Key points
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Preoperative recognition of anemia is essential to provide a systems approach to treatment.
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The decision to transfuse a patient with blood products should be based on the entire clinical picture and not the absolute laboratory value.
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Coexisting diseases of leukocytes can alter anesthetic care. Careful preoperative evaluation helps avoid complications from obstructive tumor and radiation and chemotherapy side effects.
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Thrombocytopenia and diseases related to platelets present special anesthetic challenges; preoperative evaluation is necessary to assess the potential for bleeding and guide treatment, including possible transfusion.
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Alterations in the coagulation cascade can result in thrombosis or hemorrhage and should be closely monitored and evaluated.
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Point-of-care testing is useful to determine the patient’s transfusion needs and quickly evaluate the coagulation profile.
The hematologic system plays a central role in maintaining homeostasis, although its importance is often overlooked by many clinicians. The consideration of pathologies that affect hemostasis is critical in caring for a patient in a perioperative setting. This chapter highlights both common and uncommon abnormalities of the hematologic system and provides treatment strategies. Anesthesiologists are often faced with the daunting task of caring for patients with coagulation abnormalities and must balance the risk of surgical bleeding versus potential thrombosis. An understanding of these diseases will improve patient care.
Anemias
Anemia is defined as hemoglobin (Hb) concentrations less than 11.5 grams per deciliter (g/dL) in females and 12.5 g/dL in males. It is a common finding, occurring in 35% to 56% of patients presenting for surgery and 84% to 90% of patients postoperatively. Preoperative testing is often the only way to diagnose patients with anemia because many are asymptomatic. Patients with more severe anemia may refer to a number of clinical symptoms, including fatigue, depression, anorexia, nausea, menstrual abnormalities, tachycardia, and exertional dyspnea.
In the preoperative period the causes of anemia are multifactorial, and the clinician is responsible for investigating possible causes of low Hb concentrations. Potential causes of anemia during this period are iron deficiency, renal insufficiency, malignancy, chronic disease, gastrointestinal (GI) bleeding, and decreased red blood cell (RBC) life span. To aid in the differential diagnosis, erythrocyte indices are used to help categorize anemias and pinpoint probable causes of anemia ( Table 11-1 ). Erythrocyte (RBC) indices are defined as follows ( Hct, hematocrit):
Mean corpuscular hemoglobin: MCH = Hb × 10/RBC
Mean corpuscular volume: MCV = Hct × 10/RBC
Mean corpuscular hemoglobin concentration: MCHC = Hb/Hct
| Anemia | RBC Size | Chromatic | MCH/MCV | Reticulocytes | Serum Iron |
|---|---|---|---|---|---|
| Thalassemia | Microcytic | Hypo- | ↓ | ↓ | ↑ |
| Myelodysplastic syndrome | Microcytic | Hypo- | ↓ | ↓ | ↑ |
| Iron deficiency | Microcytic | Hypo- | ↓ | ↓ | ↓ |
| Inflammation-infection | Micro/normocytic | Hypo/normo- | ↓/↑ | ↓ | ↓ |
| Tumor | Micro/normocytic | Hypo/normo- | ↓/↑ | ↓ | ↓ |
| Hemolytic anemia | Normocytic | Normo- | Normal | ↑ | Normal |
| Hemorrhage | Normocytic | Normo- | Normal | ↑ | Normal |
| Aplastic anemia | Normocytic | Normo- | Normal | ↓ | Normal |
| Renal failure | Normocytic | Normo- | Normal | ↓ | Normal |
| Megaloblastic | Macrocytic | Hyper- | ↑ | Normal | Normal |
| Hypochromatic Microcytic Anemia | Normochromatic Normocytic Anemia | Hyperchromatic Macrocytic Anemia |
|---|---|---|
| MCH + MCV reduced | MCH + MCV normal | MCH + MCV increased |
| Serum iron increased: thalassemia, myelodysplastic syndrome | Reticulocytes increased: hemolytic anemia, hemorrhage | Normal reticulocytes: megaloblastic anemia |
| Serum iron decreased: iron Deficiency anemia | Reticulocytes decreased: aplastic anemia, renal anemia | Iron decrease and ferritin increase: inflammatory, infection, and tumor anemia |
Anemia in the postoperative setting is common and often the result of diminished erythropoiesis during early recovery period, frequent phlebotomies, and untreated surgical bleeding. Predictors of perioperative anemia include African ancestry, female gender, low preoperative serum levels, and smaller body size. Anemia complicates patient care in the perioperative period by decreasing oxygen (O 2 ) content in circulating blood, which in turn can reduce O 2 delivery to peripheral tissues. To avoid hypoxia, the cardiovascular system must compensate by increasing cardiac output.
