The Journal of ExtraCorporeal Technology No 58-1 | Page 41

A. Saini et al.: J Extra Corpor Technol 2026, 58, 32 – 38 35
Table 2. Patient demographics and clinical characteristics stratified by hyperoxia severity. Variables
Normoxia PaO 2 100 mmHg( n = 48)
Mild hyperoxia PaO 2 101 – 200 mmHg( n = 94)
Moderate hyperoxia PaO 2 201 – 300 mmHg( n = 62)
Severe hyperoxia PaO 2 > 300 mmHg( n = 25)
Age( months)
0.5( 0.1, 2.9)
2.5( 0.3, 18.3)
7.9( 0.5, 50.7)
3.2( 0.4, 9.6)
0.001
Age group
0.01
Neonates
42( 87.5 %)
69( 73.4 %)
37( 59.7 %)
20( 80.0 %)
Pediatrics
6( 12.5 %)
25( 26.6 %)
25( 40.3 %)
5( 20.0 %)
Weight( kg)
3.4( 2.9, 4.4)
4.3( 3.2, 11.4)
7.4( 3.5, 19.2)
4.4( 3.0, 8.1)
0.001
BSA( m 2)
0.2( 0.2, 0.3)
0.2( 0.2, 0.5)
0.3( 0.2, 0.7)
0.3( 0.2, 0.4)
0.007
Race
0.2
Black
29( 60.4 %)
37( 39.4 %)
104( 45.4 %)
104( 45.4 %)
White
3( 6.3 %)
15( 16.0 %)
87( 38.0 %)
87( 38.0 %)
Hispanic
3( 6.3 %)
6( 6.4 %)
26( 11.4 %)
26( 11.4 %)
Other
13( 27.1 %)
36( 38.3 %)
12( 5.2 %)
12( 5.2 %)
Sex
0.7
Female
21( 43.8 %)
47( 50.0 %)
33( 53.2 %)
14( 56.0 %)
Male
27( 56.3 %)
47( 50.0 %)
29( 46.8 %)
11( 44.0 %)
ECLS Indication
< 0.001
Cardiac
16( 33.3 %)
44( 46.8 %)
37( 59.7 %)
15( 60.0 %)
ECPR
9( 18.8 %)
28( 29.8 %)
20( 32.3 %)
8( 32.0 %)
Pulmonary
23( 47.9 %)
22( 23.4 %)
5( 8.1 %)
2( 8.0 %)
Time from admission to ECLS Initiation
105.0( 25.0, 593.0)
49.0( 14.0, 353.0)
78.5( 5.5, 257.0)
111.5( 24.0, 313.0)
0.57
Duration of ECLS( hours)
118.0( 43.5, 248.0)
112.0( 65.0, 185.0)
101.0( 68.0, 158.0)
125.0( 72.0, 186.0)
0.68
ECLS Complications: Cardiovascular
18( 45.0 %)
28( 37.8 %)
26( 51.0 %)
15( 60.0 %)
0.21
Hemorrhagic
16( 40.0 %)
33( 44.6 %)
25( 49.0 %)
12( 48.0 %)
0.84
Mechanical
20( 50.0 %)
32( 43.2 %)
13( 25.5 %)
10( 40.0 %)
0.09
Renal
21( 52.5 %)
39( 52.7 %)
26( 51.0 %)
17( 68.0 %)
0.52
Neurologic
5( 12.5 %)
21( 28.4 %)
11( 21.6 %)
9( 36.0 %)
0.12
Metabolic
5( 12.5 %)
11( 14.9 %)
8( 15.7 %)
5( 20.0 %)
0.88
Infection
4( 10.0 %)
3( 4.1 %)
1( 2.0 %)
1( 4.0 %)
0.33
AKI Stage II or III
34( 75.6 %)
63( 74.1 %)
43( 71.7 %)
20( 95.2 %)
0.17
Mortality
19( 39.6 %)
41( 43.6 %)
27( 43.5 %)
16( 64.0 %)
0.23
Results depicted as n(%), median( Interquartile range). AKI: Acute Kidney Injury, BSA: Body Surface Area, ECLS: Extracorporeal Life Support; VA: Veno-Arterial. p- value mortality and worse neurological outcomes in patients with traumatic brain injury, and infants with hypoxic ischemic encephalopathy exposed to a PaO 2 level greater than 200 mmHg [ 1, 3 ]. In the critical care setting, exposure to high PaO 2 levels correlates with increased mortality in both adult and pediatric populations [ 18 – 20 ]. Additionally, after cardiac arrest or E – CPR, hyperoxia is associated with worse outcomes, with one study demonstrating a 24 % increase in mortality per 100mmHgincreaseinPaO 2 [ 4, 5, 21 ].
Hyperoxia during ECLS has been linked to worse outcomes. In a study of 93 infants undergoing cardiac surgery, a PaO 2 of > 193 mmHg on VA ECLS within the first 48 post-operative hours was associated with higher 30-day mortality in both unadjusted( OR: 16.6, 95 % CI: 3.17 – 305, p = 0.001) and adjusted( OR: 9.79, 95 % CI: 1.18 – 81, p = 0.03) regression analysis. Moreover, patients exposed to hyperoxia had a higher incidence of renal replacement therapy, with an overall in-hospital mortality rate of 49 % [ 10 ]. In another multi-centric study including 484 patients on VA( 86.7 %) and veno-venous( VV)( 13.3 %) ECLS, hyperoxia defined as PaO 2 > 200 mmHg during the first 48 h was associated with higher mortality( OR 1.03, 95 % CI:
1.01 – 1.04). However, no significant differences in functional status scale or renal complications were observed. Notably, patients exposed to hyperoxia were more likely to have a cardiac indication for ECLS. The in-hospital mortality was 45 % in this study [ 9 ]. Similar findings have been reported in adult patients undergoing VA ECLS [ 22, 23 ]. Comparable to prior studies, the overall in-hospital mortality in our study was 45 % and patients with PaO 2 > 200 mmHg were older and more likely to have a cardiac indication for ECLS. This observation likely reflects the more stringent PaO 2 targets typically adopted by the neonatal intensive care units compared to pediatric or cardiac intensive care units. Although severe hyperoxia was noted to be associated with in-hospital mortality in univariable analysis, this association did not remain significant in multivariable regression analysis, likely due to the small number of patients in this group. However, severe hyperoxia was significantly associated with the composite outcome of cardiovascular or renal complications during ECLS. The association between severe hyperoxia and Stage II or higher AKI trended towards significance, suggesting a potential link that requires further investigation. Consistent with the prior study by Cashen et al. [ 9 ], no difference in the