388 SECTION IV Pediatric Critical Care Cardiovascular Cardiac Tamponade The infant’s crowded mediastinum makes compression of the heart and cardiac tamponade an ever present possibility after chest cl[.]
388 S E C T I O N I V Pediatric Critical Care: Cardiovascular Cardiac Tamponade The infant’s crowded mediastinum makes compression of the heart and cardiac tamponade an ever-present possibility after chest closure, despite patent drainage tubes and surgical resection of the anterior pericardium The warning signs of tamponade frequently are subtle in small children, even minutes before cardiovascular collapse Any significant deterioration in hemodynamics after chest closure should first be attributed to tamponade if ventilation and cardiac rhythm are adequate The signs of tamponade include tachycardia, hypotension, narrow pulse pressure, and high filling pressures on both the left and right sides of the heart Acute myocardial perforation with tamponade occasionally occurs during interventional cardiac catheterization procedures Prompt support of the circulation with volume infusions and pressor support, along with immediate catheter drainage of the pericardial space, are essential in the event of this complication Hemopericardium after ventricular puncture usually is selflimited, as the muscular ventricle seals the perforation after the responsible wire or catheter is removed However, laceration of the thin-walled atrium may require suture repair under direct vision in the operating room Other causes of cardiac tamponade are seen in patients with CHD; treatment frequently requires the assistance of an intensivist for either pericardiocentesis or sedation and monitoring for that definitive procedure Postoperative tamponade from bleeding immediately after operation, as discussed earlier, is best handled by facilitation of chest tube drainage or reopening the sternotomy Some children develop pericardial effusions during later phases of their illness because of hydrostatic influences (e.g., patients with modified Fontan operations) or postpericardiotomy syndrome Fluid in the pericardial space may accumulate under considerable pressure and to the point at which filling of the heart is impaired If this problem is left unattended, the transmural pressure in the atria diminishes as intraatrial pressures rise, and diastolic collapse of the atria can be observed echocardiographically Patients become symptomatic with a narrow pulse pressure, pulsus paradoxus, tachycardia, respiratory distress, decreased urine output, hyperkalemia, metabolic acidosis, and hypotension with tremendous endogenous catecholamine response Diaphragmatic Dysfunction, Effusions, and Pulmonary Issues Diaphragmatic paresis (reduced motion) or paralysis (paradoxical movement) may precipitate and promote respiratory failure, particularly in the neonate or young infant who largely relies on diaphragmatic function for breathing; older infants and children can recruit accessory and intercostal muscles if diaphragmatic function proves inadequate Injury to the phrenic nerve may occur during operations that require dissection of the branch pulmonary arteries well out to the hilum (e.g., TOF repair, ASO), arch reconstruction from the midline (e.g., Norwood operation), manipulation of the superior vena cava (SVC; Glenn shunt), takedown of a systemic-to-pulmonary shunt, or after attempted percutaneous central venous access Phrenic nerve injury occurs more frequently at reoperation, when adhesions and scarring may obscure anatomic landmarks Extensive thymectomy during neonatal operations to improve exposure also can result in phrenic nerve injury Topical cooling with ice during deep hypothermia may cause transient phrenic palsy Increased work of breathing on low ventilator settings, increased Paco2, and a chest radiograph revealing an elevated hemidiaphragm suggest diaphragmatic dysfunction However, the chest radiograph may be misleading if it is obtained at the end of inspiration during positive-pressure ventilation when lung volume is at its highest Ultrasonography is most useful for identifying reduced diaphragmatic motion or paradoxical excursion Diaphragmatic dysfunction may be transient and resolve over time However, a patient who fails repeated extubation attempts despite optimizing cardiovascular and nutritional status, and in whom diaphragmatic dysfunction persists with lung volume loss in the affected side, necessitates surgical plication of the diaphragm.57 Although only a temporary effect is gained from plication, the prevention of collapse and volume loss in the affected lung from paradoxical movement of the diaphragm often provides the critical advantage needed for liberation from positive-pressure ventilation Pleural effusions and ascites may occur in patients after any type of cardiothoracic surgical procedures, especially following the Fontan operation or repairs involving a right ventriculotomy (e.g., TOF, truncus arteriosus) with transient RV dysfunction Especially in young patients, pleural effusions and increased interstitial lung water may be a manifestation of right heart failure This seems logically