When interpreting the formula in Box 11-1 , one sees that physically dissolved oxygen (Pa o 2 × 0.003) results in only a fraction of the total oxygen content (Ca o 2 ) found in blood. The vast majority of oxygen is bound chemically to hemoglobin. This makes it easy to understand why in states of hypoxemia, the clinician should treat the anemic patient, provided a normal arterial oxygen partial pressure (Pa o 2 ) exists, with the administration of erythrocytes, most often given in form of packed red blood cells (PRBCs). Increasing the fraction of inspired oxygen (Fi o 2 ) and thus increasing Pa o 2 only leads to slight increases in Ca o 2 .
Do 2 = CO × ( Hb × Sao 2 × 1. 34 + Pao 2 × 0.003 )
where D o 2 = oxygen delivery; CO = cardiac output; Hb = hemoglobin concentration; Sa o 2 = percent of oxygenated hemoglobin; 1.34 = Hüfner number (constant 1.34-1.36); and 0.003 = dissolved oxygen (mL/mm Hg/dL)
One of the controversial topics in recent years has been determining the threshold at which anesthesiologists should transfuse patients in the perioperative setting. The best hematocrit at which the O 2 -carrying capacity is ideally matched with the rheologic properties of blood is approximately 27%. However, the “10/30 rule” (10 g/dL Hb or 30% Hct), once thought to be the “gold standard” by many clinicians, has been challenged by recent studies. There is some evidence linking low preoperative Hb with adverse events such as increased risk of death, increased risk of transfusion, and prolonged hospitalization. The risk of a low value for starting Hb must be balanced with the known complications of allogenic blood transfusion. In fact, patients who receive transfusion are at high risk for perioperative infection due to the immunomodulating effects of transfusion. Thus, transfusing RBCs solely on the basis of Hb concentration or Hct is no longer considered proper care. It is prudent to investigate the cause of anemia and treat the underlying condition rather than transfusing PRBCs to reach a target Hb. Indications for transfusion of RBCs should be based on the O 2 supply/demand ratio in the individual patient. Decreased mixed venous oxygen saturation (S 
o 2 ), serial measurements of lactate showing progressively increasing concentrations, and electrocardiographic changes suggestive of myocardial ischemia are appropriate indications for transfusion of RBCs. For example, Nelson et al. found that Hct less than 27% was associated with an increased incidence of myocardial ischemia and infarction in patients undergoing infrainguinal bypass surgery.
Despite great advancements in transfusion medicine, life-threatening complications still do occur. Transfusion reactions can be divided into three major pathophysiologic groups. The most common complication is the transfusion of immunologic incorrectly matched blood, resulting in hemolysis. The ABO and Rhesus antigens are responsible for this reaction. Patients under general anesthesia will present with hypotension, tachycardia, and hemoglobinuria, possibly progressing to acute renal failure (acute kidney injury). Second, febrile nonhemolytic reactions are seen in 0.5% to 5% after transfusion of blood products. These reactions are caused by leukocyte and thrombocyte antigens. Third, transmission of infectious diseases, including hepatitis B and C viruses and human immunodeficiency virus (HIV), is a rare phenomenon but has serious and long-lasting consequences for the patient.
The complications of blood product transfusion should always make the clinician weigh benefits against potential risks. Strict indications for the transfusion of blood products should be employed. Transfusion solely to achieve volume expansion or to raise Hct to a certain value cannot be recommended. Finally, in a society becoming more and more conscious of the financial burden brought on by its health care system, avoiding unnecessary transfusions poses a major source of potential savings.
