Apex Unit 9 FLuid / Blood Flashcards

Question

A septic patient undergoing exploratory laparotomy has developed bleeding from the wound and around his IV sites. He has a platelet count of 40,000 mm3, fibrinogen of 95, and an elevated D-dimer. What is the BEST treatment for this patient? Heparin infusion Fresh frozen plasma Tranexamic acid Albumin

Answer 1

Fresh frozen plasma DIC is characterized by disorganized clotting and fibrinolysis that lead to the simultaneous occurrence of hemorrhage and systemic thrombosis. Definitive treatment of DIC is reversal of the cause, which in this case is sepsis. In the meantime, treatment is supportive. Although some consider it "feeding the beast," failure to replace platelets, FFP, and cryoprecipitate will lead to diffuse coagulopathy and hemorrhage.

Answer 2

Bivalirudin Heparin is contraindicated in the patient with type II HIT, so a test dose shouldn't be given. Remember that the immune response is a process of amplification. Think of the child with a peanut allergy, even a single peanut can yield devastating consequences. Bivalirudin is a direct thrombin inhibitor that can be used as an alternative to heparin. In this context, it is a suitable alternative for cardiopulmonary bypass. Enoxaparin is a low molecular weight heparin and can't be used for CPB. Warfarin requires 36 - 72 hours to achieve anticoagulation, so it isn't used for CPB.

Answer 3

Pain Dehydration Sickle cell disease is an inherited disorder that affects erythrocyte geometry. Understanding the triggers helps you plan your anesthetic. Triggers include: ``` Pain Dehydration Hypoxemia Acidosis (not alkalosis) Hypothermia (not hyperthermia) ```

Answer 4

O + A, B, AB, O A + A, AB B + B, AB AB + AB

Answer 5

Tests for ABO, Rh-D compatibility, and most clinically significant antibodies Typing determines the presence of ABO and Rh-D antigens in the recipient's blood. This takes five minutes. Screening determines the presence of the most clinically significant antibodies. This takes 45 minutes. Crossmatching provides the most accurate determination of compatibility by mixing the recipients plasma with blood in the actual unit that will be transfused. This takes 45 min.

Answer 6

Cryoprecipitate Although whole blood and FFP contain fibrinogen, cryoprecipitate contains the highest concentration of fibrinogen. A five bag pool is expected to increase fibrinogen by 50 mg/dL.

Answer 7

2275 – 2625 The maximum allowable blood loss calculation requires you to determine the estimated blood volume and then use this value in the MABL equation. Since this patient is 70 kg, we can estimate that his blood volume is 4900 mL (70 mL/kg). MABL = EBV x (Starting hgb - Target hgb) / Starting Hgb = 2275 - 2625. We took a range of answers to account for the fact that some books say adult blood volume is 65 - 75 mL/kg.

Answer 8

Citrate + Anticoagulant Dextrose + Substrate for glycolysis Phosphate + Buffer Adenine + Substrate for ATP synthesis

Answer 9

Cytomegalovirus + 1 Hepatitis B + 2 Hepatitis C + 3 HIV + 4

Answer 10

Give a crystalloid bolus Administer sodium bicarbonate This patient is experiencing an acute transfusion reaction after receiving AB blood. Remember, that O blood contains anti-A and anti-B antibodies. Immediate treatment includes stopping (not slowing) the transfusion. Free hemoglobin obstructs the renal tubules, which can cause acute tubular necrosis. Increasing UOP with a fluid bolus helps move things through the renal tubules. Sodium bicarbonate alkalizes the urine, which reduces hemoglobin precipitation. You should send a serum hemoglobin, platelets, PT, fibrinogen, and a urine sample to the lab. A liver panel does nothing to aid in the treatment of this patient.

Answer 11

Multiparous women TRALI is believed to result from HLA and neutrophil antibodies present in donor plasma. Some donor populations possess a higher concentration of antibodies, and blood products from these populations increase the likelihood that the recipient will develop TRALI. Donors that increase risk: multiparous women, history of blood transfusion, organ recipient Recipients at greatest risk: critical illness, sepsis, burns, post-CPB Jehovah witness patients will not accept blood transfusion. Creutzfeldt Jakob disease (mad cow) is a prion disease that can be spread through infected blood products.

Answer 12

Hypercalcemia Citrate intoxication is a complication of massive transfusion. As you’ll recall, citrate binds calcium and this can cause myocardial depression, coagulopathy, and impair nerve transmission.

Answer 13

Anterior hip arthroplasty Living donor kidney transplant Sometimes you'll see several answers that are correct. In this instance, you'll have to identify those that are the most correct. In this question, there are conceivably three acceptable answer choices, however one of these is clearly not as attractive as the others. The use of cell saver for cesarean section remains controversial due to the risk of amniotic fluid embolism, although two systematic reviews failed to show an increase in morbidity and mortality when cell saver was used during c-section. Intraoperative blood salvage is absolutely contraindicated with neoplastic disease. The Whipple procedure is performed on patients with pancreatic cancer.

