Download (somatic) near-infrared spectroscopy

Cardiac Intensive Care
Change in regional (somatic) near-infrared spectroscopy is not
a useful indictor of clinically detectable low cardiac output in
children after surgery for congenital heart defects
Utpal S. Bhalala, MD; Akira Nishisaki, MD; Derrick McQueen, MD; Geoffrey L. Bird, MD;
Wynne E. Morrison, MD, MBE; Vinay M. Nadkarni, MD; Meena Nathan, MD; Joanne P. Starr, MD
Objective: Near-infrared spectroscopy correlation with low cardiac output has not been validated. Our objective was to determine role of splanchnic and/or renal oxygenation monitoring using
near-infrared spectroscopy for detection of low cardiac output in
children after surgery for congenital heart defects.
Design: Prospective observational study.
Setting: Pediatric intensive care unit of a tertiary care teaching
hospital.
Patients: Children admitted to the pediatric intensive care unit
after surgery for congenital heart defects.
Interventions: None.
Measurements and Main Results: We hypothesized that
splanchnic and/or renal hypoxemia detected by near-infrared
spectroscopy is a marker of low cardiac output after pediatric cardiac surgery. Patients admitted after cardiac surgery to the pediatric intensive care unit over a 10-month period underwent serial
splanchnic and renal near-infrared spectroscopy measurements
until extubation. Baseline near-infrared spectroscopy values were
recorded in the first postoperative hour. A near-infrared spectroscopy event was a priori defined as ≥20% drop in splanchnic and/or
renal oxygen saturation from baseline during any hour of the study.
Low cardiac output was defined as metabolic acidosis (pH <7.25,
lactate >2 mmol/L, or base excess ≤–5), oliguria (urine output <1
A
predictable fall in cardiac output
(CO), referred to as low cardiac
output (LCO) syndrome, occurs
after congenital heart surgery and
is one of the major causes of perioperative
From the Department of Anesthesiology and Critical
Care (USB, AN, GLB, WEM, VMN), The Children’s
Hospital of Philadelphia, University of Pennsylvania,
Philadelphia, PA; Division of Pediatric Critical Care
Medicine (DM) and Pediatric Cardiothoracic Surgery
(JPS, MN), Children’s Hospital of New Jersey at Newark
Beth Israel Medical Center, University of Medicine and
Dentistry of New Jersey, Newark, NJ.
The authors have not disclosed any potential conflicts of interest.
For information regarding this article, E-mail:
[email protected]
Copyright © 2012 by the Society of Critical Care
Medicine and the World Federation of Pediatric
Intensive and Critical Care Societies
DOI: 10.1097/PCC.0b013e3182389531
Pediatr Crit Care Med 2012 Vol. 13, No. 5
mL/kg/hr), or escalation of inotropic support. Receiver operating
characteristic analysis was performed using near-infrared spectroscopy event as a diagnostic test for low cardiac output. Twenty
children were enrolled: median age was 5 months; median Risk
Adjustment for Congenital Heart Surgery category was 3 (1–6); median bypass and cross-clamp times were 120 mins (45–300 mins)
and 88 mins (17–157 mins), respectively. Thirty-one episodes of
low cardiac output and 273 near-infrared spectroscopy events
were observed in 17 patients. The sensitivity and specificity of a
near-infrared spectroscopy event as an indicator of low cardiac
output were 48% (30%–66%) and 67% (64%–70%), respectively.
On receiver operating characteristic analysis, neither splanchnic
nor renal near-infrared spectroscopy event had a significant area
under the curve for prediction of low cardiac output (area under
the curve: splanchnic 0.45 [95% confidence interval 0.30–0.60],
renal 0.51 [95% confidence interval 0.37–0.65]).
Conclusions: Splanchnic and/or renal hypoxemia as detected
by near-infrared spectroscopy may not be an accurate indicator
of low cardiac output after surgery for congenital heart defects.
(Pediatr Crit Care Med 2012; 13:529–534)
Key Words: cardiac surgery; cardiopulmonary bypass; congenital
heart defect; low cardiac output syndrome; near-infrared spectroscopy; renal; splanchnic
morbidity and mortality (1, 2). Studies
have shown that a LCO state occurs in as
many as 25% of patients (1). Wernovsky et
al (3) reported that 25% of neonates with
transposition of the great arteries who underwent an arterial switch operation had
a drop in cardiac index to <2.0 L/min/m2
between 6 and 18 hrs after surgery. Early
detection of LCO may allow pediatric intensive care unit (PICU) practitioners to
prevent further deterioration during this
critical postoperative period (4).
