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Venous thromboembolism (VTE) can present in a variety of different clinical settings and in a diverse, comorbid patient population, both of which will guide the clinician toward the appropriate therapeutic response. Patients who present with pulmonary embolism are at risk for hemodynamic instability, recurrence of VTE, cardiac comorbidities, and increased risk of overall mortality. Prognostication models have been clinically validated for risk stratification and prediction of mortality. Similar to pulmonary embolism, patients with deep vein thrombosis carry a higher risk of VTE recurrence and cardiac comorbidities. Consequently, VTE can be treated by a variety of methods such as anticoagulants or inferior vena cava filters, which bear their own risks and benefits. It is imperative that clinicians monitor patients for complications from VTE and the chosen therapy.

Venous thromboembolism (VTE) has a wide range of clinical presentations. Deep venous thrombosis may occur in upper or lower extremities or in visceral veins. Extremity deep venous thrombosis usually manifests with unilateral painful swelling in the limb, while visceral deep venous thrombosis manifestations vary on the basis of the involved organ. Pulmonary embolism classically manifests with sudden pleuritic chest pain and unexplained dyspnea. Superficial thrombophlebitis usually presents with acute inflammation around a palpable thrombosed superficial vein. Risk factors of VTE are either inherited or acquired. The inherited causes of VTE tend to be familial and more common in younger patients. The common acquired risk factors of VTE include previous history of venous thrombosis, immobilization, recent surgery or trauma, malignancy, and pregnancy. Identifying high-risk patients for VTE based on these risk factors is the cornerstone to provide the prophylactic treatment to prevent thrombotic events.

Venous thromboembolism includes both deep vein thrombosis and pulmonary embolism. They pose a significant risk for morbidity and mortality. In an appropriate clinical setting, invasive interventions, including administration of thrombolytics, anticoagulation, and placement of vena cava filter, are warranted. Bleeding, postthrombotic syndrome, recurrence, and filter-associated complications are few of the complications of this disease. More recently, chronic thromboembolic pulmonary hypertension has gained clinical interest in patients with pulmonary embolism and has warranted close follow-up.

Hemoptysis, or coughing of blood, oftentimes triggers anxiety and fear for patients. The etiology of hemoptysis will determine the clinical course, which includes watchful waiting or intensive care admission. Any amount of hemoptysis that compromises the patient's respiratory status is considered massive hemoptysis and should be considered a medical emergency. In this article, we review introduction, definition, bronchial circulation anatomy, etiology, and management of massive hemoptysis.

Pulmonary embolism covers a wide spectrum of presentation from an asymptomatic individual to a life-threatening medical emergency. It is of paramount importance to appropriately risk stratify patients with pulmonary embolism, particularly with those who present without hypotension. Right ventricular dysfunction can evolve after a patient has received a diagnosis of pulmonary embolism, necessitating aggressive measures rather than simple anticoagulation. In this review, we discuss definition, risk stratification, pathogenesis, diagnostic approach, and management, with particular focus on massive pulmonary embolism.

A 66-year-old woman presented with acute onset of fever, chills, and productive cough associated with right-sided chest pain. During a recent hospitalization for dyspnea, she had been diagnosed with Coombs-positive autoimmune hemolytic anemia and had been taking a tapering dose of prednisone starting approximately 6 weeks prior to admission. In the interim, her dyspnea had resolved on treatment with steroids. At the time of presentation, her prednisone dose was 40 mg. Additional medical history included VTE, for which the patient was receiving anticoagulation therapy, and steroid-induced diabetes mellitus. Many years earlier, she had been treated for TB in her home country. The patient had immigrated to Queens, New York, from a Nepalese village 8 years prior. While still in Nepal, she had worked on a farm and had been in close proximity to cows. In Queens, she lived with her family in a house with a small garden but had no pets. Recent travel included a visit to Nepal 9 months ago and a trip to Syracuse, New York, one month prior to presentation. She was a never smoker and did not consume alcohol.

A 47-year-old man with no significant past medical history, originally from Indonesia, was brought to the ED of an urban US medical center after being found collapsed on the sidewalk in respiratory distress and with an altered sensorium. Upon arrival to the ED, he was tachypneic, with increased work of breathing and an oxygen saturation of 88% on 100% nonrebreather mask, so he was immediately intubated. Following intubation, he became profoundly hypotensive, requiring aggressive crystalloid resuscitation and vasopressor support. Broad-spectrum antimicrobials were administered, including ceftriaxone, vancomycin, levofloxacin, and oseltamivir. Further history elicited subsequently from family members revealed that the patient had returned from a 2-week vacation in Indonesia 6 days prior to presentation. According to relatives, he appeared to be in his usual state of health upon his return and was not seen by anyone thereafter, but in the interim he reportedly had an episode of epistaxis, and text messages received from him became progressively more bizarre.