Apex Unit 9 FLuid / Blood Flashcards
What is the plasma volume of a 70-kg male?
3 liters
5 liters
7 liters
9 liters
Three liters
On a question like this, many students expect to be asked about blood volume. We tried to be a bit tricky and asked about plasma volume instead. It’s always a good idea to reword the question in your mind before moving on to the answer choices.
In a 70 kg adult, the total blood volume is ~ 5 L, while the plasma volume is ~ 3 L.
Whenever you’re confronted with a body water question, we want you to remember: 60/40/20 (15/5)
In the average 70 kg male, classic teaching suggests that water represents 60 percent of the total body weight. This equals 42 L.
The total body water (TBW) can be divided into:
1. Intracellular volume = 40 percent of total body weight or 28 L
2. Extracellular volume = 20 percent of total body weight or 14 L
The ECV can be further divided into:
1. Interstitial fluid = 16 percent of total body weight or 11 L
2. Plasma fluid = 4 percent of total body weight or 3 L
*If it’s easier to remember 15 percent and 5 percent instead of 16 percent and 4 percent, that’s okay. Either way, you would’ve arrived at the same answer.
Match each term with its definition.
Osmosis
Osmolality
Osmolarity
Osmosis + Movement of water across a semipermeable membrane
Osmolality + Number of osmoles per kilogram of solvent
Osmolarity + Number of osmoles per liter of solution
Calculate the plasma osmolarity.
Sodium = 150 mEq/L Glucose = 108 g/dL BUN = 14 mg/dL
(Enter your answer as mOsm/L and round to the nearest whole number)
311 mOsm/L
Plasma osmolarity = (Na+ x 2) + (Glucose / 18) + (BUN / 2.8)
(2 x 150) + (108 / 18) + (14 / 2.8)
300 + 6 + 5 = 311 mOsm/L
We made the math easy. You’re welcome.
The normal plasma osmolarity is 280 - 290 mOsm/L. In this patient, hypernatremia is responsible for the hyperosmolar state.
Rank the tonicity for each fluid. high to low
NaCl 3%
D5W
Albumin 5%
D5 + NaCl 0.45%
NaCl 3% + 1
D5 + NaCl 0.45% + 2
Albumin 5% + 3
D5W + 4
Hypotonic solutions have an osmolarity lower than the plasma.
Isotonic solutions have an osmolarity roughly equal to the plasma.
Hypertonic solutions have an osmolarity higher than the plasma.
Choose the statements that MOST accurately describe colloids. (Select 3.)
They are proinflammatory.
Colloids are associated with better outcomes than crystalloids.
Dextran reduces blood viscosity.
Albumin causes hypocalcemia.
Albumin can cause hyperchloremic metabolic acidosis.
Hetastarch dose should not exceed 20 mL/kg.
Hetastarch dose should not exceed 20 mL/kg
Albumin causes hypocalcemia
Dextran reduces blood viscosity
Some synthetic colloids (hetastarch and dextran but not voluven) increase the risk of coagulopathy. Their dose should not exceed 20 mL/kg.
Albumin binds calcium and can contribute to hypocalcemia.
Dextran reduces blood viscosity. It is used to improve microcirculatory flow during some vascular surgeries.
Sodium chloride (not albumin) can cause hyperchloremic metabolic acidosis, although you should also keep in mind that most colloids are prepared with NaCl.
Albumin has anti-inflammatory (not pro-inflammatory) properties.
When comparing colloids to crystalloids, outcomes are the same (not better).
Loss of deep tendon reflexes is MOST likely a consequence of:
hypomagnesemia.
hypermagnesemia.
hypocalcemia.
hypercalcemia.
Hypermagnesemia
One of the first clear signs of magnesium toxicity is loss of deep tendon reflexes. Think about this in the patient being treated for preeclampsia.
