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Acute hemorrhage may not immediately affect measured hemoglobin levels.
Blood component therapy should be tailored to restore both oxygen carrying capacity and hemostasis.
Hemostasis may be promoted by replacing depleted coagulation factors and platelets or by the administration of antifibrinolytic agents.
Postoperative bleeding is a common problem, representing 2.6% of all postoperative complications in one survey.[1] Bleeding may be observable, but often it is occult and may not be identified until sufficient intravascular volume-depletion has developed to cause hypotension. Since postoperative hypotension occurs frequently owing to diverse etiologies, clinical recognition of hemorrhage may be delayed. Diagnosis is made more difficult by the fact that hypovolemia from hemorrhage can be obscured by residual anesthetic effects and physiological changes associated with the surgical procedure. In the Post-Anesthesia Care Unit (PACU), clinicians should remain vigilant to the possibility of ongoing blood loss as a cause of postoperative hypovolemia. Frequently, it is necessary to institute therapy for hypotension before hemorrhage has been identified as the cause. Preparations for return to operating room should begin as soon as hemorrhage is suspected, since the availability of the proper personnel and operating room may require a significant time to coordinate.
Perioperative hemorrhage is the most common reason for blood transfusion.[2] Everyone involved in perioperative care of the surgical patient must be aware of the indications and complications of transfusion therapy.
Presentation and diagnosis
Occult hemorrhage typically presents as unexplained hypotension. Occasionally, anemia discovered incidentally on postoperative laboratory evaluation without associated hypotension will trigger further investigation for blood loss. Other more obvious signs of ongoing bleeding, such as bloody dressings or increased output from surgical drains, can be quickly identified, while laboratory and radiological assessments are made to confirm ongoing blood loss.
With acute blood loss in otherwise healthy patients, signs and symptoms may not appear until significant blood loss has occurred. Hypotension may not occur until >40% of the blood volume has been lost in young patients without cardiovascular disease.[3] In patients with significant co-existing disease, or of advanced age, much smaller amounts of blood loss can result in hypotension. Other signs of hypovolemia and inadequate perfusion include reduced urine output, narrow pulse pressure, cool or mottled extremities, and poor capillary refill. These signs may precede hypotension and should not be ignored.
Intravascular hypovolemia may be due to inadequate fluid replacement because of evaporation, urine output, and edema formation intraoperatively, or the result of previous hemorrhage. If continued bleeding is suspected, the cause should be sought immediately. Postural hypotension and tachycardia usually precede frank hypotension, but may not be apparent in the supine patient after surgery. As blood loss increases, signs of decreased end-organ perfusion and hypovolemic shock may become apparent. These may include confusion, dyspnea, palor, diaphoresis, hypotension, and tachycardia. Typical physiological changes during recovery from anesthesia and anticholinergic or anti-adrenergic medications may obscure this clinical picture.
In evaluating hypovolemia in the PACU, anemia may not always be evident. Acute bleeding will not be reflected by a decreased hematocrit, if the intravascular volume loss has not been replaced. Once adequate resuscitation has been achieved using intravenous (IV) fluids, the hematocrit will reflect blood loss. Occasionally, overzealous fluid administration intraoperatively results in dilutional anemia that does not indicate blood loss. Serial measurement of hematocrit or hemoglobin concentration should be obtained, to follow the trend rather than the absolute value in determining whether bleeding is ongoing.
The causes of postoperative hemorrhage can broadly be broken down into technical (i.e. surgical) or non-technical (coagulopathy). Evaluation for both should take place simultaneously. Some estimate that early postoperative hemorrhage is due to inadequate surgical hemostasis in 75 to 90% of cases.[4] This is the so-called “silk deficiency.” If bleeding from the surgical site is suspected, a thorough physical exam is warranted. Dressings should be examined for bleeding, and may require removal to inspect the wounds. If surgical drains are present, the output should be noted serially. If the patient has undergone an abdominal procedure, the abdomen may be distended or firm in cases of ongoing hemorrhage. The retroperitoneal space can accumulate a significant volume of blood, and signs such as Grey Turner’s sign (flank ecchymosis) should be sought. The thighs can also hide a significant volume of lost blood before this becomes visually apparent. Furthermore, patients who have undergone orthopedic procedures may have splints/wraps that obscure inspection. If extremity hemorrhage is suspected, dressings should be removed for investigation as a limb-threatening compartment syndrome may develop.
A chest X-ray is sensitive for diagnosing hemothorax following thoracic or upper abdominal surgery or central venous access placement. CT scan should be considered in evaluating possible hemorrhage after abdominal and pelvic surgery, where plain X-ray films may not reveal even large collections of blood, especially if the bleeding is retroperitoneal. Angiography can be particularly useful for diagnosis of acute bleeding, as endovascular intervention can be performed immediately once the source is found. Bedside abdominal ultrasound has been validated to detect hemorrhage after trauma in the Emergency Department,[5] but does not yet have demonstrated efficacy in detecting postoperative hemorrhage.
Rarely, emergent interventions may be required in the PACU for hemorrhage unrelated to hypovolemia. Airway obstruction from hematoma following thyroid or anterior cervical spine surgery may require immediate opening of the incision to allow decompression of the airway obstructing hematoma. This responsibility may fall on PACU personnel if the surgeon is not immediately available. However, in less severe cases, the management may consist of a controlled return to the operating room for surgical exploration. The most important intervention to be made for bleeding is volume replacement with IV fluids and blood transfusion to maintain organ perfusion, while attempting to correct the underlying cause of bleeding.
