Fetal Asphyxia: A Pathologist’s Perspective

Robert W. Bendon, M.D.

Clinical Professor of Pathology and Pediatrics (retired)

University of Louisville, KY


Mailing Address:

295 Highway A1A, Apt 308

Satellite Beach, FL 32937




502 797 5081





Objective: This review reflects on the frequent failure to find an anatomic cause of death in stillborn infants with anatomic evidence of asphyxia and in the placenta of newborn infants with intrapartum asphyxia.

Methods: This perspective is based on over thirty years of perinatal pathology practice. The history of research on fetal asphyxia is briefly reviewed to give context to the anatomical observations. The evidence for the diagnosis of asphyxia in the fetus and placenta is presented. The likely anatomic mechanism is compromised umbilical blood flow as demonstrated by the discovery that fetal thrombotic vasculopathy is often a marker of umbilical cord compromise with chronic lesions.

Results: If certain conditions of the umbilical cord are persistent, they may be detectable or treatable. Anatomic causes of fetal asphyxia include cord wrapping that produces a short cord vulnerable to twisting, occult compression, and intrinsic vasoconstriction.

Conclusion: The anatomic causes of fetal asphyxia in stillborn infants and in intrapartum asphyxia are often viewed as a black box. Improvements in preventing or treating fetal asphyxia need to be based on a better anatomic understanding of the mechanisms that can compromise umbilical cord blood flow.


Keywords: Fetal asphyxia, Umbilical cord, Cord wrapping, Fetal thrombotic vasculopathy, Stillbirth, Placenta



This review is based on over thirty years dedicated to the practice of perinatal pathology encompassing over 75,000 placental examinations, approximately 2,000 perinatal autopsies and over 600 medico-legal consultations performed by the author. The goal is not to present this material in detail, but rather to convey thoughts as to why an anatomic cause of stillbirth or intrapartum asphyxia is often not revealed by the autopsy or placental examination. This is true even though the pathologic evidence points to fetal asphyxia as the cause of fetal death or brain injury. The hope is that a better understanding of the anatomic causes of fetal asphyxia might lead to better prevention.

Fetal asphyxia is the equivalent of suffocation, which is the blockage of respiratory gas exchange. That blockage can occur anywhere from the maternal uterine blood supply through to the placenta and umbilical circulation. Asphyxia may be sudden and complete, partial, or intermittent. Clinically significant asphyxia results in fetal hypoxia that causes anaerobic metabolism, and hence acidosis in blood and fetal tissue. Experimental and clinical studies show that the effects vary in different fetal tissues. The brain and heart are the most vulnerable and asphyxia of these organs can lead to death or permanent encephalopathy.


History of clinical and experimental understanding of fetal asphyxia

Our understanding of how fetal asphyxia causes harm has grown both by clinical observations and experimental studies. The association of brain injury and fetal asphyxia was first made by Dr. John Little, a surgeon who performed tenotomy to release spastic limbs. He took careful histories and saw many patients with congenital contractures and spasticity. In 1862 he presented his observations of the high prevalence birth complications in his patients, and postulated that birth asphyxia was the cause of the palsy1. More than a century later, experimentally produced immediate neonatal suffocation was found to produce neuronal necrosis beginning after 14 minutes of complete asphyxia2. This proved to be an incomplete explanation, as the most common brain lesion in children with cerebral palsy was not the isolated neuronal necrosis observed experimentally, but extensive white and gray matter destruction.

A better explanation of Little’s observations of cerebral palsy following birth asphyxia, was made by Dr. Ron Myers. He repeated the acute asphyxial studies in monkeys, and found the same neuronal necrosis. Then by chance, he discovered the circumstances that produced cerebral palsy like brain lesions in newborn monkeys. Monkey 796 had suffered from maternal acidosis that caused a moderate fetal acidosis that was still present at birth 3. This newborn was then subjected to the same experimental routine of immediate postpartum asphyxia as his peers, only his response was very different. He had a prolonged post-asphyxial neurological deficit including seizures and eventually developed symptoms consistent with cerebral palsy. He was sacrificed at 6 months of age and the brain showed cortical atrophy and gliosis, and basal ganglia gliosis similar to that seen in human cerebral palsy. Dr. Myer reasoned that it was the pre-delivery acidosis prior to complete asphyxia that made the difference.

