Jeffrey M. Perlman, MB. Traumatic injury following a motor vehicle accident during pregnancy has an enormous potential for fetal injury and demise. With the ...
Perinatal/Neonatal Case Presentation Extensive Brain Injury in a Premature Infant Following a Relatively Minor Maternal Motor Vehicle Accident with Airbag Deployment Prameela Karimi, MD Ronald Ramus, MD Jill Urban, MD Jeffrey M. Perlman, MB
Traumatic injury following a motor vehicle accident during pregnancy has an enormous potential for fetal injury and demise. With the advent of seat belts, shoulder restraints and airbags, and improved maternal survival, the most common cause of fetal loss is placental injury. However, the safety of airbag deployment during pregnancy and in particular during the latter stages, and the potential for fetal trauma remains unclear. We report a case of extensive neurological injury of a premature infant with minimal maternal trauma associated with deployment of an airbag following a minor motor vehicle accident. Journal of Perinatology (2004) 24, 454–457. doi:10.1038/sj.jp.7211143
INTRODUCTION Trauma during pregnancy occurs in up to 3% of all pregnancies and is an important cause of adverse fetal and maternal outcomes.1,2 The leading cause of fetal death related to maternal trauma is motor vehicle accidents.2 Previously, the most common cause of fetal death was maternal death. With the advent of seat belts, shoulder restraints and airbags, and improved maternal survival, the most common cause of fetal loss is placental injury.3,4 However, the safety of airbag deployment during pregnancy and in particular during the latter stages, and the potential for fetal trauma remains unclear.5,6 To heighten awareness to this potential safety hazard, we report a case of extensive neurological injury of a premature infant with minimal maternal trauma associated with deployment of an airbag following a minor motor vehicle accident.
Departments of Pediatrics, Obstetrics and Gynecology and Pediatric Pathology (P.K., R.R., J.U., J.M.P.), University of Texas, Southwestern Medical Center, Dallas, TX, USA Address correspondence and reprint requests to Jeffrey M. Perlman, MB, Division of Newborn Medicine, 525 East 68th Street, N-506, New York, NY 10021, USA
CASE HISTORY The patient was a 1425 g, 29 week, appropriate for gestational age, male infant, born to a 22-year-old mother with a history of seizure disorder treated with phenytoin (dilantin). The mother was a restrained (lap and shoulder belt per maternal history) right front seat passenger who was involved in an isolated motor vehicle accident (a 1998 compact model), that is, the automobile struck a guard rail that caused the vehicle to veer into an opposite guard rail before stopping (per police report). The accident resulted in deployment of the airbag that struck the mother. She never lost consciousness and had minimal evidence of trauma characterized by some generalized bruising to the abdominal wall. The mother was admitted to labor and delivery for observation. Her vital signs remained stable. There was no evidence of vaginal bleeding but was having some mild contractions. However, within a few hours of the incident, the infant began to exhibit fetal heart rate decelerations with loss of variability and was delivered via emergency Cesarean section without any difficulty. Rupture of membranes was noted at delivery with bloody amniotic fluid. A Kleinhauer Betke test was positive for fetal blood in the maternal circulation (KB 0.25%), and was estimated to represent 6.2% of the fetal blood volume. The infant was delivered flaccid and pale with no respiratory effort. Resuscitation included bag mask positive pressure ventilation followed by intubation. The Apgar scores were 3, 4 and 7 at 1, 5 and 10 minutes, respectively. The cord pH was 7.31, pCO2 45 mmHg and base deficit 4 meq/l. Upon admission to the intensive care unit, the infant was noted to be hypotensive with a blood pressure (BP) 26/14 mmHg (mean BP 20 mmHg) with poor peripheral perfusion; the hematocrit was 27%. Treatment included volume re-expansion with normal saline, a blood transfusion and the initiation of a dopamine infusion. The initial chest X-ray was consistent with hyaline membrane disease and surfactant replacement therapy was administered. Also noted were bilateral clavicular fractures. A sepsis work up was performed and antibiotics initiated. The physical examination was pertinent for bilateral cephalhematomas with lethargy, hypotonia and hyporeflexia. At approximately 18 hours of life, the infant was noted to have seizures characterized by jerking of all extremities with eye deviation and mouthing movements. Treatment included the administration of phenobarbital and phosphenytoin without success. The infant underwent a cranial ultrasound scan which revealed a small focal intraparenchymal lesion involving left Journal of Perinatology 2004; 24:454–457 r 2004 Nature Publishing Group All rights reserved. 0743-8346/04 $30
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fronto-parietal white matter with diffuse echogenicity on that side. The infant underwent a MRI at 36 hours of age which demonstrated extensive cerebral edema throughout both cerebral hemispheres with superimposed areas of parenchymal and intraventricular hemorrhage (Figure 1). In addition large bilateral supratentorial as well as infratentorial subdural hematoma were noted with slight shift of midline structures to the left (Figure 2). Furthermore, large biparietal cephalhematoma with underlying calvarial fractures were noted (Figure 3). A MRI arteriogram showed no evidence of large vessel arterial occlusive disease. The condition of the infant continued to worsen with progressive respiratory failure, thrombocytopenia and persistent anemia requiring multiple transfusion and uncontrolled seizures. Care was redirected at 48 hours of life.
