Pulmonary Disorders and COVID-19
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COVID-19 Pulmonary Complications Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2] Usman Ali Akbar, M.B.B.S.[3]
Overview
Covid-19 infection is associated with pulmonary complications such as acute respiratory distress syndrome, pneumonia, pulmonary embolism, hypoxemia, superinfection, respiratory failure, and increased mortality in patients with an underlying pulmonary disease such as chronic obstructive pulmonary disease (COPD).
Complications
Acute respiratory distress syndrome
Pneumonia
Pulmonary embolism
In May 2020, various autopsies studies revealed pulmonary embolism to be the common cause of death in COVID-19 infected patients. These patients in their mid-70s had preexisting medical conditions such as cardiac diseases, hypertension, diabetes, and obesity. These studies highlight the role of hypercoagulability as the main contributor to the fatality in these patients. Various studies have described Virchow's triad to be the main component of the hypercoagulable state in these patients.
Pathogenesis
As data on COVID-19 has been incomplete and evolving, the pathogenesis of pulmonary embolism has not yet been completely understood. Various contributors to the pathogenesis of pulmonary embolism in these patients are listed as follows
Endothelial cells dysfunction
- It has been proposed that endothelial cells contribute towards the initiation and propagation of ARDS by changing the vascular barrier permeability, increasing the chance of procoagulative state that leads to endotheliitis and infiltration of inflammatory cells in the pulmonary vasculature.
- It has been proposed that COVID-19 can directly affect endothelial cells leading to widespread endotheliitis. SARS-CoV-2 also binds to the ACE2 receptors which alter the activity of ACE2.
- Reduced ACE2 activity leads to activation of kallikrein-bradykinin pathway, which increases vascular permeability.
- The activated neutrophils migrate towards the pulmonary endothelial cells and produce cytotoxic mediators including reactive oxygen species.
Stasis
Most hospitalized critically ill immobile COVID-19 patients are prone to stasis of blood flow leading to another contributor towards the pathogenesis of pulmonary embolism.
Hypercoagulable state
Various clinical studies have reported different prothrombotic factors in patients who are critically ill and are hospitalized due to COVID-19. These studies report various key lab factors that play an important role in the pathogenesis of pulmonary embolism.
- Elevation of d-dimers
- Elevation of C-reactive protein
- Elevated factor VIII and von Willebrand factor
- Decrease in Antithrombin level
- Increased fibrinogen levels
Clinical Features
Pulmonary embolism can present with no symptoms to shock and even sudden cardiac arrest. The most common symptoms that were observed in Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) trial include
- dyspnea that is sudden in onset at rest or exertion (73%)
- pleuritic pain (44%)
- calf or thigh pain (44%)
- calf or thigh swelling (41%)
- cough (34%)
Diagnosis
Prompt diagnosis of PE in COVID-19 patient is difficult in this regard that various symptoms of COVID-19 overlap with that of pulmonary embolism. American Society of Hematology provides following guidelines regarding the diagnosis of pulmonary embolism.
- Normal d-dimers level in a patient with low to moderate pretest probability is sufficient to rule out the diagnosis of PE. D-dimers level is usually elevated in COVID-19 patients. This is not applicable in a patient with a gh pretest probability.
- In patient with suspected PE with symptoms like hypotension, tachycardia and sudden drop in oxygen saturation with a high pretest probability of PE, computed tomography with pulmonary angiography is used for the diagnosis. Contraindication to the use of CTPA warrants investigation with ventilation/perfusion scan.
Treatment
Prophylaxis
All hospitalized patients with COVID 19 should get proper venous thromboembolism prophylaxis in the absence of any contraindication of anticoagulation.
- In ICU setting, empiric use of intermediate or therapeutic dose anticoagulation should be instituted.
- In non-ICU setting, all hospitalized patients should be treated with prophylactic low dose molecular weight heparin.
Acute Pulmonary embolism
- Full dose anti-coagulation is appropriate for diagnosed pulmonary embolism. Fibrinolytic therapy is usually started unless there is contraindication. e.g, massive PE, acute stroke and acute myocardial infarction.
Outpatient treatment
- Critically ill patients that have recovered from COVID-19 and had a documented VTE are usually given a minimum 3 months of anticoagulation.
- Patient not admitted to hospitals but at risk of VTE, such as prior VTE episode, recent surgery, prolonged immobilization are usually given prophylactic dose of Rivaroxaban 10 mg daily for 31 days or 39 days.
Hypoxemia
Superinfection
Pulmonary hypertension
Respiratory failure
Increased mortality in COPD patients
- According to a study conducted in China, having an underlying comorbidity such as chronic obstructive pulmonary disease (COPD) conferred a mortality hazard ratio of 2.681, even after adjusting for smoking status.