A 5-year-old girl is brought to the pediatric clinic by her mother. She reports that for the past week, her daughter has been very tired, lacks energy, sleeps more than usual, and has not had much of an appetite. Furthermore, there are unexplained bruises on her arms and legs. She was a full-term infant from an uncomplicated pregnancy and delivery. All immunizations are current. She has had only one childhood disease, measles, at 2 years of age.

A 29-year-old woman is admitted to the critical care unit following multiple traumatic injuries sustained in a motor vehicle accident. In the emergency department, her wounds are thoroughly debrided, cleansed, and sutured, and skeletal traction is applied for bilateral femoral fractures. During the first 24 hours of hospitalization, she remains in shock, requiring vasopressor support with dopamine as well as multiple transfusions of packed red blood cells.

Over the first several days, her condition stabilizes. However, on the fifth hospital day, staff observes new bleeding from multiple sites. Previously healed lacerations begin to ooze dark-red blood, and there is continuous bleeding from venipuncture and skeletal traction pin sites. She appears somnolent but remains oriented, though in moderate distress. Her vital signs show:

Peripheral pulses are present but weak, and scattered rhonchi are heard throughout the lung fields.

Laboratory testing reveals a platelet count of 66 ×10⁹/L, prolonged prothrombin and partial thromboplastin times, decreased fibrinogen, and markedly elevated fibrin degradation products and D-dimer. These findings, in the context of trauma and new bleeding, support a diagnosis of DIC.

Management focuses on supportive care and treatment of the underlying trauma-related triggers. The patient's hemodynamic status and bleeding are closely monitored, with serial laboratory evaluation of platelet counts, fibrinogen, and coagulation parameters. Because her presentation is dominated by bleeding rather than thrombosis, anticoagulation is not initiated. Instead, transfusion support is provided with platelets, fresh frozen plasma, and cryoprecipitate to replace clotting factors and stabilize hemostasis.

Throughout this period, the nursing team plays a central role in frequent assessment, ensuring comfort, monitoring for further bleeding, and promptly alerting the medical team to any changes in condition.

A 62-year-old man presents to the emergency department with sudden onset of abdominal discomfort followed by the passage of several large, black, tarry stools. He becomes diaphoretic and develops chest discomfort, reminiscent of his recent myocardial infarction.

Three weeks earlier, he sustained a non-ST-elevation myocardial infarction (NSTEMI), which was managed without complication. A submaximal exercise treadmill test before discharge revealed no residual ischemia. At discharge, he was prescribed aspirin, clopidogrel, and metoprolol.

On examination, the patient appears pale, diaphoretic, and uncomfortable. Physical examination notes:

The physician orders laboratory and cardiac testing, with the following results:

Based on the results of the assessment, the patient appears to be experiencing acute upper gastrointestinal bleeding, most likely from peptic ulcer disease exacerbated by dual antiplatelet therapy. His profound anemia (hemoglobin 5.9 g/dL) and orthostatic hypotension confirm significant blood loss leading to hemorrhagic anemia, complicated by myocardial ischemia due to reduced oxygen delivery.

The immediate focus in this patient is stabilization. Because he presents with profound anemia, orthostatic hypotension, and signs of cardiac strain, rapid intervention is required. Two large-bore intravenous lines should be placed, and isotonic fluids initiated to support perfusion while awaiting blood products. Given his hemoglobin level and the presence of ischemic symptoms, transfusion of cross-matched packed red blood cells is essential. In this setting, the threshold for transfusion is lower than in patients without cardiac disease, as the risk of ongoing ischemia outweighs the risks of transfusion.

Continuous cardiac monitoring is critical, as reduced oxygen delivery in the setting of recent myocardial infarction greatly increases the chance of recurrent ischemia or arrhythmia. Serial cardiac biomarkers should be followed to assess for evolving myocardial injury.

Because dual antiplatelet therapy contributes to his bleeding risk, aspirin and clopidogrel must be carefully reassessed in consultation with cardiology. Temporary interruption of clopidogrel may be necessary to control bleeding, but this decision must balance the risk of stent thrombosis or recurrent infarction against the acute risk of hemorrhage.

