- Email: [email protected]
Delayed traumatic intracerebral hemorrhage in children
Delayed Traumatic Intmcerebral Hemorrhage in Children Vijaya Atluru, MD*, Leon G. Epstein, MD~, and Albert Zilka, MD* This report describes delayed traumatic intracerebral hemorrhage in five pediatric patients. The phenomenon has been considered extremely rare in children. Cranial computed tomography preceding and following the ictal hemorrhages provides the best documentation of this phenomenon and suggests some insights into the pathogenic mechanism.
A
Atluru V, Epstein LG, Zilka A. Delayed traumatic intracerebral hemorrhage in children. Pediatr Neurol 1986;2:297-301.
Introduction Delayed traumatic intracerebral hemorrhage (DTICH) was described initially by Bollinger [1] using clinical criteria: the absence of pre-existing vascular disease, a definite history of trauma, an asymptomatic interval, and a subsequent apoplectiform episode. This entity is rare, especially in children, with only 18 cases recorded [2-5]. In one-half of these patients, the diagnosis was made at surgery or at autopsy; more recently reported cases were diagnosed by computed tomography (CT) as in our series. The "interval" between the traumatic episode and the onset of hemorrhage in previous reports ranged from two days to three weeks [3]. It is difficult to be certain that a preexisting hematoma with subsequent swelling or extension did not account for the delayed deterioration. All prior studies have been hampered by limited diagnostic means to evaluate intracerebral hematoma. The advent of CT has been a major asset in this regard. We report five children with DTICH who had CT scans preceding and following delayed hemorrhage.
From the *Division of Pediatric Neurology and ~Division of Neuroradiology; Nassau County Medical Center; East Meadow, New York; and the ~Departments of Neurosciences and Pediatrics; University of Medicine and Dentistry of New Jersey; Newark, New Jersey.
Figure 1. (A) Patient 1. Initial CT scan is normal. (B) CT scan 35 days later reveals an intracerebral hematoma in the right temporal /obe.
Case Reports Patient 1. This 6-year-old boy fell from a pick-up truck. He was unconscious for several minutes, but was able to respond purposefully to verbal stimuli on arrival at the hospital. Skull x-rays and cranial CT (Fig 1A) were normal. The child was discharged after three days of observation without neurologic deficit. He remained well until three weeks later when he developed a right-sided headache, with vomiting and drowsiness. Neurologic examination revealed a lethargic child with a left Babinski sign as the only focal finding. A repeat CT scan demonstrated a large intracerebral hematoma in the right temporal
Communications should be addressed to: Dr. Atluru; Nassau County Medical Center; 2201 Hempstead Turnpike; East Meadow, NY 11554. Received April 25, 1986; accepted May 7, 1986.
Atluru et al: Delayed Intracerebral Hemorrhage
297
A
B
Figure 2. (.4) Patient 2. CT scan demonstrates a cerebral contusion in the left p a m t a l lobe. (B) CT scan three days later depicts two hematomas 2 em in length and several small blood densities in the left hemisphere. t
region (Fig 1B). The hematoma was surrounded by a hypodense region indicating cerebral edema, and was associated with a slight right-to-left shift of midline structures. Prothrombin and partial thmmboplastin times were normal. Cerebral angiography demonstrared an avascular mass corresponding to the right temporal hematoma, but no evidence of an aneurysm or arretiovenous malformation. Neurosurgical consultation was obtained; it was decided to manage the patient conservatively with steroids and osmotic diuretics. The child demonstrated no further deterioration and gradually improved over two weeks. Three serial follow-up CT scans revealed a gradual decrease in the size of the hematoma. A C T scan performed four months later documented complete resolution of the hematoma with a small residual hypodense area remaining. Nenmlogic examination eight months following discharge was normal. Patient 2. This 14-year-old boy was struck in the left parietal region. CT scan on admission was interpreted as normal, but rermspectively may have revealed a cerebral contusion in the left parietal lobe (Fig 2A). The child was minimally lethargic, but was oriented and had no focal neurologic deficit. Three days later he developed severe headaches, appeared confused, and was mildly dysphasic. On examination he had a moderate tight hemiparesis. Repeat CT scan demonstrated two adjacent 2 cm hematomas in the left hemisphere (Fig 2B). Coagulation studies were normal. He was treated conservatively with steroids. He gradually improved over two weeks and was transferred to an intermediate care facility for rehabilitation and was discharged after five weeks. At that time he had a normal mental status examination, normal speech, and a mild right hemiparesis. Patient 3. This infant girl was born by spontaneous, breech, vaginal delivery after a 36-week uncomplicated gestation, weighing 1,890 grams. Apgar scores were 4,7, and 9 at 1,5, and 10 minutes, respectively, and she required supplemental oxygen for one hour after birth. After discharge she was readmitted to the hospital four weeks later with diarrhea diagnosed as milk intolerance. The child was afebrile and not dehydrated. Laboratory studies, including electrolytes, BUN, creatinine, and glucose were normal. Three weeks later the baby was found by the nursing staff to have a large left subgaleal hematoma. The precise mechanism of trauma was never ascertained.
