e136 SECTION XV Pediatric Critical Care Board Review Questions the goal would be to increase the percentage of hemoglobin A to 70% 2 A 15 year old patient with hemoglobin SS and prior history of chron[.]
e136 S E C T I O N XV Pediatric Critical Care: Board Review Questions the goal would be to increase the percentage of hemoglobin A to 70% A 15-year-old patient with hemoglobin SS and prior history of chronic transfusion therapy is admitted to the PICU with acute chest syndrome and impending respiratory failure The patient recently relocated to your state and has never been cared for at your facility Her hemoglobin on admission is 7.6 g/dL In addition to providing respiratory support, you plan to transfuse the patient with packed red blood cells (pRBCs) Her type and screen on admission reveals the presence of anti-Fya and anti-Jkb antibodies Her extended red cell phenotype and/or genotype are not yet available Of the following, the MOST appropriate orders to the blood bank at this time are as follows: A Cross-match units ABO/RhD compatible, Fya -, Jkb-, pRBCs B Cross-match units ABO/RhD compatible, Fya -, Jkb-, irradiated pRBCs C Cross-match units ABO/RhD compatible pRBCs D Cross-match units ABO/RhD compatible, Fya -, Jkb-, C-, E-, Kell -, irradiated pRBCs E Cross-match units ABO/RhD compatible, Fya -, Jkb-, C-, E-, Kell -, pRBCs Preferred response: E Rationale The patient described in the vignette has developed alloimmunization and has demonstrated antibodies with specificity to Duffy (anti-Fya) and Kidd (anti-Jkb) antigens Alloimmunization to C, E, and Kell are common in patients with sickle cell disease and can be prevented by selecting blood matched for those antigens when the patient’s phenotype is known For the patient in the vignette, neither the phenotype or genotype are known, therefore C-, E-, and Kell blood should be selected Irradiation of blood is done to inactivate viable donor lymphocytes and prevent transfusion-associated graft-versus-host disease in susceptible individuals Patients with sickle cell disease not fall into the category of patients that require irradiated blood products Which of the following characteristics is typical of children with b-thalassemia? A Acute chest syndrome B Macrocytic anemia C Thickening of the cortex of long bones D Thrombotic events Preferred response: D Rationale The sine qua non for diagnostics for thalassemia is a microcytic anemia with the demonstration of an a- to b-globin chain imbalance; however, this is not practical for routine testing Most clinical laboratories rely on a variation of a thalassemia screen The screen helps distinguish thalassemia from iron deficiency, and afrom b-thalassemia In thalassemia, free globin chains increase reactive oxygen species, whereas decreased glutathione and antioxidant stores result in oxidative damage to the fragile red cell membrane, as well as to apoptosis in a Fas-mediated process The result is a cadre of processes contributing to the heterogeneity of disease presentation Phosphatidyl serine moves to the outer leaf of the red cell membrane, enhancing macrophage-mediated destruction in the spleen and marrow and acting as a substrate for factor V and VIII binding, enhancing the generation of thrombin, which together with decreased protein C and S levels and increased platelet activation and adhesion leads to increased thrombosis In an attempt to compensate for the hemolysis and ineffective erythropoiesis, medullary and extramedullary erythropoiesis leads to skeletal abnormalities such as the thalassemic facies and thinning of the cortex of long bones, which, along with endocrine abnormalities, lead to increased fractures High levels of nontransferrin-bound iron from red cell destruction, increased intestinal absorption from inappropriately low levels of hepcidin, and transfusions lead to iron deposition, resulting in liver, cardiac, and endocrine dysfunction Although previous focus was on hepatic iron overload and cirrhosis, there is increasing awareness of iron overload in the heart, pituitary, and endocrine organs leading to dysfunction (the following section), and excessive melanin production leading to “bronze” pigmentation Cardiac failure due to iron overload, defined as a low ejection fraction with a component of cardiomyopathy, is the major cause of ICU admission and death in thalassemic patients A thalassemic patient in failure should be assumed to have cardiac iron overload until proved otherwise Risk factors include transfusion history and underchelation Untreated overload can also lead to dysrhythmias including atrial fibrillation and ventricular tachycardia, as well as conduction disturbances and heart block Which of the following two life-threatening complications of sickle cell disease can present with subtle manifestations? A Acute chest syndrome and aplastic crises B Acute chest