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[.]
Trang 1Cardiac 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
hemody-namics 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
pres-sure, 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 self-
limited, 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
inten-sivist 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
postpericar-diotomy syndrome Fluid in the pericardial space may
accumu-late 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
pres-sures rise, and diastolic collapse of the atria can be observed
echocardiographically Patients become symptomatic with a
nar-row pulse pressure, pulsus paradoxus, tachycardia, respiratory
distress, decreased urine output, hyperkalemia, metabolic
acido-sis, and hypotension with tremendous endogenous
catechol-amine response
Diaphragmatic Dysfunction, Effusions,
and Pulmonary Issues
Diaphragmatic paresis (reduced motion) or paralysis (paradoxical
movement) may precipitate and promote respiratory failure,
par-ticularly in the neonate or young infant who largely relies on
dia-phragmatic function for breathing; older infants and children can
recruit accessory and intercostal muscles if diaphragmatic
func-tion proves inadequate Injury to the phrenic nerve may occur
during operations that require dissection of the branch
pulmo-nary 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
neo-natal 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 dys-function However, the chest radiograph may be misleading if it
is obtained at the end of inspiration during positive-pressure ven-tilation when lung volume is at its highest Ultrasonography is most useful for identifying reduced diaphragmatic motion or paradoxical excursion Diaphragmatic dysfunction may be tran-sient and resolve over time However, a patient who fails repeated extubation attempts despite optimizing cardiovascular and nutri-tional 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 Espe-cially 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 imped-ing lymphatic return to the venous circulation Pleural or perito-neal 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 end- expiratory 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 under-stood, but new insights are emerging.61
The thoracic duct ascends to the right of the vertebral col-umn, crosses over to the left hemithorax at the fifth thoracic vertebral body, and drains into the venous circulation at the re-gion of the left subclavian and left jugular veins In general, chylothorax can be classified as traumatic or nontraumatic Di-rect 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
Trang 2Multiple diagnostic and therapeutic algorithms have been
re-ported 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
re-sumed However, a milky appearance alone is insufficient to
diag-nose 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;
uncer-tain cases with values 50 to 110 mg/dL may require additional
testing, such as lipoprotein analysis for the demonstration of
chy-lomicrons In children who are not on enteral feeds or are
mal-nourished, a lipoprotein analysis is suggested even with
triglycer-ides less than 50 mg/dL Typical pleural fluid in chylothorax has
a white cell count greater than 1000/mL with lymphocytic
pre-dominance (.80%), and a low lactate dehydrogenase level.65 In
addition, chyle has a high protein (.20 g/L) and
immunoglobu-lin content.66 , 67 Atypical fluid characteristics—such as
transu-dates, 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
chylo-thorax can be challenging and includes both conservative and
in-terventional 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
gener-ally started on a high medium-chain triglyceride (MCT), low
long-chain triglyceride diet for 7 days The high MCT diet is
con-tinued for 6 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
gener-ally treated with enteral fasting and parenteral nutrition for 7 to
10 days, with consideration for concomitant initiation of
soma-tostatin or its synthetic analog octreotide, administered
intrave-nously or subcutaneously.68 , 69 Absence of response to this strategy
after 2 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 do not, an
ad-ditional 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
me-dian 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
lym-phangiography and intranodal lymlym-phangiography, have provided
further insight and therapeutic options for this complex
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 plan-ning early extubation are given in Table 36.2
A number of published reports have described successful tra-cheal extubation in neonates and older children following con-genital heart surgery either in the operating room or soon after in the cardiac ICU.77 This has been possible without adversely affect-ing patient care and with a low incidence of reintubation or hemodynamic instability Such a process can reduce complica-tions 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
36.2 Considerations for Planned Early Extubation 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 hypothermiaLevel of hemodilution
Myocardial protection Modulation of the inflammatory response and reperfusion injury
Postoperative management Myocardial functionCardiorespiratory interactions
Neurologic recovery Analgesia management
Trang 3Separation 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
Ex-tubation 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
atten-tion during and following separaatten-tion from mechanical
ventila-tion that may compete for attenventila-tion with concurrent issues
affecting other patients in the unit The decision to extubate
ul-timately must take these factors into account, and, when
neces-sary, 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
accompa-nied 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
coordi-nation.79 Later, these deficits are manifested by cognitive and
speech and language dysfunction, impaired visual-motor
coordina-tion, 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
ge-netic, 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
chil-dren 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
associ-ated 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
ar-rest) have been implicated as potential causes of brain injury.87