Treatment
The treatment options for a patient with anemia first focus on discovering the etiology of the disease. The use of transfusion is only indicated in symptomatic patients or in those patients who would benefit from a higher O 2 -carrying capacity.
Iron Deficiency Anemia
Iron deficiency anemia is the most-often diagnosed anemia in the industrialized world. Its cause is usually chronic blood loss (e.g., menstruation, chronic GI bleeding) or increased requirements seen in pregnancy or infancy. An adult has approximately 3000 mg (45 mg/kg) of elemental iron in their body. An adult man requires daily iron intake of 12 mg to absorb 1 mg, to compensate for losses, and a woman requires 15 mg to absorb 2 mg. During pregnancy, iron intake must be doubled to compensate for approximately 3 mg of daily iron losses.
Iron deficiency anemia is a microcytic, hypochromatic anemia with increased serum transferrin, low serum ferritin, and low serum iron concentrations. Microscopic examination of bone marrow reveals low to missing iron depots. The differential diagnoses for iron deficiency anemia are listed in Table 11-2 . Clinically, these patients have general anemia symptoms as well as symptoms from skin and mucous membrane problems. Koilonychia, hair loss, Plummer-Vinson syndrome, and perlèche are all symptoms associated with iron deficiency.
| Disorder | Serum Iron | Transferrin | Serum Ferritin |
|---|---|---|---|
| Iron deficiency | ↓ | ↑ | ↓ |
| Myelodysplastic syndrome | ↑ | ↓ | ↑ |
| β-Thalassemia | Normal-↑ | Normal-↓ | Normal-↑ |
| Inflammatory or tumor associated | ↓ | ↓ | ↑ |
Treatment
Patients with iron deficiency anemia receive oral or parenteral iron replacement therapy, as the source of chronic blood loss is located. The goal of treatment is to return Hb levels and restore MCV to normal. A complete investigation should be performed to determine the etiology of the microcytic anemia and prevent further iron loss. The supplementation of iron is with ferrous sulfate, 200 mg three times daily; alternatively, ferrous gluconate or ferrous fumarate is used. Ascorbic acid can be given concomitantly to enhance iron absorption. An Hb increase of 2 g/dL should occur within 3 to 4 weeks of initiating treatment.
Thalassemia
Thalassemia consists of a group of inherited disorders resulting in the inability to produce structurally normal globin chains. This results in an abnormal hemoglobin molecule with subsequent hemolysis. The disorder can affect synthesis of both the alpha (α) and the beta (β) globin chain, and depending on whether the bearer is homozygous or heterozygous, the disease is called major or minor. β-Thalassemia major (Cooley’s anemia) is rare and carries a poor prognosis. Patients of Mediterranean descent present with this illness in early stages of life. Patients have prehepatic jaundice, hepatosplenomegaly, and an increased susceptibility to infection. Because of multiple blood transfusions, patients also develop secondary hemochromatosis and die of complications related to cardiac hemochromatosis (e.g., arrhythmias, congestive heart failure). β-Thalassemia is not compatible with life.
Patients with minor thalassemias show mild anemic states with microcytic, hypochromatic erythrocyte indices. Iron stores are normal or increased. The diagnosis is confirmed by Hb electrophoresis.
Treatment
In its mild form, thalassemia rarely requires an intervention. With more severe disease, folic acid and possible RBC transfusion may become necessary. Patients with advanced disease require frequent transfusions and folic acid; some require splenectomy and bone marrow transplantation. It is important to avoid iron supplementation.
Megaloblastic Anemias
Megaloblastic anemias are anemias with macrocytic, hyperchromatic erythrocyte indices. The two most common forms are vitamin B 12 deficiency and folic acid deficiency. Both vitamin B 12 and folic acid are important cofactors in the synthesis of DNA. A deficiency of either vitamin leads to an insufficient amount of DNA, resulting in the inability of bone marrow to produce an adequate amount of blood cells. This in turn results in large blood cells, each packed with an abnormally high amount of hemoglobin.
