Estimated Cerebral Blood Flow in Term Infants with Hypoxic-Ischemic Encephalopathy

Sankaran, K; Peters, Kathrine L.; Finer, Neil N.

doi:10.1203/00006450-198111000-00005

Cited by 29 publications

(10 citation statements)

References 27 publications

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“…The low CBF values in our patients could be consistent with the values described in the literature which succeeded the initial phase of hy- peremia [14] after perinatal asphyxia. The study of Shakaran et al [14] demonstrated low blood flow values up to 4 days after a hypoxic-ischemic event. However, these data are in contrast to Doppler studies demonstrating increased cerebral blood flow velocities up to 4 days after the hypoxic injury [15,16].…”

Section: Discussionsupporting

confidence: 80%

“…But their study included ventilated neonates with severe respiratory distress syndrome or persistent pulmonary hypertension which may lead to low CBF values [2,13] even in the absence of a neurological disturbance [7]. The low CBF values in our patients could be consistent with the values described in the literature which succeeded the initial phase of hy- peremia [14] after perinatal asphyxia. The study of Shakaran et al [14] demonstrated low blood flow values up to 4 days after a hypoxic-ischemic event.…”

Section: Discussionsupporting

confidence: 77%

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Impaired Chemical Coupling of Cerebral Blood Flow Is Compatible with Intact Neurological Outcome in Neonates with Perinatal Risk Factors

et al. 1998

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Early detection of pathophysiological factors associated with permanent brain damage is a major issue in neonatal medicine. The aim of our study was to evaluate the significance of the CO₂ reactivity of cerebral blood flow (CBF) in neonates with perinatal risk factors. Fourteen ventilated neonates with perinatal risk factors (pathological cardiotocogramm, low cord pH, postpartal encephalopathy) were enrolled into this prospective study. The study was performed 18–123 h after birth. CBF was measured using the nonivasive intravenous ¹³³Xe method. Two measurements were taken with a minimal PaCO₂-difference of 5 mm Hg. From the two CBF values the CO₂ reactivity was calculated. Outcome was evaluated 1 year after birth. The CBF values at a lower PaCO₂ ranged from 6.6 to 115.2 ml/100 g brain issue/min (median = 18.2) and at a higher PaCO₂ level from 7.1 to 125.7 ml/100 g brain tissue/min (median = 18.75). The calculated CO₂ reactivity ranged from –9.6 to 6.6% (median 1.1%) change in CBF/mm Hg change in PaCO₂. CO₂ reactivity correlated with lowest pH (r² = 0.35, p = 0.02). Two infants died, one of neonatal sepsis, the other of heart failure. Neurological outcome at the age of 1 year was normal in 11 patients, 1 had severe cerebral palsy. From the 12 surviving patients the patient with severe neurological deficit showed the highest CBF values (125.7 ml/100 g/min). Impaired chemical coupling of cerebral blood flow is compatible with intact neurological outcome in neonates with perinatal risk factors. CO₂ reactivity in these newborns correlates with the lowest pH and may reflect the severity of perinatal asphyxia.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionsupporting

confidence: 77%

Impaired Chemical Coupling of Cerebral Blood Flow Is Compatible with Intact Neurological Outcome in Neonates with Perinatal Risk Factors

et al. 1998

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“…In contrast, studies with arterial oxygen saturations as low as 20-25% have demonstrated that the oxygenation and function of the heart, brain, adrenal glands, and diaphragm appear to be preserved because of a redistribution of the circulation with increased blood flows to these organs (12,14,30). Thus, hypoxemia does not reduce blood flow or oxygenation in the heart, brain, adrenal glands, or diaphragm as would be expected if hypoxemia could explain the necropsy data demonstrating ischemic/hypoxic injury after birth asphyxia (5,(8)(9)(10).…”

Section: Discussionmentioning

confidence: 79%

“…Asphyxia also is frequently associated with metabolic disturbances such as hypoxemia and acidemia (6,7). As clinical and necropsy data from asphyxiated newborns have suggested that the organ injury of birth asphyxia is consistent with perinatal ischemia and/or tissue hypoxia (5,(8)(9)(10), experimental studies have focused on the relationship between the metabolic abnormalities that occur during asphyxia and total cardiac output as well as regional organ blood flows. Many studies have demonstrated that neonatal and fetal ovine hypoxemia results in reductions in renal, gastrointestinal, splenic, and hepatic blood flows (11-13).…”

mentioning

confidence: 99%

Comparative Effects of Metabolic Acidemia and Hypoxemia on Cardiac Output and Regional Blood Flows in Unanesthetized Newborn Lambs