298
PEDIATRIC NEUROLOGY
Vol. 2 No. 5
The baby was alert and feeding well. A skull x-ray demonstrated a diastatic fracture in the left parietal region extending to the right parietal and occipital bones. A C T scan revealed a hypodense area underlying the fracture and a small (1 cm) hyperdense lesion of blood density (Fig 3A). The neurologic examination remained normal until two days later when she developed right partial motor seizures with secondary generalization. These episodes were controlled with intravenous phenobarbital and phenytoin The following morning she remained lethargic and unwilling to eat. A repeat CT scan depicted a large left hemispheral intracerebral hematoma i n v o l ~ the basal ganglia with rupture into the left lateral ventricle (Fig 3B), The neurologic examination was normal except for lethargy and a tense anterior fontanel which improved over the next two days. Coagulation studies were normal. A repeat CT scan after eight weeks demonstrated resolution of the intracerebral hematoma, but revealed porencephalic and leptomeningeal cysts. The child was discharged from the hospital after surgical repair of the leptomeningeal cysts. She had a mild right hemiparesis. She has remained seizure-free on a modest dose of phenobarbital The child was re-evaluated periodically and at 16 months of age had considerable developmental delay. Gross motor development was assessed at a 5-month le*el, and fine motor and adaptive functions at a 10-month level. Neurologic examination revealed marked right hemiparesis and secondary microcephaly. Patient 4. This 12-year-old boy was struck by an automobile. Minutes later, when examined in the emergency room, he exhibited weak withdrawal of all his extremities to noxious stimuli. Both pupils were fully dilated and unresponsive to light. Cold caloric stimulation of each side produced only abduction of the ipsilateral eye. Corneal reaction was positive in both eyes. Deep tendon reflexes were 2 + to 3 + and plantar responses were extensor. The child had sustained multiple fractures of the lower extremities. ACT scan revealed partial obliteration of the quadrigeminal cistern, suggesring midbrain swelling and small lateral ventricles (Fig 4A). He was treated with steroids and osmotic diuretics. An intracranial pressure monitor was not required. On the second hospital day, the patient exhibited purposeful withdrawal to noxious stimuli of all extremities, with no change in the rest of the neurologic examination. Coagulation studies were normal. On the seventh hospital day the patient developed
A
B
Figure 3. (A) Patient 3. CT scan demonstrates a left parietal diastatic fracture with an underlying cerebral contusion and a small hyperdense area of blood density. (t3) CT scan three days later reveals a large left hemisp heral intracerebral hematoma. hypertension with a blood pressure in the range of 150-220 systolic and 100-130 diastolic. A repeat CT scan that day demonstrated a discrete hemorrhage in the paramedian midbrain tegmentum (Fig 4B). The hypertension persisted for several days in spite of therapy with multiple antihypertensive medications, with no deterioration of the patient's neurologic examination. The patient continued to improve. After four weeks, he was aroused easily, responding to his name by opening his right eye. A repeat CT scan demonstrated mild cerebral atrophy with complete resolution of the midbrain hemorrhage. By five weeks he was following commands. He remained mute, with only an occasional outburst of speech when upset. His speech improved gradually, and after nine weeks he was fairly fluent. The patient was walking with assistance. Six months after his ac-
A
cident, the patient was attending school on a regular basis. Psychometric testing showed his performance to be at, or slightly below, his grade level in all areas. He had residual bilateral third nerve palsies with mild bilateral hemiparesis, slightly more severe on the right. Patient 5. This 10-year-old boy was struck by an automobile. He was unconscious and exhibited decerebrate posturing on the right and decorticate posturing on the left to noxious stimuli. A right third nerve paresis was present. He had multiple pelvic and right femoral fractures. Skull x-ray revealed a right parietal fracture and two basal fractures. CT scan demonstrated a right temporal contusion with compression of the right lateral ventricle (Fig 5A). The patient was treated with steroids and osmotic diuretics in the intensive care unit.
