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 (