Answer 14

Magnesium Phosphate ``` The major extracellular ions: Na+ Ca+2 (see below for explanation) Cl- HCO3- The major intracellular ions: K+ Mg+2 PO4-2 Free Ca+2 is higher in the extracellular compartment. It's important to recognize, however, that there is a large quantity of Ca+2 that is sequestered inside cells (think sarcoplasmic reticulum in myocytes). ```

Answer 15

Intracellular + 28 L Extracellular + 14 L Interstitial + 11 L Plasma + 3 L Sixty percent of the adult's body weight is attributed to water. Two thirds of the water exists inside cells and one third of the water exists outside of cells. The examples below assume a 70 kg male. Total body water = 60% or 42 L Intracellular volume = 40% or 28 L Extracellular volume = 20% or 14 L The extracellular volume can be divided into 2 more compartments: Interstitial volume = 16% or 11 L Plasma volume = 4% or 3 L Understand that the total blood volume is ~ 5 L. The plasma accounts for 3 L and the water inside the blood cells (part of the ICV) accounts for 2 L.

Answer 16

5% albumin + 1 0.9% NaCl + 2 D5W + 3 The volume of distribution (Vd) describes the relationship between a drug's plasma concentration following a specific dose. It is a theoretical measure of how a drug distributes throughout the body. In the context of this question, the 3 IV fluids distribute to different body compartments. Albumin Remains in the intravascular space, so it has the smallest Vd. You could also say that it distributes to a single compartment. Normal saline Distributes throughout the entire extracellular space (plasma volume + interstitial space). D5W (glucose) Distributes into the total body water, so it has the largest Vd.

Answer 17

12 mmHg The plasma is in direct contact with the interstitial fluid by way of pores in the capillaries. The movement of fluid between the intravascular space and interstitial space is determined by Starling forces and the glycocalyx. A key exception to this rule is fluid transfer across the blood-brain-barrier - more on this in a bit... Net filtration pressure = (Pc - Pif) - (πc - πif). It is a function of 2 opposing forces: 1. Forces that move fluid from the capillary → interstitium Capillary hydrostatic pressure (Pc) Interstitial oncotic pressure (πif) 2. Forces that move fluid from the interstitium → capillary Plasma oncotic pressure (πc) Interstitial hydrostatic pressure (Pif) *only if Pif > Pc It's important to understand that the net filtration pressure is different at different points along the capillary: Arterial side of capillary = net filtration pressure pushes fluid into the interstitial fluid Venous side of capillary = net filtration pressure pulls fluid back into the intravascular space And finally back to the calculation... (Pc - Pif) - (πc - πif) (35 - 0) - (26 - 3) = 12 mmHg

Answer 18

5% Albumin + 1 Plasmalyte + 2 Lactated ringers + 3 We've ranked the osmolarity for the common IV solutions from highest to lowest (mOsm/L): ``` Hypertonic Solutions: NaCl 3% = 1026 D5NS = 560 D5LR = 525 D5 1/2NS = 405 ``` ``` Isotonic Solutions: NS 0.9% = 308 Albumin 5% = 300 Plasmalyte = 294 Lactated ringers = 273 Hypotonic Solutions: D5W = 253 NaCl 0.45% = 154 ```

Answer 19

240 mOsm/L Because cell membranes are freely permeable to water, the osmolarity of the ECF is assumed to equal the osmolarity of the ICF. Therefore, we can use plasma osmolarity as an estimate of the intracellular osmolarity. This is an important concept to understand, because changes in intracellular osmolarity can affect cellular volume and function. Plasma osmolarity = 2 [Na+] + (Glucose / 18) + (BUN / 2.8) Normal = 280 - 290 mOsm/L You can see that in plasma the Na+ concentration is the most heavily weighted variable of this equation, and by extension, it is also the most important. We multiply [Na+] by 2 to account for its major anions. The patient in this question has SIADH. You know that this disease process increases ADH secretion. Here's the pathophysiology: ↑ ADH → V2 receptor stimulation in collecting ducts → aquaporin insertion → ↑ solute-free water reabsorption → ↓ plasma osmolarity This patient's plasma osmolarity = (2 x 115) + (90 / 18) + (14 / 2.8) = 240 mOsm/L Therefore, this patient has excess free water, which dilutes plasma Na+. This places the patient at risk for the complications of hyponatremia.

Answer 20

0.9% Sodium Chloride + 154 mEq/L Plasmalyte + 140 mEq/L Lactated ringers + 130 mEq/L Any solution that contains 0.9% NaCl has a sodium concentration of 154 mEq/L. These include: 5% albumin, NS, and D5NS. Any solution that contains LR has a sodium concentration of 130 mEq/L. These include: LR and D5LR. Plasmalyte has a sodium concentration of 140 mEq/L. If you are asked which IVF is most physiologic, then plasmalyte is the answer.