Common medical causes of early postoperative bleeding include dilutional coagulopathy, inherited or acquired platelet disorders, hyperfibrinolysis, and inherited coagulation disorders. Dilutional thrombocytopenia is common after surgery owing to fluid resuscitation and blood transfusion. After transfusion of one blood volume, only 35% to 40% of platelets remain in circulation.[4] It should be noted that fibrinogen is also sensitive to hemodilution, and hypofibrinogenemia should always be considered as a medical cause for postoperative bleeding.[6] Loss of plasma coagulation factors can result in impaired thrombin generation, reflected by prolonged coagulation times.
Hyperfibrinolysis can be the result of large areas of tissue injury from trauma or extensive surgery, with resultant massive activation of the coagulation system.
The injured tissues release tissue factor, resulting in intravascular activation of coagulation and formation of thrombin and subsequent fibrin clots.[7] Fibrinolysis, which is feedback activated by thrombin generation, can become so avid as to cause premature breakdown of formed clot, resulting in further bleeding. Thus, massive clotting can result in massive fibrinolysis. Consequently, coagulation factors, platelets, and fibrinogen are further consumed, promoting further blood loss.
Assessment of platelet count, prothrombin time (PT), partial thromboplastin time (PTT) or activated partial thromboplastin time (aPTT), and fibrinogen concentration should be performed to detect coagulopathy when ongoing hemorrhage occurs. If the PT or PTT are prolonged more than 1.5 times normal values, the platelet count is less than 75K, or the fibrinogen is below 150 mg/dl, transfusion therapy should be considered to correct coagulopathy. Viscoelastic tests of coagulation, such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM), can be used in the diagnosis of coagulopathy, when available, and can be particularly useful for identifying hyperfibrinolysis.[8,9]
Hypothermia is also common in the postoperative setting and contributes to thrombocytopenia through platelet sequestration in liver and spleen.[7] In addition, platelet surface molecules are altered, leading to impaired functioning of platelets that remain in circulation. A vicious cycle may result in which hypothermia causes more bleeding, which causes more hypothermia as room temperature fluids are administered during volume resuscitation. Rewarming of the patient causes desequestration of platelets and improved bleeding time. Plasma coagulation proteins are also sensitive to the effects of hypothermia. At 33 °C, the clotting deficiency seen is equivalent to a factor IX deficiency at 33% of its normal level.[10]
Metabolic derangements during surgery may also result in coagulation disturbance. Hypotension and hypoperfusion of end organs during surgery may result in lactic acidosis, which can impair the enzymatic processes of the coagulation cascade. There is a strong correlation between the duration of hypotension and coagulation abnormalities. One study demonstrated that shock-induced acidosis lasting greater than 150 minutes resulted in an increase in aPTT and decreased factor V activity.[11]
Blood component transfusion
Blood component transfusion has essentially replaced fresh whole blood (FWB) transfusion in the United States, with the exception of military use of FWB in austere settings. FWB may be the ideal transfusion product for traumatic or postoperative bleeding, but comes with significant safety and convenience concerns compared with blood component therapy.[12] Blood components available for transfusion include red blood cells (RBCs), fresh frozen plasma (FFP), platelets, and cryoprecipitate.
Units of whole blood are collected from volunteers and are treated with additive solutions to keep the blood product fluid and prolong storage. The separation of plasma and cellular components is accomplished by centrifugation. There are several commercial additives available. Common to these solutions is citrate, which binds to calcium ions in the collected blood, effectively anticoagulating the product, as calcium is then unavailable as a cofactor to the proteins of the coagulation system. Adenosine, phosphate, and dextrose are added to provide substrates for anaerobic metabolism, ATP synthesis, and buffering. The administration of blood products to the patient always includes the administration of the additive solution as well. Citrate toxicity can result when blood components are given rapidly, manifested by acute hypocalcemia.[13]
Hypothermia from rapid administration of cold blood products can worsen hemostasis further and has other adverse consequences for the patient. Therefore, when FFP and RBCs are transfused quickly (less than 1 hour per unit) in the PACU, a fluid warming system should be used. Slow infusions of blood products over several hours generally do not require fluid warming unless the patient is already hypothermic.
Red blood cells: In the United States, about 12 million units of RBCs are transfused annually.[2] The best indication for RBC transfusion is to improve oxygen carrying capacity. Blood transfusion is not indicated for purely intravascular volume expansion. Controversy surrounds the application of specific transfusion “triggers.” Medical judgment continues to play a key role in the decision to initiate transfusion despite a hemoglobin concentration above or below a recommended threshold.
The beneficial effects of red cell transfusion are most evident in acute hypovolemia due to bleeding. The administration of red cells in response to acute blood loss provides needed intravascular volume and increases the oxygen carrying capacity. The use of volume replacement with crystalloid or colloid solutions in acute bleeding results in the anemia usually associated with blood loss.
Recommendations for specific hemoglobin and hematocrit values necessitating transfusion were developed during the NIH Health Consensus Conference.[14] These recommendations have changed little over the past 20 years. The authors recommended that acutely anemic patients with hematocrit values less than 21% will likely require RBC transfusion in the perioperative period. However, chronically anemic patients may safely tolerate lower values. Patient co-morbidities must be considered: many disease states, such as coronary artery disease, may require higher values owing to increased oxygen requirement. Clinical judgment plays a key role in these decisions.
The American Society of Anesthesiologists Practice Guidelines offered these recommendations in 2006[2]:
1. Transfusion is rarely indicated with hemoglobin values greater than 10 g/dl and almost always indicated if it is less than 6 g/dl, especially when acute.
2. Deciding whether or not to transfuse patients between these values should take patient risk into consideration.
3. The use of any specific transfusion “trigger” that does not take the patient’s physiology into account is not recommended.
4. When appropriate, preoperative autologous blood donation, intraoperative and postoperative blood recovery, acute normovolemic hemodilution, and measures to decrease blood loss may be beneficial.
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