Loss of DTR tends to occur when serum Mg+2 is either:
4 – 6.5 mEq/L
10 – 12 mg/dL
Indeed, different books use different units of measurement. You should know both
Match each acid-base disturbance with its arterial blood gas.
pH 7.30, PaCO2 = 50, HCO3 = 24
pH 7.21, PaCO2 = 36, HCO3 = 17
pH = 7.50, PaCO2 = 31, HCO3 = 26
pH = 7.49, PaCO2 = 41, HCO3 = 28
Respiratory acidosis + pH 7.30, PaCO2 = 50, HCO3 = 24
Metabolic acidosis + pH 7.21, PaCO2 = 36, HCO3 = 17
Respiratory alkalosis + pH = 7.50, PaCO2 = 31, HCO3 = 26
Metabolic alkalosis + pH = 7.49, PaCO2 = 41, HCO3 = 28
Which acid-base disorder is MOST likely to occur in response to untreated pain in the postanesthesia recovery unit?
Respiratory alkalosis
Metabolic acidosis
Respiratory acidosis
Metabolic alkalosis
Respiratory alkalosis
Untreated pain leads to hyperventilation and respiratory alkalosis.
Complications of respiratory alkalosis include:
Dysrhythmias
Decreased cerebral blood flow
Decreased P50 (oxyhemoglobin dissociation curve shifts to left)
Decreased serum calcium (muscle spasm or tetany if severe)
The MOST likely etiologies of metabolic alkalosis include: (Select 2.)
large volume resuscitation with NaCl.
massive transfusion.
vomiting.
diabetic ketoacidosis.
Vomiting
Massive transfusion
Metabolic alkalosis is characterized by a pH > 7.45. It is caused by increased bicarbonate and/or a loss of nonvolatile acids.
Vomiting produces H+ loss from the stomach.
Massive transfusion can produce metabolic alkalosis, because the liver converts citrate to bicarbonate.
Diabetic ketoacidosis and large volume resuscitation with NaCl produce metabolic acidosis. This explains why we don’t use large volumes of NaCl in the trauma patient.
Identify the components of the enhanced recovery after surgery program that are believed to improve postsurgical outcomes. (Select 2.)
Insertion of nasogastric tube
Carbohydrate drink two hours before surgery
Avoidance of premedication
Isoflurane instead of desflurane
Carbohydrate drink two hours before surgery
Avoidance of premedication
The primary objective of ERAS is to enhance postsurgical outcomes with a standardized approach to perioperative care.
Match each mediator with its primary function in the blood.
von Willebrand factor
Protein C
tPA
Plasminogen activation inhibitor
Procoagulant
Antifibrinolytic
Fibrinolytic
Anticoagulant
von Willebrand factor + Procoagulant
Protein C + Anticoagulant
tPA + Fibrinolytic
Plasminogen activation inhibitor + Antifibrinolytic
The blood contains factors that favor clot formation (procoagulants) and those that hinder clot formation (anticoagulants).
The blood also contains factors that break down clot (fibrinolytics) and those that impair the clot break down process (antifibrinolytics).
Platelets contain all of the following components EXCEPT:
actin.
adenosine diphosphate.
calcium.
deoxyribonucleic acid.
Deoxyribonucleic acid
Platelets don’t have a nucleus; therefore, they don’t contain DNA and they can’t undergo cell division.
Platelets are produced by megakaryocytes in the bone marrow.
Which substance is responsible for adhering the platelet to the damaged vessel?
Tissue factor
von Willebrand factor
Thromboxane A2
ADP
von Willebrand factor
Primary hemostasis describes the formation of the platelet plug. This process requires that the platelet adhere, activate, and aggregate at the site of vascular injury.
You should associate platelet adhesion with von Willebrand factor.
You should associate platelet activation and aggregation with ADP and thromboxane A2.
Match each coagulation factor with its pathway.
Tissue factor
Hageman factor
Prothrombin
Calcium
Extrinsic pathway
Affects all of the pathways
Final common pathway
Intrinsic pathway
Tissue factor + Extrinsic pathway
Hageman factor + Intrinsic pathway
Prothrombin + Final common pathway
Calcium + Affects all of the pathways
Which factors are specific to the classical intrinsic pathway? (Select 3.)
IV VI VII VIII IX XI
VIII
IX
XI
Factors specific to the intrinsic pathway include: VIII, IX, XI, XII (8, 9, 11, 12)
Factors specific to the extrinsic pathway include: III, VII (3, 7)
Calcium (factor IV) is a cofactor in both coagulation pathways.
