Umbilical Cord Blood Gases and Hypoxic Ischemic Encephalopathy | Birth Injury Diagnosis
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Birth injuries related to fetal oxygen deprivation are both complicated and dangerous. Because of the severity and complexity of these injuries, confronting a loved one’s new hypoxic ischemic encephalopathy (HIE or birth asphyxia) diagnosis can feel overwhelming. At Reiter & Walsh, P.C., we aim not only to provide unparalleled legal services to our birth injured clients, but to make complex information on birth injury easier to access. Throughout this page, we’ll discuss everything you need to know about fetal circulation, hypoxic ischemic encephalopathy and neonatal brain damage. We’ll explain the causes of fetal oxygen deprivation, how umbilical cord blood gases help diagnose HIE, how umbilical cord blood gases are used in birth trauma lawsuits and more. Should you have any legal questions or case inquiries as you read through this page, please contact our team for a free consultation in whichever way best suits your needs:
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Fetal Circulation: Understanding How Babies Breathe in the Womb
A fetus depends on the mother for oxygen and carbon dioxide exchange during pregnancy. In the womb, a fetus does not breathe in the same way humans do outside the womb (although “practice breathing” occurs from time to time). Rather, “breathing” (gas exchange) occurs in the intervillous space in the placenta. The placenta is an organ that connects the developing fetus to the uterine wall to allow for nutrient uptake, waste elimination and gas exchange via the mother’s blood supply. The intervillous space is a space in the placenta where maternal blood travels. Oxygenated blood from the mother diffuses into capillaries in the placenta. The vein in the umbilical cord, called the umbilical vein, picks up this oxygenated blood from the capillaries, and carries it to the baby’s heart, which pumps the blood throughout the baby’s body. Once the fetus uses this blood, it is carried away from the heart and back to the placenta by both umbilical arteries. In the intervillous space, carbon dioxide diffuses into the mother’s circulation so the mother can eliminate it by exhalation, and oxygen diffuses into the baby’s circulation. The two primary functions of gas exchange are:
- Oxygen intake for use during cellular metabolism/respiration
- To eliminate carbon dioxide, which is an end product of metabolism
Umbilical Artery Blood and Birth Asphyxia
Blood in the umbilical vein reflects uteroplacental status, which is determined primarily by maternal conditions such as anemia, hypoxia, hypertension, hypotension, ruptured uterus, placental abruption or inadequate placental size. On the other hand, blood in the umbilical arteries reflects uteroplacental status as well as fetal status. Fetal tissue oxygenation is influenced by umbilical venous blood flow and problems intrinsic to the fetus, such as heart failure and anemia.
To determine if a baby has suffered an oxygen-depriving event, called an anoxic or hypoxic-ishemic event, it is best to examine umbilical artery blood because this is the blood coming from the baby (as opposed blood going to the baby through the umbilical veins). If umbilical artery blood is acidemic (often called acidosis, which refers to acid in the tissues), it typically suggests that anaerobic metabolism occurred. Anaerobic metabolism occurs when oxygen is not available, and is therefore an indicator that an anoxic event occurred. Anoxic/hypoxic ischemic events can cause a condition called hypoxic ischemic encephalopathy (HIE), which is permanent brain damage that can lead to cerebral palsy and seizure disorders.
Normal values in an umbilical arterial sample in a term newborn:
- PH: 7.18 – 7.38
- PCO2: 32 – 66 (mmHg)
- HCO3: 17 – 27 (mmol/L)
- PO2: 6 – 31 (mmHg)
- Base excess: -8 – 0 (mmol/L); (Base deficit: 0 – 8)
Normal umbilical arterial values in a preterm newborn:
- PH: 7.14 – 7.4
- PCO2: 32 – 69 (mmHg)
- HCO3: 16 – 27 (mEq/L)
- Base excess: -7.6 – 1.3 (mEq/L)
*The “P” in PCO2 and PO2 stands for “partial pressure,” which is how these umbilical cord blood gases are measured.
