adequate hemodynamic support and tissue oxygenation is essential in preventing or combating end-organ damage.
Close monitoring of vital signs, hemodynamic parameters, intake and output, and appropriate laboratory values assists the critical care nurse in administering and titrating appro-priate agents.2
Initiating Bleeding Precautions
Awareness of the patient’s bleeding potential necessitates adjustments to normal nursing interventions. The nurse avoids unnecessary venipunctures that may result in bleed-ing, bruisavoids unnecessary venipunctures that may result in bleed-ing, or hematomas by drawing blood from and administering medications through existing arterial or venous lines. The use of manual or automatic blood pressure cuffs is avoided whenever possible. If tracheal or oral suction-ing is necessary, the use of low-level suction is recommended.6 Meticulous skin care is advised, keeping the skin moist and using specialty mattresses and beds as appropriate to prevent breakdown. Gentle care should be used when bathing or turning the patient to prevent bruising or hematoma formation.
Providing Comfort and Emotional Support
The development of DIC in the already critically ill patient can be stressful for the patient and his or her significant others. It is imperative to provide psychosocial support throughout this crisis. Calm reassurance and uncomplicated explanations of the care the patient is receiving can help to allay much of the anxiety experienced. The critical care nurse must answer all questions and provide information in terms best understood by all parties. The use of an interpreter when English is not the primary language can enhance understanding and help avoid misconceptions. Providing spiritual support as requested may also be of assistance. Col-laborative management of the patient with DIC is outlined in Box 27-3.
HEPARIN-INDUCED THROMBOCYTOPENIA
• Identify and eliminate the underlying cause.
• Provide hemodynamic support to prevent end-organ ischemia.
• Intravenous fluids
• Positive inotropic agents
• Administer blood and blood components.
• Fresh-frozen plasma
• Platelets
• Cryoprecipitate
• Antithrombin III
• Administer medications.
• Heparin
• Aminocaproic acid
• Protein C
• Antithrombin III
• Initiate bleeding precautions.
• Maintain surveillance for complications.
• Hypovolemic shock
• Peripheral ischemia
• Central ischemia
• Multiple organ dysfunction syndrome (MODS)
• Provide comfort and emotional support.
BOX 27-3 COLLABORATIVE MANAGEMENT
Disseminated Intravascular Coagulation
exposure to heparin, but the onset can occur within hours of a reexposure to heparin.9-12 Depending on the source of the disorder, reported mortality rates are as high as 30%.8
Pathophysiology
The thrombocytopenia that occurs with immune-mediated HIT is related to the formation of heparin-antibody com-plexes. These complexes release a substance known as platelet factor 4 (PF4). PF4 attracts heparin molecules, forming immunogenic complexes that adhere to platelet and endothe-lial surfaces (Figure 27-2). Activation of platelets stimulates the release of thrombin and the subsequent formation of platelet clumps.9
Patients with immune-mediated HIT are at greater risk for thrombosis than bleeding. Vessel occlusion can result in the need for limb amputation, stroke, acute myocardial infarction, and even death.9-12 The resultant formation of fibrin-platelet-rich thrombi is the primary characteristic of HIT that distinguishes it from other forms of thrombocy-topenia and gives rise to its more descriptive name: white clot syndrome.10
Assessment and Diagnosis
HIT can be associated with severe consequences. Rapid rec-ognition of risk factors and subsequent development of signs and symptoms is essential in treating this condition.
FIG 27-2 Pathogenesis of Heparin-Induced Thrombocytopenia (HIT). (1) Activated platelets release procoagulant proteins from α-granules, including platelet factor 4 (PF4). Administered heparin binds PF4 (2), which undergoes a conformation change and expresses a new antigen (neoepitope). Individuals with HIT produce an immunoglobulin G (IgG) antibody that specifically reacts (3) with multiple identical neoepitopes on the heparin-PF4 complex. The reaction forms heparin-PF4-IgG immune complexes. Platelets express FcγRIIa receptors (Fcγ receptor) that react (4) with the Fc portion of IgG in immune complexes. Cross-linking of Fc receptors (5) results in FcγRlIa-dependent platelet activation. The activated platelets mediate a series of events that lead to further activation of the coagulation cascade, resulting in thrombin generation.