There is no factor VI.
Place the events of the final common pathway in the correct sequence.
1st event
2nd event
3rd event
Prothrombin activator activates thrombin
Activated fibrin stabilizing factor crosslinks fibrin
Thrombin activates fibrin monomer
1st event + Prothrombin activator activates thrombin
2nd event + Thrombin activates fibrin monomer
3rd event + Activated fibrin stabilizing factor crosslinks fibrin
Identify the true statements regarding fibrinolysis. (Select 2.)
Alpha-2 antiplasmin inhibits the action of plasmin on fibrin.
Plasminogen is synthesized in the endothelium.
tPA inhibitor inhibits the conversion of fibrinogen to fibrin.
D-dimer measures fibrin split products.
D-dimer measures fibrin split products
Alpha-2 antiplasmin inhibits the action of plasmin on fibrin
Plasminogen is synthesized in the liver (not the endothelium). It is converted to plasmin by tPA, and plasmin converts fibrin to fibrin degradation products. These are measured by D-dimer.
Alpha-2 antiplasmin inhibits the action of plasmin on fibrin.
tPA inhibitor inhibits the conversion of plasminogen to plasmin (not fibrinogen to fibrin).
Match each phase of the contemporary model of coagulation with its key event.
Initiation
Amplification
Propagation
A large quantity of thrombin is produced
The TF/VIIa reaction activates the final common pathway
Platelets are activated
Initiation + The TF/VIIa reaction activates the final common pathway
Amplification + Platelets are activated
Propagation A large quantity of thrombin is produced
Identify the BEST predictor of bleeding during surgery.
Bleeding time
PT/INR
History and physical
Thromboelastogram
History and physical
History and physical is the best predictor of bleeding during surgery.
Heparin inhibits the:
extrinsic pathway.
intrinsic pathway.
extrinsic and final common pathway.
intrinsic and final common pathway.
Intrinsic and final common pathway
Heparin inhibits the intrinsic and final common pathways.
Heparin binds to antithrombin and accelerates the anticoagulant ability of AT by 1,000.
The heparin-AT complex neutralizes thrombin and factors X, XII, XI, and IX. It also inhibits platelet function.
Warfarin inhibits:
factors III and X.
factors II, VII, IX, X.
factors II, VII, IX, X and protein C.
factors II, VII, IX, X and protein C and S.
Factors II, VII, IX, X and protein C and S
Warfarin is a vitamin K antagonist, so it inhibits production of all the vitamin K dependent factors (II, VII, IX, and X). It also inhibits protein C and S.
Match each medication with its mechanism of action.
Clopidogrel + ADP receptor antagonist
Abciximab + GIIb/IIIa receptor antagonist
Warfarin + Vitamin K antagonist
Enoxaparin + Antithrombin catalyst
A patient scheduled for coronary revascularization is diagnosed with type III von Willebrand disease. What is the BEST treatment for this patient?
DDAVP
Platelets
vWF/factor VIII concentrate
Cryoprecipitate
vWF/factor VIII concentrate
There are three types of Von Willebrand disease:
Type I: Mild-moderate reduction in the amount of vWF produced.
Type II: The wWF that is produced doesn’t work well.
Type III: Severe reduction in the amount of vWF produced.
Since this patient has type III disease, giving DDAVP will have no effect. DDAVP would’ve been the correct answer if the patient has type I disease. It does not pose a risk of transfusion-related infection.
The rest of the answers are suitable choices, but they’re not the best. Platelets and cryoprecipitate contain vWF, however they also carry the risk of transfusion related infection.
Which coagulopathies present with a prolong PTT and normal PT? (Select 2.)
Factor II deficiency
Hemophilia A
Hemophilia B
Factor X deficiency
Hemophilia A
Hemophilia B
Even if you didn’t know that hemophilia A is factor 8 deficiency and hemophilia B is factor 9 deficiency, you should be able to use other pieces of the stem and answer choices to guide you down the right path.
PT measures the classical extrinsic (tissue factor) pathway.
PTT measures the classical intrinsic pathway.
