Surgical Bleeding and Hemostasis 8

8

Surgical Bleeding and Hemostasis

Gregory R. Brevetti, Lucy S. Brevetti, and Rocco G. Ciocca

Objectives

1. To describe the differential diagnosis:

• To differentiate between surgical and nonsurgi- cal causes of bleeding.

• To describe the treatment options for both sur- gical and nonsurgical bleeding.

• To identify the indications, risks, and benefits of blood product transfusions.

2. To describe factors that can lead to abnormal bleed- ing postoperatively and to discuss the prevention and management of postoperative bleeding:

• Inherited and acquired factor deficiencies.

• Disseminated intravascular coagulation (DIC), transfusion reactions.

• Operative technique.

3. To discuss priorities [airway, breathing, circula- tion (ABC)] and goals of resuscitation:

• To defend choice of fluids.

• To discuss indications for transfusion.

• To discuss management of acute coagulopathy.

Case

You are asked to evaluate a 70-year-old woman who has had a femoral- peroneal artery bypass with in-situ saphenous vein because of brisk bleeding from the incision. She is anxious and has a pulse of 109 and a blood pressure of 89/45 mm Hg.

Introduction

Coagulation relies on multiple interrelated steps. The process can be broken down into three main phases:

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• Phase I (vasoconstriction): Vascular injury results in the constriction of vascular smooth muscle and the early decrease in local blood flow.

• Phase II (platelet aggregation): In the presence of disrupted endothelium, thromboplastin is released, which stimulates the adherence and aggregation of platelets to subendothelial tissue.

• Phase III (coagulation cascade activation): Although hemostasis may occur solely through vasoconstriction and platelet aggregation, the generation of thrombin through the coagulation cascade is criti- cal in the formation of fibrin clot. Hemostasis and fibrin clot forma- tion work through the intrinsic and/or extrinsic pathways. Both pathways lead to a common enzyme, factor Xa, that then is followed by the common pathway (Fig. 8.1).

When first evaluating a bleeding patient, two crucial questions must be addressed:

1. Is the patient hemodynamically stable?

2. Why is the patient bleeding and how can it be stopped?

Is the Patient Hemodynamically Stable?

Whether or not the patient is hemodynamically stable can be deter- mined quickly by looking at the patient’s general appearance and by obtaining a set of vital signs. In the case presented at the beginning of this chapter, hemodynamic instability (a heart rate of 109 and blood pressure of 89/45) is caused by hypovolemia, which can be corrected with intravenous fluids. Despite the simple treatment for hypovolemia, the initial evaluation always should begin with the ABCs. Assuring adequate ABCs provides stabilization and permits a full history and a physical examination, thereby allowing question 2 to be answered.

Airway

The patient’s ability to maintain a patent airway should be evaluated, and rapid endotracheal intubation should be considered if the patient is unconscious or otherwise unable to maintain a clear airway. The patient in our case was “anxious,” which also means conscious, prob- ably communicative, and able to protect her airway.

Breathing

Adequate breathing should be confirmed by physical exam and pulse oximetry. Oxygen by nasal cannula, face mask, or endotracheal tube may be indicated.

Circulation

Heart rate and blood pressure are good indicators of circulatory

volume. Loss of less than 15% of blood volume may result in no change

in blood pressure or heart rate. Hemorrhage of 15% to 30% of blood

volume results in a decreased pulse pressure and tachycardia. Loss of

greater than 30% will result in a decrease in systolic pressure, reflex

tachycardia, and possibly other signs of shock, such as acidosis, tachyp- nea, oliguria, and decreased sensorium. The patient in our case has lost over 30% of her blood volume. (In an average-sized woman, that would be over 1500 cc.)

If there is an obvious site of active bleeding, direct pressure is most helpful. Our patient has brisk bleeding coming from her incision. Direct digital pressure should provide temporary hemostasis, while the circulating volume can be restored easily with adequate intravenous access. The maximum rate of delivery is limited by the length and gauge of the intravenous (IV) catheter. Therefore, two large (18 gauge or larger) IVs in the antecubital veins are recommended. The antecubital veins are large and easily accessible when rapid access is needed.