B
Figure 4. (A) Patient 4. CT scan demonstrates partial obliteration of the quadrigeminal cistern. (t3) Enhanced CT scan six days later depicts a discrete hyperdense lesion in the paramedian midbrain tegmentum.
Atluru et al: Delayed Intracerebral Hemorrhage
299
A
t/
FigureS. (A) Patient S. A CT scan reveals a contusion in the right temporM lobe. (B) CT scan eight days later depicts a discrete 1.8 cm hematoma in the rtght tempora/ lobe.
On the second hospital day he had some spontaneous movement of his extremities bilaterally, alternating on the left with spontaneous decorticate posturing. On admission, prothrombin time was 11 / 10 sec, partial thromboplastin time 27.2/30 sec, and on the following day they were 14/11 and 75/35 sec, respectively. Platelet count dropped from 275,000 to 75,000/ram3. The patient was treated with a transfusion of blood and fresh frozen plasma. During the first week he demonstrated no further improvement. The right third nerve dysfunction persisted and a left hemiparesis became more apparent, A repeat CT scan revealed a 1.8 cm discrete hematoma deep in the right temporal lobe adjacent to the area of contusion noted on the initial scan (Fig 5B). The intracranial pressure monitor, in place from the day of admission, documented no significant rise in pressure, nor was there any abrupt deterioration in clinical status. The child improved gradually over the next seven weeks. He was discharged eight weeks after admission with a right third nerve paresis and a mild left hemiparesis. Six months later he was attending regular school and his neurologic examination was normal with the exception of a partial right third nerve paresis.
Discl188ion Although delayed traumatic intracerebral h e m a t o m a s are said to be rare, particularly in children, the true incidence is not known. In a review o f the literature through 1970, Morin and Pitts [2] cited only four cases occurring in patients less than 20 years o f age and added two additional cases. Batatham and Dennyson [3] reported the largest series, with 21 patients, o f w h o m 3 were below age 20 years. The details of the clinical presentation are not described. In these nine childhood cases, the definitive diagnosis of intra. cerebral h e m a t o m a was m a d e at the time o f surgery or by autopsy. Nine other childhood cases of D T I C H were reported that were d o c u m e n t e d by CT scans [4,5]. On clinical grounds, the incidence could either be overestimated by including patients with a significant h e m a t o m a at the time of initial injury and subsequent deterioration due to e d e m a or extension o f the
300
PEDIATRICNEUROLOGY
Vol. 2 No. 5
hemorrhage, or be underestimated in earlier reported series of intracerebral h e m a t o m a s when serial CT scans were not obtained. The five patients reported here had initial scans which did not demonstrate a significant intracerebral h e m a t o m a . Following clinical deterioration, a repeat CT scan demonstrated delayed hemorrhage. Currently serial CT scans provide the best documentation of this p h e n o m e n o n m children. Larger studies utilizing CT scans will more accurately determ i n e the incidence of D T I C H in all age groups. Although the present study confirms the occurrence of D T I C H , the pathogenesis remains undetermined. Bollinger [1], in his original paper, hypothesized that hemorrhage was a result of direct damage to an arterial vessel wall with necrosis later leading to rupture. Alternatively, Baratham and Dennyson [3] proposed that local changes in blood flow or vessel wall integrity caused a gradual diapedesis and oozing which accumulated and coalesced to form a larger hemorrhage. They reviewed the prior autopsy studies by Evans and Scheinker [6] revealing "vasoparalysis" and the more recent data from experimental animal models d e m o n . strating local increase in cerebral blood flow following trauma [7], and speculated that a loss of local autoregulation would allow an increase in systemic blood pressure to be transmitted to small veins, facilitating diapedesis. In addition, hypertension, hypoxia, carbon dioxide retention, or any factor resulting in an elevation o f venous pressure, would exacerbate this tendency [5]. In some cases D T I C H may be due to gradual bleeding into a previously unrecognized area o f brain contusion. Delayed intracerebral hematom_as have been discovered after evacuation of traumatic extracerebral h e m a t o m a s [10], suggesting that such bleeding may be