related to raised systemic venous pressure impeding lymphatic return to the venous circulation Pleural or peritoneal fluid and intestinal distension compete with intrapulmonary gas for thoracic space Evacuation of the pleural space, drainage of ascites, and bowel decompression facilitate restoration of lung volume Pulmonary edema, pneumonia, and atelectasis are common causes of abnormal postoperative gas exchange and hypoxemia If a bacterial pathogen is identified in the respiratory secretions, antibiotics should be initiated promptly If pulmonary edema is responsible for the gas exchange abnormality, therapy is aimed at lowering the LA pressure through diuresis and pharmacologic means to reduce afterload and improve the lusitropic state of the heart For infants, fluid restriction frequently is incompatible with adequate nutrition; therefore, an aggressive diuretic regimen is preferable to restriction of caloric intake Adjustment of endexpiratory pressure and mechanical ventilation serve as supportive therapies until the alveoli and pulmonary interstitium are cleared of the fluid that interferes with gas exchange Chylothorax Chylothorax develops in 0.25% to 9.2% of children after cardiac surgery and is associated with negative outcomes, including longer LOS, higher hospitalization costs, and increased risk of in-hospital mortality.58–60 The etiologies and pathophysiology of lymphatic dynamic disorders in these children are poorly understood, but new insights are emerging.61 The thoracic duct ascends to the right of the vertebral column, crosses over to the left hemithorax at the fifth thoracic vertebral body, and drains into the venous circulation at the region of the left subclavian and left jugular veins In general, chylothorax can be classified as traumatic or nontraumatic Direct injury to the thoracic duct or its tributaries causes traumatic chylothorax, whereas processes that elevate the central venous pressure (e.g., RV diastolic dysfunction, Fontan physiology, thrombosis or obstruction of the subclavian or internal jugular veins) may lead to nontraumatic chylothorax from alterations in the Starling forces.62 CHAPTER 36 Critical Care After Surgery for Congenital Cardiac Disease Multiple diagnostic and therapeutic algorithms have been reported in the literature.63,64 Initial investigation includes a chest radiograph or ultrasound to confirm the presence of an effusion, followed by diagnostic and/or therapeutic thoracentesis with pleural fluid analysis and an echocardiogram Vascular ultrasound imaging or cardiac catheterization may be needed to delineate the etiology further in select cases Typically, chylothorax should be suspected when a “milky” exudate or unilateral effusion is noted in the postoperative period, classically after enteral feeding is resumed However, a milky appearance alone is insufficient to diagnose chylothorax.65 Fluid triglyceride levels and cell count with differential are required to further establish the diagnosis Fluid triglycerides greater than 110 mg/dL or less than 50 mg/dL essentially confirm or exclude the diagnosis, respectively; uncertain cases with values 50 to 110 mg/dL may require additional testing, such as lipoprotein analysis for the demonstration of chylomicrons In children who are not on enteral feeds or are malnourished, a lipoprotein analysis is suggested even with triglycerides less than 50 mg/dL Typical pleural fluid in chylothorax has a white cell count greater than 1000/mL with lymphocytic predominance (.80%), and a low lactate dehydrogenase level.65 In addition, chyle has a high protein (.20 g/L) and immunoglobulin content.66,67 Atypical fluid characteristics—such as transudates, neutrophil-predominance, or high lactate dehydrogenase measurement—signal another etiology, such as heart, liver, or kidney dysfunction, or infection Prolonged chylothorax increases the risk of infection, poor wound healing, malnutrition, fluid and electrolyte imbalances, and delayed separation from respiratory support, all of which may lead to worse outcomes.58,66 Management of postoperative chylothorax can be challenging and includes both conservative and interventional treatments, with considerable institutional practice variation.63,64 In general, treatment begins with the insertion of a chest tube to drain the effusion, confirm the diagnosis, and provide symptomatic relief Postoperative chylothorax can be divided into low volume (#20 mL/kg per day) or high volume (.20 mL/kg per day) output Children with low-volume chylothorax are generally started on a high medium-chain triglyceride (MCT), low long-chain triglyceride diet for days The high MCT diet is continued for weeks in those patients who respond with a decrease in output to less than 10 mL/kg per day Those who fail this initial dietary modification or have high-volume chylothorax are generally treated with enteral fasting and parenteral nutrition for to 10 days, with consideration for concomitant initiation of somatostatin or its synthetic analog octreotide, administered intravenously or subcutaneously.68,69 Absence of response to this strategy after weeks should prompt consideration