Hematologic disorders associated with COVID-19: a review.

Coronavirus disease 2019 is caused by severe acute respiratory syndrome coronavirus 2. Primarily an infection of the lower respiratory tract, it is now well known to cause multisystem abnormalities. Hematologic manifestations constitute a significant area of concern. Severe acute respiratory syndrome coronavirus 2 infects monocytes and endothelial cells leading to a complex downstream cascade, cytokine storm, and eventual intravascular thrombosis. Coronavirus disease 2019 causes lymphopenia, neutrophilia, and thrombocytopenia. Prophylactic anticoagulation is vital in patients with coronavirus disease 2019, as its effect on the coagulation system is associated with significant morbidity and mortality. The disease can cause both arterial and venous thromboses, especially pulmonary embolism and pulmonary microthrombi. A high index of suspicion is indispensable in recognizing these complications, and timely institution of therapeutic anticoagulation is vital in treating them. Virus-induced disseminated intravascular coagulation is uncommon but shares some similarities to sepsis-induced disseminated intravascular coagulation. Marked elevations in hematologic biomarkers such as lactate dehydrogenase, D-dimer, ferritin, and C-reactive protein are associated with worse outcomes. Understanding the pathophysiology and recognizing factors associated with poor prognosis are crucial in improving patient outcomes with coronavirus disease 2019.

Disseminated Mycobacterium abscessus infection and native valve endocarditis.

Mycobacterium abscessus is a rapidly growing mycobacterium. It rarely causes disseminated infection or endocarditis. A 55-year-old male with a history of hepatitis C, liver cirrhosis, intravenous drug use (last use was four years ago), and chronic back pain presented with a three-week history of a right calf nodular lesion. He did not have a fever, chills, rash, dyspnea, or cough. Laboratory data showed mild leukocytosis. Computed tomography of the chest revealed bilateral cavitating nodules. Skin biopsy, sputum, and blood cultures grew Mycobacterium abscessus. Therapy with meropenem, tigecycline, and amikacin was initiated. He was re-admitted with worsening lower back pain. A lumbar magnetic resonance imaging showed destructive changes of L4 and L5 vertebral bodies concerning for osteomyelitis. Blood culture and bone biopsy grew Mycobacterium abscessus again. An echocardiogram was performed due to persistent bacteremia, which revealed large vegetation on the tricuspid valve and small vegetation on the mitral valve. Therapy was changed to eight weeks of amikacin, with cefoxitin and imipenem for twelve months based on drug susceptibility. Treatment of disseminated Mycobacterium abscessus is challenging due to antibiotic resistance. Typically, multidrug therapy is warranted with at least three active drugs. In severe valvular endocarditis, valve replacement may be required.