Suspect acute hemolysis
STOP INFUSION IMMEDIATELY
• General ABCs
• Cardiac Monitoring
• O2 monitoring
• Recheck patient name
• Recheck typing
• Send blood and tubing to Blood Bank Fever,
tachycardia, dyspnea, back pain, hemodynamic instability
IV Fluids
• D5W with 3 amps NaHCO3 at 250 mL/hr
• Keep UOP >30–50 mL/hr
Medications
• Hydrocortisone 100 mg IV
• Diphenhydramine 50 mg IV
• Acetominophen 650 mg PO
• Epinephrine 0.3 mL of 1:1000 SC
Laboratory Tests
• CBC
• Coombs test
• Urine free hemoglobin
• Haptoglobin
• PT/PTT
• Fibrinogen
• Bilirubin
• LDH
IV, intravenous; D5W, 5% dextrose in water; UOP, PO, orally; SC, subcutaneously; CBC, complete blood count;
PT/PTT, prothrombin time/partial thromboplastin time; LDH, lactate dehydrogenase.
Haematopoeitic Disorders rTransfusion Practices 5 0 9 Nonhemolytic Febrile Reactions
Nonhemolytic febrile reactions occur in approximately 1% of transfusions and are the result of antibodies in the recipient’s serum against white blood cells in the donor’s product. This manifests acutely as an increase in body temperature and is more com- mon in patients who have been previously alloimmunized by numerous transfusions.
This reaction is treated with antipyretic medications.
Allergic Reactions
Allergic reactions occur because of transfused allergens in the donor’s product, with symptoms such as urticaria and bronchospasm; they occur in approximately 1 in 100 transfusions. This condition is treated with antihistamine medications. However, a potentially severe form may be encountered in IgA-deficient individuals who can have anaphylactic reactions to serum from non–IgA-deficient donors. This is best prevented with washed RBCs, but can be treated with high-dose corticosteroids, airway protection, and antihistamines.
Transfusion-Related Acute Lung Injury
Transfusion-related acute lung injury (TRALI) occurs by a poorly understood mech- anism, but an immune antibody-mediated process has been established in a majority of cases. A nonimmune mechanism has been postulated as well. Data from animal models and recent clinical studies suggest that both processes occur and that TRALI may be the end result of diffuse neutrophil activation and capillary leak by these mech- anisms. TRALI presents with diffuse capillary damage in the pulmonary vasculature with rapid-onset dyspnea, hypoxia, fever, and bilateral pulmonary infiltrates resem- bling acute respiratory distress syndrome, in the absence of volume overload or heart failure. Treatment is supportive as most cases are self-limiting, but patients may require mechanical ventilation.
Bacterial Infection
Blood units can be contaminated with bacterial agents, including cold-growing organ- isms such asYersinia enterocolitica, as well as various gram-negative organisms. Inci- dence of bacterial infection has dramatically decreased since the introduction of dis- posable plastic blood bags.
Long-Term Transfusion Risks Viral Infections
Infectious complications of blood transfusions are located in Table 64.2. All blood products are currently screened for hepatitis B, hepatitis C, human immunodeficiency virus 1 and 2, and human T-lymphotropic virus I and II. Other infectious risks include viruses that are not screened for, such as CMV and parvovirus B19, and the prion transmitted Creutzfeldt–Jacob disease.
Iron Overload
Although not typically an issue in the ICU setting, secondary iron overload syndromes occur in proportion to the number of blood products a patient receives. Patients at highest risk include those with multiple transfusions over long periods of time (e.g., sickle-cell disease, thalassemias, myelodysplastic syndromes). Each milliliter of packed RBCs contains approximately 1 mg of iron. Patients who are repeatedly transfused in the absence of blood loss are at risk of overwhelming the body’s ability to use iron with resultant deposition into tissues such as the myocardium, bone marrow, and liver.
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TABLE 64.2 Transfusion-Associated Infections
Risk factor Estimated frequency No. of deaths Virus (per million) (per unit) (per million units)
Hepatitis A 1 1/1,000,000 0
Hepatitis B 7–32 1/30,000–1/250,000 0–0.14
Hepatitis C 4–36 1/30,000–1/150,000 0.5–17
HIV 0.4–5 1/200,000–1/2,000,000 0.5–5
HTLV I and II 0.5–4 1/250,000–1/2,000,000 0
Parvovirus B19 100 1/10,000 0
HIV, human immunodeficiency virus; HTLV, human T-lymphotropic virus.
Adapted from Goodnough et al. (1999), with permission.
S U G G E S T E D R E A D I N G S
Drews RE. Critical issues in hematology: anemia, thrombocytopenia, coagulopathy, and blood product transfusions in critically ill patients.Clin Chest Med.2003;24:607–622.
A systematic review of diagnosis, evaluation, and treatment of blood and bleeding disorders commonly encountered in the critical care setting.
Goodnough LT, Brecher ME, Kanter MH, et al. Transfusion medicine: first of two parts. Blood transfusion.N Engl J Med.1999;6:438–441.
A review article on principles of basic transfusion medicine, including complications and indi- cations for transfusion.
Herbert PC, Wells G, Blajchman MA, et al. A Multicenter, randomized, controlled clinical trial of transfusion requirement in critical care.N Engl J Med.1999;6:409–417.