of surgical exploration to identify and repair the lymphatic injury or ligate the thoracic duct.63,70 Most high-output chylothorax resolves or significantly improves after surgical intervention For those that not, an additional week of enteral fasting and octreotide should be attempted before considering pleurodesis or placement of a pleuroperitoneal shunt.63,71 A recent analysis of the Pediatric Health Information Systems (PHIS) database reported that thoracic duct ligation or pleurodesis was performed at a median of 18 days after the cardiac surgery, and patients were discharged from the hospital at a median of 22 days after surgical treatment of chylothorax.58 More recently, percutaneous thoracic duct embolization has emerged as a less invasive alternative for the treatment of chylothorax.72–74 Newer studies, such as dynamic contrast-enhanced magnetic lymphangiography and intranodal lymphangiography, have provided further insight and therapeutic options for this complex 389 disorder.72–76 Other individualized supportive therapies include administration of 25% albumin for patients with serum albumin less than 2.5g/dL, intravenous immunoglobulin (IVIG) for those with low IgG levels, and multivitamins Separating from Mechanical Ventilation Early tracheal extubation of children following congenital heart surgery is not a new concept but has received renewed attention with the evolution of fast-track management for cardiac surgical patients Early extubation generally refers to tracheal extubation in the operating room or within a few hours (i.e., 4–8 hours) after surgery, although in practice, it means the avoidance of routine overnight mechanical ventilation Factors to consider when planning early extubation are given in Table 36.2 A number of published reports have described successful tracheal extubation in neonates and older children following congenital heart surgery either in the operating room or soon after in the cardiac ICU.77 This has been possible without adversely affecting patient care and with a low incidence of reintubation or hemodynamic instability Such a process can reduce complications such as ventilator-associated events but does not obviate meticulous attention to postoperative analgesia and sedation The judicious use of this practice has streamlined care and highlights the advances in perioperative care of infants and older children after repair of congenital heart defects.78 TABLE Considerations for Planned Early Extubation 36.2 After Congenital Heart Surgery Factor Consideration Patient Limited cardiorespiratory reserve of the neonate and infant Pathophysiology of specific congenital heart defects Timing of surgery and preoperative management Anesthesia Premedication Hemodynamic stability and reserve Drug distribution and maintenance of anesthesia on bypass Postoperative analgesia Surgery Extent and complexity of surgery Residual defects Risks for bleeding and protection of suture lines Conduct of bypass Degree of hypothermia Level of hemodilution Myocardial protection Modulation of the inflammatory response and reperfusion injury Postoperative management Myocardial function Cardiorespiratory interactions Neurologic recovery Analgesia management 390 S E C T I O N I V Pediatric Critical Care: Cardiovascular Separation from mechanical ventilation has the potential to cause important physiologic changes (e.g., increased RV preload, increased LV afterload; see Chapter 32); thus, these must be taken into consideration when planning extubation timing Extubation ideally should occur at the intersect between patient readiness and healthcare team capacity Although PICUs should strive to provide the same level of care and coverage 24 hours per day every day, it should be recognized that patients with higher complexity and risk often will require a level of undivided attention during and following separation from mechanical ventilation that may compete for attention with concurrent issues affecting other patients in the unit The decision to extubate ultimately must take these factors into account, and, when necessary, the procedure might benefit from being delayed so that it can be performed under elective conditions and with redundant staffing coverage Central Nervous System The dramatic reduction in surgical mortality has been accompanied by a growing recognition of neurologic morbidity in many survivors In the first months of life, this can manifest in altered tone, abnormal behavior, weak cry, and impaired feeding coordination.79 Later, these deficits are manifested by cognitive and speech and language dysfunction, impaired visual-motor coordination, learning disorders, and problems with executive functioning All of these contribute to decreased quality of life and increased cost to society.80 Neurologic outcomes in patients with critical CHD appear to be multifactorial, involving the interplay of genetic, prenatal, perioperative, and postoperative factors Treatment in the ICU can impact a number of these factors Prenatally, the intrauterine circulation for many critical cardiac lesions results in the delivery of less oxygenated blood to the brain, which