Traditionally, clinicians have relied on
clinical findings, such as pulse volume,
prolonged capillary refill time, widened
core-peripheral temperature difference,
hypotension, decreased urine output, and
metabolic acidosis on blood gas analysis, as
indirect markers of CO and oxygen delivery
(5). Current clinical parameters of CO and
circulatory function provide partial and
sometimes misleading information, especially in children (6). For instance, capillary
refill time and core-peripheral temperature
difference are often obscured by factors
such as fever, use of vasoactive medications, or deliberate mild hypothermia for
the management of postoperative junctional ectopic tachycardia (5). Continuous CO
measurement is either not available, cumbersome, or invasive and potentially harmful in this population. In current practice,
criteria for defining postoperative LCO in
children after surgery for congenital heart
defects (CHDs) utilize surrogate markers,
such as oliguria, metabolic acidosis and
change in inotrope support (7, 8).
It is known that splanchnic vasoconstriction is an early response to LCO as
blood is diverted to the vital organs, such
529
as the heart and brain (9). In animal experiments, it has been demonstrated that
increasing degrees of cardiogenic shock
induced by cardiac tamponade raise inferior mesenteric resistance up to four
times more than total vascular resistance
(10). In healthy adult human volunteers,
a 15% reduction in circulating blood
volume resulted in a 40% reduction in
splanchnic blood volume while heart
rate, blood pressure, and CO remained
unchanged (11).
Near-infrared spectroscopy (NIRS) is
a technique that has been used in various
clinical settings to evaluate regional tissue oxygenation in a noninvasive manner (12–19). NIRS renal and splanchnic
regional oxygenation monitoring has
been shown to positively correlate with
mixed venous saturation (17, 18) and
lactate levels (19) in children after surgery for CHD. Evidence is still lacking
to support its use in the postoperative
period to detect early LCO in children.
We therefore designed this study to assess the ability of NIRS splanchnic and/
or renal oxygenation monitoring to detect clinically detectable LCO in children
after surgery for CHD.
MATERIALS AND METHODS
The study is a prospective observational
study of children admitted to a PICU who had
surgery for congenital cardiac defects during
a 10-month period between November 2007
and August 2008. The local institutional review board approved the study, and written
informed consent was obtained from a legal
guardian of each subject.
Subjects
The study included children between 0
and 21 yrs of age who underwent surgery
for CHD requiring cardiopulmonary bypass
(CPB) and were subsequently admitted to the
PICU. Patients with clinical and/or radiologic
evidence of necrotizing enterocolitis were
excluded from the study. Patients were categorized for disease severity using the Risk
Adjustment for Congenital Heart Surgery categories (20). All operations were performed
by two surgeons during the study period.
Standard clinical practice at the institution
included intraoperative deep hypothermia to
a temperature between 18°C and 25°C, when
indicated, and a CPB circuit (Stockert-Shiley
pumps, Osterwaldstrasse, Munchen, West
Germany) with a membrane oxygenator and
roller pump. The CPB technique was similar
for all age groups, and modified ultrafiltration was used in all cases. Flow rates varied
with age from 100 to 175 mL/kg/min for
530
children weighing <10 kg and 2 to 3 L/min
for >10 kg. The pump was primed with heparin (2 U/mL of prime solution), sodium bicarbonate (15–20 mEq), 25% albumin (50 mL),
furosemide (1 mg/kg, maximum of 20 mg),
methylprednisolone (30 mg/kg, maximum
500 mg), cefazolin (30 mg/kg), one unit of
packed red cells, 150 mg of calcium chloride
for children weighing <10 kg, and PlasmaLyte A (Baxter, Deerfield, IL). Total CPB and
cross-clamp times were recorded for all patients. Patients were transferred to the PICU
after surgery. They were placed on fentanyl
infusions with or without muscle relaxant.
Postoperative inotrope management in the
PICU was at the discretion of the PICU physicians. The inotropic agents used were either
dopamine alone or in combination with epinephrine or milrinone. The inotrope score
(3) was determined in each patient at the
time of arrival to the PICU and subsequently
at the time of escalation of the inotropic support. In all the patients, point-of-care arterial
blood gases and lactate levels were measured
using iSTAT, a portable clinical analyzer device (I-stat, East Windsor, NJ), every hour
and as needed in the postoperative period
until extubation. Also, urine output was recorded every hour until extubation.