Answer 21

Hyponatremia Hyponatremia (Na+ < 130 mEq/L) is the most common electrolyte disturbance in hospitalized patients.

Answer 22

Osmotic demyelination syndrome The blood-brain-barrier does not allow ions to freely pass through it. This means that the sodium concentration in the brain is relatively stable. Since water can move across the BBB, but ions cannot, we can say that the intravascular osmolarity largely determines the water content of brain cells. There is an inverse relationship between serum osmolarity and brain water: ↑ serum osmolarity → ↓ brain water ↓ serum osmolarity → ↑ brain water Since sodium is the primary determinant of serum osmolarity, hyponatremia can lead to cerebral edema (increased brain water). And since the brain resides in a boney box, cerebral edema can increase ICP. This is reversed by increasing serum osmolarity with sodium chloride. Rapid correction of hyponatremia can cause an osmotic destruction of the myelin sheath, leading to a condition called osmotic demyelination syndrome (myelinolysis). It is more common when hyponatremia has persisted for > 48 hours. As a general rule, the serum sodium level should not change more than 1-2 mEq/L per hour. This can be accomplished with 3% NaCl at 1-2 mL/kg/hr. ``` The clinical presentation of osmotic demyelination syndrome includes: Mental status changes Seizures Spastic quadriplegia Pseudobulbar palsy Encephalopathy Coma Death ```

Answer 23

Hyperchloremic metabolic acidosis The problem with excessive 0.9% NaCl resuscitation is an iatrogenic hyperchloremic metabolic acidosis. This explains why LR is a better choice than 0.9% NaCl in the setting of massive volume resuscitation. Why does this occur? The chloride concentration in 0.9% NaCl is 154 mEq/L, which is higher than the normal plasma value. When the kidneys are faced with an increased chloride load, they excrete bicarbonate to maintain electroneutrality. As a consequence, this creates a non-gap metabolic acidosis. Remember: A gap acidosis is the result of the addition of acid. A non-gap acidosis is the result of loss of bicarbonate.

Answer 24

Stage III There are 4 stages of hemorrhagic shock (shown on the next page) This patient is experiencing stage III: ``` EBL = 1,800 mL Heart rate = 123 beats/min Blood pressure = 90/54 Urine output = 10 mL/hr ```

Answer 25

von Willebrand's factor + Procoagulant Antithrombin III + Anticoagulant Plasminogen + Fibrinolytic Alpha-antiplasmin + Antifibrinolytic Blood is a complex chemical soup. In the beginning of the Coagulation Tutorial, we gave you a paradigm to help organize these chemicals in your mind: Procoagulants → promote clot formation Anticoagulants → inhibit clot formation Fibrinolytics → promote clot breakdown Antifibrinolytics → inhibit clot breakdown Knowing the origin and function of each chemical will help you answer a wide variety of questions in the classroom and on boards!

Answer 26

Thromboxane A2 Immediately following vascular injury, the vessel (tunica media) contracts to reduce blood flow to the affected area. Contraction is the result of SNS reflexes, the myogenic response, and release of vasoactive substances, such as thromboxane A2. TXA2 also activates platelets to begin the formation of the platelet plug. vWF contributes to platelet adhesion. Nitric oxide and prostacyclin cause smooth muscle relaxation (vasodilation). They don’t contribute to vascular spasm.

Answer 27

1. Fibrinogen 2. Calcium 3. Prothrombin 4. Tissue factor 1. Factor I - fib 2. Factor IV- calcium 3. Factor II -prothrom 4. Factor III -TF

Answer 28

I II V X Extrinsic Pathway (3, 7): “The extrinsic pathway can be purchased for 37 cents” Intrinsic Pathway (8, 9, 11, 12): “If you can’t buy the intrinsic pathway for 12 dollars, you can buy it for 11.98.” Final Common Pathway (1, 2, 5, 10, 13): “The final common pathway can be purchased at the 5 and dime for 1 or 2 dollars on the 13th of the month.”

Answer 29

VII While it's a low yield strategy to memorize the half-lives for all of the clotting factors, there are a few that you should know: Factor VII: 3-6 h Antithrombin: 48-72 h Fibrinogen: 72-120 h Here's one reason why this is relevant. Hopefully you can come up with some others... The anticoagulant effect of warfarin depends on factor VII inhibition. If the half-life of factor 7 is 3-6 hours (2, 9, and 10 are even longer) and ~5 half-lives are required for warfarin to reach steady state, then it should make sense why it takes several days for warfarin to achieve a therapeutic level. If you noticed that all the answer choices represented those clotting factors inhibited by warfarin (2, 7, 9, and 10), then give yourself a high five. Hear the applause?