Vitamin B 12 deficiency is most often caused by an autoimmune disease and results in pernicious anemia. An autoantibody targeted toward the intrinsic factor leads to the inability to absorb vitamin B 12 . Intrinsic factor is produced by gastric parietal cells and is required to absorb vitamin B 12 (extrinsic factor) in the terminal ileum. Other causes are rare and include strict vegetarian diet, malabsorption syndromes, stasis (blind loop) syndrome, and tapeworm (Diphyllobothrium latum) infection ( Box 11-2 ).
Vegetarian diet
Reduction in intrinsic factor
Pernicious anemia
Subtotal or partial gastric resection
Malabsorption syndrome
Tapeworm (Diphyllobothrium latum) infection
Stasis (blind loop) syndrome
Vitamin B 12 deficiency can also lead to neurologic and gastroenterologic symptoms. An atrophic tongue, known as Hunter’s glossitis, is a typical sequela of vitamin B 12 deficiency. Degeneration of the lateral and posterior spinal cord leads toperipheral neuropathy and gait ataxia. Depression and psychotic symptoms are also seen. Clinically, the loss of sensation to vibration is an early warning sign. The diagnosis is obtained by measuring vitamin B 12 concentrations in plasma. At present, parenteral administration of vitamin B 12 is the only therapeutic option.
Folic acid deficiency is the third most common cause of anemia seen in pregnancy, resulting from increased requirements. Other risk factors for folic acid deficiency are alcoholism, abnormal dietary habits, and certain medications (methotrexate, phenytoin). Folic acid deficiency does not present with neurologic sequelae in the adult, although it has been linked to neural tube defects in early stages of pregnancy. The diagnosis is confirmed, as in vitamin B 12 deficiency, by measuring plasma concentrations. Folic acid, however, can be supplemented orally.
Nitrous oxide (N 2 O) can irreversibly oxidize the cobalt ion found in vitamin B 12 . Therefore, use of N 2 O should be avoided in patients with megaloblastic anemia, to avoid a synergistic effect. Otherwise, the same principles apply as in treating any other form of anemia.
Treatment
The treatment of patients with megaloblastic anemia consists of cobalamin and folate. It is rarely necessary to transfuse patients because the anemia develops over time, and patients tend to compensate for their low hemoglobin.
Hemolytic Anemias
Hemolytic anemias can be caused by corpuscular defects of the erythrocyte or by extracorpuscular pathologic processes. Typical corpuscular hemolytic anemias are seen with cell membrane defects (e.g., spherocytosis), hemoglobinopathies (e.g., thalassemia, sickle cell disease), or enzyme defects within the erythrocyte (e.g., glucose-6-phosphate dehydrogenase or pyruvate kinase deficiency). Extracorpuscular hemolytic anemias are immunologically mediated (Rh incompatibility, ABO transfusion reactions, autoimmune hemolytic anemias) and result from consumption of certain medications, infectious diseases, metabolic derangements (Zieve syndrome), or microangiopathic pathologic processes (hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura).
Treatment
Patients with hemolytic anemia are treated according to the cause of their disease. Options include folic acid, corticosteroids, and intravenous immune globulin (IVIG).
Spherocytosis
Spherocytosis is one of the most common inherited hemolytic anemias. It is caused by a defect in the erythrocyte membrane, which leads to an increased permeability for sodium and water, giving the erythrocyte its characteristic spherical form. This renders the erythrocytes susceptible to phagocytosis in the spleen at an early age. Patients are prone to hemolytic crisis and gallstones, formed primarily of bilirubin. Normocytic anemia accompanied by signs of hemolysis (increased indirect bilirubin, increased lactate dehydrogenase, increased reticulocytes) is the typical laboratory finding. The diagnosis is confirmed by osmotic testing of erythrocytes.
Patients with recurrent hemolytic crisis may have undergone splenectomy. The anesthesiologist must be aware that these patients, if not properly vaccinated, are at increased risk for sepsis (overwhelming postsplenectomy sepsis).
