While in labor, a 37-year-old woman developed acute dyspnea, hypoxemia, and tachycardia. Transthoracic echocardiography demonstrated severe right ventricular dilation and dysfunction, raising the suspicion of acute pulmonary embolism. The patient indeed had bilateral pulmonary embolism, necessitating percutaneous thrombectomy. Her course was complicated by another saddle pulmonary embolus, heparin-induced thrombocytopenia, and COVID-19 infection. This clinical case illustrates the importance of prompt diagnosis of acute pulmonary embolism in a peripartum female patient, the multidisciplinary approach of management, and how to approach clinical complications such as heparin-induced thrombocytopenia. Furthermore, long-term management in acute pulmonary embolism is presented.

UNASSIGNED: Heparin-induced thrombocytopenia (HIT) is an immune-mediated complication that occurs in a small percentage of patients exposed to heparin. Concerns of HIT are particularly high in patients undergoing cardiac procedures requiring cardiopulmonary bypass, as they are exposed to high doses of heparin intraoperatively. Our aim was to identify and assess the hospital courses of patients who were diagnosed with HIT during readmission following cardiac surgery.
UNASSIGNED: A retrospective review of patients who underwent open cardiac surgical procedures from June 2017 through October 2019 was performed. Of these, we identified patients who were newly diagnosed with HIT upon readmission. HIT positivity was defined as a positive anti-PF4 antibody screening test, plus a positive serotonin release assay.
UNASSIGNED: Of the 2496 patients identified, 13 patients were HIT positive on index admission and were excluded. Of the remaining 2483 patients, 351 were readmitted within 30 days. Six were newly diagnosed with HIT during readmission, 5 of whom presented with thrombotic complications. One patient was readmitted with thrombocytopenia and was started on argatroban; the remaining 5 did not have a significantly lower platelet count on readmission. Of the 12 patients readmitted for venous thromboembolism, 4 tested positive for HIT.
UNASSIGNED: HIT can have a delayed appearance following open heart surgery. Venous thromboembolism appears to be a significant indicator for HIT during readmission, even in the absence of thrombocytopenia. This may support the use of non-heparin anticoagulation for cardiac surgery patients readmitted with thromboembolism until HIT status is determined.

Anti-glomerular basement membrane disease (anti-GBM disease) associated with renal and lung lesions has a poor prognosis. Diffuse alveolar hemorrhage (DAH) is a complication that worsens anti-GBM disease prognosis. We report a rescue case using veno-venous extracorporeal membrane oxygenation (VV-ECMO) for diffuse alveolar hemorrhage due to isolated pulmonary anti-GBM disease; a rare anti-GBM syndrome. A 30-year-old Japanese female with no past medical history. Presented with acute hypoxemic respiratory failure requiring mechanical ventilation. Progressive deterioration and refractory hypoxemia prompted therapy with VV-ECMO. Serum anti-GBM antibody confirmed the diagnosis of anti-GBM disease. Multi-modal systemic therapy with pulse-dosed methylprednisolone, plasma exchange, and rituximab resulted in significant clinical improvement. VV-ECMO for 10 days was uncomplicated. Renal replacement therapy was not required. The patient was extubated on day 18 and discharged from the hospital after 45 days. VV-ECMO supportive therapy for DAH with refractory respiratory failure was demonstrated to be effective pending definitive diagnostic and therapeutic management in this case of isolated pulmonary anti-GBM disease.

UNASSIGNED: Coronavirus disease 2019 (COVID-19) is associated with a hypercoagulable state. Limited data exist informing the relationship between anticoagulation therapy and risk for COVID-19 related hospitalization and mortality.
UNASSIGNED: We evaluated all patients over the age of 18 diagnosed with COVID-19 in a prospective cohort study from March 4th to August 27th, 2020 among 12 hospitals and 60 clinics of M Health Fairview system (USA). We investigated the relationship between (1) 90-day anticoagulation therapy among outpatients before COVID-19 diagnosis and the risk for hospitalization and mortality and (2) Inpatient anticoagulation therapy and mortality risk.
UNASSIGNED: Of 6195 patients, 598 were immediately hospitalized and 5597 were treated as outpatients. The overall case-fatality rate was 2•8% (n = 175 deaths). Among the patients who were hospitalized, the inpatient mortality was 13%. Among the 5597 COVID-19 patients initially treated as outpatients, 160 (2.9%) were on anticoagulation and 331 were eventually hospitalized (5.9%). In a multivariable analysis, outpatient anticoagulation use was associated with a 43% reduction in risk for hospital admission, HR (95% CI = 0.57, 0.38-0.86), p = 0.007, but was not associated with mortality, HR (95% CI=0.88, 0.50 - 1.52), p = 0.64. Inpatients who were not on anticoagulation (before or after hospitalization) had an increased risk for mortality, HR (95% CI = 2.26, 1.17-4.37), p = 0.015.
UNASSIGNED: Outpatients with COVID-19 who were on outpatient anticoagulation at the time of diagnosis experienced a 43% reduced risk of hospitalization. Failure to initiate anticoagulation upon hospitalization or maintaining outpatient anticoagulation in hospitalized COVID-19 patients was associated with increased mortality risk.
UNASSIGNED: No funding was obtained for this study.

