In this episode, we review three hematology cases. One case illustrates the work-up and treatment of immune thrombocytopenia (ITP).

Another case demonstrates how to diagnose and manage heparin-induced thrombocytopenia (HIT). And the final case is a patient who presented with anemia, a new mitral valve murmur, and mild splenomegaly.

Host David H. Henry, MD, reviews these cases with three residents from Pennsylvania Hospital in Philadelphia – Sheila De Young, DO; Ronak Mistry, DO; and Debika Shinohara, MD, PhD.

Case 1: Suspected ITP with Sheila De Young, DO

Patient presentation: A 50-year-old female with no past medical history and incidental platelet count of 4,000/microL (normal 150,000-450,000/microL [150-450 x 109/L]).

On physical exam, there was no lymphadenopathy, and the spleen was nonpalpable. She had obvious petechiae on her legs. A urine pregnancy test was negative. Her hemoglobin and white blood cell counts were normal via complete blood count.

• ITP definition:
  • Acquired thrombocytopenia caused by autoantibodies against platelet antigens.
  • One of the most common causes of thrombocytopenia in otherwise asymptomatic adults.
• To consider: Increased destruction, decreased production, and pseudothrombocytopenia
  • To ensure the platelet count is not falsely low (in the case of pseudothrombocytopenia), looking at a peripheral smear is helpful. If red blood cells and white blood cells appear normal, we can exclude pseudothrombocytopenia.
• Work-up:
  • We need to rule out secondary causes of thrombocytopenia such as HIV, hepatitis C, chronic lymphocytic leukemia, systemic lupus erythematosus, etc.
• Management/treatment:
  • In the acute setting, the treatment for ITP is intravenous immunoglobulin and steroids.
  • Long-term management of ITP includes steroids, splenectomy, thrombopoietin receptor agonists (romiplostim/eltrombopag), and rituximab.
• Case conclusion:
  • This patient was found to have ITP. Shared decision-making led to the patient receiving a thrombopoietin receptor.

Case 2: Possible HIT with Ronak Mistry, DO

Patient presentation:  A male with ischemic leg and creatinine phosphokinase greater than 4,000 units/L. His platelet count was 101,000/microL on admission, 70,000/microL on the second day, and 60,000/microL on the third day.

The patient was on prophylactic subcutaneous heparin for 48 hours, so the surgery team considered HIT to explain the drop in platelets.

• HIT definition:
  • A life-threatening complication of exposure to heparin.
  • Results from autoantibody directed against endogenous platelet factor 4 (PF4) in complex with heparin.
• To consider:
  • Determine baseline platelet count, what type of heparin the patient received, and look at when the heparin was administered in relation to when the platelet count dropped.
  • HIT is far less common in patients who receive subcutaneous heparin versus intravenous heparin.
  • Typically, we see a 50% decrease in platelet count 5-10 days following exposure to heparin.
• Work-up:
  • In the inpatient setting, it is important to consider other causes that predispose patients to thrombocytopenia (i.e., critical illness, medications).
  • Thrombocytopenia can represent a consumptive process of platelets secondary to tissue injury in the setting of elevated creatine phosphokinase.
• Diagnosis:
  • Enzyme-linked immunosorbent assays (ELISAs) can detect the presence of PF4-heparin antibody.
  • ELISA should be followed by a confirmatory test. The serotonin release assay is preferred among diagnostic tests for HIT.
• Management/treatment:
  • Stop heparin immediately.
  • Giving more platelets is not the solution. It increases a person’s risk for thrombotic events.
  • The patient needs to be placed on different anticoagulation, such as argatroban or fondaparinux, to carry them through this procoagulant time frame.
• Case conclusion:
  • HIT was ruled out in this patient.

Case 3: Anemia case with Debika Shinohara, MD, PhD

Patient presentation: A female, age 45 years, with a 4-month history of intermittent fevers and unintentional weight loss.

Her hemoglobin was 8 g/dL, but she had otherwise unremarkable blood work. On physical exam, she was found to have a new mitral valve murmur and mild splenomegaly.

• To consider:
  • Increased destruction versus decreased production of red blood cells.
  • Low reticulocyte count (