1994-03-30-17 Subdural hematoma © Dellinger www.thefetus.net/
Eric H. Dellinger, MD, Thomas C. Wheeler, MD
Address correspondance to Eric H. Dellinger, MD, Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, Vanderbilt University Medical Center, B-1100 Medical Center North, Nashville, TN 37232-2519. Ph: 615-322-0122; Fax 615-343-8881
Synonyms: Cerebral hemorrhage, intracranial hemorrhage.
Definition: Hemorrhage between the dura mater and the arachnoid membrane in the fetus.
Prevalence: Unknown, rare.
Etiology: Multiple possible causes including in utero fetal trauma1, maternal warfarin anticoagulation2, immune thrombocytopenic purpura (ITP)3, alloimmune thrombocytopenia4, and idiopathic5,6 .
Pathogenesis: Related to the etiology; defective coagulation or trauma led to bleeding from veins in the subdural space.
Associated anomalies: Hydrocephalus, skull fractures, hydrops, porencephalic cysts, macrocephaly, microcephaly.
Differential diagnosis: Suba-rachnoid hemorrhage, intraventricular hemorrhage, intracranial neoplasm.
Prognosis: Very poor, as it usually results in profound mental deficits, seizures, hypotonia, or fetal or neonatal demise5-7.
Recurrence risk: Unknown, probably rare unless alloimmune thrombocytopenia is present, in which case the recurrence risk may approach 75%8.
Management: Exclude immune thrombocytopenic purpura, alloimmune thrombocytopenia, and maternal coagulopathy if a history of trauma cannot be obtained. Pregnancy termination should be offered if the fetus is previable.
MESH Subdural space hematoma ICD9 742.4 (772.8) CDC 772.300*
Acute subdural hemorrhage following trauma is a recognized cause of neonatal brain injury and subsequent neurologic impairment9. The incidence of antepartum subdural hemorrhage is unknown but comparatively less common. In the absence of a maternal history of trauma, the etiology may be obscure but may involve coagulation disorders, abruption, and immune or alloimmune thrombocytopenia.
We present two cases of subdural hematoma occurring in the second trimester which illustrate the two major types of hemorrhage, traumatic and atraumatic. The first case was diagnosed in a fetus and occurred for unknown reasons. The second case was discovered in a neonate following a postmortem cesarean section in a mother fatally injured in a motor vehicle accident.
A 35-year-old white woman G2P1 was referred for evaluation of refractory hyperemesis gravidarum at 16 weeks gestation. Thyroid function tests and b-hCG were normal, and sonography demonstrated normal cranial anatomy and placentation. A sonogram performed for an abnormally elevated maternal serum a-FP of 2.7 MOM at 19 weeks gestation demonstrated biometry of the long bones consistent with 19 weeks and a biparietal diameter of 23 weeks. A transvaginal scan showed a large left subdural hematoma with compression and displacement of the left hemisphere beyond the midline (fig 1).
|Figure 1: Case #1: the head is normal at 16 weeks.
Mild right-sided hydrocephalus from presumed compression of the cerebral aqueduct was noted. A fluid-fluid interface between serum and clot could be demonstrated with postural change.
The prenatal history was unremarkable, including no history of recent abdominal trauma or use of anticoagulants. The patient denied recent rash or known viral exposure. The maternal platelet count and bleeding times were normal, and assays for antiplatelet antibodies were negative. The family declined fetal assessment by cordocentesis and opted for termination at 20 weeks of gestation.
Autopsy demonstrated subdural hematomas in the left anterior and middle cranial fossae, compressing the left cerebral hemisphere (fig 2). The spinal cord also showed areas of subdural hemorrhage.
|Figure 2: Case #1: 19 weeks. A large left subdural hematoma (black arrow) and small amount of contralateral hydrocephaly (white arrow).
|Figure 3: Case #1: fluid-fluid level (arrow) in the subdural hematoma.
|Figure 4: Case #1: Autopsy: the cranium has been partially resected, and the depressed hemisphere is visible.
|Figure 5: Case #1: Additional foci of subdural hemorrhage are present in the spinal cord.
Case # 2
A 23-year-old white woman, involved in a frontal motor vehicle accident, was unconscious, hemodynamically unstable, and intubated upon arrival in the emergency room. Multiple facial fractures and a skull fracture were noted. An emergency laparotomy demonstrated a hemoperitoneum and multiple liver lacerations including a grade IV laceration. Bleeding, exacerbated by disseminated intravascular coagulation, could not be controlled, so the liver was packed and the patient was transported to the surgical intensive care unit. A second emergency laparotomy also failed to control the bleeding. The patient was repacked and closed with towel clips. In the intensive care unit, oxygenation and ventilation became increasingly difficult. The coagulopathy persisted and could not be corrected with component therapy. The fetus could not be monitored due to the large wound dressing. The patient"s condition began to deteriorate rapidly. When terminal cardiac monitor patterns were seen, the wound was quickly opened and the uterus exposed. A hysterotomy was performed and the fetus delivered. A near total placental abruption was evident.