alters growth and cerebral vascular resistance.81 The brains of many children with critical CHD demonstrate greater immaturity on brain MRI and have a higher incidence of periventricular leukomalacia (PVL).82 PVL, much like that seen in premature infants, is associated with increased vulnerability of immature oligodendrocytes to hypoxia and ischemia.83 Indeed, preoperative hypoxia and diastolic hypotension and postoperative hypotension are all associated with a greater degree of postoperative PVL.84–86 Intraoperatively, a number of support techniques used during neonatal and infant cardiac surgery (e.g., CPB, profound hypothermia, circulatory arrest) have been implicated as potential causes of brain injury.87 These include (1) the total duration of CPB, (2) extreme hemodilution during CPB to hematocrits less than 20, (3) the duration and rate of core cooling, (4) pH management during core cooling, (5) duration of circulatory arrest, (6) position and function of cannulae, and (7) depth of hypothermia However, the impact of each of these factors is not consistently seen, suggesting the multifactorial nature of CNS injury following CPB In the postoperative period, the primary factor that most consistently impacts neurodevelopmental outcomes is duration of hospital stay.88 LOS not only serves as a surrogate for complexity, it also correlates with greater number of medical errors, increased parental stress, and the development of additional morbidities LOS is also greatly impacted by sedation, prolonged ventilation, and the presence of delirium Infants and children undergoing cardiac surgery will require analgesia, sedation, and sometimes paralysis to manage pain, anxiety, oxygen delivery, and hemodynamic instability However, such agents must be optimally chosen and titrated to avoid under- and overtreatment Undertreatment can result in an increased stress response, with hemodynamic instability, delayed healing, and the development of posttraumatic stress response.89 Overtreatment can lead to hypotension, prolonged mechanical ventilation, tolerance, withdrawal, and delayed recovery This balance can be challenging in infants and young children and those on mechanical ventilation who are unable to communicate However, the use of validated pain and sedation scores for intubated and nonintubated infants and children that use clinical signs— such as alertness, agitation, muscle tone, facial expression, and response—has been shown to provide more objective measures of adequate pain and sedation management.90–92 The use of such scoring systems allows one to tailor therapy to effectively treat pain and minimize oxygen consumption in the most critically ill while also facilitating appropriate state control, early extubation, early mobility, and increased parental involvement The necessity of more targeted therapy has become increasingly evident with the growing knowledge of the impact of anesthetics, sedatives, and narcotics on the development of delirium and neurologic dysfunction in critically ill infants and children.93 Delirium has been increasingly recognized within pediatrics as a driver of prolonged LOS and has been associated with increased mortality and neurologic dysfunction.94–96 It is thought to be the consequence of underlying medical illness combined with unwanted side effects of treatment and the stressful environment of the ICU Possible mechanisms include neuronal injury due to inflammation, microemboli, and global or cellular hypoxia, all of which can be further exacerbated in the presence of critical illness and cardiac surgery with prolonged cardiopulmonary bypass.97 The incidence of delirium in the pediatric intensive care population has been estimated to be as high as 30% Those children who are younger than years, require mechanical ventilation, receive benzodiazepines, or require mechanical restraints are at highest risk In the general critically ill pediatric population, those patients with increased LOS (8 days vs days) are at greater risk, as are those with inflammatory-mediated disease processes.98 This may explain the higher incidence and earlier onset of delirium that is seen in the postcardiac surgery population as well as the increased association with duration of CPB.99 This suggests that the best approach for a postoperative cardiac patient is to: Routinely assess pain, sedation, and delirium using validated scoring systems to more effectively target therapy.100,101 Minimize narcotic and sedative use This can be achieved by the use of a standardized method of treatment of pain that routinely uses scheduled, nonopioid analgesics such as acetaminophen or nonsteroidal antiinflammatory drugs in the immediate postoperative period together with opioid agents Additionally, the use of agents such as dexmedetomidine, a highly selective a2 agonist that provides both sedation and analgesia, may have a narcotic and benzodiazepine-sparing effect.102 Further, dexmedetomidine has been demonstrated to have neuroprotective effects, though the mechanisms remain unclear.103 While its effect on decreasing heart rate can limit its use, it also has been shown to prevent and