosis – For critically ill patients with COVID-19, the prognosis is poor with mortality ranging from 25 to 50 percent that is largely driven by severe ARDS. However, death can occur from several other conditions including cardiac arrythmia, cardiac arrest, and pulmonary embolism. The highest rates of death occur in those ≥64 years. As the pandemic progresses, mortality may be decreasing for several reasons. Length of stay appears to be longer than that in patients with non-COVID-19-related ARDS. Long-term sequelae may also be higher in this population. (See 'Prognosis' above and "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")".)
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