The infant, which weighed 860g at birth, was initially without a heart beat. Resuscitation included intubation and endotracheal epinephrine. Apgar scores were one and four at one and five minutes, respectively. A coagulation profile showed evidence of subclinical disseminated intravascular coagulation with a platelet count of 101,000, fibrinogen of 72 mg/dl, and PT/PTT of 19/110 (normal 10-13/25-40). These gradually corrected with FFP infusion. A 10-second episode of tonic-clonic seizure activity was witnessed, which did not recur. A head ultrasound on day one of life showed bilateral subdural hematomas (fig 3). One week later, bilateral grade II intraventricular hemorrhages were noted, which resolved by the second week. After three weeks, the subdural hematomas had resolved. The infant developed hyaline membrane disease and required five weeks of mechanical ventilation before finally being extubated. Bilateral retinopathy of prematurity was diagnosed and treated with laser therapy. The infant was hospitalized for 68 days before being transported to an intermediate care nursery in the family"s community.
|Figure 6: Case #2: Postnatal scan: an echogenic layer of clotted blood (arrow) is seen between the cortex and the skull.
|Figure 7: Case #2: five hours after the image in fig. 6, the clot has started to lyse, and the layer is now hypoechoic.
|Figure 8: Case #2: a parasagittal view demonstrates the fluid around the cortical mantle and the paucity of gyri due to the prematurity.
A subdural hematoma is defined as a coagulum of blood which collects during hemorrhage below the dura mater and above the arachnoid membrane.
The pathogenesis of fetal subdural hematoma formation is directly related to the etiology. Cases may occur as a result of in utero fetal trauma1. Because the uterus and amniotic fluid offer effective cushioning for the fetus, fetal trauma usually occurs only with severe forms of maternal injury such as motor vehicle accidents. The maternal bony pelvis, which offers excellent protection for the fetus from blunt trauma, can ironically cause injury during rapid decelerations. The second patient probably represents such an injury, though it is also possible that the intracranial bleeding could have occurred as a result of an abruption-induced coagulopathy. We feel that it is more likely that the coagulopathy resulted from consumption of clotting factors within the hematomas.
Fetal intracranial bleeding has also been reported with maternal anticoagulation. Warfarins, which are known to cross the placenta, have been associated with the fetal warfarin syndrome as well as with fetal bleeding2. Immune thrombocytopenic purpura, in rare cases, can produce fetal thrombocytopenia severe enough to cause fetal hemorrhage3. Although rare, alloimmune thrombocytopenia is an even more predictable inducer of fetal thrombocytopenia and has been linked to cases of fetal hemorrhage prior to the onset of labor4. Vascular anomalies such as aneurysms and arteriovenous malformations can be demonstrated in some cases of intracranial bleeding. Fetal asphyxia is associated with intraventricular and intracerebral hemorrhage. Despite knowledge of the aforementioned causes, many cases of fetal intracranial bleeding have no identifiable etiology5,6.
|Figure 9: Subdural hemorrhage (in red) assumes a lenticular shape between the hard skull, and the depressed brain.
Prenatal diagnosis of fetal subdural hematoma has been reported. The characteristic appearance is one of a fluid collection just beneath the cranium which displaces and compresses brain matter. The appearance of the fluid may vary, depending on the age of the clot. Acute hemorrhage will appear homogeneous. Older clots which have undergone lysis may demonstrate a liquid-solid or liquid-liquid interface, which can be shifted by rotating the patient into different positions. The final stage of clot evolution is complete liquefaction with resolution or development of a permanent cyst. Porencephalic cysts may be an example of the final outcome of this process.
Associated findings include hydrocephalus with a characteristic enlargement of the third ventricle due to compression of the cerebral aqueduct, skull fractures, hydrops, porencephalic cysts, and macrocephaly. Because fetal sutures have not closed, the cranium frequently expands in response to intracranial hemorrhage and increased intracranial pressure.
The differential diagnosis of a subdural hematoma includes subarachnoid hemorrhage, intraventricular hemorrhage, intracranial neoplasm, hydrocephalus, Dandy-Walker malformation, and miscellaneous cysts of the brain, including arachnoid cysts and an aneurysm of the vein of Galen. The location of the subdural hematoma just beneath the cranium, the typical deformity of the brain, the layering of hemorrhagic material, and, occasionally, the patient history are most helpful in establishing the diagnosis.
The recurrence risk for fetal subdural hematoma is unknown. It is probably rare unless alloimmune thrombocytopenia is present in which case the recurrence risk may approach 75%8.
If the diagnosis of fetal subdural hematoma is suspected, immune thrombocytopenic purpura, alloimmune thrombocytopenia, and maternal coagulopathy should be excluded if a history of trauma cannot be confirmed. Cordocentesis can be used to evaluate fetal coagulopathies and to exclude chromosomal anomalies6. Blood component therapy can also be given during the same procedure, if indicated. Maternal immune globulin administration has shown some promise in cases of alloimmune thrombocytopenia8. Determination of fetal platelet counts before labor in patients with ITP will indicate fetuses at risk for hemorrhage during vaginal delivery who should be delivered by cesarean section. If a fetal subdural hematoma is diagnosed, pregnancy termination should be offered if the fetus is previable. The prognosis for the fetus is extremely poor, as profound mental deficits, seizures, hypotonia, and even fetal or neonatal demise are the usual outcome5-7.
The authors wish to acknowledge the assistance of Philippe Jeanty, MD, PhD, in the diagnosis of Case #1.
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In utero diagnosis and management of fetal subdural hematoma. Am J Obstet Gynecol 164:1246-8, 1991.
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