treat perioperative arrhythmias Optimize the environment by minimizing stressful factors and augmenting parental involvement Cycling of lights, controlling extraneous or excess noise, promoting healthy and consistent sleep, and encouraging parental presence and involvement can both decrease the need for sedation and minimize the development of delirium CHAPTER 36 Critical Care After Surgery for Congenital Cardiac Disease Renal Function and Postoperative Fluid Management Risk factors for postoperative renal failure include preoperative renal dysfunction, prolonged bypass time, hemolysis, low cardiac output, and cardiac arrest In addition to relative ischemia and nonpulsatile blood flow on CPB, angiotensin II–mediated renal vasoconstriction and delayed healing of renal tubular epithelium have been proposed as mechanisms for renal failure Postoperative sepsis and nephrotoxic drugs may further contribute to injury Serum creatinine is the most widely used test and the current gold standard for diagnosing acute kidney injury (AKI) Using creatinine measurements to diagnose AKI in children has several shortcomings, including—but not limited to—variable normal levels based on age, gender, race, muscle mass, volume status, comorbidities, and use of certain medications In addition, creatinine assesses only glomerular filtration and functional changes, and levels typically have a delayed rise over days after more than 50% of kidney function is lost in AKI, making it a poor gold standard.104–107 These limitations have provided the impetus to search for new biomarkers for the early detection of AKI prior to the functional change heralded by an increase in serum creatinine Promising new biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), cystatin C, urinary interleukin-18 (IL-18), liver-type fatty acid-binding protein (L-FABP), cell cycle marker insulin-like growth factor binding protein (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2).107–109 A landmark study of 71 children undergoing CPB showed that the concentrations in serum and urine of NGAL were sensitive, specific, and highly predictive of early AKI after cardiac surgery.4 In another prospective uncontrolled cohort study, plasma NGAL was shown to be an early predictive biomarker of AKI, morbidity, and mortality after pediatric CPB.110 Because of the inflammatory response to bypass and significant increase in total body water, judicious fluid management in the immediate postoperative period is critical Capillary leak and interstitial fluid accumulation may continue for the first 24 to 48 hours following surgery, necessitating ongoing intravascular volume replacement with colloid or blood products A fall in cardiac output and increased antidiuretic hormone secretion contribute to delayed water clearance and potential prerenal dysfunction, which could progress to acute tubular necrosis and renal failure if a low–cardiac output state persists During CPB, optimizing the circuit prime, hematocrit, and oncotic pressure; attenuating the inflammatory response with steroids; and use of modified ultrafiltration techniques have been recommended to limit interstitial fluid accumulation.111 During the first 24 hours following surgery, fluids should be restricted to 50% to 66% of full predicted maintenance and volume replacement titrated to appropriate filling pressures and hemodynamic response Oliguria in the first 24 hours after complex surgery under CPB is common until cardiac output recovers and neurohumoral mechanisms abate Although diuretics are commonly prescribed in the immediate postoperative period, neurohumoral influences on urine output are powerful and often limit diuretic response Time after CPB and enhancement of cardiac output through volume and pharmacologic adjustments are the most important factors that will promote diuresis Peritoneal dialysis, hemodialysis, and continuous venovenous hemofiltration provide alternate renal support in patients with severe oliguria and AKI Besides enabling water and solute clearance, maintenance fluids can be increased to ensure adequate 391 nutrition The indications for renal support vary but include pronounced uremia, life-threatening electrolyte imbalance (such as severe hyperkalemia), ongoing metabolic acidosis, fluid restrictions limiting nutrition, and increased mechanical ventilation requirements secondary to persistent pulmonary edema or ascites A peritoneal dialysis catheter may be placed preemptively at the completion of surgery for selected cases or as a bedside procedure later in the ICU, when necessary Indications include the need for renal support or for reducing intraabdominal pressure from ascites that may compromise mechanical ventilation and splanchnic perfusion Drainage may be voluminous in the immediate postoperative period as third space fluid losses continue Replacement of these losses with albumin or FFP may be necessary to treat hypovolemia and hypoproteinemia Gastrointestinal Issues Adequate nutrition is important following cardiac surgery in neonates and children These patients often have decreased caloric intake and increased energy demand after surgery; the