Interpreting Umbilical Cord Blood Gases | Detecting Birth Asphyxia
The following can cause a low pH and fetal acidosis:
- High PCO2: Respiratory acidosis (or alkalosis) defines the contribution of PCO2 to the acid-base status. An elevated PCO2 means that the fetus is producing more carbon dioxide than can be eliminated through circulation. In other words, carbon dioxide is not readily diffusing from the umbilical artery and capillaries into the maternal placenta and maternal circulation. An accumulation of carbon dioxide is most commonly seen in cases of umbilical cord compression, which hinders or prevents the movement of blood to and from the baby. When this occurs, both venous and arterial cord blood PCO2 will typically be high, although the venous PCO2 will be more in the high normal range. PO2 will typically be low, and if this condition persists, there will be progression to metabolic acidosis with accumulation of lactic acid.
- HCO3-: HCO3- (bicarbonate) is a buffer that neutralizes acidity in the blood. Increased carbon dioxide can cause acidosis (respiratory acidosis). However, if HCO3- increases, it can buffer the carbon dioxide and prevent the blood from being acidic (acidemia). If a cord gas shows an elevated PCO2 with a normal or close to normal pH, the normal pH will have been caused by an increase in HCO3-; this is called compensated or partially compensated respiratory acidosis.
- Metabolic acidosis: The majority of conditions in which fetal acidosis is present are associated with fetal hypoxemia and the accumulation of lactic acid in the fetal tissues and blood. When the cells are not receiving adequate oxygen, they revert to anaerobic metabolism, which produces acidic byproducts, such as lactic acid; when too many acid byproducts are in the blood, acidosis occurs. While respiratory acidosis means the acidosis is due to impaired gas exchange (elevated carbon dioxide), metabolic acidosis is acidosis caused by metabolic reasons, such as a low HCO3- or the occurrence of anaerobic metabolism. In simplest terms, HCO3- represents the metabolic component and PCO2 represents the respiratory component of acid base status.
- Mixed acidemia: Mixed acidemia is metabolic acidosis that develops when respiratory acidosis is prolonged. What happens with mixed acidemia is that initially, the baby is not getting rid of enough carbon dioxide, which causes acidosis (respiratory acidosis). Then, the prolonged oxygen deprivation causes anaerobic metabolism, which produces a metabolic acidosis. This is the most common pattern seen after prolonged end-stage bradycardia.
HCO3- and Base Excess / Base Deficit
Many blood gas analyzers do not accurately calculate HCO3- in the presence of a PCO2 that significantly deviates from the normal value. Thus, the base excess or base deficit should be examined instead of HCO3- when the PCO2 is abnormal.
Base excess is defined as the amount of acid required to titrate the blood gas sample to a normal pH (7.4) at a normal PCO2 (40) at normal body temperature. (These are adult normal values.) In other words, base excess is a reflection of non respiratory (non carbon dioxide) factors affecting the pH. If base excess is normal, there is no metabolic component affecting the pH. If there is a base deficit of 25 (which would be written as base excess of –25), for example, it means there is a metabolic component to the acidosis. Most severely acidotic babies have a base deficit of 12 or greater.
Causes of Fetal Hypoxemia
Fetal hypoxemia occurs in three ways, which we will explain in detail below.
1. Reduced Delivery of Oxygen to the Placenta | Fetal Hypoxemia
Research shows that the probable mechanism for acidosis in the normal term fetus is most likely decreased perfusion (blood flow) of the intervillous space. This can be caused by the following conditions:
- Tetanic uterine contractions, tachysystole, hyperstimulation or hypertonic contractions: During labor, uterine contractions cause pressure increases in the uterus (womb), and this pressure is exerted on the vessels in the placenta that supply blood to the baby. The pressure on the vessels impedes blood flow. In between contractions, blood flows freely and oxygen-rich blood is delivered to the baby. Labor induction drugs such as Pitocin (oxytocin) and Cytotec can cause contractions to be too fast and strong (hyperstimulation), leaving little or no time for the placenta to recharge with oxygen-rich blood for the baby. When contractions are excessively strong, too frequent, too long, or if there is poor resting tone between contractions, the flow of oxygen-rich blood to the baby can be substantially decreased, and this can cause fetal hypoxia. Hyperstimulation (tachysystole) leads to tetanic (hypertonic) contractions. Tetanic uterine contractions occur when stimulation causes normal muscle twitches to run together, which produces what is essentially a continuous contraction or constant contracted state of the uterus. When tetanized, the contracting tension in the muscle remains constant in a steady state. This can cause severe fetal hypoxia and asphyxia.