A randomized trial of 838 ICU patients to receive transfusions for hemoglobin levels of less than 10 g/dL, or 7 g/dL. Overall 30-day mortality was similar in the two groups, but there was significantly less in-hospital mortality in patients transfused for hemoglobin levels less than 7 g/dL (22.2% vs. 28.1%, p 0.05), demonstrating that a “restrictive” transfusion strategy is well tolerated and potentially superior to liberal transfusion strategies.
McLellan SA, McClelland DB, Walsh TS. Anaemia and red blood cell transfusion in the critically ill patient.Blood Rev.2003;17:195–208.
A review of anemia and transfusion strategies in critically ill patients.
Pajoumand M, Erstad BL, Camamo JM. Use of Epoetin Alfa in critically ill patients. Ann Pharmacother.2004;38:641–648.
A review of the use of Epoetin Alfa for reduction of red blood cell transfusions in critically ill patients with anemia.
Triulzi DJ. Transfusion-related acute lung injury: an update.Hematology Am Soc Hematol Educ Program.2006;497–501.
Review of current research and proposed mechanisms of TRALI.
Uy GL. Transfusion medicine. In: Lin TL, ed.Hematology and Oncology Subspecialty Consult.
Baltimore: Lippincott, Williams & Wilkins; 2004:73–79.
Book chapter focusing on basic transfusion medicine and practical information about blood products and proper use.
Vincent JL, Baron JF, Reinhart K, et al. Anemia and blood transfusion in critically ill patients.
JAMA.2002;12:1499–1507.
A prospective observational study of patients in European ICUs evaluating the prevalence of anemia and transfusion use in this setting.
65 Hypercoagulable States
James C. Mosley, III
Hypercoagulable states are a heterogeneous group of inherited or acquired disor- ders that predispose individuals to the inappropriate formation of a clot in the venous or arterial circulation. The inappropriate formations of thrombi occur in the presence of Virchow’s triad of hypercoagulability, stasis, and endothelial dam- age. Embolization of these clots can occur, resulting in pulmonary embolism (PE) in the case of venous embolic disease, or emboli to vital organs in the setting of arterial thrombosis.
Various manifestations of hypercoagulability are demonstrated in the intensive care unit (ICU) setting. Patients are at an increased risk of venous thromboembolic disease because of their prolonged immobilization, the numerous procedures that they are exposed to, and their underlying disease states. Patients in the ICU setting may have only transient risk factors for thromboembolic disease, or may also have underlying conditions that increase their risk. Listed in Table 65.1 are common causes of hypercoagulability.
D E E P V E N O U S T H R O M B O S I S A N D P U L M O N A R Y E M B O L I S M
Deep venous thrombosis (DVT) and PE are very common in the ICU and are likely under-diagnosed. Some observational studies have demonstrated a 20% to 40% inci- dence of DVT in the ICU setting.
Diagnosis of DVT and PE in the ICU can be difficult (Algorithms 65.1 and 65.2). Various studies have demonstrated that 10% to 100% of DVTs diagnosed by ultrasound in this setting were not found on physical examination. Furthermore, patients in the ICU setting have a number of factors confounding the diagnosis, including their numerous comorbid conditions, inability to communicate symptoms, numerous procedures and medications, and inability to undergo various diagnostic tests. Table 65.2 lists the diagnostic modalities for DVT and PE.
Treatment of DVT and PE should commence when clinically suspected. As previously mentioned, diagnosis can be difficult in the ICU setting, but delay in treatment can lead to increased morbidity and mortality. Clinically suspected DVT or PE should be treated with weight-based unfractionated heparin or with low-molecular- weight heparin. Dosing guidelines for unfractionated heparin and alternatives are listed in Tables 65.3 and 65.4.
DVT prophylaxis decreases the incidence of PE and venous thromboembolism in the ICU patient. In general, all patients in the ICU should receive DVT prophylaxis if no contraindication exists.
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TABLE 65.1 Causes of Hypercoagulability
Acquired causes Inherited causes
Trauma/surgery Factor V Leiden mutation
Malignancy Prothrombin G20210A mutation
Immobilization Protein C deficiency
Nephrotic syndrome Protein S deficiency
Obesity Antithrombin deficiency
Pregnancy Increased factor VIII activity
Oral contraceptive use Congestive heart failure Myeloproliferative disorders Antiphospholipid antibodies Lupus anticoagulant Anticardiolipin antibodies
A R T E R I A L T H R O M B O E M B O L I S M
Acute arterial thrombosis can be secondary to embolization of material (e.g., from the atria in atrial fibrillation or from a proximal source secondary to a damaged artery), or anin situformation of clot. Symptoms are generally related to the territory served by the artery that has thrombosed, and generally is noted as a painful, pale, and cool extremity, or an acute neurologic deficit in the case of a stroke. However, in the ICU setting, these symptoms may be masked by the patient’s other comorbidities.
TABLE 65.2 Diagnostic Tests for Deep Venous Thrombosis (DVT) and Pulmonary Embolism (PE) in the Intensive Care Unit Setting Test Indication for testing Key points
Venous duplex ultrasound
Suspected DVT in extremities
rGood sensitivity and specificity for proximal DVT Spiral computed
tomography
Suspected PE rGood sensitivity for large rPEsContrast bolus predisposes
to nephrotoxicity Ventilation-perfusion
scanning
Suspected PE rGood sensitivity for PEs rDifficult to interpret in
setting of recent pneumonia or other infiltrative process Computed tomography
angiography/
venography
Suspected DVT or PE rNot widely available rLarge bolus of contrast
used Adapted from Cook et al. (2005), with permission.
Haematopoeitic Disorders rHypercoagulable States 5 1 3