Answer 30

Urgent reversal of warfarin therapy Antithrombin deficiency Indications for FFP: Urgent reversal of warfarin therapy Correction of uncontrolled bleeding when PT and/or PTT are > 1.5x normal Replacement of coagulation factor when no specific concentrate is available Ok...so you might be asking why AT was a correct answer when there is a specific concentrate available for it. While this is true, the rules are different on the NCE. You have to pick the best answer(s) of those provided. Although it may not be the very best answer in real life, it's a much better choice than those that are clearly incorrect. This is a very important concept to understand. FFP is NOT indicated for: Plasma volume expansion Hypoalbuminemia

Answer 31

Fibrinogen Von Willebrand factor Factor 8 Fibrinogen (factor I) is required for clot stabilization. It also plays a role in platelet activation and aggregation. We use cryoprecipitate to replace fibrinogen. A single dose of cryoprecipitate (5 pooled bags) increases fibrinogen by 50 mg/dL. You should consider fibrinogen replacement when the fibrinogen level is < 80 - 100 mg/dL. Cryoprecipitate also contains: von Willebrand factor (helps platelet adhesion) Factor 8 (missing in patients with hemophilia A) Factor 13 Fibronectin

Answer 32

Sickle cell disease Indications for the use of cryoprecipitate: Disseminated intravascular coagulation: fibrinogen < 80 - 100 mg/dL Massive transfusion (dilutional coagulopathy): fibrinogen < 100 - 150 mg/dL Cryoprecipitate is also indicated for prophylaxis for the following conditions: Hemophilia A von Willebrand disease Congenital dysfibrinogenemia

Answer 33

24 mcg Von Willebrand's disease is categorized into 3 types: Type I: Mild-moderate reduction in amount of vWF produced Type II: The vWF that is produced doesn't work well Type III: Severe reduction in vWF production Desmopressin (0.3 mcg/kg IV) restores vWF function in patients with type I and sometimes with type II disease. Since patients with type III disease do not have an endogenous supply of vWF, DDAVP isn't useful. 80 kg x 0.3 mcg/kg = 24 mcg

Answer 34

Factor VIII concentrate Cryoprecipitate Patients with type III von Willebrand disease and patients that do not respond to desmopressin should be treated with cryoprecipitate or factor VIII concentrate. The latter is preferred due to the risk of transfusion-transmitted infection with cryoprecipitate.

Answer 35

Thrombocytopenia Increased fibrin split products Disseminated intravascular coagulation is characterized by disorganized clotting and fibrinolysis that lead to the simultaneous occurrence of systemic thrombosis and hemorrhage. Generalized thrombin formation creates microvascular clots that impair tissue perfusion, resulting in tissue hypoxia and acidosis. The body attempts to break down these clots by activating its anticoagulant system, however this leads to the widespread consumption of its coagulation factors, fibrinogen, and platelets. ``` Common lab results in DIC: ↓ Platelets (consumption) ↓ Fibrinogen (consumption) ↑ PT/PTT (inadequate supply of procoagulants) ↑ D-dimer (increased clot breakdown ```

Answer 36

Reversal of the underlying cause DIC is not a disease in itself, but rather it’s a manifestation of some other underlying problem. Indeed, the definitive treatment for DIC is reversing the underlying cause. Otherwise, treatment is supportive: Hypovolemia: Treat with IV fluids Coagulopathy: Replace consumed blood components with FFP, platelets, and cryoprecipitate (it's ok to "feed the beast") Severe microvascular thrombosis: IV heparin or LMWH

Answer 37

Sepsis Amniotic fluid embolism Malignancy There are three conditions that you should associate with a high risk of developing DIC: Sepsis: (highest risk = gram-negative bacilli) Obstetric complications: (highest risk = preeclampsia, placental abruption, and amniotic fluid embolism) Malignancy: (highest risk = adenocarcinoma, leukemia, and lymphoma) Trauma, burns, and pancreatitis do not commonly cause DIC.

Answer 38

VIII Hemophilia A is an X-linked chromosomal disorder (more common in males). The severity of hemophilia A corresponds with factor VIII activity. Since factor VIII is part of the intrinsic pathway, you can predict that the PTT will be prolonged in patients with hemophilia A. Treatment aims to restore factor VIII: Factor VIII concentrate Recombinant factor VII FFP (risk of viral transmission) Cryoprecipitate (risk of viral transmission) Patient's should receive a type & crossmatch prior to surgery. Hemophilia B patients lack factor IX. These patients will also have a prolonged PTT. Hemophilia B is generally believed to be less severe than hemophilia A.

Answer 39

Hemophilia By now you know that: Factor 8 deficiency → Hemophilia A Factor 9 deficiency → Hemophilia B So why is recombinant factor 7 the correct answer? Sometimes patients with hemophilia A or B develop inhibitors that prevent exogenous factor 8 or 9 from achieving their therapeutic goals. For a clot to form, the missing coagulation factor must be replaced or "bypassed". Recombinant factor 7 is a “bypass” agent, because it skips over factor 8 or 9 in patients with inhibitors, ultimately allowing the patient to form clot. The dose is 90 - 120 mcg/kg. Although the exact mechanism is unclear, both the classic and contemporary cell-based theories of coagulation suggest that factor 7 contributes to thrombin generation by facilitating tissue factor at the site of vascular injury and on the surface of the platelet. Recombinant factor 7 can increase the risk of arterial thrombosis (MI and embolic stroke) as well as venous thrombosis (DVT or pulmonary embolism), so the risk/benefit ratio must be considered in patients at risk for these complications. Recombinant factor 7 is also used as a "last-ditch" treatment for bleeding without an identifiable cause (this is off label). The dose is 20 - 40 mcg/kg.