Outcome
This study’s primary outcome was the
occurrence of LCO. Previous studies in children after cardiac surgery have used surrogate markers like oliguria, tachycardia, cool
extremities, arterio-venous oxygen difference, occurrence of metabolic acidosis, initiation of a new inotropic agent, escalation
of existing pharmacologic support, and initiation of extracorporeal membrane oxygenation to define LCO syndrome (7, 8). Similar
to these pediatric studies, we defined LCO
as one or more of the following surrogate
markers: need for fluid bolus, occurrence
of metabolic acidosis (pH <7.25, lactate >2
mmol/L, base excess ≤–5), oliguria (urine
output <1 mL/kg/hr), and/or escalation in
inotropic support.
Measurement of Somatic
Regional Oxygen Saturation
Using NIRS
Somatic regional oxygen saturation
(rSo2) was monitored until extubation using
a multichannel NIRS device (Somanetics,
Troy, MI). Regional oxygen saturation at
splanchnic and renal regions were measured
by applying age- and weight-appropriate
NIRS probes over the anterior abdominal
wall above the umbilicus and over the flank
at the renal angle, respectively. The NIRS
device measured splanchnic and renal oxygen saturations every 6 to 30 secs. Probes,
cables, and monitors were placed and maintained by study personnel and nursing staff.
The bedside medical team was not responsible for NIRS setup and maintenance, and
clinical management was not altered based
on the display. The NIRS values recorded in
the first postoperative hour were used to define each subject’s baseline.
Statistical Analysis
All data were analyzed in hourly epochs
during the postoperative phase until extubation. A NIRS event (NE) was a priori defined
as a relative drop in splanchnic and/or renal
oxygen saturation (SrSo2 and RrSo2, respectively) by ≥20% from baseline value as in a
prior study (21). For example, when a patient
with baseline renal NIRS at 80% dropped renal
NIRS down to 64%, this event is calculated as
a 20% drop from the baseline. Sensitivity and
specificity of NE as a diagnostic test of LCO
was performed using 2 × 2 table. Receiver
operating curve (ROC) analysis was then performed to determine whether any other percent drop from baseline in NIRS values was a
better predictor of LCO. Sensitivity analyses
were performed using a limited LCO definition without fluid bolus as well as for subjects below 5 months of age. Summary data
are described as range, interquartile range,
or 95% confidence interval (CI). All analyses
were performed with Stata version 11 (Stata,
College Station, TX).
RESULTS
We enrolled 20 patients for the study,
and three were excluded due to technical challenges in obtaining complete
NIRS data. The remaining 17 patients
provided 828 hrs of postoperative measurements. Demographics and surgical background data are summarized in
Table 1. There were six univentricular lesions – one with pulmonary atresia status
post Blalock-Taussig shunt, two with tricuspid atresia and pulmonary atresia status post Blalock-Taussig shunt, two with
hypoplastic left heart syndrome, and one
with double outlet right ventricle. There
were 11 biventricular lesions – one with
secundum atrial septal defect, one with
transposition of great arteries with intact
ventricular septum, six with tetralogy of
Fallot, two with large perimembranous
ventricular septal defect, and one with
common atrioventricular canal defect.
Six patients underwent intraoperative
transesophageal echocardiograms, all of
which demonstrated good ventricular
function. Baseline postoperative data are
summarized in Table 2. Using a cutoff of
≥20% drop in SrSo2 and/or RrSo2 from
baseline during any study hour for NE,
Pediatr Crit Care Med 2012 Vol. 13, No. 5
Table 1. Demographic and surgical data of the patients
Parameter
Median
Range (Interquartile
Range)
Age (months)
Gender
Weight (kg)
Height (cm)
Risk Adjustment for Congenital Heart Surgery-1
Cardiopulmonary bypass time (min)
Cross-clamp time (min)
Type of lesion
  5
Not applicable
  5
 55
  3
120
 88
Not applicable
0.06–180 (1.2–8.0)
Male 14, Female 3
2–63 (3.6–6.3)
43–150 (51–66.5)
1–6 (2–3)
45–300 (92.5–225)
17–157 (54–108)
Univentricular 6 Biventricular 11
Table 2. Baseline postoperative data of the patients
Parameter
Median
Range (Interquartile
Range)
Temperature (°F)
Heart rate (per minute)
Systolic blood pressure (mm Hg)
Diastolic blood pressure (mm Hg)
Inotrope score
pH
Base deficit (mEq/L)
Lactate (mmol/L)
Splanchnic regional oxygen saturation
Renal regional oxygen saturation
98.5
160
96
54
10
7.36
0
3.20
65
65
94.1–100.9 (96–98.3)
108–209 (151–176)
68–132 (89–104)
33–67 (47–62)
0–17.5 (9.6–13.1)
7.28–7.42 (7.31–7.38)
–5 to +3 (–1.75–1.75)
1.62–9.33 (2.2–3.6)
30–90 (51.5–84)
27–90 (62–87.5)
273 NEs and 31 episodes of LCO were observed in 17 patients. Figure 1 shows an
example of NE and LCO episodes during a
24-hr record of SrSo2 and RrSo2 in one of
the patients.