Both pathways arrive at the final common pathway.
Factors II and X are part of the final common pathway. Therefore, a deficiency of factor II and X will prolong both PT and PTT.
Since hemophilia A and B affect the intrinsic, but not the extrinsic pathway, these coagulopathies will prolong the PTT only.
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
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.
A patient with a history of type II heparin induced thrombocytopenia requires anticoagulation for cardiopulmonary bypass. What is the BEST treatment?
Heparin test dose
Bivalirudin
Enoxaparin
Warfarin
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.
Triggers of sickle cell crisis include: (Select 2.)
hyperthermia.
dehydration.
alkalosis.
pain.
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)
Match each donor blood group to the recipient(s) who can receive it.
O + A, B, AB, O
A + A, AB
B + B, AB
AB + AB
Type and screen:
takes five minutes.
mixes the recipients plasma with donor blood.
tests for ABO and Rh-D compatibility only.
tests for ABO, Rh-D compatibility, and most clinically significant antibodies.
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.
Which blood product contains the HIGHEST concentration of fibrinogen?
Whole blood
Fresh frozen plasma
Packed red blood cells
Cryoprecipitate
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.
What is the maximum allowable blood loss in a 70-kg patient with a hemoglobin of 12 g/dL? The transfusion trigger is a hemoglobin of 6 g/dL.
(Enter your answer as a whole number in mL)
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.
Match each blood additive with its function.
Citrate + Anticoagulant
Dextrose + Substrate for glycolysis
Phosphate + Buffer
Adenine + Substrate for ATP synthesis
Rank each infectious complication of transfusion from MOST common to LEAST common.
(One is most common, and four is least common)
Cytomegalovirus + 1
Hepatitis B + 2
Hepatitis C + 3
HIV + 4
A patient with O blood received AB blood during surgery. Within five minutes, you observe hemoglobinuria, hypotension, and increased surgical bleeding. What actions should you perform at this time? (Select 2.)
Give a crystalloid bolus.
Slow the rate of transfusion.
Send an AST/ALT to the lab.
Administer sodium bicarbonate.
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.
Fresh frozen plasma from which donor population imparts the HIGHEST risk of transfusion-related acute lung injury?
Jehovah witness
Creutzfeldt Jakob
Organ recipient
Multiparous female
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.
Consequences of massive transfusion include all of the following EXCEPT:
alkalosis.
hypercalcemia.
hyperkalemia.
hyperglycemia.
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.
Intraoperative blood salvage is MOST appropriate for: (Select 2.)
anterior hip arthroplasty.
cesarean section.
Whipple procedure.
living donor kidney transplant.
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.
Identify the major intracellular ions. (Select 2.)
Chloride
Sodium
Phosphate
Magnesium
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).
Match each fluid compartment with its approximate volume in a 70-kg adult.
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.
Rank each substance in terms of its volume of distribution.
(1 is the smallest, and 3 is the largest)
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.
Use the following data to calculate the net filtration pressure in the capillary.
Plasma oncotic pressure = 26 mmHg Plasma hydrostatic pressure = 35 mmHg Interstitial oncotic pressure = 3 mmHg Interstitial hydrostatic pressure = 0 mmHg
(Enter your answer in mmHg and round your answer to the nearest whole number)
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:
- Forces that move fluid from the capillary → interstitium
Capillary hydrostatic pressure (Pc)
Interstitial oncotic pressure (πif)
- 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
Rank each intravenous solution in terms of its osmolarity.
(1 is the highest, and 3 is the lowest)
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
A patient with SIADH presents to the operating room for emergency surgery. Calculate the plasma osmolarity.
Sodium = 115 mEq/L
Glucose = 90 mg/dL
BUN = 14 mg/dL
(Enter your answer as mOsm/L, and round to the nearest whole number)
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.
Match each fluid with its sodium concentration.
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.
What is the MOST common electrolyte abnormality in hospitalized patients?
Hypernatremia
Hyponatremia
Hyperkalemia
Hypokalemia
Hyponatremia
Hyponatremia (Na+ < 130 mEq/L) is the most common electrolyte disturbance in hospitalized patients.
