COVID-19 Associated Coagulopathy/Disseminated Intravascular Coagulation

There is still much to be learned about the COVID-19 associated coagulopathy.

The first and ultimate reason for excellent documentation is improved patient care through clear communication between providers and an accurate picture of the patient’s medical situation and treatment course.

It is essential to capture all the comorbidities conditions seen in patients who are hospitalized with COVID-19. A variety of clinical scenarios appear in our hospitals across the country with symptoms ranging from mild to ventilated patients to death. Since coding advice regarding COVID-19 is frequently updated, it is recommended to check official coding sources to ensure any advice published here is still current. If the provider documents a definitive COVID-19 diagnosis but after discharge, the test results come back negative, it is recommended to query the provider for clarification.

The provider should be allowed to reconsider the diagnosis based on the new information. If the provider confirms of diagnosis of COVID-19 even though the test results are negative, confirmed COVID-19 (U07.1) should be reported.

It is essential to note that the incubation period for COVID-19  falls within 14 days following exposure, with most cases occurring approximately 4 to 5 days after exposure. Per recent studies, common comorbid conditions identified an infected patient with COVID-19 are as follows:

• Patients that are on medication that suppresses immunity, such a sore steroid usage
• Diabetes
• Cardiac disease
• Sickle cell crisis or people with preexisting lung diseases
• Diseases that involve immunosuppression

CDI professionals need to review the record for associated conditions/complications of COVID-19 such as the following:

• ARF
• ARDS
• Acute Hepatic Failure
• Cardiac Complications
• Thrombocytopenia
• Sepsis/Septic Shock
• Cytokine release syndrome
• Hemophagocytic Lymph histiocytosis (HLH)
• Coma
• Encephalopathy
• Delirium
• Coagulopathy

Furthermore, it is essential to review the record carefully for documentation and clinical indicators for all comorbid conditions. CDI professionals need to review the chart thoroughly and remember that each patient should be approached as being unique in their presentation.

Patients being admitted for novel coronavirus (COVID-19) might present with various manifestations and complications. It is important to report all of them because it impacts the severity of illness and risk of mortality. Some COVID-19 patients have been reported to experience coagulopathy and thrombosis, deep vein thrombosis, pulmonary embolism, and even stroke.

Furthermore, suppose there is evidence of both bleeding and clot formation. In that case, the patient may have DIC (disseminated intravascular coagulation), an MCC that will increase the severity of illness (SOI) and risk of mortality (ROM).

COVID-19 associated coagulopathy is reported using codes U07.1, COVID-19, and Other specified coagulation defects (D68.8). If skin failure due to the COVID-19 associated coagulopathy is documented, report COVID-19 (U07.1), Other specified coagulation defects (D68.8), and Other disorders of the skin and subcutaneous tissue in diseases classified elsewhere (L99).

If specified as disseminated intravascular coagulation (DIC) due to COVID-19, assign U07.1 and Disseminated intravascular coagulation (D65). Not all COVID-19 associated coagulopathy progresses to DIC. Up to 70 percent of the most severely ill patients with SARS-CoV2 have features of disseminated intravascular coagulation (DIC).

Unlike sepsis-associated DIC, patients with COVID-19 associated DIC have relatively mild thrombocytopenia (100 × 10⁹/L to 150 × 10⁹/L) and would usually not meet classic ISTH criteria for DIC.

It is now clear that among hospitalized patients with COVID-19, respiratory failure, pneumonia, and sepsis are frequent complications, with some patients developing multiorgan failure and severe systemic disease. The most common end-organ dysfunctions linked with sepsis:  Shock, Acute kidney injury, encephalopathy, disseminated intravascular coagulation (DIC), non-diabetic hyperglycemia, liver dysfunction, etc.

Furthermore, patients critically ill with COVID-19 would present with elevated D-dimers’ baseline characteristics and prolonged prothrombin time.  The strong association between COVID-19 and vascular coagulopathy may suggest that multiple molecular pathways are dysregulated during the diseases’ clinical progression and thus contribute to the associated thrombosis. The latest data suggest the incidence of thrombotic complications is between 16–49 percent  in patients with COVID-19 admitted to intensive care.

Critically ill patients have higher risks of developing thromboembolism because of the combination of platelet activation, immobility, systemic inflammation, and stasis of blood flow.

In some hospitalized patients with COVID-19, as occurs in sepsis more generally, an overproduction of early response proinflammatory cytokines such as interleukin (IL)-6, IL-1, and TNFα, leads to a cytokine storm. This hyperinflammatory state can cause lung injury, including damage to the microvasculature and endothelial dysfunction, which could trigger haemostatic derangements and the generation of pulmonary thrombi.

It is recommended to monitor haemostatic markers such as prothrombin time, platelet count, and D-dimers in all patients presenting with COVID-19. It is important to determine if the hemostatic changes are a consequence of severe inflammation or if they are specific effects mediated by the virus. In hospitalized COVID-19 patients with sepsis, an overproduction of early response proinflammatory cytokines such as IL-6, TNF alpha, and IL-1 leads to a cytokine storm. This hyperinflammatory state can cause lung injury, which could trigger hemostatic derangements and the generation of pulmonary thrombi. On the other hand, the virus can directly or indirectly interfere with coagulation pathways causing systemic thrombosis.

Antiviral treatments are generally effective early in the disease course, while treatment strategies targeting coagulation and inflammation might be more promising for patients with severe COVID-19. Some studies suggest that low molecular weight heparin (LMWH) can improve prognosis in patients with severe COVID-19 meeting SIC criteria or elevated D-dimers. Other anticoagulants are being tested, such as antithrombin three, factor 10 A, and complement inhibitors.

There is still much to be learned about the COVID-19 associated coagulopathy, but the fast and ongoing collaboration worldwide makes for a hopeful outcome.

Programming Note: Listen to Dr. Kuqi report this story live today during Talk Ten Tuesdays, 10-10:30 a.m. Eastern.