Further release of PF4 from newly activated platelets leads to a cycle of continuing platelet activation and (6) formation of a primary clot. The reaction can be enhanced by the release of platelet-derived microparticles that are rich in surface phosphatidylserine and increase activation of coagulation and by the binding of heparin-PF4 complexes and HIT-IgG to the vascular endo-thelium (not shown). (From McCance KL et al, eds. Pathophysiology: The Biologic Basis for Disease in Adults and Children. 7th ed. St. Louis: Elsevier; 2014.)
Activated platelet
1
2
3
4
5
6 Heparin
Platelet
Fc receptor PF4 HIT antibody Endothelium
PF4 neoepitope
Clinical Manifestations
Common signs and symptoms are listed in Table 27-3. The clinical manifestations of HIT are related to the formation of thrombi and subsequent vessel occlusion.8 Most thrombotic events are venous, although both venous and arterial throm-bosis can occur. Thrombotic events typically include deep vein thrombosis, pulmonary embolism, limb ischemia thrombosis, thrombotic stroke, and myocardial infarction.8,12 The presence of blanching and the loss of peripheral pulses, sensation, or motor function in a limb indicate peripheral vascular thrombi. Neurologic signs and symptoms such as confusion, headache, and impaired speech can signal the onset of cerebral artery occlusion and stroke. Acute myocar-dial infarction may be heralded by dyspnea, chest pain, pallor, and alterations in blood pressure. Thrombi in the pulmonary vasculature may be evidenced by pleuritic pain, rales, and dyspnea.9,10
Laboratory Findings
The key indicator for identifying HIT is the platelet count.
General consensus in the literature considers a platelet count of less than 100,000/mm3 or a sudden drop of 50% from the patient’s baseline after initiation of heparin therapy strongly to indicate HIT.10-12
Two types of assays have become available to assist in confirming the diagnosis of HIT: activation assays, based on platelet aggregation or the release of granular contents such as serotonin, and assays that identify the HIT antigen. Activa-tion assays are highly sensitive in detecting the presence of HIT. The most common assay used is heparin-induced plate-let aggregation (HIPA). Serotonin-release assay (SRA) is used by a few institutions. The enzyme-linked immunosorbent assay (ELISA) identifies the presence of the HIT antigen.10
Medical Management
Early identification is critical to managing the effects of immune-mediated HIT. Current guidelines suggest that for high-risk patients platelet count monitoring be performed every 2 or 3 days from day 4 to day 14.13 When a decrease in the platelet count is detected, heparin therapy should be discontinued immediately, and the patient should be tested for the presence of heparin antibodies.9,11-13 If the original
ELISA, Enzyme-linked immunosorbent assay; HIPA, heparin-induced platelet aggregation; SRA, serotonin release assay.
SYSTEM OR STUDY SIGNS AND SYMPTOMS
Cardiac Chest pain, diaphoresis, pallor, alterations in blood pressure, dysrhythmias Vascular Arterial: pain, pallor, pulselessness, paresthesia, paralysis
Venous: pain, tenderness, unilateral leg swelling, warmth, erythema, a palpable cord, pain on passive dorsiflexion of the foot, and spontaneous maintenance of the relaxed foot in abnormal plantar flexion (Homans sign)
Pulmonary Dyspnea, pleuritic pain, rales, chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain, syncope, hemoptysis, shortness of breath, wheezing
Renal Thirst, decreased urine output, dizziness, orthostatic hypotension Gastrointestinal Abdominal pain, vomiting, bloody diarrhea, abnormal bowel sounds
Neurologic Confusion, headache, impaired speech patterns, hemiparesis or hemiplegia, vision disturbances, dysarthria, aphasia, ataxia, vertigo, nystagmus, sudden decrease in consciousness
Laboratory Platelets <50,000/mm3 or sudden drop of 30%-50% from baseline; positive results for HIPA, SRA, ELISA
TABLE 27-3 Heparin-Induced Thrombocytopenia: Signs, Symptoms, and Laboratory Data
BOX 27-4 NURSING DIAGNOSIS PRIORITIES
• Risk for Decreased Cardiac Tissue Perfusion, p. 603
• Risk for Ineffective Peripheral Tissue Perfusion, p. 605
• Risk for Ineffective Renal Tissue Perfusion, p. 606
• Risk for Ineffective Gastrointestinal Tissue Perfusion, p. 605
• Risk for Ineffective Cerebral Tissue Perfusion, p. 604
• Powerlessness related to lack of control over the current situation or disease progression, p. 600
• Deficient Knowledge related to lack of previous exposure to information, p. 585 (see Box 27-5, Patient Education for Heparin-Induced Thrombocytopenia)