Answer 40

Pain Dehydration Sickle cell disease is a genetic disorder where valine is substituted for glutamic acid on the beta globulin chain of the hemoglobin molecule. This variant affects RBC function in several ways: HgbS contributes to sickling when it becomes deoxygenated. Sickling is a conformational change that alters the erythrocyte's geometry. In severe cases, sickling causes the RBCs to clump together, which causes mechanical obstruction of the microvasculature in the vital organs and joints. This impairs tissue perfusion and causes intense pain (particularly in the bones and joints). Sickled cells are more prone to hemolysis and removal by the spleen (lifespan = 12 - 17 days vs. normal RBC = 120 days). Triggers of sickle cell crisis: Pain Hypothermia Hypoxemia Acidosis Dehydration

Answer 41

Vaso-occlusive crisis Vaso-occlusive crisis: Occurs when sickled cells impair tissue perfusion, resulting in ischemic injury. It is the most common manifestation of sickle cell disease. Treatment includes analgesics (oral or IV) and hydration. Acute chest syndrome: Is a significant source of mortality in the patient with SCD (1-20%). It is likely the result of thrombosis, embolism, and infection. It is more common in children. Diagnosis requires new lung infiltrates on CXR and at least one of the following: chest pain, cough, dyspnea, and wheezing. It is common during the postoperative period. Potential causes include: hypoventilation, narcotics, splinting, and pain. Sequestration crisis: Occurs when the spleen removes RBCs from the circulation at a faster rate than they are produced by the bone marrow. It can lead to anemia and hemodynamic instability. Aplastic crisis: May result in response to bone marrow suppression. This is usually the result of a viral infection (parvovirus B19).

Answer 42

Hydroxyurea Hydroxyurea reduces the incidence and severity of vaso-occlusive crisis. Children with SCD are at increased risk of infection, particularly pneumococcal disease. These patients are often prescribed: Daily penicillin prophylaxis (up to 5 years of age) Pneumococcal vaccination

Answer 43

Hypoxemia Heterozygous sickle cell disease is also referred to as sickle cell trait. While homozygous SCD affects 0.5-1.0% of the African-American population, nearly 10% demonstrate sickle cell trait. As a general rule, patients with sickle cell trait do not advance to crisis. Severe hypoxemia is the exception to this rule.

Answer 44

Asthma This one was a bit tricky. Most of you know that sickle cell disease is more common in African-Americans, so this might have led you down the path of diabetes mellitus or hypertension. Surely, we couldn't make it that easy for you. Asthma occurs in 50 percent of patients with sickle cell disease. Another key association is pulmonary hypertension, which occurs in 10% of patients with SCD.

Answer 45

Aspirin + Normal PT & Normal PTT Heparin + Normal PT & Elevated PTT Warfarin + Elevated PT & Normal PTT PT measures the extrinsic and common pathways. ``` Normal value = 12-14 seconds Prolonged by warfarin Warfarin is reversed by phytonadione PTT measures the intrinsic and common pathways: Normal value = 25-32 seconds Prolonged by heparin Heparin is reversed by protamine Bleeding time measures platelet function: Normal value = 2-10 minutes Prolonged by aspirin and NSAIDs These drugs do not affect PT or PTT There are no specific reversal agents for aspirin or NSAIDs ```

Answer 46

350 mg Protamine is used to reverse heparin at the conclusion of cardiopulmonary bypass. It does this via a neutralization reaction (it forms an acid/base complex with heparin). As a general rule, 1 mg of protamine will reverse every 100 units of heparin that was given. If 35,000 units of heparin remain in the patient’s circulation, then the calculated dose of protamine is 350 mg. There are two ways to calculate the protamine dose: It is calculated from the initial heparin dose or... It is calculated from the amount of heparin that is predicted to remain in the patient’s circulation at the conclusion of cardiopulmonary bypass. Because protamine has anticoagulant properties, basing the protamine dose from the initial heparin dose (not what remains after CBP) may contribute to protamine overdose (prolonged ACT). Administering protamine over 10-15 minutes reduces the likelihood of systemic vasodilation as well as pulmonary vasoconstriction (both side effects of protamine). The rate of administration does not impact the probability of anaphylaxis.

