Learning Objectives
By the end of this section, you will be able to:
- Discuss the pathophysiology, risk factors, and clinical manifestations associated with thrombocytopenia
- Describe the diagnostics and laboratory values in thrombocytopenia
- Apply nursing concepts and plan associated nursing care for the patient with thrombocytopenia
- Evaluate the efficacy of nursing care for the patient with thrombocytopenia
- Describe the medical therapies for thrombocytopenia
Low platelet count syndrome, or thrombocytopenia, is an uncommon hematologic condition characterized by decreased numbers of platelets (thrombocytes) in the bloodstream, affecting three out of 100,000 people yearly in the United States (NORD, 2022). Platelets play an essential role in hemostasis, which is the physiological process that prevents and controls bleeding. Individuals with thrombocytopenia may have increased risk for bleeding as their platelet count decreases, resulting in difficulty creating blood clots and controlling hemostasis. Thrombocytopenia may either present as its own condition or be the result of other medical issues, including autoimmunity disorders, infections, or adverse drug reactions. The disorder may range in severity from mild cases with minimal symptoms to those posing significant risks of spontaneous bleeding. Management and treatment approaches depend upon the cause, level of platelet reduction, and associated symptoms. Consequently, early diagnosis and effective monitoring are key to providing optimal health-care services to patients with thrombocytopenia.
Pathophysiology of Thrombocytopenia
Platelet production is triggered in bone marrow by thrombopoietin, a protein released by the liver. Thrombocytopenia can have many causes: from bone marrow disorders that impair production of platelets, such as leukemia and myelodysplastic syndromes, to diseases that disrupt platelet survival over time. Immunological mechanisms may contribute to platelets being destroyed by the immune system and lead to immune thrombocytopenic purpura (ITP). Other causes include various infections, hereditary disorders, and overuse of certain medications, such as aspirin or heparin. Liver damage, from excessive alcohol intake, for example, can also cause a decrease in viable platelets, due to lower levels of thrombopoietin being produced by the liver.
Pathophysiology often includes disruption in the delicate equilibrium among platelet production, circulation, and removal, leading to fewer platelets in the bloodstream. The normal range of platelets for males and females is 150,000–400,000/μL blood) (NORD, 2022). Clinical manifestations can range from petechiae (pinpoint-sized spots on the skin) and bruising to more serious conditions like gastrointestinal or intracranial bleeding. Prompt recognition, thorough diagnostic evaluation, and targeted interventions are crucial for effectively managing thrombocytopenia and mitigating its risks of bleeding complications in affected individuals (Nicolas et al., 2023).
Heparin-Induced Thrombocytopenia
An immune-mediated side effect caused by exposure to heparin products is known as heparin-induced thrombocytopenia (HIT). HIT is characterized by a drop in platelet count and an increase in blood coagulability, which can manifest anytime from 1 to 14 days after exposure to heparin (Nicolas et al., 2023). An exaggerated immune response occurs due to antibodies produced against complexes composed of heparin and platelet factor 4 (PF4) proteins released by activated platelets. When heparin binds with PF4 proteins, an immune response triggers the production of antibodies, which attach themselves directly onto platelet surfaces, activating platelets to clot. This causes the platelet count to drop because they die off before they can be reproduced in the bone marrow. Because of its late onset in some instances, HIT may go unrecognized if a patient is discharged; therefore, occurrence may be difficult to detect.
Link to Learning
Learn more about the pathophysiology, diagnosis, and treatment of heparin-induced thrombocytopenia in this video.
Clinical Manifestations
HIT typically manifests as swelling at multiple points on the body surface, as the result of blood clot formation following the activation of PF4. HIT can be identified by an acute drop in platelet count, usually below 150,000 microliters; in severe cases, this can be as low as 50,000 microliters. Although most individuals with HIT do not experience bleeding directly, its adverse effect is an increased risk of arterial and venous thrombosis and subsequent arterial and venous clot formation resulting from hypercoagulability. These conditions may result in deep vein thrombosis (DVT), which is a type of venous thromboembolism; pulmonary embolism (PE); and potentially life-threatening conditions such as stroke or myocardial infarction (Nicolas et al., 2023). Because blood interacts with all tissues of the body, all organs and body systems may be affected, as shown in Table 16.4.
| System | Symptom |
|---|---|
| General | Fatigue |
| Integumentary | Ischemic limb necrosis and necrotic lesions Swelling and edema Warmth of skin in thrombotic areas |
| Neurologic | Anxiety, if there is a pulmonary embolism Headache, dizziness, cognitive changes, and disorientation from poor blood flow to the brain |
| Hematologic | Increased blood clotting vs bleeding |
| Cardiovascular | Hypotension |
| Respiratory | Dyspnea (shortness of breath) |
| Gastrointestinal | Abdominal tenderness |
| Renal | Hematuria |
| Musculoskeletal | Joint pain |
Diagnostics and Laboratory Values
Blood tests for markers related to hypercoagulability are used to diagnose HIT. A “4-Ts” scoring system is commonly used to estimate risk potential of disease; 4-T scores less than 3 indicate a low probability for developing HIT (Lindholm & Perrotta, 2023). The four “Ts” assess degree of thrombocytopenia, thrombocytopenia timing, thrombosis, and thrombocytopenic cause. Additionally, laboratory tests such as enzyme-linked immunosorbent assays, as well as serotonin release assays can confirm antibodies specific for HIT.