Fisher

1986

Pediatr Res

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METHODShypoxemia on cardiac output and regional organ blood flows in unanesthetized newborn lambs.Surgical technique. We operated on 24 Western newborn lambs at 1 to 8 days (5 ± 1, mean ± SE) after birth. The weight at surgery was 5.6 ± 0.2 kg. We performed a thoracotomy under halothane anesthesia in the left fourth intercostal space and inserted polyvinyl catheters (inside diameter 0.10 cm; outside diameter 0.15 cm) directly into the left atrium, and into the ascending aorta via the left internal thoracic artery (14). A pair of stainless steel pacing wires were sutured onto the left atrial appendage (A5633 hookup wires, Cooner Wire Co., Chatsworth, CA). Separate catheters were placed in a leg vein and artery, and advanced into the distal inferior vena cava and abdominal aorta, respectively. The wounds were sutured and postoperative care was given as described previously (14).Experimental protocols. Studies were performed 3 days after surgery, which is a duration that allows for the recovery of a normal cardiac output after a thoracotomy and halothane anesthesia in newborn lambs (15). The lambs were blindfolded, placed in a nylon-mesh animal sling, and a continuous recording was begun of a lead II electrocardiogram, aortic mean blood pressure, and heart rate. After the lambs had been resting quietly for 30 min, we withdrew 0.5 ml of aortic blood for the measurement of oxygen saturation, hemoglobin concentration, POz, pH, and Peoz. Immediately after obtaining the blood sample, we measured cardiac output and regional blood flows with radionuclide-labeled microspheres (16).After the control measurements were made, each lamb was subjected to 20 min of either reduced arterial blood oxygen content (hypoxemia) or reduced arterial pH (metabolic acidemia). Hypoxemia was produced in 12 lambs by placing each lamb's head in a polyethylene bag through which we administered 7% oxygen with the balance as nitrogen (14). Metabolic acidemia was produced in the other 12 lambs with an intravenous infusion of 0.5 N HCl into the distal inferior vena cava at 0.4 ml/min. We increased the infusion rate by 0.1 ml/min every ten minutes until the aortic pH was less than 7.20. The HCl infusion was discontinued at that time and the measurements were repeated after 20 min of metabolic acidemia. The arterial pH decreased by 0.02 ± 0.02 pH units during this period, but this trend was not statistically significant. The acidemia was achieved over 29 ± 2 (mean ± SE) min with a 0.09 ± 0.02 ml/kg/min of HCI.Previous studies have noted that metabolic acidemia may result in severe sinus bradycardia and an unstable preparation in experimental lambs and dogs (17,18). Consequently, we paced 756 ABSTRACT. We studied the comparative effects of HClinduced metabolic acidemia (pH = 7.11 ± 0.03, mean ± SE) and hypoxemia (PO z = 28 ± 1 torr) on cardiac output and regional blood flows in newborn lambs 3 days after the surgical placement of catheters in the left atrium and aorta and pacing wires on the left atrium. Cardiac output decreased by 49 ± 6% during metab...

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“…The infants in groups 2 and 3 suffered varying degrees of hypoxic-ischemic encephalopathy and its complications. The latter two groups had a history suggestive of fetal distress including meconium staining, fetal heart rate abnormalities, severe antepartum hemorrhage or a complicated delivery including breech extraction, difficult forceps extraction, failed forceps and/or cesarean sec tion for prolonged labor or fetal distress [9]; immediate neonatal asphyxia as evidenced by the need for immediate intubation and resuscitation; evidence of neurologic dysfunction as shown by seizures, marked abnormalities in behavioral state, posture, tone, motility and reflexes [9], Electroencephalograms and computerized tomographic scans were done on all infants and showed abnormalities compatible with hypoxic-ischemic encephalopathy. Group 2 differed from group 3 in the following manner; all infants in group 2 showed evidence of pulmonary complications such as meconium aspiration and persistent fetal circulation.…”

Section: Methodsmentioning

confidence: 99%

Hypoxic-Ischemic Encephalopathy and Plasma ß-Endorphin

Sankaran¹,

Hindmarsh²,

Watson³

1984

Dev Pharmacol Ther

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In an attempt to determine whether hypoxic-ischemic encephalopathy in and of itself or its associated pathologic conditions lead to increased concentrations of plasma ß-endorphin (ß-ED), measurements were made in three groups of term infants. Group 1 (control) consisted of 8 infants with a mean gestation of 38.6 ± (SE) 0.4 weeks, a mean birth weight of 3,420 ± 150 g, and a mean postnatal age of 1.4 ± 0.7 days. Group 2 consisted of 10 infants with a mean gestational age, birth weight and postnatal age of 40.1 ± 0.5 weeks, 3,310 ± 80 g and 3,9 ± 1.1 days, and group 3 included 6 infants with a mean gestational age, birth weight and postnatal age of 40.4 ± 1 weeks, 3,650 ± 310g, and 2.8 ± 1 days, respectively. The group 2 and 3 infants suffered clinical and neurological evidence of hypoxic-ischemic brain injury from perinatal asphyxia; however, the infants in group 2 suffered additional problems such as meconium aspiration, persistent fetal circulation with ongoing hypoxemia as measured by transcutaneous or umbilical arterial oxygen monitoring. The group 3 infants were normoxemic after resuscitation. The mean plasma ß-ED concentrations were 19 ± (SE) 2.7, 103 ± 35.7 and 25 ± 4.5 pg/ml in groups 1, 2 and 3, respectively. A significant elevation of plasma ß-ED concentration was observed in group 2 when compared to groups 1 and 3. The association of increased plasma ß-ED concentration in infants with hypoxic-ischemic encephalopathy associated with ongoing hypoxemia suggests that hypoxemia may act as a strong stimulus for plasma ß-ED release in term infants.

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Estimated Cerebral Blood Flow in Term Infants with Hypoxic-Ischemic Encephalopathy

Cited by 29 publications

References 27 publications

Impaired Chemical Coupling of Cerebral Blood Flow Is Compatible with Intact Neurological Outcome in Neonates with Perinatal Risk Factors

Impaired Chemical Coupling of Cerebral Blood Flow Is Compatible with Intact Neurological Outcome in Neonates with Perinatal Risk Factors

Comparative Effects of Metabolic Acidemia and Hypoxemia on Cardiac Output and Regional Blood Flows in Unanesthetized Newborn Lambs

Hypoxic-Ischemic Encephalopathy and Plasma ß-Endorphin

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