syndrome and pulmonary hypertension C Multiorgan failure and acute chest syndrome D Vasoocclusive events and aplastic crises Preferred response: B Rationale Although all of the listed complications can be life threatening, multiorgan failure, vasoocclusion, aplastic crisis, and splenic sequestration tend to be associated with significant laboratory findings, signs, or symptoms Whereas acute chest syndrome (ACS) and pulmonary hypertension can present with dramatic findings, they also can be diagnosed despite a normal physical examination and laboratory findings and subtle symptoms What underlying process must be aggressively assessed and treated when a thalassemic patient presents in cardiac failure? A Anemia B Iron overload C Myocarditis D Pulmonary hypertension Preferred response: B Rationale Because of transfusional iron and increased gastrointestinal absorption, virtually all thalassemic patients have iron overload Iron overload is either one major factor or the major factor contributing to cardiac failure in persons with thalassemia Aggressive treatment with chelation can rapidly reduce iron overload, significantly improving cardiac function CHAPTER 136 Board Review Questions Which of the following processes is a potent inhibitor of hemoglobin S polymerization and resultant sickling? A Acidosis B Dehydration C Hemoglobin F D Hypoxia Preferred response: C Rationale Hemoglobin S is a soluble compound when oxygenated However, when oxygen tension decreases at the tissue level, oxygen is released from the hemoglobin molecule, causing polymerization or aggregation of the molecule and production of gels or crystals inside the cell Crystallization is enhanced by a high hemoglobin concentration, low pH, and low temperature A key determinant of sickling is the capillary transit time The longer a red cell is exposed to the relatively deoxygenated, cold, and acidotic environment of the capillary and postcapillary venule, the more time exists for hemoglobin S polymerization Hemoglobins F and A2 are potent inhibitors of hemoglobin S polymerization Which of the following is the first process responsible for the initiation of a vasoocclusive crisis in a child with sickle cell disease? A Endothelial activation B Interaction of sickle erythrocytes with leukocytes C Recruitment of leukocytes D Vascular occlusion Preferred response: A Rationale Vasoocclusion can be described as a four-step process starting with endothelial activation, which can be triggered by several processes, including the generation of oxygen radicals, adhesion, and infection These various activating factors can induce expression of the endothelial adhesion molecule and, in step 2, promote the recruitment of adherent leukocytes In step 3, sickle erythrocytes interact with adherent leukocytes, and in step they cause vascular clogging Which of the following conditions is the most common cause of hospitalization and death in patients with sickle cell disease? A Aplastic crisis B Acute chest syndrome C Hemolysis D Splenic sequestration Preferred response: B Rationale Acute chest syndrome (ACS) is the number one cause of death and hospitalization among patients with sickle cell disease It is defined as fever, cough, wheezing, chest pain, tachypnea in the presence of a new pulmonary infiltrate involving at least one complete lung segment, and no atelectasis on chest radiograph Several triggers in the pathophysiology of ACS have been identified, including atelectasis, fat embolism, true thromboembolism, and infection e137 A 10-year-old patient with sickle cell disease presents to your pediatric intensive care unit with acute chest syndrome (ACS) You initiate rehydration, pain control, oxygen, and broadspectrum antibiotics and decide to transfuse packed red blood cells What other intervention has been shown to be of benefit in these cases? A Aspirin B Corticosteroids C Bronchodilators D Ibuprofen Preferred response: C Rationale Recommendations for treatment of patients diagnosed with ACS consist of general management, which includes adequate pain control, rehydration, and oxygen administration for patients with pulse oximetry measurements less than 97% or 2% to 3% below baseline More specific management of ACS consists of (1) use of broad-spectrum antibiotics including a macrolide, (2) use of bronchodilators even if no wheezing is present, (3) transfusion, (4) bronchoscopy for patients who not respond to initial therapy, and (5) aggressive ventilation or extracorporeal membrane oxygenation Corticosteroid use remains controversial Chapter 89: Coagulation and Coagulopathy A 3-year-old girl is admitted to the PICU with an acute illness for the last days, characterized by fever and increasing respiratory difficulty On physical examination, she is irritable but appropriately responsive and has the following vital signs: temperature, 39°C; respiratory