Treatment
In neonates with hereditary spherocytosis and hyperbilirubinemia, it may be necessary to initiate phototherapy to prevent kernicterus. In addition, transfusion of RBCs and exchange transfusion need to be considered. Aplastic crisis can cause a significant drop in Hb and may require blood transfusion. Folic acid (1 mg/day) is administered to sustain erythropoiesis. Splenectomy is often curative and should be considered in patients with frequent aplastic crisis.
Hemoglobinopathies
There are approximately 300 known abnormal hemoglobin molecules. Most of these pathologic globin molecules differ from the physiologic α and β chains through exchange of only one amino acid with another. This section concentrates on the illnesses most likely seen in daily practice.
Sickle Cell Anemia
Sickle cell anemia is the most common form of inherited hemoglobinopathy found in humans; 5% to 10% of African Americans are heterozygotic carriers. The mutation is in the sixth amino acid in the β chain of the Hb molecule; glutamic acid is replaced by valine. In its deoxygenated form, hemoglobin S (HbS) tends to precipitate, causing the erythrocytes to lose their normal biconcaval form and take on a sickled structure. This leads to sludging and eventually occlusion of the microvasculature, resulting in end-organ infarction.
Heterozygotic carriers are generally asymptomatic, expressing only a sickle cell trait found in laboratory testing (HbS < 50%). However, homozygotic carriers can display sickle cell crisis as early as infancy, with signs of hemolysis and painful vaso-occlusive infarctions (spleen, kidney, bones). Because of an atrophic spleen caused by recurrent microinfarctions, patients are prone to Streptococcus pneumoniae and Haemophilus influenzae infections of the respiratory tract and osteomyelitis. The diagnosis of sickle cell anemia is made through microscopic sickle cell testing or Hb electrophoresis.
Conventional anesthetic management is geared toward avoiding a sickle cell crisis during the perioperative period. Patients should be kept well hydrated, warm, and well oxygenated. Acidosis should be avoided at all costs. Sickle cell patients presenting for cardiac surgery can be appropriately managed by maintaining temperature and Hb concentration. Fast-track or early extubation protocols have been used with success. Many of the practices directed toward avoiding a sickle cell crisis are still followed in current management, but some of the classic “dogmas” have been challenged in the past decade. For example, the use of tourniquets for orthopedic procedures is no longer considered an absolute contraindication. Exchange transfusion solely with the intent to improve a laboratory value (HbS fraction < 30%) can no longer be considered proper standard of care. Griffin and Buchanan suggest that transfusion before elective surgery in children may not be necessary at all. They successfully provided anesthesia for 54 children with sickle cell disease without a transfusion and found that smaller surgical procedures could be easily performed without complication, but that pulmonary complications arose after laparotomy, thoracotomy, and tonsillectomy. Although benefits for pain management and rheology accompany neuraxial anesthesia, many investigators still believe that the patient with more complex sickle cell anemia is better managed using general anesthesia.
The anesthesiologist is sometimes asked to assist as a pain consultant in managing an acute sickle cell crisis. Adequate oxygenation, normothermia, and euvolemia are the cornerstones of management. Analgesia is achieved with opiates. Caution must be used with analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs), which can impair renal function because these patients frequently have renal microinfarctions with reduced baseline renal function. Vaso-occlusive crisis of the lower extremities can be managed with continuous neuraxial blocks. Occasionally a partial exchange transfusion with PRBCs is performed to increase the fraction of HbA greater than 50%. For rheologic reasons, Hct should not exceed 35%.
In parturients with sickle cell disease, transfusion therapy is recommended to treat the complications of the disease, especially those associated with chest pain syndromes, pre-eclampsia, and multiple gestations. Antibiotic prophylaxis for both mother and newborn should be actively practiced. The avoidance of adverse events during labor does not seem to be associated with the type of analgesia provided (regional vs. systemic) but appears more related to careful monitoring for the known consequences of the disease.
Newer therapies are being investigated for the anesthetic management of patients with sickle cell disease. Cytotoxic agents such as hydroxyurea stimulate the production of fetal hemoglobin and are being studied in the prevention of vaso-occlusive crises. Inhaled nitric oxide (iNO) and other investigational drugs have shown promise in reducing the sickling process and even unsickling cells.