Crystalloid, such as normal saline or lactated Ringer’s, is indicated for the initial volume replacement. In adults, transfusion of blood products is indicated if signs of hypovolemic shock persist after approximately 2 L are infused (see Treatment, below). Laboratory tests also are done during this initial assessment (see Diagnostic Studies, below).

Figure 8.1. Critical steps in the coagulation cascade. The central pathway involves the activation of factors X to Xa and prothrombin to thrombin. In surgery, tissue factor (TF) generation is probably the initiating event, leading to Xa activation both through the intrinsic pathway (tenase complex) and by direct activation of X by the TR-VIIa complex. Subsequently, Xa assembles on the platelet phospholipid membrane to form the prothrombinase complex, which converts prothrombin to thrombin.

Factor XII

Factor XI

Factor IX

Factor VIII Factor X

Factor II (prothrombin)

Factor I (fibrinogen)

Factor V Factor VII

Intrinsic Pathway Extrinsic Pathway

Why Is the Patient Bleeding and How Can It Be Stopped?

To address this question, a complete history and a physical examina- tion should be performed. A few specific questions and diagnostic tests may help narrow the differential diagnosis and guide treatment.

Algorithm 8.1 addresses the emergency management of bleeding.

History

Review of Systems

Does the patient report any previous spontaneous bleeds (i.e., epis- taxis) or easy bruising? Does the patient report bleeding during simple daily activities, such as brushing his/her teeth? These simple items may provide a clue to an underlying tendency to bleed.

Past Medical History

Is there a history of liver dysfunction, such as hepatitis or cirrhosis (with associated decrease in synthetic function and decrease in coagu- lation factors in the intrinsic pathway), or a history of renal failure with its associated dysfunctional platelets?

Medications

Multiple medications affect coagulation by a variety of mechanisms (Table 8.1). Many patients are unaware of the anticoagulant effect of some medications (i.e., nonsteroidal antiinflammatory drugs, NSAIDs, such as ibuprofen). The NSAIDs, including aspirin, irreversibly acety- late platelet cyclooxgenase, thus preventing the synthesis of throm- boxane A

. This effect is overcome only by new platelet synthesis over a period of 7 to 10 days.

Family History

Many coagulopathies are hereditary. Hemophilia A (factor VIII defi- ciency) and hemophilia B (factor IX deficiency or Christmas disease) are sex-linked recessive traits; other hereditary clotting abnormalities include factor I, V, VII, and X deficiencies and hereditary telangectasias (Table 8.2). Deficiencies of the various factors generally must be moderate to severe to affect clinically on bleeding.

Operative History

A complete understanding of what operation was performed and the

technical details is critical in dealing with a postoperative bleeding

problem. Did the patient have adequate hemostasis at the time of

surgery? (This history should be obtained from the operating surgeon.)

Diffuse microvascular bleeding and failure to form adequate clot is

suggestive of an underlying clotting abnormality. Significant, bright

red bleeding from a surgical wound might represent a suture line leak

and require reexploration. Alternatively, if there were many adhesions

that were divided at the time of surgery, these can be a source of

postoperative bleeding. What medications or blood products did the

patient receive while in the operating room? If the patient received

large-volume transfusions with packed red cells, clotting factors and

Apply direct pressure if possible.

Ensure adequate airway and ventilation Begin volume resuscitation with 3L of crystalloid Obtain history, perform physical examination, and send for initial laboratory tests: • Hematocrit • Platelet count

• PT/PTT • Type and crossmatch Bleeding is surgically correctable Patient is unstable Systolic hypotension should initiate the transfusion of red blood cells; start with 2 units.