His further research confirmed that this severe pattern of brain injury followed prolonged partial asphyxia, defined as interference with placental gas exchange sufficient to cause fetal hypoxia, and a mixed respiratory and metabolic acidosis. This occurred when fetal partial pressure of oxygen fell to or below 13-14 mm Hg. Experimentally this could be produced by various manipulations including maternal hypotension from fluorothane4, oxytocin hyperstimulation of the uterus, carbon monoxide administered to the mother5, partial placental separation, and most consistently by mechanical compression of the aorta below the level of the renal arteries6. If the mean maternal blood pressure perfusing the uterus fell below 40 mg Hg of pressure, partial fetal asphyxia occurred with fetal death in 0.5 to 1 hour. The degree of hypoxia producing fetal death was very close to that producing cerebral palsy. Fetal partial asphyxia could also be caused by maternal infusions of catecholamines that led to a 60-80% increase in blood pressure and visceral vasoconstriction. Maternal stress during handling could cause sufficient partial fetal asphyxia, presumably from endogenous catecholamine release7. This model was a combination of partial asphyxia that was followed by a severe decompensation and fetal death or brain necrosis.

Subsequently other researches focused on the effects of various degrees and patterns of asphyxia on the fetus, mostly in sheep, produced by inflatable ring occluders of the umbilical cord. The goal was not to determine the natural clinical causes of asphyxia, but instead to relate patterns of asphyxia to fetal physiologic changes, particularly heart rate to patterns of cord compression and decreased umbilical blood flow. One surprising conclusion of this research was that after repetitive umbilical cord occlusions, the fetal heart rate monitoring did not consistently predict the severe fetal acidosis that developed in the lamb8-10.

.           Obstetricians are very familiar with repetitive late decelerations of fetal heart rate as indicators of hypoxemia, and with deep variable decelerations as evidence of umbilical cord compression, as well as more ominous patterns such as loss of beat-to-beat variability or of bradycardia. The goal of fetal heart rate monitoring is to deliver the infant before there is death or brain injury and yet minimize unnecessary operative delivery. The criteria for the diagnosis of intrapartum asphyxia after birth based on clinical events, umbilical cord blood gases, Apgar scores, and neonatal symptoms are reviewed in a recent publication11. Based on the many medical legal cases that I have reviewed in which it was argued that a brain injured neonate met the clinical criteria of birth asphyxia, I have to conclude that current practice can not predict when to intervene to prevent brain damage or death. The introduction of fetal heart rate monitoring did not cause a significant reduction of cerebral palsy, which has been interpreted as evidence for an onset of cerebral palsy prior to the intrapartum period12, but could also be interpreted as evidence that such fetal heart rate monitoring cannot predict the onset of fetal brain injury. Possibly more direct monitoring of fetal brain acidosis or another modality could improve the accuracy of predicting the risk of damaging asphyxia to the fetus.

If we cannot accurately and quickly predict when an infant will suffer cerebral palsy or death by fetal monitoring, perhaps the difficulty can be circumvented by understanding and correcting the underlying cause of the fetal asphyxia. The anatomic cause of asphyxia is often treated as a “black box”, usually attributed to “umbilical cord accident”, or simply as unknown. Some anatomic causes are known, such a premature placental separation, and can often be verified pathologically or clinically. It is the unknown causes of fetal asphyxia that this review will consider.


Anatomic evidence of fetal asphyxia in stillborn infants

.           Before considering what might be the anatomic causes of the “black box” of asphyxia, I will first present the anatomic evidence implicating asphyxia as the cause of death in the stillborn infant. The pathologist performing an autopsy tries to deduce the cause of death based on a chain of plausible mechanisms based on the details of the history and the anatomy. This approach differs from that of the epidemiologist. A statistically significant association of stillbirth with maternal obesity or diabetes does not explain how a particular fetus died. Instead the pathologist identifies anatomic findings for the particular infant that fit well-established clinical and experimental physiologic mechanisms. The problem is how did maternal obesity or diabetes cause the death of this infant as opposed to other infants whose mothers had a similar clinical history but did not die.

To identify anatomic evidence of asphyxia, a useful model is the experimental airway occlusion in end-expiration of a primate13. I n this situation the monkey attempts to expand its chest with the lungs at end expiratory volume, and hence creates a large negative intrathoracic pressure that ruptures intrathoracic surface capillaries. Infants succumbing to Sudden Infant Death Syndrome (SIDS) show similar intrathoracic petechiae14. The association of SIDS with sleeping face down suggests that airway obstruction from bedding that occurs after end expiration with an attempted new inspiration would be similar to the primate experimental model15. A similar pattern of intrathoracic petechiae occurs with complete or near complete premature placental separation16 (Fig 1). Early experimental studies demonstrated that acute fetal or immediate neonatal asphyxia results in fetal gasping, and that this is associated with a glottic stop that assists expansion of the uninflated lung 17,18. Thus gasping in response to in utero asphyxia also results in large intrathoracic negative pressure and a temporarily occluded airway. In stillborn infants with a pattern of intrathoracic petechiae, a reasonable deduction is that their death was associated with acute asphyxia and intrauterine gasping.