rate (RR), 44 breaths per minute, unlabored; heart rate, 132 beats per minute Pulmonary auscultation revealed scattered fine rales with scattered wheezes The rest of the physical examination was unremarkable Initial laboratory studies revealed hemoglobin (Hb), 11.1g/dL; white blood cell count (WBC), 15,300 per microliter with 57% neutrophils, 17% bands, 2% metamyelocytes; platelets, 212 103 per microliter Serum electrolytes are as follows: creatinine, 0.4 mg/dL; blood urea nitrogen (BUN), 16 mg/dL; lactate, mg/dL; normal aspartate transaminase (AST) and alanine transaminase (ALT) Prothombin time (PT), activated partial thromboplastin time (aPTT) and fibrinogen were all within normal limits Central venous and peripheral arterial lines were placed with heparin in the arterial line solution She received supplemental oxygen via facemask Over the next 36 hours, her respiratory status worsened with increased RR and decreased O2 saturation by pulse oximetry Urine output was noted to decrease in spite of adequate intravenous fluid intake and repeat serum creatinine was found to be 0.7 mg/dL Complete blood count (CBC) demonstrated Hb, 10.2 g/dL; platelets, 36 103 per microliter; WBC, 22,700 per microliter Coagulation panel demonstrated PT, 3.4 seconds; aPTT, 26.2 seconds; fibrinogen, 189 mg/dL The test most likely to identify the underlying process is: A ADAMTS13 B Heparin-dependent antiplatelet antibodies by ELISA C Serum C3 D Thrombin-antithrombin complex Preferred response: A e138 S E C T I O N XV Pediatric Critical Care: Board Review Questions Rationale Elements against heparin-induced thrombocytopenia (HIT) include time frame for the development of thrombocytopenia (too soon) and degree of thrombocytopenia (lower than usual for HIT) While the decrease in urine output and the development of renal insufficiency are consistent with atypical hemolytic uremic syndrome (HUS), the presence of significant respiratory dysfunction is not typical for this diagnosis A finding of a low ADAMTS13 would confirm a diagnosis of thrombocytopeniaassociated multiorgan failure (TAMOF), as low ADAMTS13 is not an element of HUS TAMOF is a recently described entity characterized by clinical signs of sepsis, a microangiopathic blood smear with marked thrombocytopenia, and clinical course with rapid development of multi-organ failure and poor prognosis Etiology of this disorder is unclear, but the pathophysiology involves consumption of the vWf-cleaving protease ADAMST13 with consequent enhancement of platelet deposition in the microvasculature Plasma exchange to replace the depleted ADAMST13 has been found to reduce morbidity and mortality A 17-year-old male weighing approximately 90 kg is brought to the emergency room unconscious following a motor vehicle accident involving alcohol He demonstrates active bleeding from a compound fracture of the left tibia and from a left parietal head wound He is normothermic, hypotensive (blood pressure, 85/50 mm Hg) and tachycardic (heart rate, 157 beats per minute) Urine obtained at the time of catheterization is grossly bloody He received units of packed red blood cells (pRBCs) on admission to the emergency room Central venous and peripheral venous and arterial lines are placed and oozing is noted at the insertion sites The Glasgow Coma Scale (GCS) is Complete blood cell count reveals Hb, 7.2 g/dL; WBC, 17,700 per microliter; platelets 22 103 per microliter Peripheral blood smear revealed “myelocytes and metamyelocytes,” “giant platelets,” and “schistocytes.” Coagulation profile is PT, 15.2 seconds; aPTT, 33.7 seconds; fibrinogen, 122 mg/dL Chemistry panel reveals BUN, 22 mg/dL; creatinine, 1.0 mg/dL; lactate dehydrogenase, 210 units/L; aspartate transaminase (AST or SGOT), 58 units/L; alanine transaminase (ALT or SGPT), 66 units/L The most likely diagnosis is: A Coagulopathy secondary to alcoholic liver disease B Coagulopathy of trauma C Disseminated intravascular coagulation D Massive transfusion syndrome Preferred response: C Rationale The presence of schistocytes strongly points toward the presence of a microangiopathic process such as that present in disseminated intravascular coagulation (DIC) While alcohol was involved in the motor vehicle accident, there is no information to suggest that the patient had a history of chronic alcohol use or liver disease While both ALT and AST are mildly elevated, these levels are also consistent with acute liver trauma Given the patient’s estimated blood volume, a coagulopathy caused by the transfusion of units of pRBCs in the emergency room is unlikely The coagulopathy of trauma is ill-defined but usually considered to be due to factors such as hypothermia and acidosis 3 A 4-year-old male with known cystic fibrosis presents with a 5-day history of increasing diarrhea and new onset fever, bruising, and bloody diarrhea Physical exam