Rapid correction of serum sodium in the patient with hyponatremia is MOST likely to cause:
osmotic demyelination syndrome.
water intoxication.
glucose-6-phosphate deficiency.
kernicterus.
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
A consequence of massive volume resuscitation with 0.9% sodium chloride solution is:
hyperchloremic metabolic acidosis.
hyperchloremic metabolic alkalosis.
hypochloremic metabolic acidosis.
hypochloremic metabolic alkalosis.
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.
A 70-kg victim of a shark attack presents to the operating room. Use the data below to classify the stage of hemorrhagic shock.
Estimated blood loss = 1,800 mL
Heart rate = 123 beats/min
Blood pressure = 90/54 mmHg
Urine output = 10 mL/hr
Stage I
Stage II
Stage III
Stage IV
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
Match each mediator with its classification.
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!
Which mediator promotes vasoconstriction in response to vascular injury?
Nitric oxide
Thromboxane A2
von Willebrand factor
Prostacyclin
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.
Match each coagulation factor with its other name.
- Fibrinogen
- Calcium
- Prothrombin
- Tissue factor
- Factor I - fib
- Factor IV- calcium
- Factor II -prothrom
- Factor III -TF
Identify the coagulation factors in the final common pathway. (Select 4.)
I II III V VII VIII X XII
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.”
Which clotting factor has the SHORTEST half-life?
II
VII
IX
X
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?
Indications for fresh frozen plasma transfusion include: (Select 2.)
plasma volume expansion.
antithrombin deficiency.
hypoalbuminemia.
urgent reversal of warfarin therapy.
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
Cryoprecipitate contains: (Select 3.)
fibrinogen. von Willebrand factor. tissue factor. platelets. factor 11. factor 8.
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
Indications for the use of cryoprecipitate include all of the following EXCEPT:
von Willebrand disease.
sickle cell disease.
massive transfusion.
disseminated intravascular coagulation.
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
An 80-kg patient with type I von Willebrand disease is scheduled for a right hip arthroplasty. How much desmopressin should be administered prior to surgery?
(Enter your answer in micrograms)
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
Identify the BEST treatment options for a surgical patient with type III von Willebrand disease. (Select 2.)
Factor VIII concentrate
Cryoprecipitate
Platelets
Recombinant factor IX
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.
Which laboratory results suggest a diagnosis of disseminated intravascular coagulation? (Select 2.)
Hyperfibrinogenemia
Normal aPTT
Thrombocytopenia
Increased fibrin split products
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
What is the definitive treatment for disseminated intravascular coagulation?
Platelets
Reversal of the underlying cause
Fresh frozen plasma
Heparin
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
Which conditions confer the GREATEST risk of developing disseminated intravascular coagulation? (Select 3.)
Trauma Malignancy Pancreatitis Sepsis Hemolysis Amniotic fluid embolism
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.
The severity of hemophilia A corresponds with the activity of factor:
II.
III.
VIII.
IX.
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.
Which condition is an indication for recombinant factor VII?
Idiopathic thrombocytopenic purpura
Hemophilia
Thalassemia
von Willebrand disease
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.
Triggers of sickle cell crisis include: (Select 2.)
alkalosis.
pain.
dehydration.
hyperthermia.
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
What is the MOST common major complication of sickle cell disease?
Aplastic crisis
Splenic sequestration
Acute chest syndrome
Vaso-occlusive crisis
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).
Which drug reduces the incidence of vaso-occlusive crisis in the patient with sickle cell disease?
Penicillin
Labetalol
Pneumococcal vaccination
Hydroxyurea
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
Which condition is MOST likely to precipitate sickle cell crisis in a patient with heterozygous sickle cell disease?
Infection
Dehydration
Hypoxemia
Hypothermia
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.
What is the MOST common comorbidity associated with sickle cell disease?
Asthma
Diabetes mellitus
Hypertension
Obesity
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.
Match each drug with its effects on laboratory tests of coagulation.
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
At the conclusion of cardiopulmonary bypass, the perfusionist estimates that 35,000 units of heparin remain in the patient’s circulation. How much protamine should the patient receive to restore the activated clotting time to baseline?
