Fatal iliopsoas and rectus sheath hemorrhage in a critically ill patient with COVID-19 on therapeutic anticoagulation.

Pulmonary embolism and thrombosis are two common postmortem findings in novel coronavirus disease 2019 (COVID-19), the fact which led experts to include anticoagulants in the standard management of COVID-19. However, at least until now, no guidelines stated the exact safe yet optimal dose of anticoagulants. We report a case of a 65-year-old man admitted to our hospital with severe acute respiratory distress syndrome due to COVID-19. He showed remarkable improvement during the first 10 days of treatment at our facility but subsequently developed spontaneous iliopsoas hemorrhage (IPH). We discontinued antithrombotic and anticoagulant agents as soon as we confirmed the IPH from the abdominal computed tomography scan. His condition worsened even after he received adequate blood transfusion sets and eventually developed disseminated intravascular coagulation. Due to the limitation of our hospital, we could not perform stent grafting and angiographic embolization. He finally died 6 days after the occurrence of IPH. To the best of our knowledge, this is the first case of COVID-19 with IPH in Indonesia. As a developing country, many hospitals in Indonesia do not have stent grafting and angiographic embolization. This condition urges the dose recommendation for anticoagulant therapy to provide safe and efficient management for COVID-19.

Pulmonary embolism in patients with severe COVID-19 treated with systemic low-dose thrombolytic therapy: A case series.

Coronavirus disease 2019 (COVID-19) has been associated with respiratory failure and high mortality. Hypercoagulability and thromboembolic complications have been found in a high percentage of patients amongst which, pulmonary embolism (PE) is the most common. Currently, there are no guidelines on using thrombolysis therapy in COVID-19 patients who developed PE. We present five survivors aged 30-75 years old with confirmed COVID-19. All cases were proven by computed tomography pulmonary angiogram (CTPA) to have PE treated with low-dose recombinant tissue plasminogen activator (rtPA). PE should be suspected in all COVID-19 patients with rapid worsening of dyspnea, desaturation, unexplained shock, and increased level of D-dimer and fibrinogen. In our cases, PE developed despite preventative anticoagulation regimens with low molecular weight heparin. After thrombolytic therapy, all patients showed improvement in partial-arterial-oxygen-pressure to inspired oxygen-fraction ratio (arterial partial pressure of oxygen/inspired oxygen fraction ratio). D-dimer showed elevation after thrombolytic therapy and decreased in the following days. Fibrinogen levels decreased following thrombolytic therapy. Current anticoagulation regimens seem insufficient to halt the course of thrombosis, and thrombolytic therapy may be beneficial for patients with severe COVID-19 and PE. Systemic thrombolysis therapy is a double-edged sword, and clinicians must balance between benefit and risk of bleeding.

Case reports of cerebral sinus venous thrombosis in COVID-19 patients.

BACKGROUND: Coronavirus disease 2019 (COVID-19) pandemic has started in December 2019 and still ongoing. The disease has been expanding rapidly with a high variety of phenotypes from asymptomatic, mild respiratory tract infection, multiple organ system dysfunction, and death. Neurological manifestations also appear in patients with COVID-19, such as headache, seizures, a decrease of consciousness, and paralysis. The hypercoagulable state in patients with COVID-19 is associated with the thromboembolic incident including ischemic strokes, venous thromboembolism, pulmonary artery embolism, and many further. Cerebral sinus venous thrombosis (CSVT) is a rare neurovascular emergency that is often found in critically ill patients. We report two cases of CSVT with different onsets, neurologic manifestations, and prognoses. CASE PRESENTATION: Two cases of cerebral sinus venous thrombosis in COVID-19 patients were reported, following respiratory, hematology, and coagulation disarrangements, which was triggered by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The first patient, which was presented with a seizure, had hypertension and diabetes mellitus as comorbidities. The latter case had no comorbidity but showed more severe presentations of COVID-19 such as brain and lung thrombosis, although already had several days of intravenous anticoagulant administrations. These two cases also have a different course of disease and outcomes, which were interesting topics to study. CONCLUSIONS: CSVT is one of the neurological complications of the COVID-19 when the brainstem venous drainage is involved. Despite successful alteration to the negative result of SARS-CoV-2 through the rt-PCR test, thrombogenesis and coagulation cascade continuing. Therefore, a high level of neutrophil to lymphocyte ratio (NLR), D-dimer, fibrinogen, and C-reactive protein (CRP) are paramount indicators of poor prognosis.

Progressive COVID-19-Associated Coagulopathy Despite Treatment with Therapeutic Anticoagulation and Thrombolysis.

BACKGROUND Coronavirus Disease 2019 (COVID-19) has been associated with a hypercoagulability state. Clinical presentation can range from asymptomatic to severe illness and mortality. Thrombotic complications in COVID-19 have been associated with mortality. The incidence of systemic hypercoagulation in COVID-19 is associated with the process of severe inflammation. The majority of severely ill patients have developed coagulopathy, and this condition is associated with poor outcomes. CASE REPORT A 72-year-old man presented with respiratory symptoms and was diagnosed with a COVID-19 infection. He presented with tachypnea, tachycardia, increased blood pressure, and 74% peripheral oxygen saturation under 15 L/min oxygen per non-rebreather mask. Initial laboratory test results showed severe hypoxemia as per blood gas analysis (pH 7.42, pCO2 23 mmHg, pO2 43 mmHg, HCO3 15 mmol/L, base deficit -9 mmol/L), with increased procalcitonin, high-sensitivity C-reactive protein, D-dimer, fibrinogen, creatine kinase myocardial band, and Troponin I. He subsequently developed thrombosis of the pulmonary arteries and multiple branches of the pulmonary vein despite therapeutic anticoagulation. We initiated heparin therapy (average dose 25 191 units per day, mean activated partial thromboplastin time, 64.35 seconds). Radiological investigations revealed multiple thromboses on pulmonary arteries and pulmonary veins, as well as multiple locations of brain infarction. Rescue thrombolytic therapy was given, but unfortunately, the patient died due to multiple end-organ failures. CONCLUSIONS Controlling coagulopathy, and thrombolytic therapy type and timing, are critical issues, and new strategies must be sought to lower its morbidity and mortality rates further.