- Prolonged second stage of labor: More than 30 minutes in the second stage of labor is associated with a predominantly metabolic contribution to the fall in pH.
- Delivery by vacuum extraction or low forceps has been shown to result in lower pH and higher PCO2 in umbilical cord blood, but these changes were associated with the indication for instrument delivery (maternal exhaustion, prolonged second stage of labor, medications given to mother that inhibit her effort to push, breech delivery) and not primarily with the instrument delivery.
- Vasoconstriction (which causes high blood pressure) caused by medications/anesthesia or factors intrinsic to the mother.
- Low maternal blood pressure (hypotension)
- Cardiorespiratory failure in the mother (failure of the heart and breathing)
- Maternal hypertensive disease (chronic high blood pressure)
2. Reduced Transfer of Oxygen Across the Placenta from the Maternal to the Fetal Side | Fetal Hypoxemia
When reduced levels of oxygen transfer from the mother to the fetus through the placenta, fetal hypoxemia can occur. Conditions that can cause this include the following placental complications:
3. Reduced Transport of Oxygen by the Fetal Circulation | Fetal Hypoxemia
Decreased fetal oxygen transport can occur when the following conditions are present:
- Fetal anemia
- Fetal bradycardia
- Umbilical cord prolapse
- Placental abruption
- Nuchal cord
- Fetal acidosis
Severity of Acidosis and Brain Damage: New Research
In 2010, authors of an important systematic review that analyzed data from multiple studies concluded that low arterial pH in umbilical cord blood was strongly associated with long-term adverse outcomes. Some of these outcomes included HIE (hypoxic ischemic encephalopathy), periventricular leukomalacia (PVL), intracranial hemorrhages, cerebral palsy and death. What was unclear, at that point, was what pH constituted clinically significant acidemia. A study by Yeh et al of 51,519 singleton, term neonates published in BJOG last year found the ideal cord arterial pH to be 7.26 – 7.30 for all outcomes. The risk for adverse neurological outcomes starts to rise below a pH of 7.10, with the risk being highest below a pH of 7.0. Another key finding of this study is that most neonates with adverse outcomes, even that of seizures in the first 24 hours, are not born acidemic. In addition, the authors concluded that “it appears as though the lowest risk of any adverse outcome occurs at 7.26 – 7.30, rather than ‘the higher the better’, for there may be a higher risk at higher pH levels.” All arterial cord samples in this study were validated with, among other items, a paired venous sample, and this cohort study was far larger than has been used before.
The American College of Obstetricians and Gynecologists suggests that the arterial cord blood’s pH should be less than 7.0 if it is going to be used as a factor establishing a link between birth asphyxia and neurological injury. This view is not supported by the literature. Multiple studies confirm that birth asphyxia can cause brain damage even when umbilical cord arterial pH is greater than 7.0. Yeh et al (whose study excluded infants with major congenital abnormalities) found that 10 – 15% of the subjects had adverse neurological outcomes at a pH between 7.0 and 7.11; even for subjects with seizures and encephalopathy within the first 24 hours of life, at least half had a pH > 7.10, whereas 39% had a pH above 7.20.
The following has been observed:
- Many babies with birth asphyxia (who often have low Apgar scores) often have a normal pH.
- Neonates with low Apgar scores who are acidemic may do better in the long term than those who are not.
- Catastrophic intrapartum events can occur without acidemia.