Answer 47

Decreased bile synthesis Vitamin K is a fat soluble vitamin that plays an integral role in the coagulation cascade. It comes from diet (50%) and GI tract bacteria (50%). Bile salts are required for the GI tract to absorb vitamin K. Vitamin K is required for the liver to synthesize factors 2, 7, 9, and 10. Warfarin inhibits the actions of vitamin K, which explains why warfarin inhibits factors 2, 7, 9, and 10. Causes of vitamin K deficiency include: Inadequate dietary intake Hepatocellular disease (decreased bile synthesis) Biliary duct obstruction (decreased bile release) Antibiotics that kill vitamin K producing bacteria in the GI tract Vitamin K deficiency will manifest as a prolonged PT (same as warfarin therapy). Bile is synthesized in the liver and stored in the gallbladder. Increased cholecystokinin causes gallbladder contraction, which promotes bile flow into the small intestines. Bile facilitates vitamin K absorption. Sphincterotomy of the sphincter of Oddi improves the release of bile into the duodenum, assisting in fat soluble vitamin absorption (DAKE). While blockage to the pancreatic duct and hyperinsulinemia are serious issues, they don't relate to this question.

Answer 48

20 minutes Warfarin inhibits vitamin K dependent clotting factors (2, 7, 9, and 10). Sometimes you’ll have to reverse the effects of warfarin in order to proceed with surgery. Options include: FFP Recombinant factor VIIa Phytonadione (exogenously administered vitamin K) Given the risk of complications associated with FFP and the cost of recombinant factor VIIa, phytonadione is a reasonable option for non-emergency surgery. The dose is 10 - 20 mg PO, IM, or IV. IV administration is NOT recommended, because it can cause life-threatening anaphylaxis. If you give phytonadione IV, then the rate should not exceed 1 mg/min (20 mg over 20 min).

Answer 49

Cimetidine Ranitidine Warfarin reduces the risk of thromboembolism in patients with atrial fibrillation. The problem is that warfarin increases the risk of GI bleeding, and this is particularly problematic in the patient with concurrent peptic ulcer disease. Indeed, hemorrhage is the most common cause of mortality in the patient with peptic ulcer disease. Gastric acid suppression with an H2 blocker reduces the incidence of GI bleeding, however there is a key drug interaction between warfarin and some H2 blockers. Cimetidine and ranitidine are hepatic enzyme inhibitors, and they inhibit the same hepatic P-450 enzymes that metabolize warfarin. This can augment warfarin’s anticoagulant effects, increasing the risk of hemorrhage. Famotidine and nizatidine do not inhibit the same P-450 enzymes, making either of these a better choice in the patient on warfarin.

Answer 50

Clopidogrel + ADP receptor inhibitor Abciximab + GIIb/IIIa receptor antagonist Bivalirudin + Direct thrombin inhibitor Tranexamic acid + Plasmin activation inhibitor

Answer 51

Clopidogrel + 7 days Ticlopidine + 14 days Prasugrel + 3 days Ticagrelor + 1 day Adenosine diphosphate (ADP) receptor inhibitors are a class of antithrombotic agents. How long to discontinue each drug prior to surgery? Ticlopidine = 14 days Clopidogrel = 7 days Prasugrel = 2-3 days Ticagrelor = 1-2 days *Nagelhout incorrectly states that ticlopidine should be discontinued 7 days before surgery. All of these drugs are metabolized by the liver.

Answer 52

180 - 200 mL Here are the estimated blood volumes across the lifespan: Premature neonate: 90 - 100 mL/kg Full term neonate: 80 - 90 mL/kg Infant: 80 mL/kg Adult: 70 mL/kg At 34 weeks gestation, this patient is premature. She weighs 2,000 grams. 2,000 g = 2 kg 2 kg x 90 mL/kg = 180 mL or 2 kg x 100 mL/kg = 200 mL We accepted the entire range of answers (180 - 200 mL).

Answer 53

1,657 - 1,913 mL The maximum allowable blood loss calculation requires you to first estimate the patient's blood volume and then use this value in the MABL equation. Since this patient is 85 kg, we can estimate that his blood volume is 5,950 mL (EBV = 70 mL/kg). MABL = EBV x [(Starting Hgb - Target Hgb) / Starting Hgb] Step 1: Calculate the estimated blood volume: 85 kg x 70 mL/kg = 5,950 Step 2: Calculate the maximum allowable blood loss: 5,950 x [10 - 7) / 10] = 1785 mL Since the textbooks say the adult EBV is 65 - 75 mL/kg, we accepted all of the possible answers using these values (1,657 - 1,913 mL). Some texts use hematocrit instead of hemoglobin for this calculation. On your exam, just use whatever variable they give you in the question. Don't try to convert one to the other, because you'll likely introduce a rounding error.

Answer 54

8 g/dL For every unit of PRBCs administered, the hemoglobin and hematocrit should increase by 1 g/dL and 2-3% respectively. This question required you to convert Hct to Hgb. Hemoglobin can be estimated as 1/3 of the hematocrit. Pretransfusion Hct = 18% Pretransfusion Hgb = 18% / 3 = 6 g/dL Each unit of PRBCs increases Hgb 1 point. Therefore, if the starting Hgb is 6 g/dL, then transfusing 2 units of PRBCs can be expected to increase the patient's Hgb to 8 g/dL.

