Page 1249 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

856 PART 7: Hematologic and Oncologic Disorders

■ HEMOLYSIS, ELEVATED LIVER ENZYMES, LOW PLATELETS SYNDROME TABLE 90-10 Distinguishing Features of Coagulopathies

Hemolysis with microangiopathic hemolytic anemia, elevated liver Other
enzymes, and low platelets (HELLP) is a syndrome which occurs in PT, aPTT Platelets Fibrinogen D-Dimer Features
pregnancy and resolves with delivery. The etiology is unknown; however,
there are associations with preeclampsia, hepatic inflammation, and ITP Normal Decreased Normal normal Normal RBC
activation of the complement system that respond to treatment with TTP-HUS normal decreased normal normal Schistocytes
eculizumab. 146,147 HELLP is relatively rare, developing in fewer than 1% DIC prolonged decreased decreased elevated Schistocytes
of all pregnancies. Common presenting symptoms include hyperten-
sion, abdominal pain, vomiting, and headache. Laboratory criteria for HELLP normal decreased normal to normal Pregnancy
diagnosis include microangiopathic hemolytic anemia, thrombocytope- increased Elevated LFT
nia with platelet count <100 × 10 /L, LDH >600 IU/L, total bilirubin Massive Transfusion/ prolonged decreased decreased normal Hypothermia,
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≥1.2 mg/dL, and AST ≥70 IU/mL. Treatment of HELLP includes Trauma acidosis
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management of hypertension, prompt delivery, and supportive transfu-
sion for platelet counts <20 × 10 /L. 149 plasminogen which results in stabilization of fibrin clot. The Clinical
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■ COAGULOPATHY OF TRAUMA AND MASSIVE TRANSFUSION Randomization of Antifibrinolytic Therapy in Significant Hemorrhage-2
trial (CRASH-2) evaluated the effect of an initial loading dose of
Coagulopathy is present on hospital admission in almost one-third of all tranexamic acid followed by an 8-hour infusion administered within
trauma patients and uncontrolled, posttraumatic bleeding is a leading 3 hours of trauma. Mortality was significantly reduced without an
cause of death. 150,151 Despite fundamental differences in cause, the prin- increase in thrombosis or other complications. These results have led
159
ciples developed from trauma hemorrhage management are relevant to the endorsement of tranexamic acid in massive trauma resuscitation
to massive transfusion in medically ill patients with massive bleeding guidelines. 154
and other patients who have atraumatic vascular rupture (eg, ruptured
aneurysm). Multiple factors converge in the massively transfused patient PLATELET TRANSFUSION, BLOOD COMPONENTS,
to cause coagulopathy: acute injury-associated inflammation, systemic AND PROCOAGULANT TREATMENTS
activation of hemostasis and fibrinolysis, dilutional coagulopathy,
hypocalcemia, acidosis, and hypothermia. 152,153 Particularly because the ■ PLATELET TRANSFUSION
coagulopathy of massive transfusion limits the effectiveness of intra-
vascular volume resuscitation, it directly increases treatment require- There are two main indications for platelet transfusion: to promote
ments, prolongs shock, and is associated with higher degrees of organ hemostasis in bleeding patients with thrombocytopenia or functional
dysfunction and mortality. Clinical guidelines and systematic reviews of platelet disorders and to prevent bleeding in patients with profound
the literature on massive transfusion emphasize early clinical identifica- thrombocytopenia. Indications for platelet transfusion are related to
tion of all bleeding sources, physical control of the hemorrhage sites the underlying disease, presence or absence of active bleeding, anticipa-
wherever possible, maintenance of normothermia, monitoring and cor- tion of invasive procedures, and platelet count. In general, patients with
rection of electrolyte disturbances, intensive monitoring of coagulation active life-threatening bleeding, intracranial hemorrhage, or undergoing
function, and early blood component therapy. 154 neurological or vascular surgery should receive platelet transfusion to
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Massive transfusion has been clinically defined as replacement of maintain concentrations over 100 × 10 /L. For most bleeding situations,
more than 50% of a patient’s blood volume within 24 hours. Alternative general surgical procedures, and routine endoscopies with biopsies;
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definitions range from replacement of 100% blood volume within however, lower thresholds (50 × 10 /L) are adequate; 20 × 10 /L is an
12 hours to administration of more than 10 units of packed red blood adequate platelet threshold for most bedside, needle-based procedures
cells within 24 hours. Any patient receiving massive transfusion including central venous catheterization and lumbar puncture. 160,161
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should have INR, aPTT, fibrinogen, and platelets measured immediately While the role of prophylactic platelet transfusion in patients with
on presentation and periodically throughout the entire resuscitation hematologic malignancy has been debated, there appears to be some
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period. Because calcium is an essential cofactor for coagulation factor benefit when a transfusion threshold of 10 × 10 /L is used. 162,163
function, ionized calcium levels should be monitored and maintained In clinical practice, each unit of pooled, random donor platelets
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within normal range throughout the resuscitation period. Particularly increases the circulating platelet count by 5 to 10 × 10 /L in patients
in patients with preexisting renal disease, serum potassium should also with average body size. For this reason, random donor platelets are
be monitored closely. pooled and typically given as a “six pack.” By comparison, one single-
Regardless of the rate of hemorrhage, coagulopathy must be identi- donor pheresis platelet unit may increase the platelet count by 30 to
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fied and treated. FFP should be administered to patients with clinically 60 × 10 /L and these are administered singly. Routine monitoring of
significant bleeding who have INR or aPTT exceeding 1.5 times control. platelet transfusion should include posttransfusion platelet count to
Platelet transfusion is indicated in any bleeding patient with dysfunctional determine transfusion responsiveness. Failure of the circulating platelet
platelets (eg, receiving clopidogrel) or having severe thrombocytopenia count to increase may result from destruction of the transfused platelets
(platelet count ≤50 × 10 /L). Cryoprecipitate or fibrinogen concentrate or consumption of the platelets at sites of injury or clot activation. Risks
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should be administered for plasma fibrinogen concentration less than 1.5 for ineffective platelet transfusion include ITP, presence of antiplate-
to 2.0 g/L. Patients who have shock and clearly visible massive hemor- let antibodies, DIC, drug-induced thrombocytopenia, and sepsis. In
rhage should immediately receive red blood cell transfusion and should general, platelet transfusions are ineffective if the cause of thrombo-
be considered for inclusion in clinical treatment protocols that specify cytopenia is enhanced destruction, since the transfused platelets are
ratios of red blood cell transfusion to plasma and platelets. These proto- destroyed through the same mechanism.
of blood products, but may increase wastage of prepared but unused ■ FRESH-FROZEN PLASMA
cols are feasible and facilitate timely bedside arrival and administration
components. Particularly for patients with trauma requiring massive FFP contains all of the coagulant factors and coagulation inhibitors
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hemorrhage, a ratio of blood:plasma:platelets of approximately 1 : 1 : 1 in normal blood. By convention, 1 mL of FFP is equivalent to 1 unit
improves survival and subsequent transfusion needs. 154,157,158 of blood coagulation factor activity. The typical dosage of FFP is 10
Emerging therapies in coagulopathy of massive trauma include to 15 mL/kg which should restore coagulation factors to 25% to 30%
antifibrinolytic agents. Tranexamic acid is a competitive inhibitor of normal levels. It has been suggested that this dosage level is inadequate
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