The aforementioned events can occur because neonates without acidemia might still have been hypoxic but may have been unable to develop acidemia as a response. This can occur due to a number of reasons. If a fetus has poor circulation and perfusion (blood flow), the acid products that occurred due to anaerobic metabolism will not be moving through the baby’s body via normal circulation and blood flow. A look back at the baby’s fetal heart tracings will often show heart problems that can cause decreased circulation and perfusion.
A catastrophic even that can occur without acidemia is complete umbilical cord occlusion. This brief but intense insult may cause brain injury with comparatively low acidemia or no acidemia at all.
In an Asphyxiated Newborn, an Artery Cord Blood Samples May Significantly Underestimate the Acidosis in the Fetus or Newborn
In almost all severely asphyxiated newborns, perfusion at the time of birth is poor to nonexistent. Poor perfusion includes the umbilical circulation as well. The umbilical arteries will only reflect fetal tissue status up until the flow in them stops. Lactic acid produced from hypoxia or anoxia at the tissue level will not be cleared to the central circulation and subsequently to the umbilical arteries. Thus, in an asphyxiated fetus or newborn, the cord gas sample may grossly underestimate the acidosis in the fetus/newborn. As the baby is resuscitated, circulation improves and tissue lactic acid is cleared into the central circulation. Due to the lactic acid entering the central circulation, the postnatal base deficit obtained from an asphyxiated newborn within the first hour after delivery is frequently found to be higher (worse) than in the umbilical cord blood gas. This blood gas is one of the most accurate predictors of neurological outcome.
Umbilical Cord Blood Gases and Birth Injury Litigation
Umbilical cord blood gases are frequently used in birth trauma litigation. A hospital may attempt to use normal umbilical cord gas results to defend their case on causation. There are many reasons why a fetus who suffered asphyxia or hypoxia can have a normal cord gas. The fetus may have had very poor circulation and perfusion right before birth, the fetus may have suffered a severe and sudden head injury during delivery that caused ischemia (lack of blood flow) in the brain, or the results may be invalid due to error in drawing, storing or analyzing the blood. The blood may have been drawn from the wrong vessel, or it may have been improperly stored in the collection tube. There are a number of technical errors that can affect the validity of umbilical cord gas results, and approximately 18 – 20% of cord gas results are, in fact, invalid due to technical error.
Due to the importance umbilical cord gas results play in litigation, it is imperative to have an attorney with experience in this area. A skilled and experienced attorney will know what to look for in medical records to determine if a sample is valid and an accurate reflection of the baby’s condition at the time of birth. An experienced attorney will work with the best experts to find the cause and timing of the birth injury.
Video: How Do You Pronounce Umbilical Cord?
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- Hypothermia Treatment (Brain Cooling)
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- Yeh, P., Emary, K., & Impey, L. (2012). The relationship between umbilical cord arterial pH and serious adverse neonatal outcome: analysis of 51 519 consecutive validated samples. BJOG: An International Journal of Obstetrics & Gynaecology, 119(7), 824-831.
- Malin, G. L., Morris, R. K., & Khan, K. S. (2010). Strength of association between umbilical cord pH and perinatal and long term outcomes: systematic review and meta-analysis. BMJ: British Medical Journal, 340.
- ACOG Committee on Obstetric Practice. ACOG Committee Opinion No. 348, November 2006: Umbilical cord blood gas and acid-base analysis. Obstet Gynecol 2006; 108:1319.
- Armstrong L, Stenson BJ. Use of umbilical cord blood gas analysis in the assessment of the newborn. Arch Dis Child Fetal Neonatal Ed 2007; 92:F430.
- Nageotte, MP, Gilstrap, LC III. Intrapartum fetal surveillance. In: Creasy & Resnik’s Maternal-Fetal Medicine Principles and Practice, 6th ed, Creasy, Resnik, Iams, Lockwood, Moore (Eds), Saunders, Philadelphia, PA 2009. p.397.
- Page FO, Martin JN, Palmer SM, et al. Correlation of neonatal acid-base status with Apgar scores and fetal heart rate tracings. Am J Obstet Gynecol 1986; 154:1306.