Ian Garrahy

Coronavirus disease of 2019 (COVID-19) is the respiratory viral infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Despite being a primary respiratory illness, it is commonly complicated by systemic involvement of the vasculature leading to arterial and venous thrombosis. In this review, we will focus on the association between COVID-19 and thrombosis. We will highlight the pathophysiology of COVID-19 coagulopathy. The clinical manifestations of COVID-19 vasculopathy will be discussed with a focus on venous and arterial thromboembolic events. COVID-19 vasculopathy and disseminated intravascular coagulation (DIC) are distinguished within, as well as areas of controversy, such as “long COVID”. Finally, the current professional guidelines on prevention and treatment of thrombosis associated with SARS-CoV-2 infection will be discussed.

Autoimmune hemolytic anemia (AIHA) is a well-recognized phenomenon of non-Hodgkin lymphoma, albeit with only few cases described with mantle cell lymphoma (MCL). The characteristics of such cases can improve understanding and management of AIHA in this type of lymphoma. To that end, we describe herein two cases of patients with MCL who presented with AIHA, with comparison to nine previously described cases in literature.

Acute portal vein thrombosis represents a less common type of venous thromboembolism, even among the prothrombotic complications of coronavirus disease 2019 (COVID-19). Such complications are primarily reported during the active phase of infection. The case here describes acute portal vein thrombosis following resolution of COVID-19 in a 44-year-old male who presented with abdominal pain. Abdominal imaging identified portal and other splanchnic vein thromboses. Studies for hypercoagulable conditions were negative. Polymerase chain reaction was negative for severe acute respiratory syndrome coronavirus-2; however, IgG serology was positive. The case highlights the importance of considering thrombotic complications, particularly splanchnic vein thromboses, in patients with recent COVID-19.

We report a case of a middle-aged female who presented with altered mental status, hypotension, and hypoglycemia and was diagnosed with secondary adrenal insufficiency. She was also found to have elevated troponin I on initial evaluation with diffuse T wave inversions on electrocardiogram. Transthoracic echocardiogram revealed ejection fraction of 38% with apical akinesia. Subsequent left heart catheterization revealed clean coronary arteries. She was diagnosed with typical Takotsubo cardiomyopathy secondary to adrenal insufficiency. She was managed with IV hydrocortisone with resolution of symptoms. This article adds to the select few cases in the literature of the association of Takotsubo cardiomyopathy resulting from secondary adrenal insufficiency.

Langerhans cell histiocytosis (LCH) is a rare malignancy most commonly characterized by histiocytic infiltration of bone. LCH lesions in the skull place the adjacent central nervous system (CNS) at risk for involvement, which can manifest as central diabetes insipidus (CDI) when there is infiltration of the hypothalamic-pituitary axis. We present a case of a 39-year-old female who presented with polyuria and polydipsia for 1 year and left-sided hearing loss, gait instability, and nystagmus for 5 days. She was found on laboratory evaluation to have CDI and underwent left cortical mastoidectomy for a destructive peripherally enhancing mastoid lesion seen on MRI brain. Pathology revealed CD1a and S100+ LCH and the patient was subsequently discharged to begin outpatient chemotherapy with vinblastine and prednisone. The patient’s CDI was diagnostic of CNS involvement, making her LCH multisystem through the infiltration of both the skull and hypothalamic-pituitary structures. As CDI can be seen in up to 25% of single-system LDH, and up to 50% of multisystem cases, radiologic studies to evaluate for osteolytic skull lesions must be considered as part of the evaluation for LCH when CDI has been diagnosed.

AL amyloidosis is due to deposition of protein derived from immunoglobulin light chain fragments. It is a systemic disorder in which deposition of plasma proteins can adversely affect function of the heart, liver, kidneys, and peripheral nerves. Deposition in the heart results in a decrease in the amplitude of the electrical activity of the heart and can be an early clue to the diagnosis. A 63-year-old male admitted for volume overload was found to have nephrotic range proteinuria, progressive renal insufficiency (Creatinine 4.0 increased from his baseline 0.9), and hypoalbuminemia. On exam, he had diffuse anasarca and peripheral neuropathy. A renal biopsy showed AL amyloidosis, lambda related, involving the glomeruli, interstitium, and arterial walls. Bone marrow biopsy showed 30% plasma cells with lambda light chain predominance. Serum free light chains were elevated. Lamda was 11.50 mg/dL and kappa was 5.12 mg/dL. In retrospective review of his chart, an EKG with low voltage and anterior pseudo-infarct pattern was first apparent on an admission for stroke two years prior. Echocardiogram showed mild concentric left ventricular hypertrophy. The patient was started on chemotherapy with Bortezomib. The differential of a low-voltage EKG includes many common pulmonary and chest wall (COPD, obesity) as well as pericardial diseases (effusions), but also important rarer infiltrative diseases including sarcoidosis and amyloidosis. Amyloidosis of the heart can cause progressive irreversible heart failure, but its progress can be altered if identified early. Physicians should consider amyloidosis when faced with a low-voltage EKG along with systemic symptoms including nephrotic range proteinuria, peripheral neuropathy, hepatosplenomegaly, and macroglossia.

Radiation recall dermatitis (RRD) is an inflammatory skin reaction that develops in a previously quiescent radiation field triggered most commonly by chemotherapy, particularly anthracyclines and taxanes. Radiation-recall dermatitis secondary to antibiotic therapy is quite rare. The patient is 61-year-old female with a history of squamous cell carcinoma of the left breast treated with neoadjuvant carboplatin, paclitaxel, and anthracycline chemotherapy followed by surgery and subsequent whole breast radiation 6040 cGy. Eight years after completion of her radiation she developed diffuse redness of the left breast after two doses of nitrofurantoin taken for a urinary tract infection. On examination, vital signs were stable and she had an erythematous and excoriated rash on her left breast that clinically appeared to be cellulitis. Given her clinical history, coupled with the temporal relationship of starting an antibiotic, strong consideration was given for antibiotic-induced RRD. Nitrofurantoin was discontinued, and the rash resolved completely within several days. This case demonstrates an example of RRD which is the development of an acute inflammatory skin reaction of a previously irradiated area most commonly triggered by chemotherapeutic agents. This case highlights antimicrobial therapy as a rare cause of RRD and underscores the importance of considering RRD in a patient presenting with an acute rash over a previously irradiated area while on antimicrobial therapy.