reveals a thin though otherwise well-appearing child in no acute distress with mild tachycardia but otherwise normal vital signs Laboratory studies reveal hemoglobin of 9.2 g/dL, a platelet count of 189 103 per microliter, normal white blood cell count and red blood cell (RBC) morphology, prothrombin time (PT) of 42.6 seconds, and activated partial thromboplastin time (aPTT) of 34.2 seconds Comprehensive metabolic panel is unremarkable What is the most likely diagnosis? A Disseminated intravascular coagulation (DIC) B Hemolytic uremic syndrome (HUS) C Liver disease D Vitamin K deficiency Preferred response: D Rationale The isolated prolonged PT places the defect in the “extrinsic” component of the traditional clotting cascade The only single clotting factor deficiency that would produce this pattern is a deficiency of factor VII Factor VII is a vitamin K–dependent clotting factor that requires vitamin K for the posttranslational modification, enabling it to be efficiently activated to activated factor VII (factor VIIa) Vitamin K is a fat-soluble vitamin, and children with cystic fibrosis may not adequately absorb vitamin K from their diet, particularly if they are having increased diarrhea during an exacerbation of their disease Although the absence of thrombocytopenia and prolongation of the aPTT not rule out DIC, their absence, along with normal RBC morphology, makes this diagnosis less likely The normal chemistry profile points against liver disease or HUS A 12-year-old autistic child is admitted to the PICU following scoliosis repair The patient was estimated to have a total of 1500 mL of blood loss during the procedure, and he received six units of stored packed red blood cells (RBCs) intraoperatively Immediately before wound closure he received one unit of fresh frozen plasma (FFP) and one unit of apheresis platelets (equivalent to the platelets derived from eight units of whole blood donation) Upon arrival to the PICU, he was mildly tachycardic but with normal blood pressure Physical exam demonstrated bloody surgical dressings but no blood on suctioning of the endotracheal tube Urine output was mL/kg/ hr during and following the surgical procedure (urinary catheter in place); no hematuria was noted Preoperative weight was 37.5 kg and preoperative hematology evaluation was within normal limits (hemoglobin (Hb), 12.3 g/dL; platelets, 221 103 per microliter; prothrombin time (PT), 11.8 seconds; and activated partial thromboplastin time (aPTT), 32.1 seconds) Laboratory studies obtained in the operating room before transfer to the PICU were as follows: Hb, 11.6 g/dL; platelet count, 88 103 per microliter; PT, 22.1 sec; aPTT, 47.7 sec; and fibrinogen, 91 mg/dL The patient’s mother admits that her son’s grandfather had given the boy ibuprofen (400 mg) the evening before because of a headache What is the most likely cause for this clinical/laboratory picture? A Disseminated intravascular coagulation (DIC) B Drug-induced platelet defect C Liver disease D Massive transfusion syndrome Preferred response: D CHAPTER 136 Board Review Questions Rationale Intraoperatively, this child received approximately 60% to 65% of his estimated blood volume in the form of stored RBCs Packed RBCs contain neither platelets nor sufficient amounts of clotting factors to support clot formation Although he did receive a large platelet transfusion and a single unit of FFP at the end of the procedure, this was not sufficient to reconstitute his hemostatic balance This syndrome could have been prevented if platelets and FFP were transfused in a ratio of close to 1 : 1 : 1 (RBC : FFP : platelets) Although DIC can develop in the context of massive transfusion, this diagnosis is less likely given the clinical context Although a markedly increased D-dimer assay might increase the possibility of DIC contributing to the clinical picture, one would expect D-dimer to be elevated in the immediate postoperative period, limiting its usefulness in this setting The thrombocytopenia would not be explained by an anesthesia-induced hepatic insult or acute exacerbation of underlying liver disease An acquired (or congenital) platelet defect would not explain the abnormal coagulation parameters present Chapter 90: Thrombosis in Pediatric Critical Care A 4-year-old child who presented with severe sepsis and circulatory collapse and was resuscitated via a femoral central venous access device (CVAD), has developed a swollen tense leg The most appropriate next investigation is: A Contrast magnetic resonance venography (MRV) B D-dimer levels D Thrombophilia screen E Ultrasound Preferred response: D Rationale Ultrasound is usually reliable and accurate for below groin deep venous thrombosis (DVT) and is easy to perform in sick children MRV will confirm the diagnosis but is not required for a femoral vein clot in most cases MRV has added