The Effect of Decreasing Flow Rate on Cerebral Hemodynamics During Veno-Arterial Extracorporeal Membrane Oxygenation in Piglets.

To explore the influence of decreasing flow rate on cerebral hemodynamics during veno-arterial extracorporeal membrane oxygenation (va-ECMO), six normoxemic and six hypoxemic piglets were put on va-ECMO. The ECMO flow rate was decreased from the maximal achievable level to 50 mL min1 with steps of 50 mL min1 every 2 minutes. Changes in mean arterial blood pressure (MABP), left common carotid artery blood flow (Qcar), and other physiologic variables were continuously measured. Changes in concentrations of oxyhemoglobin and deoxyhemoglobin were measured using near infrared spectrophotometry (NIRS). Changes in difference between cerebral oxygen hemoglobin and deoxyhemoglobin concentration (ΔcHbD) and total hemoglobin concentration (ΔctHb) were calculated. ΔcHbD represents changes in cerebral blood flow (CBF), and ΔctHb reflects changes in cerebral blood volume (CBV). Data analysis was performed using mixed models and demonstrated a significant positive correlation between ECMO flow and, respectively, MABP (r = 0.7, p < 0.001), Qcar (r = 0.7, p < 0.001), cHbD (r = 0.8, p < 0.001), and ctHb (r = 0.7, p < 0.001). There was no significant relation between oxygenation state preceding ECMO and Qcar, cHbD, and ctHb during decreasing ECMO flow rate. We conclude that decreasing ECMO flow rate ultimately leads to concurrent decrease in MABP, CBF, and CBV.

Omphalocele and alveolar capillary dysplasia: a new association.

OBJECTIVE: First report of an infant with coexistent omphalocele and alveolar capillary dysplasia. DESIGN: Descriptive case report. SETTING: Neonatal intensive care unit of a tertiary care children's hospital. PATIENT: We describe a term infant with omphalocele and respiratory insufficiency attributable to pulmonary hypertension. The patient was placed on extracorporeal membrane oxygenation, but the pulmonary hypertension persisted. After 10 days on extracorporeal membrane oxygenation, a lung biopsy was performed. It showed alveolar capillary dysplasia. Because of the lethal prognosis, extracorporeal membrane oxygenation was withdrawn and the patient expired. CONCLUSIONS: This is the first description of an association between omphalocele and alveolar capillary dysplasia. In newborns with omphalocele who have severe respiratory insufficiency and pulmonary hypertension, alveolar capillary dysplasia should be considered.

Effect of bladderbox alarms during venoarterial extracorporeal membrane oxygenation on cerebral oxygenation and hemodynamics in lambs.

To determine the effects of bladderbox alarms during venoarterial extracorporeal membrane oxygenation (va-ECMO) on cerebral oxygenation and hemodynamics, six lambs were prospectively treated with va-ECMO and bladderbox alarms were simulated. Changes in concentrations of oxyhemoglobin (deltacO2Hb), deoxyhemoglobin (deltacHHb), and total Hb (deltactHb) were measured using near infrared spectrophotometry. Fluctuations in Hb oxygenation index (deltaHbD) and cerebral blood volume (deltaCBV) were calculated. Heart rate (HR), mean arterial pressure (MAP), blood flow in the left carotid artery (Qcar), and central venous pressure (CVP) were registered. Bladderbox alarms were simulated by increasing the ECMO flow or partially clamping the venous cannula and resolved by decreasing the ECMO flow, unclamping the cannula, or intravascular volume administration. CBV, HbD, MAP, and Qcar decreased significantly during bladderbox alarms, whereas HR and CVP increased. After the bladderbox alarms, CBV and HbD increased significantly to values above baseline. For HbD, this increase was higher during intravascular volume administration.MAP, Qcar, and CVP recovered to preexperiment values but increased further with volume administration. HR was increased at the end of our measurements. We conclude that Bladderbox alarms during va-ECMO treatment result in significant fluctuations in cerebral oxygenation and hemodynamics, a possible risk factor for intracranial lesions.

Intravascular volume administration: a contributing risk factor for intracranial hemorrhage during extracorporeal membrane oxygenation?

OBJECTIVE: The objective of this study was to determine the relationship between the frequency and total volume of intravascular volume administration and the development of intracranial hemorrhage during venoarterial extracorporeal membrane oxygenation. METHODS: In a retrospective, matched, case-control study, 24 newborns who developed an intracranial hemorrhage during venoarterial extracorporeal membrane oxygenation treatment were compared with 40 control subjects. Both groups were analyzed for gestational age, gender, race, Apgar scores at 1 and 5 minutes, birth weight, cardiopulmonary resuscitation before venoarterial extracorporeal membrane oxygenation, age at the start of treatment, duration of treatment, worst arterial blood gas sample preceding treatment, activated clotting time values, need for platelet transfusions, mean blood pressure, and the use of inotropics and steroids before the treatment. For both groups, total number and volume of intravascular infusions of normal saline, pasteurized plasma protein solution, erythrocytes, and platelets during the first 24 hours of treatment were determined. Variables were analyzed in their relationship to intracranial hemorrhage by using univariate and multivariate conditional logistic regression. RESULTS: The only statistically significant difference in patient characteristics between the case patients and control subjects was arterial blood gas values. Newborns who developed intracranial hemorrhage during the treatment received both a statistically significantly higher number and a statistically significantly higher total volume of intravascular volume administrations compared with control patients. After adjustment for pH, Paco(2), and Pao(2) in the multivariate analysis, we found a significant relation between the development of intracranial hemorrhage and >8 infusions or >300 mL of volume infusion in the first 8 hours and >10 infusions in the first 24 hours of treatment. CONCLUSIONS: The number and total volume of intravascular volume administration in the first 8 and 24 hours of venoarterial extracorporeal membrane oxygenation treatment are statistically significantly related to the development of intracranial hemorrhage.

Epileptiform activity during rewarming from moderate cerebral hypothermia in the near-term fetal sheep.

Moderate hypothermia is consistently neuroprotective after hypoxic-ischemic insults and is the subject of ongoing clinical trials. In pilot studies, we observed rebound seizure activity in one infant during rewarming from a 72-h period of hypothermia. We therefore quantified the development of EEG-defined seizures during rewarming in an experimental paradigm of delayed cooling for cerebral ischemia. Moderate cerebral hypothermia (n=9) or sham cooling (n=13) was initiated 5.5 h after reperfusion from a 30-min period of bilateral carotid occlusion in near-term fetal sheep and continued for 72 h after the insult. During spontaneous rewarming, fetal extradural temperature rose from 32.5 +/- 0.6 degrees C to control levels (39.4 +/- 0.1 degrees C) in 47 +/- 6 min. Carotid blood flow and mean arterial blood pressure increased transiently during rewarming. The cooling group showed a significant increase in electrical seizure events 2, 3, and 5 h after rewarming, maximal at 2 h (2.9 +/- 1.2 versus 0.5 +/- 0.5 events/h; p <0.05). From 6 h after rewarming, there was no significant difference between the groups. Individual seizures were typically short (28.8 +/- 5.8 s versus 29.0 +/- 6.8 s in sham cooled; NS), and of modest amplitude (35.9 +/- 2.8 versus 38.8 +/- 3.4 microV; NS). Neuronal loss in the parasagittal cortex was significantly reduced in the cooled group (51 +/- 9% versus 91 +/- 5%; p <0.002) and was not correlated with rebound epileptiform activity. In conclusion, rapid rewarming after a prolonged interval of therapeutic hypothermia can be associated with a transient increase in epileptiform events but does not seem to have significant adverse implications for neural outcome.