A young woman presented with an acute ST-segment elevation myocardial infarction. Her clinical course was complicated by cardiogenic shock and acute renal failure. Work-up revealed thrombocytopenia and hemolytic anemia. A diagnosis of atypical hemolytic-uremic syndrome was made on the basis of clinical and pathological findings. (Level of Difficulty: Intermediate.).

A 54-year-old woman with a mechanical mitral valve replacement presented with recurrent admissions for pneumonia and pulmonary edema. Multimodality imaging revealed mobile masses on the prosthesis and discrepant point of care and inpatient international normalized ratio levels owing to antiphospholipid antibody cross-reactivity on the outpatient assay. The prosthetic valve thromboses resolved with therapeutic anticoagulation. (Level of Difficulty: Beginner.).

The recognition of the rare but serious and potentially lethal complication of vaccine induced thrombotic thrombocytopenia (VITT) raised concerns regarding the safety of COVID-19 vaccines and led to the reconsideration of vaccination strategies in many countries. Following the description of VITT among recipients of adenoviral vector ChAdOx1 vaccine, a review of similar cases after Ad26.COV2·S vaccination gave rise to the question whether this entity may constitute a potential class effect of all adenoviral vector vaccines. Most cases are females, typically younger than 60 years who present shortly (range: 5-30 days) following vaccination with thrombocytopenia and thrombotic manifestations, occasionally in multiple sites. Following initial incertitude, concrete recommendations to guide the diagnosis (clinical suspicion, initial laboratory screening, PF4-polyanion-antibody ELISA) and management of VITT (non-heparin anticoagulants, corticosteroids, intravenous immunoglobulin) have been issued. The mechanisms behind this rare syndrome are currently a subject of active research and include the following: 1) production of PF4-polyanion autoantibodies; 2) adenoviral vector entry in megacaryocytes and subsequent expression of spike protein on platelet surface; 3) direct platelet and endothelial cell binding and activation by the adenoviral vector; 4) activation of endothelial and inflammatory cells by the PF4-polyanion autoantibodies; 5) the presence of an inflammatory co-signal; and 6) the abundance of circulating soluble spike protein variants following vaccination. Apart from the analysis of potential underlying mechanisms, this review aims to synopsize the clinical and epidemiologic features of VITT, to present the current evidence-based recommendations on diagnostic and therapeutic work-up of VITT and to discuss new dilemmas and perspectives that emerged after the description of this entity.

We report the case of a 35-year-old pregnant woman (gravida 3, para 1) with antithrombin deficiency who was successfully treated with apixaban. She had a history of heparin-induced thrombocytopenia and venous thromboembolic events. Pregnancy was confirmed while the patient was having anticoagulant therapy for a persistent thrombus. Choice of anticoagulation during her pregnancy was limited because of her antithrombin deficiency: heparin was not an option because of her history of heparin-induced thrombocytopenia; antithrombin-dependent anticoagulant drugs were not an option because of her antithrombin deficiency, and she preferred outpatient management. Despite the fact that there are no reports of its use in pregnant women, we selected apixaban (10 mg/day), a direct Xa inhibitor, as the best solution. No progression of thrombus was noted during the pregnancy. The newborn baby had no external congenital anomalies, intracranial hemorrhage, or bleeding tendency. Thus, apixaban may be a candidate for anticoagulant therapy in pregnant women with a history of venous thromboembolic events and heparin-induced thrombocytopenia.