expense, complexity of performance, and requires contrast Thrombophilia screen has no role in the diagnosis of DVT and does not contribute to the care of a child with a CVAD-associated DVT D-dimer will be likely elevated due to the sepsis and also does not contribute Normal D-dimer has some negative predictive value in previous well teenagers with venous thromboembolism but is of no use in a sick child with CVAD-associated symptomatic DVT A 1-day-old infant post-cardiac surgery is discovered to have a large intracardiac clot on echocardiogram on admission to the PICU The clinical decision is to anticoagulate and monitor, with a plan to perform thrombectomy if circulatory difficulties arise The best drug to use in this child is A Apixaban B Bivalirudin C Dalteparin D Enoxaparin E Unfractionated heparin Preferred response: E Rationale This child is clinically unstable and may require urgent surgical intervention Both enoxaparin and dalteparin are given subcutaneously e139 every 12 hours with no easy reversal option Direct oral anticoagulants (DOACs) like apixaban lack adequate data on neonatal dosing, are oral, and not reversible Intravenous bivalirudin has a rapid onset and short half-life but is not easily reversible Intravenous unfractionated heparin has a short half-life, is titratable, and reversible, and there is considerable experience of using the drug in this age group Unfractionated heparin is preferred choice in this scenario The most common cause of death due to heparin-induced bleeding for neonates is: A Accidental overdose due to error in vial concentration used B Concomitant use of antiplatelet agents C Failure to dose adjust in renal failure D Performing monitoring assays less than 12 hourly E Titrating in 20% dose increments instead of 10 % increments Preferred response: A Rationale Optimal titration amounts will depend on clinical circumstance and how much below target range monitoring assays are Increments of 10–20% are commonly employed The optimal frequency of monitoring in children and neonates remains unclear, but once stable most children can be monitored once daily Heparin dose adjustment is certainly required in renal failure but it is rarely a cause of death Concurrent antiplatelet agents increase the risk of bleeding, and the use of multiple agents should always be carefully considered Heparin is packaged in a wide range of concentrations ranging from 50 U/mL to up to 5000 U/mL and given the weight range of patients and variety of uses of heparin in pediatric ICU (arterial line flushing compared to extracorporeal circulation support) then multiple concentrations are usually stored in the ward drug cupboard All units must ensure adequate systems to minimize this risk The coagulation system in children compared to adults is vastly different and should be considered as: A Pro-thrombotic in infancy due to low levels of antithrombin B Pro-bleeding in infancy due to low levels of vitamin K dependent factors C Pro-bleeding in infancy due to low levels of VWF D Pro-thrombotic in infancy due to reduced TFPI levels E Neither pro-thrombotic nor pro-bleeding Preferred response: E Rationale While there are a multitude of changes in the coagulation proteins and inhibitors of coagulation throughout childhood, with most marked changes being noted during the newborn period, these changes not render infants pro-thrombotic nor pro-bleeding compared to adults In fact neonates and children tolerate many stimuli that cause clinical complications in adults without any clinical consequence in terms of abnormal bleeding or clotting While antithrombin levels are low in infancy, this seems balanced by increased levels of alpha-2-macroglobulin, which does most of the thrombin inhibition in this age group Without vitamin K supplementation, then infants would be vitamin K deficient and the rates of severe bleeding are around in 10,000; however, in Western countries the majority of babies receive intramuscular vitamin K shortly after birth and this ameliorates the bleeding e140 S E C T I O N XV Pediatric Critical Care: Board Review Questions risk Von Willebrand factor levels are high in infancy with increased high molecular weight multimers, such that the diagnosis of von Willebrand disease is very difficult in the first months of life Total tissue factor pathway inhibitor (TFPI) is similar in neonates and adults Free TFPI is reduced in neonates, but the impact on overall on coagulation is unknown What is the most common cause of thromboembolic disease in children? A Factor V Leiden B Protein C deficiency C Sepsis D Vascular access devices Preferred response: D Rationale The most common cause of thromboembolic disease in children is vascular access devices Protein C deficiency is a rare thrombophilia of childhood Factor V Leiden mutation, although more common than protein C deficiency, is rarely