At the same time, urgent gastroenterology consultation is warranted for endoscopic evaluation and intervention. Endoscopy allows both identification of the bleeding source—likely a peptic ulcer given his medication history—and targeted therapy, such as epinephrine injection, thermal coagulation, or clip placement. A proton pump inhibitor infusion should be started promptly to promote clot stabilization and reduce the risk of rebleeding.

Overall, successful management requires close coordination between emergency medicine, gastroenterology, and cardiology teams to stabilize the patient, address the source of bleeding, and minimize the competing risks of hemorrhage and cardiac ischemia.

A 52-year-old man presents to his primary care physician with complaints of progressive fatigue over the past four to five months. Although he remains physically active, he has recently noticed shortness of breath during his daily jogs. He denies orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, melena, hematochezia, or hematemesis. He reports vague, intermittent left-sided abdominal discomfort unrelated to meals and acknowledges occasional use of over-the-counter ibuprofen for joint pain. There is no history of fever, chills, nausea, vomiting, or significant unintentional weight loss.

On physical examination, the patient weighs 205 lbs and is afebrile. He appears pale, with conjunctival and palmar pallor. There is no lymphadenopathy. Cardiac exam reveals a regular rate and rhythm with a soft systolic ejection murmur, likely flow-related. Lungs are clear to auscultation. The abdomen is soft, nontender, and without organomegaly. No peripheral edema, cyanosis, or clubbing is noted. Peripheral pulses are symmetric.

A 25-year-old African American man with a known history of sickle cell disease presents with a vaso-occlusive pain episode. He has required six hospital admissions over the past year for similar crises, most recently two months ago. Today, he reports severe abdominal and bilateral lower extremity pain, consistent with his prior episodes.

On assessment, he is febrile to 101°F, with a respiratory rate of 25 breaths per minute, blood pressure within normal limits, and a heart rate of 100 beats per minute. Lung auscultation reveals bronchial breath sounds and egophony at the right lung base. His oxygen saturation on 2 L/min oxygen via nasal cannula is 92%. In addition to his usual pain, he now reports pleuritic chest pain that worsens with inspiration.

Physical examination shows tenderness on palpation of the extremities but is otherwise unremarkable. Laboratory studies demonstrate leukocytosis, elevated reticulocyte count, and hemoglobin and hematocrit values slightly lower than his baseline. A peripheral smear reveals sickled and target cells.

Given the presence of chest pain, fever, hypoxemia, and abnormal lung findings, acute chest syndrome is suspected in addition to vaso-occlusive crisis.

The clinical presentation prompts an urgent diagnostic workup. A chest radiograph is ordered to assess for new infiltrates, as pulmonary involvement would confirm acute chest syndrome. Blood cultures are obtained to evaluate for possible infectious triggers, because infection is a frequent precipitant of both vaso-occlusive crisis and acute chest syndrome. Oxygenation is closely monitored with pulse oximetry, and arterial blood gases are considered to further assess the degree of hypoxemia. Laboratory studies, including a complete blood count, reticulocyte count, bilirubin, lactate dehydrogenase, and renal function, are obtained to establish a current baseline and guide ongoing management.

The initial management plan focuses on stabilizing the patient while addressing both pain and pulmonary complications. Supplemental oxygen is administered with a goal of maintaining oxygen saturation above 94%. Broad-spectrum intravenous antibiotics are initiated promptly in light of the fever and pulmonary findings, to cover both typical and atypical respiratory pathogens. Intravenous fluids are started to improve microvascular circulation, though careful monitoring is required to avoid fluid overload, which could worsen pulmonary status. Opioid analgesia is provided on a scheduled basis to ensure effective pain control, with close monitoring for respiratory depression. Incentive spirometry is introduced to promote lung expansion and reduce the risk of atelectasis, which is a known contributor to acute chest syndrome. The team prepares for possible red blood cell transfusion, either simple or exchange, should the patient's hypoxemia worsen, his hemoglobin fall significantly, or chest imaging reveal progressive infiltrates. Throughout care, hematology and pulmonology are engaged to provide coordinated, multidisciplinary management.