(Enter your answer as a whole number in milligrams
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.
During preoperative evaluation, a patient presents with an INR of 2.1. He denies taking anticoagulant medications. Which of the following is the MOST likely explanation for this finding?
Hyperinsulinemia
Increased production of cholecystokinin
Blockage of the pancreatic duct
Decreased bile synthesis
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.
When administered intravenously, what is the MINIMUM amount of time 20 mg of phytonadione should be infused?
(Enter your answer in minutes)
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).
A patient with atrial fibrillation and peptic ulcer disease is on warfarin therapy. Co-administration of which of the following drugs will increase the risk of hemorrhage? (Select 2.)
Ranitidine
Famotidine
Cimetidine
Nizatidine
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.
Match each drug with its drug class.
Clopidogrel + ADP receptor inhibitor
Abciximab + GIIb/IIIa receptor antagonist
Bivalirudin + Direct thrombin inhibitor
Tranexamic acid + Plasmin activation inhibitor
Match each ADP receptor inhibitor with the number of days it should be discontinued prior to elective surgery.
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.
Estimate the blood volume for a neonate born at 34-weeks gestation. She weighs 2,000 grams.
(Enter your answer as a whole number in mL)
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).
What is the MAXIMUM allowable blood loss in an 85-kg adult with a hemoglobin of 10 g/dL? Use a transfusion trigger of 7 g/dL.
(Enter your answer as a whole number in mL)
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.
A patient’s hematocrit is 18%. If two units of packed red blood cells are transfused, what is the expected post transfusion hemoglobin concentration?
(Round your answer as a whole number and enter as g/dL)
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.
If a patient’s erythrocytes express B antigen, then the patient has: (Select 2.)
type A blood.
type B blood.
anti-A antibodies in the plasma.
anti-B antibodies in the plasma.
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
What blood type is the universal donor for plasma?
O
A
B
AB
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?
A patient suffering from acute hemorrhage requires an emergency transfusion. There is no crossmatch available. What is the BEST intervention at this time?
Transfuse type O uncrossmatched blood
Transfuse type-specific uncrossmatched blood
Transfuse type-specific partially crossmatched blood
Hold transfusion until a full crossmatch is obtained
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.
Match each blood component with its shelf life.
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
Consequenceses of citrate intoxication following massive transfusion include:
hypocalcemia.
hypercalcemia.
hyperkalemia.
hypokalemia.
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).
Which physiologic changes occur as a result of the red blood cell storage lesion? (Select 2.)
Hyperkalemia
Altered erythrocyte morphology
Increased aerobic metabolism
Right shifted oxyhemoglobin dissociation curve
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
Match each blood component processing procedure with its function.
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.
What is the MOST common viral complication associated with transfusion?
Human immunodeficiency virus
Hepatitis B
Cytomegalovirus
Hepatitis C
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.
What is the MOST common cause of transfusion related mortality in the United States?
Transfusion-related acute lung injury
Bacterial contamination
Transfusion associated circulatory overload
Acute hemolytic reaction
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
All of the following suggest a diagnosis of transfusion-related acute lung injury EXCEPT:
left atrial hypertension.
PaO2/FiO2 ratio < 300 mmHg.
onset within 6 hours following transfusion.
bilateral infiltrates on chest x-ray.
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
Identify the blood products that are associated with the highest incidence of transfusion-related acute lung injury. (Select 2.)
Cryoprecipitate
Fresh frozen plasma
Platelets
Packed red blood cells
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.
Transfusion-associated circulatory overload can be distinguished from transfusion-related acute lung injury by the presence of: (Select 2.)
left ventricular dysfunction.
hypervolemia.
aortic regurgitation.
tachypnea.
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.
A patient under general anesthesia received two units of packed red blood cells. Within 15 minutes, he becomes tachycardic and hypotensive. There is hematuria and oozing in the surgical field. What are the BEST interventions at this time? (Select 2.)
Slow the transfusion
Mannitol
Normal saline
Acidify the urine
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?
The “lethal triad” of trauma consists of all of the following EXCEPT:
hypothermia.
coagulopathy.
acidosis.
traumatic brain injury.
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.