Patient is stable after administration of 3L of crystalloid No further support of hemostatic system is necessary. Patient requires continued transfusion Include plasma in transfusion fluids; start with 2 units. Search for coagulopathy: Measure fibrinogen levels, fibrin split products, and bleeding time; obtain factor assay. Administer replacement products Give platelets and cryoprecipitate as indicated.

Patient regains hemodynamic stability. No treatment of coagulopathy is necessary.

Bleeding is diffuse Search for coagulopathy: measure fibrinogen levels, fibrin split products, and bleeding time; obtain factor assay. Continue therapy without waiting for results. Patient is stable after administration of 3L of crystalloid No further support of hemostatic system is necessary.

Patient is unstable Systolic hypotension should initiate the transfusion of red blood cells; start with 2 units. Patient requires continued transfusion Include plasma in transfusion fluids; start with 2 units.

Patient regains hemodynamic stability No treatment of coagulopathy is necessary. As results of earlier laboratory tests become available, review indications for administration of platelets and cryoprecipitate Patient has acquired bleeding disorder from anticoagulation Discontinue anticoagulant. Consider giving protamine. Consider giving vitamin K (10mg I.V.)

Patient has coagulation defect Give specific factor, cryoprecipitate, or FFP.

Patient has undergone massive transfusion Give platelets and FFP.

Patient has primary fibrinolysis Consider using fibrinolytic inhibitors (EACA) if condition is adequately differentiated from DIC.

Patient has DIC Treat underlying disorder. Algorithm 8.1.Algorithm for emergency management of bleeding.

platelets may be diluted. In addition, large-volume transfusions (over one blood volume, i.e., 5 L) may cause a patient to become calcium depleted. Citrate used to anticoagulate banked blood binds calcium, and calcium is necessary as a cofactor in multiple steps of both the intrinsic and extrinsic pathways (Fig. 8.1).

Physical Examination

Patients with abnormal bleeding often develop ecchymoses and hematomas at IV catheter or venipuncture sites. Bright red blood (well oxygenated) from the surgical incision suggests an arterial source. In the patient in our case, a leak from the anastomosis is pos- sible. If this does not resolve with local compression, reexploration may be indicated. Darker blood suggests venous bleeding or old hematoma. Postoperative venous bleeding may cease with local com- pression. Not all postoperative bleeding complications involve bleeding that is external. If bleeding is suspected, a complete phys- ical exam may yield clues to occult bleeding. However, in obese patients, soft tissues can mask a significant amount of bleeding. Fur- thermore, the chest, abdomen, pelvis, and retroperitoneum all may hold significant amounts of blood, with only subtle clues to the exam- ining healthcare practitioner. If a thoracic operation was performed, the chest should be auscultated carefully and percussed for dullness, and the chest tube output should be inspected for quality (sanguinous vs.

serosanguinous) and volume. If an abdominal operation was per- formed, abdominal pain, girth, and signs of flank ecchymosis should be evaluated.

Table 8.1. Alterations of hemostasis by common drugs.

Severity of

Drug Mode of action Duration effect

Warfarin Inhibits synthesis of factors 5–7 days Major II, VII, IX, XI

Heparin Inhibits clotting factor 4–6 hours Major activators; immune

thrombocytopenia 2–4 days Variable Aspirin Blocks platelet secretion, 5–7 days Major

aggregation

Ticlopidine Unknown 5–7 days Major

Nonsteroidal Blocks platelet section, 1–2 days Moderate antiinflammatory aggregation

drugs

Dipyridamole Inhibits platelet aggregation 1–2 days Mild Dextran Impairs platelet adhesion, 3–5 days Moderate

aggregation

Calcium channel Inhibits platelet aggregation 1 day Mild blockers (in large doses)

Vasodilators Inhibits platelet aggregation Short Mild Quinidine Immune thrombocytopenia 2–4 days Variable Various antibiotics Inhibits platelet aggregation Few days Variable Source: Reprinted from Sobel M, Dyke CM. Hemorrhage and thrombotic complications of cardiac surgery. In: Baue AE, Glenn A, Geha AS, eds. Glenn’s Thoracic and Cardio- vascular Surgery. Stamford: Appleton and Lange, 1996, with permission.