Answer 55

Type B blood Anti-A antibodies in the plasma Blood type is determined by specific glycoproteins expressed on the erythrocyte's cell membrane. These glycoproteins have an immunogenic potential, so administering blood of the wrong type risks a catastrophic outcome. We'll begin with a conceptual framework, then we'll give you examples of how to apply this framework. If an antigen is expressed on the erythrocyte, then there will NOT be an antibody against that specific antigen in the patient's plasma. If an antigen is NOT expressed on the erythrocyte, then there will be an antibody against that specific antigen in the patient's plasma. Now that you know the conceptual framework, let's apply this to the ABO system: A blood has anti-B antibodies in the plasma B blood has anti-A antibodies in the plasma O blood has anti-A and anti-B antibodies in the plasma AB blood has no antibodies in the plasma In this question, the patient's erythrocytes expressed B antigen, therefore this patient has: Type B blood Anti-A antibodies in the plasma

Answer 56

AB Nothing gets past you! We tried to trip you up with the universal donor for plasma (not PRBCs), but you're way too slick for our cheap tricks. Universal Donors: PRBCs: O negative (donor cells do not contain RBC antigens) Plasma: AB positive (donor plasma does not contain plasma antibodies) Universal Acceptors: PRBCs: AB positive (patient already has both RBC antigens) Plasma: O negative (patient already has both plasma antibodies present) See the pattern?

Answer 57

Transfuse type-specific partially crossmatched blood In the setting of acute hemorrhage, there may not be time to complete a full crossmatch. Here is the recommended order of administering uncrossmatched blood (ordered from most to least favorable): 1. Type-Specific Partially Crossmatched Blood: Tests for ABO compatibility as well as a few antibodies. 2. Type-Specific Uncrossmatched Blood: Tests for ABO compatibility only. 3. Type O Uncrossmatched Blood: No lab test is required. Type O is the universal donor for erythrocytes, because these cells do not express A or B antigen. It’s important to note, however, that the bag of PRBCs will contain some of the anti-A and anti-B antibodies found in the plasma of type O blood. Can you switch back to the patient's blood type (type-specific blood) if you've already transfused type O blood? After two or more units of type O blood are transfused, you must continue to use type O blood even if the patient is identified to be a different blood type! In this situation, you must wait to transfuse type-specific blood until the blood bank has determined that the transfused anti-A and anti-B antibodies have decreased to a safe level.