neonate, in particular, has limited metabolic and fat reserves Total parenteral nutrition can provide adequate nutrition in the hypercatabolic phase of the early postoperative period However, achieving proper caloric intake may be challenging in critically ill patients for whom limited fluid intake and an aggressive fluid removal strategy are a priority (e.g., to facilitate chest closure) For these patients, delaying initiation of parenteral nutrition might be advantageous.112 Gastritis, ulcer formation, and upper gastrointestinal bleeding may occur following the stress of cardiac surgery in children and adults There are limited reports of the efficacy of proton pump inhibitors, histamine H2 receptor blockers, sucralfate, or oral antacids in pediatric cardiac patients, although their use is common in most PICUs Hepatic failure may occur after cardiac surgery, particularly after the Fontan operation, and typically is characterized by elevated liver enzymes, hyperammonemia, and coagulopathy Necrotizing enterocolitis, although typically a disease of premature infants, is seen with increased frequency in neonates with CHD Risk factors include (1) left-sided obstructive lesions, (2) umbilical or femoral arterial catheterization/angiography, (3) hypoxemia, and (4) lesions with wide pulse pressures (e.g., systemic-to-pulmonary shunts, severe aortic regurgitation) resulting in diastolic runoff in the mesenteric vessels Frequently, multiple risk factors exist in the same patient, making a specific etiology difficult to establish Treatment includes intestinal decompression through continuous nasogastric suction, parenteral nutrition, and broadspectrum antibiotics Bowel exploration or resection may be necessary in severe cases with impending or established perforation Infection Low-grade (,38.5°C) fever is common during the immediate postoperative period and may be present for up to to days, even without a demonstrable infectious etiology However, one ought not to simply disregard the occurrence of fever in the days following surgery, as it might signal an infection, especially in the multiply-instrumented patient CPB activates complement and other inflammatory mediators but also can lead to derangements of the immune system that increase the likelihood of infection Sepsis and nosocomial infection after cardiac surgery contribute substantially to overall morbidity Despite the increased use of 392 S E C T I O N I V Pediatric Critical Care: Cardiovascular broad antibiotic coverage with third-generation cephalosporins, these agents not seem to be more effective in decreasing postoperative infections Most centers use prophylactic coverage with a first-generation cephalosporin (i.e., cefazolin) with the first dose administered in the operating room and continued for the first 24 hours Type and duration of prophylactic antibiotic coverage may be altered depending on contributing factors (e.g., chest reexploration, transthoracic ECMO cannulation, delayed sternal closure), but these decisions are best made as part of clinical protocols and a robust antibiotic stewardship program to decrease variability and minimize unnecessary exposure Meticulous catheter insertion and daily care routines, along with early removal of indwelling catheters in the postoperative patient, are important in reducing the incidence of sepsis.113 Optimal head positioning, mouth care, sedation management, and consideration of an early-extubation strategy can reduce the rates of ventilator-associated events Mediastinitis occurs in up to 2% of patients undergoing cardiac surgery Risk factors include delayed sternal closure, particularly beyond days, early reexploration for bleeding, or reoperation.114 Mediastinitis is characterized by persistent fever, redness, dehiscence, and purulent drainage from the sternotomy wound, instability of the sternum, and leukocytosis Staphylococcus is the most common offending organism Treatment usually involves debridement and irrigation, along with parenteral antibiotic therapy The duration of therapy depends on the organism and severity of the infection and is generally between and weeks Hyperglycemia Hyperglycemia is a frequent occurrence in the PICU.115,116 As many as 97% and 78% of patients exhibit at least one blood glucose measurement above 125 mg/dL and 200 mg/dL, respectively, following surgical repair of congenital cardiac defects.115,116 The duration of postoperative hyperglycemia in these patients has been strongly and independently correlated with increased morbidity and mortality rates.115,116 Correlation does not signify causation; however, strict glycemic control with insulin administration has been shown to reduce morbidity and mortality rates significantly for adult patients admitted to a surgical ICU,117 and in one small pediatric study,118 two large randomized controlled pediatric trials of glycemic control failed to show improvement in meaningful primary outcomes (number of days alive and free from mechanical ventilation,119 rate of healthcare-associated infection120) In addition, patients assigned to strict glycemic control targeting fasting euglycemia experienced