Table 8.2.Hereditary hemorrhagic disorders not involving factor VIII. Deficient factorInheritanceType of bleedingAssaysTreatment Factor IX (Christmas disease,Sex-linkedIdentical to that in factor Long PTTFFP or factor IX conc PTC deficiency, VIII deficiencySpecific assayBiologic half-life 20–24hr hemophilia B) Factor XI (PTAdeficiency)Autosomal recessiveLess severe than that in Long PTTFFP hemophilia Aor BSpecific assayBiologic half-life is 60hr Factor XIIAutosomal recessiveNoneLong PTTNone Specific assay Factor V (parahemophilia)Autosomal recessivePostoperative andLong PTT, PTFFP spontaneous bleedingNormal P and PBiologic half-life is 60hr Rarely hemarthrosisSpecific assay menorrhagia Factor XAutosomal recessive Epistaxis, hemarthrosis,Long PT, PTT, PFFP (only homozygotesecchymoses,and PBiologic half-life is 48hr bleed)menorrhagiaSpecific assay Factor VIIAutosomal recessive Epistaxis, hemarthrosis,Long PT, P and PFFP (only homozygotesecchymoses, Normal PTTBiologic half-life is 4–6hr bleed)menorrhagiaSpecific assay Factor IIAutosomal recessiveEpistaxis, hemarthrosis,Long PT, P and PFFP ecchymoses,Specific assayBiologic half-life is 72hr menorrhagia Factor IAutosomal recessiveVariable, deep tissueLong PTCryoprecipitate: each bag hemorrhageLow fibrinogen levelcontains 400–500 Fibrinogen; 100mg/dL required for hemostasis Biologic half-life is 100hr Factor XIIINot clearUmbilical bleeding,Clot solubility inFFP posttraumatic and late5M ureaBiologic half-life is 120hr postoperative bleeding Wound heals slowly w/keloid formation FFP, fresh frozen plasma; PT, prothrombin time; Pand P, prothrombin proconvertin; PTA, plasma thromboplastin antecedent; PTC, plasma thromboplastin component; PTT, partial thromboplastin time. Source:Reprinted from Addonizio VP, Stahl RF. Bleeding in emergency care. In: Wilmore DW, Cheung LY, Harken AN, et al, eds. Scientific American Surgery. New York: WebMD Corporation, 1989.

Diagnostic Studies

After taking a history and performing a physical exam, the clinician should have narrowed the differential diagnosis. Laboratory tests will be helpful in confirming the diagnosis and managing the patient appropriately with respect to blood loss.

Complete Blood Count (CBC)

A preoperative CBC is obtained in most patients. Postoperative levels should be compared with preoperative levels. The amount of blood loss usually is well represented by the decrease in hemoglobin and hematocrit. However, in the setting of acute blood loss, the hemo- globin and hematocrit are not accurate, as they take some time to equi- librate after acute blood loss. For example, the patient in our case may have a hemoglobin of 10 g/dL (intraoperative hemoglobin of 11 g/dL), low urine output, and significant bloody drainage from an incision site.

However, once her intravascular volume has been restored and the hemodyamics are corrected with crystalloid, she will have a much lower hemoglobin.

Platelet Counts

Platelet counts are affected by a variety of causes as well as medica- tions (Table 8.3). Heparin, ranitidine, or cimetidine cause thrombocy- topenia in some patients and should be discontinued if platelet counts decline during their use. Postoperative bleeding in the setting of moderate to severe thrombocytopenia mandates platelet transfusions.

However, a normal platelet count is not synonymous with normally functioning platelets. As mentioned above, aspirin affects the platelet function without a change in platelet count.

