An Emergency Department Approach to Thrombocytopenia
Aside from the hematocrit, the platelet count tends to be the second most ignored lab value that is displayed on a CBC. This is often the case because most of the time the platelet count is normal or close enough to normal that it does not really change management of our patients. It’s not until that lab value comes back in red or abnormal that we pay any attention to it, but even then the etiologies for low platelet count is so vast that we often do not know how to approach it.
Platelets as First Responders:
In our bloodstream, we have anywhere between 150,000 to 450,000 platelets/ mm^3 circulating around. They originate from our bone marrow through megakaryocytes, which are the precursor to platelets. One megakaryocyte can produce upwards to 1,000 to 5,000 platelets each. Our bone marrow receives signal from the immune system via thrombopoietin and IL-6 to stimulate more production. Their job requires them to be the first responders to any vascular insult or damage to blood vessels by forming that temporary plug in primary hemostasis.
Thrombocytopenia is not necessarily what brings the patient to the ED, unless they were referred by their primary care physician it or made aware of it prior to arrival. This is because the presentation for thrombocytopenia ranges widely. Patients can present with vague symptoms like fever and loss of appetite or present with the more classic petechiae1/purpura2, mucosal bleeding, or spontaneous bleeding. There is no predilection for age or gender as any patient can present with low platelets.
Before launching into further investigation for thrombocytopenia, it is important to look at the patient’s previous lab results to ascertain their baseline platelet count. The platelet count can often times qualify as thrombocytopenic in patients with sepsis, so these patients need their platelet count trended daily, however this is something that is hard to do in the Emergency Department and more suited for the floors.
Decreased Megakaryocyte Production (EtOH, thiazide diuretics, chemotherapy, linezolid, toxin, infections, leukemia)
Review past medical history, social history, and medication
Decreased Thrombopoietin (Liver Disease)
History Assess for manifestations of cirrhosis Hepatic Panel, PT/PTT
Splenic Sequestration 1. Portal HTN (Liver Disease) 2. Felty Syndrome (Rheumatoid arthritis)
Portal HTN: 1. Same as above Felty Syndrome: 1. Detailed history / physical 2. Rheumatoid Factor and anti-cyclic citrullinated peptide antibodies
Disseminated Intravascular Coagulopathy (DIC): systemic activation of blood coagulation that results in generation of microthrombi diffusely eventually leading to end organ dysfunction.
Detailed History and Physical exam Labs: PT/PTT, INR, Fibrinogen, D-Dimer
Thrombotic Thrombocytopenic Purpura: ADAMSTS13 is a metalloproteinase that cleaves multimers of von Willebrand Factor (vWF). vWF is a protein that links platelets and the blood vessel wall in coagulation. Without proper ADAMSTS13 function, there are large multimers of vWF that are prone to coagulation, especially in small vessels.
Labs: CBC, ADAMSTS13 activity assay, LDH, Haptoglobin Call Hematology to assess for microangiopathic hemolytic anemia (MAHA) Tx: plasmapheresis
Hemolytic Uremic Syndrome: Triad of MAHA, thrombocytopenia, and acute renal failure seen in children and adults. Caused by shiga-toxin producing bacteria, such as E.coli.
History and Physical Exam; CBC, Chem 8, GI pathogens panel, LDH, Haptoglobin Treatment: Supportive Care
Heparin Induced Thrombocytopenia: Heparin administration leads to formation of Heparin- Platelet Factor 4 complexes. Immune system produces antibodies against HPF4 complexes. Typically seen 4 days after Heparin is started.
Review medications list Labs: Serotonin Release Assay, Anti Platelet 4 antibody test Tx: Stop Heparin. Start Argatroban or Bivalirudin
Massive Fluid Resuscitation/Exchange Transfusion/ECMO
Immune Thrombocytopenic Purpura (ITP): Body produces antibodies that attack platelets. There are numerous autoimmune causes such as Systemic Lupus Erythematous (SLE).
Diagnosis of exclusion Acute: seen more often in children after a viral infection. Treatment is supportive care. If actively bleeding: Steroids, IVIG Chronic: seen more often in adults. Supportive Care If life threatening, then consider platelet transfusion, steroids, IVIG
Medications (Non Immune ITP)
Culprits: beta lactam antibiotics, NSAIDs, Sulfonamides, Phenytoin, Valproic Acid, Gold
Malfunctioning Cardiac Valves
Gestational Thrombocytopenia: This is the most common cause of thrombocytopenia in pregnancy. Typically occurs in the 3rd trimester with spontaneous resolution after delivery. However, low platelets can be associated with other diseases in pregnancy such as pre-eclampsia, HELLP syndrome. If you are able to rule out HELLP and pre-eclampsia, then there is no need to further investigate gestational thrombocytopenia.
Leukemia: CBC will show either leukocytosis or leukopenia. However, if there is low WBC and evidence of DIC, then the diagnosis becomes acute promyelocytic leukemia, which is an oncologic emergency. These patients need to be started on All-Trans Retinoic Acid, receive a consultation from Hematology/Oncology. Tranfusion is indicated here if the platelet count is < 10 or < 50 with bleeding and invasive procedures.
Pseudothrombocytopenia: in-vitro sampling problem. Occurs when the anticoagulant used for testing blood samples causes a clumping of platelets, which mimics a low platelet count. Hematology/Oncology can review blood smears and help rule out pseudothrombocytopenia.
The decision to admit rarely depends on the platelet count. The whole patient presentation needs to be taken into account before a patient is admitted. However, there are certain criteria that might help you decide between admission vs discharge. These are listed as follows:
1. Severe Thrombocytopenia (< 20 )
2. Platelet count >50% from baseline
3. Suspected leukemia, TTP/HUS, or DIC
4. Active bleeding
Williamson DR, Albert M, Heels-Ansdell D, et al. Thrombocytopenia in critically ill patients receiving thromboprophylaxis: frequency, risk factors, and outcomes. Chest 2013; 144:1207.
Darshak Vekaria, MD is a current PGY-1 in Emergency Medicine at Stony Brook University Hospital.