Of 31 LCO episodes observed, 17 were
in the form of fluid boluses, two were oliguria, five were the occurrence of metabolic acidosis, and seven were an escalation
of inotropic support. Among seven LCO
events that were identified as escalation of
inotrope support, two were in the form of
escalation of epinephrine infusion (change
in inotrope score from 14.5 to 15.5 and 13
to 14, respectively), two as escalation of
dopamine infusion (change in inotrope
score from 11 to 13 and 5 to 7, respectively), one as escalation of milrinone infusion
(change in inotrope score from 5 to 7.5),
and two as restarting of the dopamine infusion (change in inotrope score from 0 to
5 in each). NEs were observed with 48%
(15 of 31) of LCO events. The sensitivity
and specificity for LCO were 48.3% (95%
CI: 30.5%–66.6%) and 67.6% (95% CI:
64.2%–70%), respectively. Table 3 presents sensitivity, specificity, positive predictive value, and negative predictive value of
NE as a diagnostic test for LCO using NE
cutoff as ≥5%, 10%, 15%, 20%, 30%, and
40% drop from the baseline. ROC analysis
revealed that neither splanchnic nor renal
NE had a significant area under the curve
Pediatr Crit Care Med 2012 Vol. 13, No. 5
(AUC) for prediction of LCO (splanchnic:
AUC 0.45, 95% CI 0.30–0.60; renal: AUC
0.51, 95% CI 0.37–0.65). The diagnostic
ability of NIRS (with ≥20% drop from
baseline as cutoff value) did not change
when we used a limited LCO definition after eliminating fluid bolus as a criterion for
LCO (sensitivity, 42.8% [95% CI 18–70],
specificity, 67.1% [95% CI 63–70]), and
also when we performed analysis of data
for subjects below 5 months of age only
(n = 8) (AUC for splanchnic NE = 0.51
[95% CI 0.33–0.69], AUC for renal NE =
0.48 [95% CI 0.31–0.65]). When we used
≥20% drop in NIRS saturation as a cutoff for detection of LCO, only 5.4% (95%
CI 3.2–9.0) of NEs had an association
with clinical LCO, whereas 97.1% (95%
CI 95.2–98.2) of NEs were not associated
with clinical LCO events. There was one
patient out of the 17 patients with a high
baseline lactate level of 9.33 mmol/L and
low renal and splanchnic baseline NIRS
values of 27 and 30, respectively. This
patient belonged to Risk Adjustment for
Congenital Heart Surgery category 2, with
a CPB time of 120 mins and baseline inotrope score of 10. There was no intraoperative transesophageal echocardiogram
record available for this patient, however.
The remaining 16 patients had baseline
lactate level <3 mmol/L. A sensitivity analysis with and without this patient did not
change the direction or significance of our
findings. The diagnostic characteristics
did not improve when we used an absolute NIRS measurement cutoff instead of a
relative percent drop from baseline values
(AUC for splanchnic NIRS: 0.58 [95% CI
0.43–0.73], AUC for renal NIRS: 0.50 [95%
CI 0.37–0.63]).
DISCUSSION
To our knowledge, this is one of the
few studies that examined the sensitivity
and specificity of NIRS splanchnic and/
or renal tissue oxygenation monitoring
for detection of LCO in children following
surgery for both single- and two-ventricle
reconstruction of CHDs. Since splanchnic and/or renal tissue hypoxemia can be
an early indicator of LCO, NIRS regional
oxygen monitoring has been proposed as
an early marker of LCO. Our data, however, show that NIRS monitoring for renal and splanchnic oxygenation has poor
predictive validity as an indicator of LCO.
This result is surprising because previous
studies demonstrated a better correlation
between somatic NIRS and indirect measures of CO, such as mixed venous saturation (17, 18) and lactate levels (19).