Prothrombin Time (PT) and Partial Thromboplastin Time (PTT) (Table 8.3)

Prothrombin time evaluates the extrinsic pathway. Elevations are caused by liver dysfunction or Coumadin use. Liver dysfunction may result in abnormal synthesis of prothrombin and factors VII, IX, and X.

Coumadin inhibits synthesis of these factors, which are vitamin K dependent. The international normalized ratio (INR) is a method used to measure the degree of anticoagulation and is a ratio of the patient’s PT to the control PT. Partial thromboplastin time tests the intrinsic pathway. Elevations in PTT are caused by deficiencies in factors XII, XI, IX, and VIII as well as factors in the common pathway. Also, PTT is used to monitor the degree of anticoagulation on heparin. Heparin accelerates the binding of thrombin to antithrombin III, thus potenti- ating its anticoagulant effect.

Bleeding Time (Table 8.3)

A very good index of a patient’s coagulation is the bleeding time. A

standardized injury at the skin level is created with an automatic lancet,

and the amount of time necessary to clot is the bleeding time. (Ivy

forearm method normal is 2 to 9.5 minutes.) The test is somewhat cum-

bersome to perform and probably is underutilized. It measures the

adequacy of coagulation factors as well as platelet function, thus taking

into account all of the components necessary to achieve hemostasis. For example, aspirin use may affect bleeding and bleeding time, yet platelet count and PT/PTT will be normal. Also, patients with uremia may have platelets that do not function properly, yet their platelet count may be normal.

Liver Function Tests (LFTs, Including AST/ALT/Total Bilirubin/Alkaline Phosphatase)

Abnormalities in coagulation factors made in the liver (factors II, VII, IX, and XI) affect bleeding. Hepatitis, passive liver congestion, cir- rhosis, and hepatic ischemia all can result in hepatic dysfunction, decreased protein synthesis, and abnormal coagulation. Abnormal LFTs can alert the physician to one of these conditions and the propen- sity to bleed. An elevated alkaline phosphatase may suggest biliary obstruction and an associated decrease in vitamin K–dependent factors.

Table 8.3. Common causes for abnormalities in coagulation screening tests and sugges- tions for initial further analysis.

Finding Potential cause Further test

Thrombocytopenia Immune thrombocytopenia (ITP) Antiplatelet antibodies, thrombopoietin

Impaired platelet production Complete blood cell count and bone marrow analysis

Disseminated intravascular aPTT, PT, fibrin degradation

coagulation products

Heparin-induced HIT test

thrombocytopenia

Prolonged bleeding Von Willebrand disease or Platelet aggregation tests and von

time thrombocytopathic Willebrand factor

Uremia, liver failure, — myeloproliferative disorder,

etc.

aPTT prolonged, Coagulation factor deficiency Measure coagulation factor PT normal (factor VIII, IX, XI, or XII)

Use of heparin —

PT prolonged, Coagulation factor deficiency Measure coagulation factor aPTT normal (factor VII)

Vitamin K deficiency Measure factor VII (vitamin K–dependent) and factor V (vitamin K–independent) or administer vitamin K and repeat after 1–2 days

(Mild) hepatic insufficiency —

Both aPTT and PT Coagulation factor deficiency Measure coagulation factor prolonged (factor X, V, II or fibrinogen)

Use of oral anticoagulants —

Severe hepatic insufficiency Measure coagulation factors

Disseminated intravascular Platelets, fibrin degradation products coagulation

Loss/dilution caused by excessive — bleeding/massive transfusion

aPTT, activated PTT; HIT, heparin induced thromcytopenia.

Source: Reprinted from Levi M, van der Poll T. Hemostasis and coagulation. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence, New York: Spinger-Verlag, 2001, with permission.

Blood Urea Nitrogen (BUN)/Creatinine

Patients with uremia have dysfunctional platelets and are more likely to bleed. Platelet dysfunction in uremia is extremely complex and involves multiple qualitative defects, including defects in adhe- sion, aggregation, and proteins responsible for platelet contractile function.