In stillborn infants with less complete but greater than 50% premature placental separation, there is often a different pattern of findings16. The heart chambers are dilated and there are small pleural and pericardial effusions. These are the common findings of heart failure in any individual regardless of cause. In the case of partial but lethal placental separation, a reasonable interpretation is that the initial fetal hypoxia leads to a positive feedback of tissue acidosis causing myocardial dysfunction causing progressively less placental perfusion, more hypoxia and finally death. The findings of heart failure in these fetuses differs from the chronic failure found in non-immune fetal hydrops, in that the later have more severe effusions with anasarca, and have pulmonary hypoplasia from the mass effect of the effusions19. With the findings of acute heart failure, the diagnosis of asphyxia requires excluding other mechanisms such as septic shock or exsanguination.

In many normally formed stillborn infants with either anatomic evidence of acute gasping or of acute heart failure, no known anatomic or clinical cause of asphyxia can be found. Yet, by a process of elimination of known causes, the conclusion of fetal asphyxia from an “umbilical cord accident” is a plausible diagnosis. Until a few years ago, no more direct evidence was available. Other indirect and often controversial markers of asphyxia were intrauterine passage of meconium and increased nucleated red blood cells in the fetus20-23. Then a seminal observation was made, namely that stillborn infants without an identified cause of death had statistically increased prevalence of fetal thrombotic vasculopathy in the placenta24. This discovery built on prior studies showing that the placental lesions recognized as hemorrhagic endovasculosis were caused by proximal thrombi in the fetal circulation25-27. These lesions and direct observation of thrombi in placental vessels were combined into the concept of fetal thrombotic vasculopathy that was then shown to be associated with a mixed group of umbilical cord abnormalities28.

The discovery of fetal thrombosis as a marker of fetal asphyxia from umbilical compromise raises questions. The first question is what is the mechanism that links decreased umbilical blood flow to fetal thrombotic vasculopathy? Virchow’s triad is invoked (stasis, vascular injury and hypercoagulability) as the explanation with umbilical cord occlusion causing local endothelial injury as well as stasis of umbilical blood flow. This explanation does not explain the focal distribution of fetal thrombi in chorionic vessels. The second question is: why do some of the vasculopathy lesions appear chronic in that they require cell proliferation or collagen secretion? These more chronic lesions of fetal thrombotic vasculopathy can be found in in stillborn infants with short intrauterine postmortem retention, in living asphyxiated infants, and in apparently normal infants. A logical hypothesis is that the umbilical cord configuration causes a partial or intermittent occlusion of umbilical blood flow over a prolonged period of time(Fig 2). Eventually either the level of acidosis leads to cardiovascular collapse or a more complete occlusion of blood flow supervenes to cause death. This prolonged period of exposure to intermittent asphyxia is consistent with pathological reports of finding neurologic lesions from asphyxia already progressing in stillborn infants29. If death had been from sudden complete asphyxia, no lesions would be seen pathologically. If the antecedent umbilical cord anatomy that predisposes to stillbirth and intrapartum asphyxia can be identified, then that configuration might be reversed before causing fetal harm. At the least, it may make decisions about emergency operative delivery or of elective preterm delivery more rational.


Possible anatomic causes of compromised umbilical cord blood flow

The hope for intervention leads to the next question, what anatomic conditions decrease fetal blood flow? One answer can be deduced from some very basic experiments showing physical principles applicable to the umbilical cord. Personal experience demonstrates that it is very difficult to stop the flow of water in a garden hose by applying pressure directly to the sidewall. However if the gardener makes a small loop and then pulls it slightly, the lumen will collapse and flow stops. This phenomenon is all too well known to gardeners whose hose spontaneously develops such loops from a combination of torsion and pull that causes sudden loss of water pressure. Torsion alone can also collapse the lumen. We did a simple experiment in vitro with umbilical cords30. Fluid at 50 cm of water pressure was perfused through the umbilical vein, then a portion of the cord was wrapped around a pipe of a diameter mimicking fetal limbs and body. The distal portion, that is the end after the wrapping, was twisted until fluid flow stopped. The amount of twist needed to stop flow was directly proportional to the length of the distal segment. The explanation was simple mathematics in that a twist produces a greater pitch (twists per centimeter of cord length) in a short segment than in a longer segment of cord. (The coiling index of the cord as measured after delivery is more complex since early in development the vessels twist because they are free to move in Wharton’s jelly, and the flow in the vessels forces them to spiral along the inner wall. Later in development the vessels become tightly fixed within the cord and then external torsion and likely remodeling all play a role in determining the visible pitch of the vessels) The result seemed trivial until we realized that the distance from the placenta to the beginning of the cord wrapping was an important parameter that was often overlooked clinically. Yet this short distance would restrain the infant at delivery resulting in some loops becoming tight nuchal cords at the introitus. Tight nuchal and multiple cord wrapping have a correlation with clinical evidence of mild fetal asphyxia 31,32 and are reported in stillborn infants 33,34. The high frequency of nuchal cords and the low frequency of diagnosed fetal asphyxia make a prospective study difficult. A more feasible study could examine the outcome of prenatally detected cases of a very short distance between the start of cord wrapping and the placental insertion.