Treatment
As stated, treatment of sickle cell anemia includes hydroxyurea and folate. Investigational treatments include NO, oral glutamine, butyrate, and arginine. Exchange or simple transfusion should be considered, depending on the type and complexity of surgery and individual patient needs.
Enzyme deficiency anemias
Enzyme defects within erythrocytes can lead to hemolysis. The two most common defects are glucose-6-phosphate dehydrogenase (G6PD) deficiency and pyruvate kinase (PK) deficiency.
Glucose-6-Phosphate Dehydrogenase Deficiency
G6PD deficiency is the most common enzyme deficiency anemia and is seen in individuals of African, Asian, or Mediterranean descent. The illness is inherited recessively on the X chromosome. Patients with this defect have erythrocytes containing a reduced amount of glutathione, leading to oxygenation injury of the cell membrane. A hemolytic crisis can be induced through infections or ingestion of beans and certain medications (e.g., sulfonamides, aspirin, quinidine). No specific therapy for G6PD deficiency exists. Avoiding trigger substances is the only recommendation available at present.
Pyruvate Kinase Deficiency
The PK deficiency is the most common defect of the glycolysis pathway. It has an autosomal recessive pattern of inheritance. The normal erythrocyte does not have mitochondria and relies on glycolysis to produce adenosine triphosphate (ATP) to maintain cellular integrity. Homozygous carriers for PK deficiency present with hemolytic anemia, splenomegaly, and acanthocytes.
Treatment
Patients with enzyme deficiency anemias are treated with removal of the precipitating agent. Supportive care with bed rest and oxygen are helpful while the patient’s Hb levels return to baseline. In those with the most severe forms of enzyme deficiency anemia, transfusion and splenectomy must be considered.
Antibody-induced hemolysis
Antibodies can result in two major reactions: hemolysis and agglutination. Antibodies directed against erythrocytes are either immunoglobulin M (IgM) or IgG in structure. IgM antibodies are larger (molecular weight, 900,000 daltons) and can act as a bridge between two erythrocytes. The term complete antibodies is sometimes used. Examples of IgM antibodies are ABO isoagglutinins and cold agglutinins. IgG antibodies are smaller in size (150,000 D) and cannot form a bridge between two erythrocytes (incomplete antibodies). Examples of IgG antibodies are Rhesus (Rh) agglutinins and warm antibodies. The Coombs test is used to diagnose the presence of incomplete antibodies either already attached to the surface of erythrocytes (direct Coombs) or in the patient’s serum (indirect Coombs).
Autoimmune Hemolytic Anemia
Autoimmune hemolytic anemias can be caused by either warm (IgG) or cold (IgM) antibodies; 70% of all autoimmune hemolytic anemias are caused by warm antibodies. Warm autoimmune hemolytic anemias are seen in patients with non-Hodgkin’s lymphoma, systemic lupus erythematosus, viral infection, and after ingestion of certain drugs (penicillin, α-methyldopa). These antibodies bind to the surface of erythrocytes at body temperature without causing hemolysis. The erythrocytes undergo phagocytosis in the spleen. The erythrocyte survival time can be diminished to only a few days, with erythropoiesis increased tenfold. About 15% of all patients with autoimmune hemolytic anemia present with cold antibodies. These antibodies are seen in patients after Mycoplasma pneumonias or mononucleosis. These antibodies lead to a Raynaud-like syndrome (acrocyanosis) and hemolysis as soon as intravascular temperature drops to below 25° to 30° C (77°-86° F).
Treatment
Patients with cold-agglutinin antibodies can often be managed with temperature regulation. Glucocorticoids are occasionally administered to patients with warm-antibody-induced hemolysis, but are of limited benefit with IgM cold antibodies. Chemotherapy and immunosuppressive therapy are generally reserved for patients with underlying malignancies. Plasmapheresis is useful in temporarily removing and reducing levels of IgM antibodies from plasma and can be used before a patient undergoes a hypothermic surgical procedure.