Heparin-Induced Thrombocytopenia
indication for heparin still exists or new thrombosis occurs, an alternative form of anticoagulation is usually necessary.13 Direct Thrombin Inhibitors
Direct thrombin inhibitors (DTIs) are being used with increasing frequency to treat HIT. DTIs bind directly to the thrombin molecule, thereby inhibiting its action.12 Currently, the only medication approved for use in the United States is argatroban. Warfarin, although commonly used to treat deep vein thrombosis, is not indicated as a sole agent in treating HIT because of its prolonged onset of action. Studies have shown that the use of warfarin without concomitant use of DTIs can significantly increase the incidence of thrombosis in patients with HIT.8,10-12
Nursing Management
Nursing management of the patient with HIT incorporates a variety of nursing diagnoses (Box 27-4). Nursing priorities are directed toward 1) decreasing the incidence of heparin exposure, 2) maintaining surveillance for complications, 3) providing comfort and emotional support, and 4) initi-ating patient education. The critical care nurse plays a pivotal role in prevention and detection of HIT. Initial assess-ment is crucial to identifying those patients at risk for HIT.
Ascertaining a medical history that includes previous heparin therapy, deep vein thrombosis, or cardiovascular surgery that
(Hb AS), and a 25% chance of having a child with entirely normal hemoglobin (Hb AA).15,16
This genetic trait is primarily found in people of West African descent. The disease has also been linked to persons of sole European or Middle Eastern ancestry; however, this is extremely rare. The disease is not prevalent in persons of Asian or Pacific Islander descent.15 SCA is usually diagnosed during the first few years of life due to manifestation of initial symptoms. Prenatal screening is now available for at-risk couples.16 This consists of DNA analysis from fetal cells. This should be offered as part of their prenatal counseling. There are more than 40 states that undergo universal neonatal screening for hemoglobinopathies.16
Pathophysiology
Sickle cell disease (SCD) is a chronic inflammatory condition characterized by hemolysis and vasoocclusion. The cause of SCA is a mutation in the genetic sequence in the beta chain gene of the hemoglobin. This results in a sequence of the replacement of valine with glutamic acid at the N-terminal amino acid position 6 of the protein chain.15,16 This substitu-tion leads to the production of hemoglobin S.
Normal RBCs contain hemoglobin that are flexible, bicon- cave disks. When deoxygenated, RBCs containing predomi-nantly Hb S distort into a crescent or sickle shape. In this form, the hemoglobin becomes rigid and friable, causing vasoocclusion in the small vessels of the circulatory system.
This tends to happen during times of physiologic stress, such as physical overexertion, muscle tissue ischemia, dehydra-tion, infection, or extreme temperatures.16 Even though these conditions have a tendency to exacerbate the condition, the majority of the sickling events have no identifying cause.15
The RBCs become lodged in the vasculature and the micro-circulation causing stasis and obstruction of blood flow and damage to the surrounding organs, tissue ischemia, infarction, and if not corrected eventually, necrosis (Figure 27-3).16 In addition, hemolysis of the RBCs occurs, resulting in anemia.
included the use of cardiopulmonary bypass can alert the nurse to potential problems.
Decreasing the Incidence of Heparin Exposure
Ensuring that all heparin has been removed from the patient’s hemodynamic pressure monitoring system, avoiding the use of heparin-coated catheters, and discontinuing heparin flushes to maintain the patency of other intravenous lines are essential elements of nursing management.
Maintaining Surveillance for Complications
Patients with HIT remain at high risk for thrombotic complica- tions for several days or weeks after cessation of heparin. Vigi-lant monitoring, early recognition of signs and symptoms, deep vein thrombosis prevention strategies, and prompt notification of the physician are key roles of the critical care nurse.
Educating the Patient and Family
Prevention of subsequent episodes in patients sensitized to heparin incudes education of the patient and family (Box 27-5). Education should include measures to avoid future exposure to heparin. The use of medical alert bracelets and listing heparin allergies in the medical record are neces- sary to avoid this serious complication in the future. Collab-orative management of the patient with HIT is outlined in Box 27-6.