Fibrin Degradation Products (FDP) and Fibrinogen

Disseminated intravascular coagulation (DIC) is a frequently encountered consumptive coagulopathy in which platelets and fi- brinogen are consumed. It involves an activation of the coagulation system with a concomitant activation of fibrinolysis. As a result, platelet counts and fibrinogen levels decrease, and fibrin split products increase.

Treatment

As mentioned earlier, the treatment of hypovolemia occurs simulta- neously with the evaluation for its cause. If a surgical etiology is identified, local pressure may result in hemostasis. Bleeding that fails control by local pressure may require a second operation for suture repair or cauterization of bleeding sites. If a nonsurgical etiology is suspected, therapy should be directed toward the specific abnormality.

Fluid resuscitation is accomplished by the use of three main types of volume expanders: crystalloid solutions, colloid solutions, and blood products. Each category has specific indications, advantages, and dis- advantages.

Crystalloid Solutions

A wide variety of crystalloid solutions exists and constitutes the first line of therapy for patients who are hypovolemic. Lactated Ringer’s solution and normal (0.9%) saline are used most frequently. These solu- tions are isotonic and can be given in large amounts without causing significant electrolyte aberrations (Table 8.4). Hypertonic saline is used occasionally in emergency situations with the intention of mobilizing interstitial fluid intravascularly, thus increasing circulating volume.

Although crystalloid equilibrates with the interstitium almost imme- diately, it has few disadvantages other than hemodilution and fluid overload.

Table 8.4. Volume resuscitation.

Effect on intravascular

Sodium pH volume Cost Volume

Normal saline 140 5.7 + + 1000 cc

Ringer’s lactate 130 6.7 + + 1000 cc

6% hetastarch 154 3.5–7.0 +++ ++ 500 cc

5% albumin 130–160 6.4–7.4 ++ +++ 250–500 cc Packed red cells 135–145 6.6–7.6 +++ ++++ Approx. 300cc

Colloid Solutions

The use of colloids is common in clinical practice; however, the true value of colloid use remains controversial. Colloid is very expensive when compared to crystalloid. It has the advantage of containing larger molecules (i.e., protein or starch), and thus it remains in the intravas- cular space longer than crystalloid. However, despite that advantage, colloid molecules eventually do equilibrate with the interstitial space, thus that short-term advantage is lost.

Blood Products

Transfusion of blood products exposes the recipient to a number of risks, minimized by stringent blood bank protocols, but it is indicated for a number of reasons discussed in this section. Risks include febrile reactions, allergic reactions, hemolytic reactions, and infectious com- plications. Simple febrile reactions are thought to be due to leukocyte antigens, whereas hemolytic reactions are caused by ABO incompati- bility. Allergic reactions are much less frequent. Most of these reactions occur in patients with a prior transfusion history. Hemolytic reactions may be severe and potentially fatal if the amount of infused blood is large. Thus, any suspicion of a possible transfusion reaction must result in an immediate cessation of blood product infusion and in further workup to delineate the type of reaction.

A significant degree of public anxiety is directed at the possibility of blood-borne infection. Realistically, the risk of transmitting various blood-borne infections is low with current antigen screening. The risk of hepatitis B is estimated at 16/1,000,000, hepatitis C at 10/1,000,000, and HIV at approximately 1/500,000.

Whole blood is available, but component blood products allow treatment for specific deficiencies without volume overload. Compo- nent therapy also avoids the use of scarce blood fractions that might not be needed in the specific circumstance.

Packed Red Blood Cells (PRBCs): Packed red blood cells have a typical hematocrit of about 70%. One unit measures approximately 250 cc. It is important to know that in an average-sized adult (70 kg), one unit of PRBCs raises the systemic hematocrit approximately 3%. Posttransfu- sion hemoglobin and hematocrit levels that do not increase appropri- ately may indicate ongoing, possibly occult, blood loss. In a critically ill patient, a hematocrit of about 30% to 35% is desired for optimal oxygen-carrying capacity and oxygen delivery. This is used as a general guideline to determine the amount of PRBCs necessary. PRBCs also are associated with fewer febrile and allergic reactions than whole-blood preparations.