Idiopathic Thrombocytopenic Purpura
More frequently referred to as immune thrombocytopenia, idiopathic thrombocytopenic purpura (ITP) is an autoimmune condition marked by an abrupt and significant drop in platelet count, leading to increased risks of bleeding and anemia. With ITP, the immune system erroneously recognizes platelets as foreign and produces antibodies to destroy them in the spleen and liver, which are key organs for filtering blood. Children typically experience acute ITP; in contrast, adult-onset ITP typically manifests chronically and requires ongoing management.
Clinical Manifestations
ITP may be related to other autoimmune disorders; therefore, it is important for providers to conduct a comprehensive evaluation and follow-up for patients exhibiting signs of ITP. Clinical presentation includes uniquely notable petechiae. Large, discolored, purple areas called purpura may also be seen on the body, due to internal bleeding. Ecchymosis and spontaneous bleeding from mucous membranes, gums, nosebleeds, and even the intestines may occur, resulting in nausea and vomiting.
Diagnostics and Laboratory Values
Laboratory and diagnostic tests for ITP are similar to those for other types of thrombocytopenia. They include measuring CBC and platelet counts, as well as autoimmune antibodies to rule out other autoimmune conditions (Nicolas et al., 2023). Additional tests such as a bone marrow biopsy can help identify bone causes of thrombocytopenia and distinguish the etiology from the other types.
Alcoholic Thrombocytopenia
A condition in which excessive alcohol consumption results in decreased platelet count in the blood is known as alcoholic thrombocytopenia, which leads to decreased clotting mechanisms and increases the risk for bleeding and bruising. Chronic alcohol consumption can impair platelet production from bone marrow and has other consequences, direct and indirect, on platelet production and function. Alcohol abuse is one of the main contributors of liver diseases such as alcoholic liver disease and cirrhosis. Given the importance of liver cells to platelet storage, liver damage from alcohol abuse can contribute to thrombocytopenia by disrupting clotting factor synthesis and thrombopoietin. Moreover, alcoholic thrombocytopenia is compounded by nutritional deficiencies in folate, thiamine, and vitamin B12 (Silczuk & Habrat, 2020).
Clinical Manifestations
Alcohol abuse often manifests with signs of thrombocytopenia that include easy bruising and petechiae, along with prolonged bleeding from minor injuries. With advanced liver disease, thrombocytopenia can be enhanced through the development of esophageal varices, which are dilated veins that generate under the mucosa of the lower esophagus and gastrointestinal tract, making the patient at risk for hemorrhage (Meseeha & Attita, 2023). Other symptoms include nose bleeds, bleeding gums, or prolonged bleeding times after minor invasive procedures (Silczuk & Habrat, 2020).
Diagnostics and Laboratory Values
Diagnostic tests are the same as for the other two types of thrombocytopenia; however, a careful social history of the patient may reveal alcohol use disorder, which can help clarify the cause of thrombocytopenia. Management then includes the same medical treatments, with the addition of patient education and support and resources to decrease alcohol consumption.
Nursing Care of the Patient with Thrombocytopenia
Nursing care for the patient with thrombocytopenia focuses on avoiding bleeding complications, creating a safe environment, and supporting overall patient well-being. Nurses should monitor laboratory tests and vital signs, administer medication, take safety precautions, and educate the patient about their condition. Effective communication and collaboration between the patient and members of the health-care team are crucial in optimizing treatment of this disorder and increasing overall quality of life for everyone affected by it.
Recognizing and Analyzing Cues
Nurses should maintain a level of clinical judgment when treating patients at risk for thrombocytopenia, such as those with an underlying hematologic disorder, liver disease, or recent use of medication associated with platelet depletion. It is vitally important to work closely with all members of the health-care team, but particularly hematologists, to provide timely diagnoses and interventions and ongoing management. A careful physical exam from head to toe may reveal cues that point to decreased platelet count and possibly thrombocytopenia. These cues include bruising, purpura, petechiae, excessive bleeding from minor cuts or injuries, bleeding from gums, hematomas, hematuria, heavy menstrual bleeding, frequent or spontaneous nosebleeds, and blood blisters in the mouth or on the body. Other cues to analyze are downward trends in platelet counts and vital sign deviations such as tachycardia, hypotension, and, in severe cases, hypoxia. A past medical and social history may reveal recent exposure to heparin or heavy alcohol use, which may cause thrombocytopenia.