a significant increase in the occurrence of iatrogenic hypoglycemia,119,120 which is just as deleterious, if not more so, than hyperglycemia.121,122 Therefore, strict glycemic control with insulin infusion aimed at fasting euglycemic targets cannot be routinely recommended following cardiac surgery It may be reasonable to administer an insulin infusion to address severe and persistent postoperative hyperglycemia while targeting the more permissive range, such as the one used in the control arm of the pediatric glycemic trials (150–180 mg/dL).120 Critical Care Management of Selected Specific Lesions Single-Ventricle Anatomy and Physiology For a variety of anatomic lesions, the pulmonary and systemic circulations are in parallel with complete mixing, with a single ventricle effectively supplying both systemic and pulmonary blood flow The proportion of ventricular output to either the pulmonary or systemic vascular bed is determined by the relative resistance to flow in the two circuits The pulmonary arterial and aortic oxygen saturations are equal Assuming equal mixing, normal cardiac output, and full pulmonary venous saturation, Sao2 of 80% to 85%, with MVo2 of 60% to 65%, indicates Qp/Qs ≈1 and, hence, a balance between systemic and pulmonary flow Although “balanced,” the single ventricle still must receive and eject twice the normal amount of blood: one part to the pulmonary circulation and one part to the systemic circulation A Qp/Qs greater than implies a volume burden on the heart that may have a clinical impact depending on the degree, duration, and myocardial reserve Though lesion-specific considerations are important in the various types of single-ventricle physiology, common management principles to balance flow and augment systemic perfusion apply Neonatal Preoperative Management Changes in PVR have a significant impact on systemic perfusion and circulatory stability, especially preoperatively when the ductus arteriosus is widely patent In preparation for surgery, it is important that systemic and pulmonary blood flow be as well balanced as possible, especially in the patient who may have accompanying systemic ventricular dysfunction For example, a newborn with HLHS who has an arterial oxygen saturation greater than 90%, a wide pulse pressure, oliguria, cool extremities, hepatomegaly, and metabolic acidosis has severely limited systemic blood flow Even though ventricular output is increased, the blood flow that is inefficiently partitioned back to the lungs is unavailable to the other vital organs Immediate interventions are necessary to prevent imminent circulatory collapse and end-organ injury In this “overcirculated” state, PVR is falling as it should in the normal postnatal state, and the ductus arteriosus is maintained widely patent to mitigate outflow obstruction from the RV to the systemic circulation Blood flow manipulation by mechanical ventilation and inotropic support may temporarily stabilize the patient; this should accelerate the timeline for surgical intervention Similarly, in a patient with pulmonary atresia and an intact ventricular septum, LV-dependent pulmonary circulation occurs Ductal patency is necessary for pulmonary blood flow As PVR falls, pulmonary blood flow will be excessive and eventually will steal from the systemic circulation Preoperative management should focus on the adequacy of systemic oxygen delivery This is best achieved by thorough and continuous reevaluation of the clinical examination for cardiac output state and perfusion; evaluation of chest radiograph for cardiac size and pulmonary congestion; review of laboratory data for alterations in gas exchange, acid-base status, and end-organ function; and echocardiographic imaging to assess ventricular function and AV valve competence In a patient with a good systemic ventricular function, even high pulmonary blood flow (as manifested by higher saturations) is well tolerated for a few days However, in the patient without good systemic ventricular function, an assessment of the balance between pulmonary (Qp) and systemic flow (Qs) becomes important Qp/Qs is equal to the systemic arteriovenous saturation difference (systemic saturation – central venous saturation) divided by the pulmonary venoarterial saturation difference (pulmonary venous saturation [usually estimated] – pulmonary arterial saturation) In all single-ventricle physiologies, the systemic arterial saturations and pulmonary arterial saturations are equal by definition If this ratio is greater than ... processes.98 This may explain the higher incidence and earlier onset of delirium that is seen in the postcardiac surgery population as well as the increased association with duration of CPB.99 This suggests... synthetic analog octreotide, administered intravenously or subcutaneously.68,69 Absence of response to this strategy after weeks should prompt consideration of surgical exploration to identify and repair... lymphangiography and intranodal lymphangiography, have provided further insight and therapeutic options for this complex 389 disorder.72–76 Other individualized supportive therapies include administration