Traumatic hemolysis
Traumatic injury to erythrocytes leading to premature RBC destruction can be seen in patients with mechanical heart valves, intra-aortic balloon pumps, or after severe physical exertion (e.g., extreme hiking, runner’s anemia). Whenever feasible, remove the cause of hemolysis as quickly as possible. Other options are supportive treatment, and in the most severe cases, consider transfusion.
Renal anemia
Patients presenting for surgery with chronic kidney disease (CKD, chronic renal failure), with glomerular filtration rate (GFR) less than 30 mL/min, frequently have a normochromic, normocytic anemia (see Table 11-1 ) because of inadequate production of erythropoietin. Hb concentration is generally found to be about 9 g/dL. Transfusion of PRBCs is necessary should signs of ischemia develop. These patients are frequently treated with recombinant human erythropoietin to raise baseline Hb values. Patients often tolerate anemia caused by CKD. The need for transfusion should be reserved for those requiring increased O 2 -carrying capacity or expected blood loss. The use of epoetin alfa and more recently darbepoetin alpha are helpful options to increase Hb levels.
Acute blood loss/hemorrhagic shock
One of the most challenging situations for the anesthesiologist is to induce anesthesia for a patient in hemorrhagic or hypovolemic shock. A further complication is that acute hemorrhage is often difficult to diagnose. Laboratory values for hemoglobin are normal immediately after an acute blood loss. Loss of half the circulating blood volume will result in no change in Hb concentration unless fluid with a different Hb concentration is added. In clinical practice, fluids are administered parenterally after obtaining access to the circulatory system. Advanced Trauma Life Support protocols advise administering 2 L of crystalloid solution to patients in suspected hypovolemic shock. This will lead to dilution of the original Hb concentration. If intravenous (IV) fluids are not administered, anemia will result within hours through movement of interstitial fluid into the intravascular space. Because of this delay, Hb and Hct are not ideal parameters for detecting acute blood loss.
In addition to laboratory problems with diagnosis of acute blood loss, the volume state of a patient is also extremely difficult to assess clinically. Especially in young patients, the sympathetic nervous system is capable of masking even extreme states of hypovolemia, giving the clinician a false sense of security. Subtle signs such as orthostatic hypotension, tachycardia, narrowing pulse pressure, alterations of cerebral function, and low urine output must be sought before induction of anesthesia is indicative of hypovolemia. In an attempt to maintain adequate perfusion to the brain and myocardium, the autonomic nervous system compromises perfusion to the kidneys, skeletal muscular system, and gut. This redirection in blood flow is achieved by increasing the sympathetic adrenergic tone of the vegetative nervous system, resulting in increased heart rate, systemic peripheral resistance (SVR), and narrowing pulse pressure. As a result of impaired tissue perfusion, lactate concentrations increase while urine output and S 
o 2 decrease.
The treatment of acute blood loss is primarily aimed at replacing lost volume. This can be achieved by administering either crystalloid or colloid solutions. Whether primarily crystalloid or colloid solutions should be employed to replace lost blood volume is controversial. Blood products need to be administered because of the rapid dilution of RBCs and coagulation factors. The goal of therapy is aimed at restoring adequate perfusion and O 2 delivery to all organ systems. A successful course of treatment can be seen by normalization of vital signs, urine output, lactate concentrations, and S 
o 2 . Vasopressors should be used only as a temporary resort in maintaining perfusion pressure to the myocardium and cerebrum until adequate volume replacement can be achieved.
Inducing a hypovolemic patient is especially challenging to anesthesiologists because all induction agents can potentially reduce the adrenergic tone needed by the organism to maintain adequate perfusion pressure to the brain and myocardium. If not corrected quickly, a vicious cycle is started that will lead to further hemodynamic deterioration. Invasive monitoring and use of induction agents with the least suppressive effect on hemodynamics are recommended; ketamine and etomidate are good choices. If perfusion pressure declines, a vasopressor might be indicated until adequate access is obtained and volume loading begins.
Treatment
As previously described, treatment of acute blood loss is with transfusion of PRBCs. The clinician should consider the benefit of blood transfusion increasing O 2 -carrying capacity against possible transfusion-related adverse effects.
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