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Autopsy Findings The findings were pertinent for biparietal subcapsular and subgaleal hemorrhage, convexity subdural hemorrhage, patchy subarachnoid hemorrhage as well as left thalamic and intraventricular hemorrhage. There were bilateral midshaft fractures of the clavicles (Figure 4). Microscopically, there was evidence of acute neuronal necrosis involving fronto-parietal cortex. Additional findings included evidence of hyaline membrane disease and bilateral dilated ureters and renal pelvises with blunting of the calyces presumed to be secondary to an obstructive uropathy. Placental pathology was normal.
Figure 3. Note the bilateral linear parietal skull fractures (arrows).
Figure 1. Diffusion weighted image from this infant. Note the increase in signal intensity periventricular and posterior parietal cortex.
Figure 2. Reflected skull demonstrating convexity subdural hemorrhage (arrow). Journal of Perinatology 2004; 24:454–457
Figure 4. Postmortem body radiograph-note the bilateral mid shaft clavicular fractures. 455
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DISCUSSION This case describes extensive brain injury with evidence of intracranial and extracranial hemorrhage as well as traumatic injury characterized by fractures of the parietal skull and clavicles in a premature infant. This followed a relatively minor motor vehicle accident with subsequent deployment of an airbag that struck the abdomen of the mother. The causes of fetal morbidity and mortality following blunt abdominal trauma in the second and third trimesters include maternal death, abruptio placentae, uterine rupture, feto-maternal hemorrhage, preterm labor and/or direct fetal injury, i.e. skull fractures, intracerebral hemorrhage, bone fractures, cord and organ rupture and cephalhematoma.4 Direct fetal injury after blunt abdominal trauma is considered a rare complication of maternal trauma for two reasons. The first relates to the protective nature of the maternal soft tissues, uterus and amniotic fluid, and the second to the mandatory use of seat belts, shoulder restraints as well as airbags. When fetal injury occurs, it usually involves fractures of the skull and associated intracerebral hemorrhage.2 However the vast majority of inutero skull fractures are related to severe maternal injury invariably with pelvic fractures, a finding absent in this case. Contrary to traditional teaching, even minor maternal trauma can result in adverse fetal outcome usually secondary to placental abruption.7 The mechanism of this injury is most likely a direct result of the blunt trauma. Thus the placenta does not have elastic tissue and does not have the capacity to expand and contract. In contrast, the uterus contains elastic tissue and can react to acceleration- deceleration forces by changing its shape generating very high intrauterine pressures. This creates a shearing effect on the placental attachment with resultant separation, and is the probable mechanism for the abruption in this case.6,8 Prematurity per se also contributes to fetal morbidity and mortality. Indeed, the intraparenchymal and intraventricular hemorrhage in this premature infant could be attributed to the abruption placenta via a mechanism of hypotension followed by a reperfusion injury within vulnerable regions such as the germinal matrix and periventricular white matter.9 However, the presence of the subdural and cephalhematoma coupled with the calvarial fractures suggests a traumatic mechanism.10 Indeed, the most common mechanism of subdural hemorrhage includes tentorial laceration with rupture principally of either the straight sinus, transverse sinus, vein of Galen, or smaller infratentorial veins, or a falx laceration with rupture of the inferior sagittal sinus and/or the superficial cerebral veins.11 What is a potential explanation for the subdural and the cephalhematoma as well as the bilateral clavicular and calvarian fractures following relatively minor blunt trauma? The mother followed the proper placement of a seat belt as recommended by ACOG and the National Highway Traffic Safety Administration. Thus, the lap belt was placed as low as possible under the 456