Prioritizing Hypotheses, Generating Solutions, and Taking Action
When deciding on hypotheses and solutions, nurses should always prioritize a patient’s airway, breathing, and circulation. Because thrombocytopenia is a circulation problem, it is important to perform a comprehensive physical exam, paying attention to potential clinical manifestations. The nurse should consider the potential causes of thrombocytopenia, including immune-mediated causes, decreased production of platelets from bone marrow or nutritional disorders, or medications such as heparin or other anticoagulants.
Taking action includes the nursing interventions of administering prescribed medications, coordinating blood transfusions and products as ordered, providing patient education on bleeding and injury prevention, and collaborating with the health-care team. Actions to reduce further bleeding include avoiding sharp objects and using an electric razor or a soft toothbrush to avoid tissue integrity issues. Safety implications include identifying patients at high risk of falling and educating patients to avoid contact sports. Dietary and nutrition interventions include avoiding alcohol (which decreases platelet production) and avoiding foods that may disrupt the intestinal lining. In the event the patient sustains a fall or trauma, imaging, such as a head CT scan, may be clinically warranted to rule out bleeding in the brain.
Thrombocytopenic conditions that have been acutely stabilized also require thorough education. Patients should be taught the pathophysiology of the disease and the importance of adhering to the treatment plan and identifying signs and symptoms of acute bleeding and hemorrhage. As demonstrated during the COVID-19 pandemic, vaccinations for COVID-19 and influenza can decrease or even eliminate risk for exacerbation of forms of ITP that have been caused by viral illness (ITP Support Association, n.d.).
Evaluation of Nursing Care for the Patient with Thrombocytopenia
Evaluation of interventions for thrombocytopenia requires an ongoing and methodological process to assess their efficacy and assess any changes that implemented measures have on the patient’s hemostasis levels. The nurse should keep the following points foremost in mind:
- The primary focus of evaluation is to monitor the patient’s platelet counts to detect improvements or declining trends.
- It is also important to evaluate the patient’s response to medications. The nurse should be aware of side effects and adverse reactions to prescribed medications, which may include nausea, vomiting, and clot formation.
- Documentation is essential to visualize trends in vital signs, blood components, and clotting times. Indications that the patient is improving include normalization of vital signs and blood tests showing stabilizing or improving platelet levels and decreasing clotting times.
Medical Therapies and Related Care
Medical treatments for thrombocytopenia depend on its cause, severity, symptoms, or complications associated with its presence. Treatment plans are individualized, requiring close collaboration among health-care providers and ongoing monitoring to assess treatment efficacy and make necessary adjustments. Patients should be taught to recognize signs of bleeding and to prioritize follow-up care.
HIT presents serious clinical challenges, so prompt recognition, appropriate management strategies, and collaboration among health-care providers are critical in mitigating its associated complications. HIT can be managed effectively by immediately stopping all forms of heparin therapy and other anticoagulant agents like direct thrombin inhibitors (e.g., argatroban, bivalirudin, fondaparinux) to avoid further thrombosis. Warfarin typically should be avoided during the acute stage of the condition due to the risk of skin necrosis. Other essential components of care for managing HIT effectively include monitoring platelet counts regularly and conducting ongoing assessment for potential complications. The removal, treatment, and return or replacement of blood and blood products, known as plasmapheresis, may be performed help remove antibodies when treating HIT.
There are several interventions for ITP, including:
- corticosteroids, such as prednisone or dexamethasone, which are immunosuppressant medicines used to moderate immune system activity and help protect from immune-mediated thrombocytopenia. They are the first-line treatment for ITP.
- immunosuppressive therapy, which is given when the patient’s immune system is attacking itself. It carries the risk of depleting the body’s ability to fight pathogens naturally, but it can be a helpful treatment for ITP, when the immune system is hypersensitive and destroying its own platelets. Medications such as azathioprine, mycophenolate mofetil, cyclophosphamide, and rituximab can help decrease the autodigestion of valuable platelets.
- intravenous immunoglobulin infusion therapy (IVIG), in which antibodies collected from multiple donors are administered intravenously over several days or weeks. IVIG treatment keeps immunity active but controlled, protecting affected tissues from further injury while the body fights infection by pathogens.
- removing the spleen, which can help decrease platelet destruction and increase platelet counts, increasing their numbers significantly. This treatment should only be considered when chronic ITP does not respond to other therapies.
- thrombopoietin receptor agonists, which form a class of medications for chronic ITP. They work by stimulating the production of platelets from the bone marrow.
Regardless of the cause, platelet transfusions can be used to directly increase the body’s platelets levels. This intervention is often used in cases such as severe bleeding or when platelet numbers have dropped dangerously low. Effective treatment is also contingent on addressing the actual cause of thrombocytopenia. If it is alcohol induced, for example, then, in addition to stabilizing platelets, alcohol cessation is key.