These include (1) the total duration of CPB, (2) extreme
hemodi-lution 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
can-nulae, and (7) depth of hypothermia However, the impact of each
of these factors is not consistently seen, suggesting the
multifacto-rial nature of CNS injury following CPB In the postoperative
period, the primary factor that most consistently impacts
neurode-velopmental 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
im-pacted 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 in-creased 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 bal-ance can be challenging in infants and young children and those
on mechanical ventilation who are unable to communicate How-ever, 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 un-wanted 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 popula-tion has been estimated to be as high as 30% Those children who are younger than 2 years, require mechanical ventilation, receive benzodiazepines, or require mechanical restraints are at highest risk In the general critically ill pediatric population, those pa-tients with increased LOS (8 days vs 4 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:
1 Routinely assess pain, sedation, and delirium using validated scoring systems to more effectively target therapy.100 , 101
2 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 acet-aminophen 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 ef-fect.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
3 Optimize the environment by minimizing stressful factors and augmenting parental involvement Cycling of lights, control-ling extraneous or excess noise, promoting healthy and consis-tent sleep, and encouraging parental presence and involvement can both decrease the need for sedation and minimize the development of delirium
Trang 4Renal 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,
co-morbidities, 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
stan-dard.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-associ-ated lipocalin (NGAL), kidney injury molecule-1 (KIM-1),
cys-tatin C, urinary interleukin-18 (IL-18), liver-type fatty
acid-bind-ing protein (L-FABP), cell cycle marker insulin-like growth factor
binding protein 7 (IGFBP7) and tissue inhibitor of
metallopro-teinases-2 (TIMP-2).107–109 A landmark study of 71 children
un-dergoing 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
in-terstitial 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
con-tribute to delayed water clearance and potential prerenal
dysfunc-tion, 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
replace-ment 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
neuro-humoral 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
clear-ance, maintenance fluids can be increased to ensure adequate
nutrition The indications for renal support vary but include pro-nounced uremia, life-threatening electrolyte imbalance (such as severe hyperkalemia), ongoing metabolic acidosis, fluid restric-tions 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 proce-dure 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 im-mediate postoperative period as third space fluid losses continue Replacement of these losses with albumin or FFP may be neces-sary to treat hypovolemia and hypoproteinemia
Gastrointestinal Issues
Adequate nutrition is important following cardiac surgery in neo-nates 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 ad-vantageous.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 com-mon 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 prema-ture 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 broad-spectrum antibiotics Bowel exploration or resection may be neces-sary 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 3 to 4 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
Trang 5broad antibiotic coverage with third-generation cephalosporins,
these agents do not seem to be more effective in decreasing
post-operative 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
re-exploration, transthoracic ECMO cannulation, delayed sternal
clo-sure), 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
cath-eters in the postoperative patient, are important in reducing the
in-cidence 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 6 days, early reexploration for bleeding, or reoperation.114
Mediastinitis is characterized by persistent fever, redness,
dehis-cence, and purulent drainage from the sternotomy wound,
insta-bility of the sternum, and leukocytosis Staphylococcus is the most
common offending organism Treatment usually involves
debride-ment and irrigation, along with parenteral antibiotic therapy
The duration of therapy depends on the organism and severity of
the infection and is generally between 2 and 4 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
glu-cose 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
addi-tion, 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
con-trol with insulin infusion aimed at fasting euglycemic targets
can-not 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, nor-mal 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 pulmo-nary circulation and one part to the systemic circulation
A Qp/Qs greater than 1 implies a volume burden on the heart that may have a clinical impact depending on the degree, dura-tion, and myocardial reserve Though lesion-specific consider-ations are important in the various types of single-ventricle physiology, common management principles to balance flow and augment systemic perfusion do 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 impor-tant 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 inef-ficiently 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 “over-circulated” state, PVR is falling as it should in the normal postna-tal state, and the ductus arteriosus is maintained widely patent to mitigate outflow obstruction from the RV to the systemic circula-tion 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; evalu-ation of chest radiograph for cardiac size and pulmonary conges-tion; 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 esti-mated] – pulmonary arterial saturation) In all single-ventricle physiologies, the systemic arterial saturations and pulmonary arte-rial saturations are equal by definition If this ratio is greater than