Fresh Frozen Plasma (FFP): Fresh frozen plasma is an acellular fraction of whole blood. One unit measures approximately 200 to 250 cc. Fresh frozen plasma contains clotting factors, fibrinogen, and other plasma proteins. However, factors V and VIII are less stable, and therefore FFP is not a good source for these factors.

Platelet Concentrates: Platelet concentrates typically come in 8 to 10

packs. Each pack measures approximately 25 to 50 cc. Platelet concen-

trates are given when thrombocytopenia exists in the setting of bleed- ing or when platelet dysfunction exists even in the presence of a normal platelet count (in patients with renal failure or post–cardiopulmonary bypass). The platelet count generally will rise 5000 to 10,000 per “pack”

transfused. Platelet counts that do not increase appropriately also may indicate ongoing blood loss or platelet consumption, that is, DIC.

Cryoprecipitate: Cryoprecipitate is a concentrate of factor VIII, fibrino- gen, and von Willebrand factor. It is given in 10 unit “packs” that are pooled from 10 different donors. Each “pack” in the 10-pack consists of 1 cc of cryoprecipitate diluted with some saline. These factors are decreased in patients with hemophilia A (because of synthetic defi- ciency), in patients who have had massive transfusions (because of factor dilution), and in patients with DIC (because fibrinogen is con- sumed).

Factor VIII or Factor IX Concentrates: Specific factors, such as factor VIII or factor IX concentrates, should be used in patients with known defi- ciencies. Hematologic consultation can greatly assist in the manage- ment of these complex patients.

Calcium: Calcium is a major cofactor of both intrinsic and extrinsic pathways. As mentioned before, calcium becomes depleted after multiple PRBC transfusions. Therefore, empiric calcium supplementa- tion with 1 g of calcium gluconate or 1 g of calcium chloride is indicated in patients with large-volume transfusions or with low calcium levels.

Case Management and Conclusion

Upon hearing the nurse’s concerns regarding the incisional bleeding of the patient in our case, you immediately go to the patient’s bedside to assess her. You find the above-stated vital signs, including a respira- tory rate of 25, oxygen saturation of 95%, and a large puddle of bright blood in her bed. You first talk with her and establish her level of con- sciousness and airway/breathing. You then make sure she has ade- quate IV access (which she does since she just had surgery earlier that day). You ask the nurse to give her a 500-cc bolus of normal saline (NS), and you ask an assistant to insert a Foley catheter so you can monitor her urine output closely. As someone else is obtaining the laboratory values of a CBC, PT/PTT, and ABG, you continue to assess the patient by checking the site of bleeding. The groin incision is continuously draining blood during this time period; a pressure dressing is placed.

However, over the next 30 minutes, the patient soaks the pressure dressing, has had minimal urine output, and has a blood pressure of 110/60. The laboratory values return with the PT/PTT minimally ele- vated; the hemoglobin is now 7.5 g/dL. You decide to transfuse her 1 unit of PRBCs. You call the attending surgeon to tell him of the events.

You also tell him that you think this is surgical bleeding and that the

patient needs to return to the operating room for a repair.

Summary

An understanding of the processes of hemostasis and thrombosis is necessary for every surgical procedure. There are a large number of biochemical events that occur in response to endothelial injury that result in the formation of a fibrin clot. Clinical bleeding may result from a defect or deficiency in any of these events or from technical error. An understanding of the specific history and physiology of a particular patient and of the intraoperative details is necessary to diagnose the etiology of postoperative bleeding. In the case discussed in this chapter, because of the large amount of bright red blood, the attending surgeon is concerned about a technical error that mandates a second trip to the operating room. The treating physician must be aware of the risks, benefits, and indications of the various treatments for postoperative bleeding.

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