Explanations for our differing results
from other studies include the possibility
that somatic rSo2 measurements using current sensors are not accurate. Greisen (22)
recently described a lack of accuracy of the
currently available NIRS instruments in
measurement of cerebral rSo2. Commercial
NIRS sensors have a signal-to-noise ratio
of 2%–3%, higher than that of pulse oximetry. According to Greisen (22), averaging
the absolute cerebral NIRS tissue oxygenation index measurements over a minute
can provide an accurate mean value and
overcome the problem of large signal-tonoise ratio. Mean values differ, however,
based on site of sensor placement, as much
as 15%. This expert review concluded that
the precision of currently available NIRS
instruments is insufficient for clinical use
(22). There are also concerns that abdominal wall thickness may exceed the sampling
depth (1.5–2 cm) of currently used NIRS
probes in patients above 4 yrs for renal and
6 yrs for splanchnic measurements (23).
We therefore performed an analysis of data
for subjects younger than 5 months of age
(n = 8) with no improvement in sensitivity
and specificity.
It is also possible that the previously
used threshold of a 20% drop in NIRS
values is not an appropriate cutoff for
531
Figure 1. Twenty-four–hour record of splanchnic and renal regional oxygen saturation (rSo2) with near-infrared spectroscopy (NIRS) event: NIRS event
(arrow) and low cardiac output (LCO) episodes (heart). At time 00:32:58, NIRS event precedes a LCO episode whereas at times 09:17:10 and 12:01:02, both
NIRS events did not precede any LCO episodes.
Table 3. Positive predictive value, negative predictive value, sensitivity, and specificity of near-infrared
spectroscopy for low cardiac output at various cutoffs
Near-infrared
Spectroscopy
Cutoff Drop
From Baselinea
≥5%
≥10%
≥15%
≥20%
≥30%
≥40%
Positive Predictive
Value (95% CI)
3.5 (2.1–5.6)
3.5 (2.1–5.7)
4.3 (2.5–7.1)
5.4 (3.2–9.0)
5.2 (2.9–8.9)
2.8 (1.0–6.9)
Negative Predictive
Value (95% CI)
95.9 (93.0–97.7)
95.9 (93.2–979.7)
96.6 (94.5–98.0)
97.1 (95.2–98.2)
96.8 (95.0–98.0)
96.8 (94.1–98.3)
Sensitivity
(95% CI)
Specificity
(95% CI)
  58 (39.2–74.9)
54.8 (36.2–72.2)
48.3 (30.5–66.6)
48.3 (30.5–66.6)
41.9 (25–60.7)
16.1 (6–34.4)
38.6 (35.2–42.1)
  42 (38.5–45.5)
58.2 (54.6–61.6)
67.6 (64.2–70)
70.2 (66.9–73.3)
78.9 (75.8–81.6)
CI, confidence interval.
a
Drop from baseline is calculated as relative proportion of drops from the admission baseline value.
For example, if a patient has a near-infrared spectroscopy value of 80% at admission, then a nearinfrared spectroscopy drop down to 64% is considered as 20% drop.
LCO. Currently, data on the normal range
of NIRS rSo2 exist only in healthy term
newborns (24). Similar to several studies (25–28), we observed substantial between-subject variability in baseline NIRS
rSo2 values (baseline SrSo2 values ranged
from 30 to 90 and baseline RrSo2 values
ranged from 27 to 90). We performed the
ROC analysis to evaluate the discriminative ability of the NIRS measurement and
to identify an appropriate cutoff for the
postoperative NIRS measurement. We
were not able to identify any appropriate
cutoff for LCO, however. To address the
issue of baseline variability in NIRS rSo2
values, we also ran a ROC analysis for the
532
absolute rSo2 values instead of the relative percent drop from baseline as a sensitivity analysis. This strategy also did not
improve the diagnostic characteristics of
the NIRS-derived splanchnic and/or renal
regional oxygenation for LCO.
One other possibility is that our surrogate markers inadequately represent
LCO. As is usually the case in clinical
practice in pediatrics, we did not have a
continuous CO measurement to correlate
with somatic NIRS values. We defined
LCO using clinical (oliguria, need of fluid
bolus, or escalation of inotrope support)
and/or laboratory (occurrence of metabolic acidosis) criteria as have previously
published studies (7, 8). Because clinicians’ decisions to provide a fluid bolus
could conceivably be affected by factors
other than a diagnosis of LCO, we conducted a sensitivity analysis with a more
limited definition of LCO excluding fluid
boluses. This yielded similar results.