Even if the fetus did produce a short cord between a wrapping and the placental insertion, how would it become twisted? The answer was suggested by the marked twisting of the cord seen in mid trimester stillbirth with prolonged gestation.  Such cords are twisted in fetuses even with a known cause of death19. The mechanism for post mortem cord twisting can be demonstrated in a simple experiment. If a smooth ovoid rock representing the fetus is suspended in a large, water-filled jar by a string fixed to the lid, the stone will begin to rotate after a brief, random shaking of the jar35. The cylindrical shape of the jar mimics the vectoral addition of forces in the ovoid intrauterine cavity. The cord must often be subjected to torsion in the uterus although less dramatically later in gestation because of less fluid..

If a short segment of cord is more likely to compromise blood flow with torsion, why are long cords associated with cerebral palsy36? This can be answered by considering first that the cord length is controlled by fetal tension of the cord37,38. Fetal akinesia results in a very short cord39. Teleologically, the cord must be long enough to allow delivery of the infant while one end is still attached to the placenta. Fetal pull on the cord provides a convenient signal for growth as the uterus enlarges. If the cord becomes wrapped and effectively shortened, this mechanism of pull would signal growth and permit a length compatible with delivery. After delivery the cord would appear long because of an approximate addition of normal length and the wrapped segment, yet in the history of the fetus there would have been a period in which a short cord persisted.

A functionally short cord may also be more vulnerable to torsion with certain types of placental insertion such at Battledore (marginal) or furcate (fork-like) insertions. In the latter, the Wharton’s jelly ends prior to insertion in the placental surface. Twisting the cord in vitro demonstrates the ease with which exposed vessels can be collapsed. I have seen stillborn infants with no other mechanism of asphyxia except the furcate insertion (Fig 3). All of these simple observations lead to a potentially testable hypothesis: functionally short cords measured from the placental insertion to the onset of wrapping around a fetal part create a risk for compromised umbilical blood flow.

This hypothesis does not preclude other anatomic causes of compromised umbilical blood flow. From my own experience, I observed the effects of direct compression on the cord. One of my daughters was having repetitive deep variable decelerations with each of my wife’s contraction. An ultrasound demonstrated an entrapped occult cord prolapse. Rather than wait for a more ominous heart rate pattern, a Cesarean section was performed. This may not be standard practice, but provides an example of how anatomic information could influence clinical management.

Cord compression as in the example above with the cord caught between a fetal part and the pelvis would seem an obvious mechanism to occlude cord blood flow. Yet we do not know how much pressure is required to directly stop flow. The experimental studies in sheep did not record the actual pressure applied. I contacted the manufacturer of the ring occluders and they do not know how much pressure is applied to the cord when the ring is inflated. Sheep experiments may also be a poor model for the human since the ovine cord has two umbilical veins. If the lower blood pressure in the vein makes it more vulnerable target to compression, a sheep may be able to by-pass a single compressed vein. Any model of cord compression must account for uneven distribution of the pressure on the cord, as well as the effects of deformation, torsion, movement, and location. The experimentalists have not described nor explicitly looked for a microscopic lesion beneath the occluder. They have not looked for downstream or upstream evidence of stasis and thrombosis. With no known histological lesion of direct injury from compression, the pathological examination of the cord seldom confirms the diagnosis of cord compression. Rarely a segment of the cord shows a compressed segment of Wharton’s jelly, which may be evidence of compression if it correlates with the clinical history (Fig 4). Further understanding of the anatomic conditions in which significant cord compression occurs might prospectively identify “at risk” fetuses.