Answer 58

``` Fresh frozen plasma = 1 year Packed red blood cells = 42 days Platelets = 5 days Packed red blood cells: Storage duration = 42 days (21 - 35 days if no preservative) Temperature = 1 - 6 C Fresh frozen plasma: Storage duration = 1 year or 7 years Temperature = < -18 C for 1 year or < -65 C for 7 years Cryoprecipitate: Storage duration = 1 year Temperature = < -18C Platelets: ``` Storage duration = 5 days Temperature = 20 - 24 C Notice that platelets stored at room temperature. This explains why their shelf life is much shorter, and it also explains why this blood product is most susceptible to bacterial contamination

Answer 59

Hypocalcemia Citrate is a calcium chelating agent that prevents coagulation in banked blood. After transfusion of at least several units, the citrate binds calcium (factor IV) in the patient's circulation, resulting in acute hypocalcemia. Other blood preservatives include: Dextrose = substrate for glycolysis Phosphate = buffer to combat acidosis Adenine = substrate that helps RBCs synthesis ATP Collectively, this is known as the CDPA preservative (citrate, dextrose, phosphate, and adenine).

Answer 60

Hyperkalemia Altered erythrocyte morphology Although the CDPA preservative extends the life of banked blood, there are several important physiochemical changes that occur during storage. This is known as the red blood cell storage lesion. Decreased 2, 3 DPG → shifts oxyhemoglobin dissociation curve to the left (left = love → decreased O2 release) Decreased ATP → shift to anaerobic metabolism Decreased pH (increased lactic acid) Increased potassium (caution in neonates and renal failure) Impaired ability to change shape (important for capillary flow) Hemolysis Increased production of proinflammatory mediators

Answer 61

Leukoreduction + Reduces risk of HLA alloimmunization Washing + Prevents anaphylaxis in IgA deficient patients Irradiation + Prevents graft vs host disease Leukoreduction Removes WBCs from RBCs and platelets. Since leukocytes are responsible for human leukocyte antigen (HLA) alloimmunization, febrile nonhemolytic transfusion reactions, and CMV transmission, it makes sense that removing leukocytes reduces these risks. Washing Washing the blood products with saline removes any remaining plasma (and antigens) from the donor RBCs (RBCs antigens are not removed). This process prevents anaphylaxis in IgA deficient patients. Irradiation Irradiation exposes donor units to gamma radiation, and this disrupts WBC DNA in the donor cells. Prevents graft vs host disease in immunocompromised patients. Populations who benefit from irradiated cells include those suffering from: leukemia, lymphoma, hematopoietic stem cells transplants, and DiGeorge syndrome.

Answer 62

Cytomegalovirus Cytomegalovirus is the most common infectious complication of transfusion. It occurs in 1 - 3% of all transfusions. Leukoreduction reduces the risk of CMV transmission (0.023% of all transfusions). Other viral complications of transfusion (Ranked from most to least common): Hepatitis B = 1 in 366,500 Hepatitis C = 1 in 1,657,700 Human immunodeficiency virus = 1,860,800 Human T-cell lymphotropic virus = 1 in 3,394,000 West Nile virus = very rare (11 cases reported from 2003 - 2010) These numbers will vary throughout the texts, but the relative incidence for each should be similar.

Answer 63

Transfusion-related acute lung injury Transfusion-related acute lung injury (TRALI) is the most common cause of transfusion related mortality in the United States. The risk is highest in critically ill patients as well as those susceptible to acute lung injury: sepsis, burns, or post-CPB. Pathophysiology of TRALI: Antibodies from donor blood product causes neutrophil activation → endothelial injury → capillary leak → pulmonary edema → impaired gas exchange → hypoxemia → acidosis → death

Answer 64

Left atrial hypertension ``` Diagnostic criteria for TRALI: Onset < 6 hours following transfusion Bilateral infiltrates on frontal CXR PaO2/FiO2 < 300 mmHg or SpO2 < 90% on RA Normal pulmonary artery occlusion pressure (no left atrial hypertension or volume overload) ``` Management is supportive and focuses on a lung protective strategy: Maximize PEEP Low tidal volume Avoid overhydration

Answer 65

Fresh frozen plasma Platelets Plasma containing products are associated with the highest incidence of TRALI. These include: Fresh frozen plasma Platelets TRALI is likely caused by HLA and neutrophil antibodies present in the donor plasma. Once these antibodies enter the recipient’s bloodstream, they activate the immune response in the lungs. Which donor populations are likely to contain these antibodies? Multiparous women (alloimmunization from pregnancy) History of transfusion History of organ transplant Indeed, plasma obtained from multiparous women is associated with the highest incidence of TRALI. For this reason, plasma obtained from male donors reduces the risk of TRALI.

Answer 66

Hypervolemia Left ventricular dysfunction Because both cause pulmonary edema in the setting of transfusion, it's easy to confuse transfusion-associated circulatory overload (TACO) with TRALI. TACO is a state of volume overload caused by expanding the plasma volume beyond the patient's compensatory ability (ex: patient with heart failure receiving four units of FFP to reverse warfarin). Signs and Symptoms of TACO: Pulmonary edema Hypervolemia Left ventricular dysfunction Mitral regurgitation secondary to volume overload Increased pulmonary artery occlusion pressure Increased brain natriuretic peptide Echocardiography can be very useful in the diagnosis.

Answer 67

Mannitol Normal saline This patient is experiencing an acute hemolytic reaction. Intravascular hemolysis is usually the result of ABO incompatibility, and the most common cause is clerical error (in the lab or the OR). General anesthesia can mask the presenting signs and symptoms, and the situation can quickly progress to disseminated intravascular coagulation, shock, and renal failure. Management plan for an acute hemolytic reaction: Stop the transfusion!!!!! Treat hypotension with liberal IV hydration. Maintain urine output 75 – 100 mL/kg with IV hydration and osmotic diuresis (mannitol 12.5 – 50 g). If mannitol does not produce a response, then administer furosemide (20 – 40 mg). Alkalize the urine with sodium bicarbonate (40 – 70 mEq). This reduces free hgb precipitation in the distal convoluted tubules. Labs: Hgb (plasma and urine), free hemoglobin, platelet count, fibrinogen, and PT/PTT. Send remaining donor blood to the blood bank for analysis. Send a patient blood sample for a repeat Coombs test. Before moving on to the next question, look away from this page, and try to envision an acute hemolytic reaction in the OR. How would you handle the situation?

Answer 68

Traumatic brain injury The “lethal triad” of trauma consists of: Acidosis Hypothermia Coagulopathy The problem begins with hemorrhage and hypoperfusion, and this ultimately impacts coagulation and acid-base balance. Hypoperfusion/Acidosis: Hypoperfusion and hypoxemia reduce oxygen delivery, so the body converts from aerobic to anaerobic metabolism. The net result is lactic acidosis. Hypothermia: Hemorrhage and hypoperfusion impair the body’s ability to regulate heat. Exposure to the elements and/or room temperature IV solutions also contribute to heat loss. Coagulopathy: All enzymatic processes are highly dependent on temperature. Coagulation is an enzymatic process, so it is impaired by hypothermia. PT and PTT are prolonged at < 34 C. Acidosis alters enzymatic structure, so acidosis also impairs the hemostatic mechanism. Massive volume resuscitation causes a dilution coagulopathy.