In recent years there has been increased interest in NIRS as a monitoring
device in various clinical settings (15–17,
29-32), but there are gaps in the understanding of NIRS regional oxygenation
monitoring. One study provided normal
NIRS values of cerebral and renal rSo2 in
a small population of healthy term newborns (24), but baseline preoperative rSo2
in children with cyanotic and noncyanotic heart defects are not known. Also, the
effects of palliative or corrective surgery
for these lesions on the rSo2 are unknown.
Hoffman et al (17) evaluated the correlation between regional (cerebral and
renal) NIRS measures and mixed venous saturations in neonates after stage
1 palliation for single-ventricle lesions.
The intrapatient correlation among rSo2
and mixed venous saturation was higher
(r2 = .53) than interpatient correlation
(r2 = .46). Therefore, the authors concluded that the NIRS measure is a reliable noninvasive indicator of mixed
venous saturations. Another study by
Chakravarti et al (19) showed a correlation between NIRS measurements
and lactate levels among children with
Pediatr Crit Care Med 2012 Vol. 13, No. 5
double-ventricle physiology undergoing
repair of CHD. In this study, they evaluated the diagnostic values of cerebral,
splanchnic, renal, and muscle rSo2 using
blood lactate as a surrogate standard for
LCOs. Measured rSo2 at each point was
averaged over 1 hr before a blood draw.
They measured lactate levels at 0, 2, 4, 6,
8, 10, 12, 14, and 24 hrs after surgery. By
using this methodological approach, they
probably missed an unknown number of
changes in NIRS rSo2 values and lactate
levels. Our study monitored blood lactate every hour with other clinical signs
of LCO, and the NE was defined as a drop
in rSo2 below baseline every hour. We believe our approach is more realistic and
close to the clinical application. In a case
series of children who underwent cardiac
surgery, the authors stated that NIRS
may herald deterioration and that there
may be a “threshold” effect that NIRS
may usefully detect (33). Our study, using
ROC analysis, failed to detect any meaningful threshold value of either renal or
splanchnic NIRS measurement to detect
early deterioration (LCO). It appears that
NIRS events are overwhelmingly associated with no change in clinical CO status,
demonstrated by an extremely low positive predictive value. Therefore, our study
results cannot support the routine use of
regional NIRS as an indicator that reliably
heralds LCO.
Our study has several limitations.
This is a prospective observational study
with a small sample size from a single
PICU, and the majority of patients belonged to low Risk Adjustment for
Congenital Heart Surgery categories.
Since the definition of LCO may be problematic, future multicentered studies
would benefit from continuous CO or
mixed venous saturation measurement
to compare to rSo2. We cannot exclude
the possibility that they may have responded to the values on the display with
interventions to potentially improve
CO, although clinicians caring for our
study subjects were not formally trained
to interpret data from the NIRS monitor. If this occurred, however, it would
have increased the likelihood that a fall
in NIRS values would be associated with
clinician interventions, biasing toward
a positive result, which we did not find.
Therefore, this is unlikely the case. We
also used a landmark approach to place
NIRS probes to detect splanchnic and renal rSo2. This might have decreased the
validity of the NIRS measures in older
patients, although those were few in our
Pediatr Crit Care Med 2012 Vol. 13, No. 5
study population. Also, if it were possible
to continuously monitor lactate, base
deficit, and instantaneous glomerular
filtration rate, then there may have been
other transient episodes of LCO that the
clinical criteria missed. We acknowledge this is a methodological challenge
when we compare an intermittent diagnostic test with continuously measured
parameters.
Some physicians have recommended
NIRS as “standard of care” in children for
postoperative management (34), recognizing that “regional saturation measured
by the NIRS technology may provide an
early indication of oxygen deficits associated with impending shock states and
anaerobiosis” (35). Our study results,
however, suggested that NIRS measurements of splanchnic and renal regional
oxygenation have limited capability to detect LCO. Further study is needed to delineate where the NIRS technology plays
an important role to manage critically ill
infants and children.
CONCLUSIONS
Splanchnic and/or renal tissue hypoxemia as detected by NIRS may not
be highly sensitive or specific for clinical
LCO after open-heart surgery in children.
ACKNOWLEDGMENTS
We thank the PICU staff at Children’s
Hospital of New Jersey for their assistance
with NIRS monitoring. We also extend
our special thanks to children and their
parents for their willingness to contribute
to the science.
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