the primary stimulus for a thromboembolic event Most often in children it is a multiple hit that results in thrombosis (i.e., sepsis factor V Leiden mutation vascular access device) In infants, which factor(s) have levels that are 33% to 50% lower than adults? A Antithrombin B Factor II, VII, IX, and X C Factor V, VIII, XIII, and von Willebrand factor D Protein C and protein S Preferred response: B Rationale Vitamin K–dependent clotting factors are the most studied group of factors in infants Factors II, VII, IX, and X have been demonstrated to have levels that are 33% to 50% lower in infants than in adults, despite vitamin K prophylaxis at birth This is a part of the complexity that is developmental hemostasis Factor V, VIII, XIII, and von Willebrand factor are elevated at birth Protein C is very low at birth, and protein S is also lower; however, the functional activity of protein S is similar to that of adults, as all of the protein S is in its active free form Antithrombin is also lower at birth, albeit to a lesser extent than the vitamin K–dependent factors A child who is in the pediatric intensive care unit for airway management and nutritional support begins bleeding unexpectedly from intravenous sites and mucous membranes Immediate coagulation studies reveal an activated partial thromboplastin time (aPTT) of 200 seconds, an international normalized ratio (INR) of 5, and a normal fibrinogen level Results of a full blood examination are normal, with a platelet count of 220,000/µL What is the most likely cause of the coagulopathy? A Accidental heparin overdose B Disseminated intravascular coagulation (DIC) C Liver disease D Platelet function disorder Preferred response: A Rationale Hemophilia and platelet function defects not prolong the aPTT and INR Severe liver disease would be associated with a low fibrinogen level DIC usually occurs in persons with sepsis, severe hypotension, or severe hypoxia, none of which exist in this child Given that fibrinogen is an acute phase reactant, it is possible to have DIC with a normal fibrinogen level Accidental heparin overdoses are common in pediatric hospitals because of selection errors Often the child is meant to be receiving a low-dose heparin line flush that may or may not even be documented in the child’s medical record A massive heparin overdose will prolong both the aPTT and INR in many laboratories, depending on the reagent/analyzer system in place In any hospitalized child with unexpected severe coagulopathy, accidental heparin overdose should be in the initial differential diagnosis Chapter 91: Transfusion Medicine Which of the following is most frequently used by pediatric intensivists to guide the use of packed red blood cell transfusion in clinical practice? A Arterial partial pressure of oxygen (Pao2) B Central venous oxygen saturation (Scvo2) C Hemoglobin concentration D Oxygen consumption (Vo2) E Near infrared spectroscopy (NIRS) Preferred response: C Rationale The hemoglobin level is the most frequently used parameter to guide red blood cell transfusion Additional studies are warranted to evaluate the appropriateness of other variables For patients in hemorrhagic shock, which is the current recommendation for transfusion of red blood cells: plasma: platelets? A 1:1:2 B 1:2:1 C 2:1:1 D 3:1:1 Preferred response: C Rationale In patients with hemorrhagic shock, the current literature supports the recommendation to transfuse red blood cells, plasma, and platelets at a ratio between 1:1:1 and 2:1:1 A lower plasma or platelet ratio (such as a 3:1) is associated with worse clinical outcome Which of the following is the most frequent cause of morbidity and mortality attributable to transfusion? A Hemolysis B Transfusion-associated circulatory overload (TACO) C Transfusion-associated graft-versus-host disease D Transfusion-related acute lung injury (TRALI) E Transfusion-transmitted infectious diseases Preferred response: B Rationale Current evidence suggests that transfusion-associated circulatory overload (TACO) is the most frequent severe adverse event attributable to transfusion, in terms of morbidity or mortality It is nearly seven times more frequent than transfusion-related acute lung injury (TRALI) and eight times more frequent than acute ... of sepsis, a microangiopathic blood smear with marked thrombocytopenia, and clinical course with rapid development of multi-organ failure and poor prognosis Etiology of this disorder is unclear,... transfusion and a single unit of FFP at the end of the procedure, this was not sufficient to reconstitute his hemostatic balance This syndrome could have been prevented if platelets and FFP were... difficulties arise The best drug to use in this child is A Apixaban B Bivalirudin C Dalteparin D Enoxaparin E Unfractionated heparin Preferred response: E Rationale This child is clinically unstable and