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protuberant portion of the abdomen and the shoulder belt was positioned off to the side of the uterus, between the breasts and over the mid portion of the clavicle. This placement results in the lowest recorded injuries.12 Moreover, investigations of automobile accidents have revealed that the most significant factor associated with fatal outcome is an accurate estimation of the crash severity.13 Given these observations, we speculate that deployment of the airbag may have contributed to the severity of the traumatic skeletal and intracranial findings. Thus under experimental conditions with frontal air bag deployment, the cushion expands with a speed of about 125 mph towards an individual.13 Consequently, a person within this expansion zone, that is, within 20 cm from the steering wheel hub is at considerable risk for injury. Did the maternal use of dilatin contribute to the hemorrhagic findings in this case? Thus maternal anticonvulsant therapy during pregnancy can affect the fetus and cause neonatal hemorrhage.14 The presumed mechanism is secondary to depression of the vitamin K-dependent coagulation factors 2, 7, 9 and 10. The commonly used anticonvulsants phenytoin, phenobarbital, carbamazepine and valproic acid all readily cross the placenta. Phenytoin, phenobarbital and carbamazepine induce microsomal mixed function oxidase enzymes in the fetal liver. It is hypothesized that these hepatic enzymes increase the rate of oxidative degradation of vitamin K, resulting in deficiency. Both inutero hemorrhage or bleeding within the first 24 hours after birth has been described. Bleeding can occur at any site, but predominantly into the skin, the gastrointestinal tract or the brain, and is often fatal. In the largest retrospective study, no evidence for increased risk of intracranial hemorrhage was observed in infants born to mothers taking anticonvulsants during pregnancy.15 Thus, we consider the use of Phenytoin a less likely cause of hemorrhage in this case. In conclusion, while major maternal injury and crash severity is strongly correlated with adverse fetal outcome, relatively minor accidents can result in severe fetal injury even in the absence of significant maternal injury. This case raises the possibility that airbag deployment may be an additional risk factor of uterine, placental and fetal injury.16
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5. Sims CJ, Boardman CH, Fuller SJ. Airbag deployment following a motor vehicle accident in pregnancy. Obstet Gynecol 1996;88:726. 6. Schultze PM, Stamm CA, Roger J. Placental abruption and fetal death with airbag deployment in a motor vehicle accident. Obstet Gynecol 1998; 92:719. 7. Fries MH, Hankins GDV. Motor vehicle accident associated with minimal maternal trauma but subsequent fetal demise. Ann Emerg Med 1989;18:301–4. 8. Connolly A, Katz VL, Bash KL, McMahon MJ, Hansen WF. Trauma and pregnancy. Am J Perinatol 1997;14(6):331–6. 9. Shalak L, Perlman JM. Hemorrhagic-ischemic cerebral injury in the preterm infantFcurrent concepts. Clin Perinatol 2002;29:745–63. 10. Volpe JJ. Neurology of the Newborn. 4th ed. Philadelphia: WB Saunders; 2001.
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11. Hartl R, Ko K. In utero skull fracture: case report. J Trauma Injury Infection Critic Care 1996;41(3):549–52. 12. Pearlman MD, Viano D. Automobile crash simulation with the first pregnant crash test dummy. Am J Obstet Gynecol 1996;175:977–81. 13. Pearlman MD, Klinich KD, Schneider LW, et al. A comprehensive program to improve safety for pregnant women and fetuses in motor vehicle crashes: A preliminary report. Am J Obstet Gynecol 2000;182:1554–64. 14. Cornelissen M, Steegers-Theunissen R, Kollee L, et al. Increased incidence of neonatal vitamin K deficiency resulting from maternal anticonvulsant therapy. Am J Obstet Gynecol 1993;168:923–8. 15. Sabers A, Rogvi-Hansen B, Dam MW, et al. H. Pregnancy and epilepsy: a retrospective study of 151 pregnancies. Acta Neurol Scand 1998;97:164–70. 16. Bjornstig U, Haraldsson PO, Polland W, Sandstrom T. Awareness of the risk of air bag-associated injuries. Lakartidningen 2002;99:3022–6.
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