The peculiarities of the umbilical circulation need to be better understood. Both umbilical and placental, arteries and veins are very muscular. Perhaps uniquely in the human circulation, the umbilical artery can maintain its contracted state for a prolonged interval. The umbilical arteries seen microscopically are tightly contracted with ridges of intimal cushion occluding the lumen long after delivery. Teleologically, this contraction prevents exsanguination of the infant after the cord is detached. The initiation of this state is not completely understood. Experimental studies in the fetal sheep on cardiac by pass have shown that temporary cessation of placental blood flow results in a markedly elevated placental vascular resistance if the fetal circulation is reattached to the placenta. This effect appears due to vascular constriction initiated and maintained by systemic vasopressin in response to the temporary loss of blood flow. Dr. Elizabeth Ramsey and colleagues demonstrated the intermittent and uneven intervillous blood flow in the monkey. Muscular control of fetal blood flow may have evolved as a mechanism to match fetal perfusion to variations in intervillous blood flow analogous to matching lung perfusion to ventilation. An overshoot of this regulation might explain cases of fetal grasping of the cord leading to decreased cord blood flow40,41. A second hypothesis for “umbilical cord accidents” is: Transient compromise of umbilical cord blood flow initiates a systemic overcompensation, possibly via vasopressin, with chorionic vascular constriction and occlusive vascular resistance in the placenta. A better understanding of the control of vascular resistance in the fetal circulation might provide pharmacologic means of improving a pathologically compromised fetal circulation.

Umbilical vein hematoma is an accepted cause of occlusion of the umbilical circulation and fetal asphyxia. Microscopically there is usually evidence of medial necrosis, variceal dilatation and rupture of the media of the umbilical vein42-46. The cause of this necrosis is not well established. Foci of necrosis and dilatation similar to that found in cord hematomas can be seen in random sections of umbilical cords that have no other pathologic lesion (Fig 5). Vascular medial necrosis can also be seen with meconium (bilirubin) staining of the dead muscle cells with prolonged meconium staining of the amniotic fluid. This can be interpreted as meconium induced vascular injury. An alternative interpretation is that fetal hypoxia causes hypoxic injury of vascular media since without a vaso vasorum oxygenation depends on diffusion from the lumen making the outer myocytes more vulnerable to hypoxia. The injured cells cannot exclude bilirubin from entering and become stained. Both the vascular medial necrosis and the meconium staining are then secondary to the underlying fetal hypoxia rather then being the cause. Vascular necrosis of the umbilical cord media could be a consequence of fetal hypoxia or may have unknown etiologic significance. Another unknown in the fetal control of the umbilical circulation is the significance of the mast cells in Wharton’s jelly47 (Fig 6) . Whatever, the mechanism of vascular necrosis, a better understanding of the effects of fetal hypoxia on the vessels of the umbilical cord may lead to better insight into the duration and systemic circulatory effects of fetal hypoxia.



The clinical and experimental evidence points to occlusion of the umbilical circulation (“cord accidents”) as a cause of fetal asphyxial injury. The exclusion of any other causes in many infants even after complete autopsy and placental examination in stillbirths and after complete clinical and placental examination in hypoxic ischemic encephalopathy suggests that fetal asphyxia from such “cord accidents” is an important mechanism leading to stillbirth and newborn encephalopathy. Myers experiments demonstrated that the sudden onset of cardiovascular collapse in the mildly acidotic fetus quickly leads to brain injury or death. The best hope is in prevention not rescue. Current practice leads to lawsuits of competent physicians and likely to unnecessary Cesarean sections for non-reassuring fetal heart rate tracings. Likewise current prenatal care does not prevent stillbirth of many normally formed infant dying at a viable gestation. Research to further open the black box of the anatomic/physiologic mechanisms that cause fetal asphyxia could expand the repertoire of interventions to prevent stillbirth and intrapartum asphyxia.




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Fig 1: The pleural surface of these lungs from a stillborn infant demonstrates numerous petechial hemorrhages.

Fig 2: An umbilical artery was injected with blue dyed barium and demonstrates the small area of placental still being perfused. The large red surface vessels are occluded. The arrows point to areas of old calcified mural thrombi. There is a marginal insertion of the umbilical cord.

Fig 3: This furcate (fork like) umbilical cord insertion demonstrates the loss of Wharton’s jelly that could make the vessels subject to collapse with the application of fetal turning. The infant was stillborn without other explanation.

Figure 4: This infant was delivered two hours after umbilical cord prolapse and fetal death. The cord closest to the body was pale and it is possible that compression squeezed the blood out of this portion of the cord prior to death.

Figure 4: This infant was delivered two hours after umbilical cord prolapse and fetal death. The cord closest to the body was pale and it is possible that compression squeezed the blood out of this portion of the cord prior to death.

Figure 6: This photomicrograph of Wharton’s jelly shows mast cells identifiable by the metachromasia that makes them appear purple with a blue dye. (Giemsa, 40x)









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