accelerated by the removal of other intracranial mass lesions which initially may tamponade intraparenchymal hemorrhage. Seven of the nine cases of CT-documented DTICH in children were recognized following extracerebral hematoma decompression [4,5]; however, none of our patients had extracerebral hematomas. Disseminated intravascular coagulation and fibrinolysis (DICF) has been reported following head injury in children [9,10]. DICF after head trauma is probably caused by the release of thromboplastic substances (e.g., phospholipoprotein membranes) from injured meninges and brain tissue into the circulation. Kaufman et al. [10] reported 12 patients with DTICH, 11 of whom had clotting abnormalities. The authors raised the intriguing possibility that DTICH may occur predominantly in head trauma victims with coagulopathy. Alternatively, DICF may be an epiphenomenon because it also occurs in patients with significant head injury, without discrete hemorrhage. In the present series only one of five patients had a clotting abnormality, and none had received aspirin; three patients were treated with osmotic diuretics that may cause a mild anticoagulant effect. Prospective studies will be necessary to determine if coagulation abnormalities are important in the development of DTICH. Four patients in this report had cerebral contusions in the area of subsequent intracerebral hematoma. These cases support the theory of prior damage to brain parenchyma, affecting blood vessel integrity and/or autoregulation, setting the stage for delayed hemorrhage. In these cases, the delayed hemorrhage occurred consistently after the second day of the head injury. It is difficult to assess whether the hypertension experienced by Patient 4 was a result of, or contributed to the midbrain hemorrhage. The facts that the oculomotor findings preceded the onset of the hypertension by several days and demonstrated no clinical worsening at the time the hypertension was identified argues against the hemorrhage resulting from hypertension. Hypertension is a frequent clinical correlate of primary midbrain hemorrhage [11]. It is possible, however, that the hypertension caused extension of smaller hemorrhages not detectable by CT scan in an area of recent contusion. Elevated intracranial pressure may have contributed to the hemorrhage, but unfortunately pressure was not monitored. Generally, the initial presentation, clinical course, and CT scan findings are most consistent with primary brainstem contusion with delayed hemorrhage. In the one child with an initially normal CT scan, the
delayed hemorrhage occurred approximately five weeks after injury. Cerebral angiography failed to reveal any evidence suggestive of carotid artery disease or preexisting arteriovenous malformation. This child's course is likely the result of a different mechanism that is similar to Bollinger's suggestion of a more discrete injury to a small cerebral blood vessel. All of the five patients survived. Of these, one recovered completely, and three recovered with mild deficits. One patient, the only infant in the series, recovered but was left with a significant motor deficit and overall delayed development. All patients recovered without the need for surgical evacuation of their hematomas. It has been suggested that the intracranial pressure monitoring may be a useful adjunct in deciding which patients with intracerebral hematomas are candidates for surgical intervention [8]. It is likely that the availability of CT scans will demonstrate that DTICH is more common than previously reported in both adults and children. Sydney Louis, MD reviewed the manuscript and Christine Kolsch provided secretarial assistance. References 11] Bollinger O. Veber traumatische span-apoplexie ein beitrag zur lehre yon der hirnershutterung. Internationale beitrage zur wissenschaftlichen medicin. Festschrift. Rudolf Virchow. Berlin: A Hirshwald, 1881;2:457-70. [2] Morin MA, Pitts FW. Delayed apoplexy following head injury (' 'Traumatische Span -Apoplexie' '). J Neurosurg 1970; 33: 542 -7. [3] Baratham G, Dennyson W. Delayed traumatic intracerebral hemorrhage. J Neurol Neurosurg Psychiatry 1972; 35:698-706. [4] Gudeman SK, Kishore PRS, Miller JD, Girevendulis AK, Lipper MH, Becker DP. The genesis and significance of delayed traumatic intracerebral hematoma. Neurosurgery 1979; 5: 309-13. [5] Ninchoji T, Uemura K, Shimoyama I, Hinokuma K, Bun T, Nakajima S. Traumatic intracerebral haematomas of delayed onset. Acta Neurochir 1984;71:69-90. [6] Evans Jp, Scheinker IM. I. Histologic studies of the brain following head trauma. If. Post-traumatic petechial and massive intracerebral hemorrhage. J Neurosurg 1946;3:101 - 13. [7] Brock M. Experimental "luxury perfusion" in the cerebral cortex of the cat. Prog Brain Res 1968;30:125. 18] Jennett B, Teasdale G. Management of head injuries. Philadelphia: FA Davis, 1981;157:172-4. [9] Miner ME, Kaufman HH, Graham SH, Haar FH, Gildenberg PL. Disseminated intravascular coagulation fibrinolytic syndrome following head injury in children: Frequency and prognostic implications. J Pediatr 1982 ; 100:687-91. [10] Kaufman HM, Moake JL, Olson JD, et al. Delayed and recurrent intracerebral hematomas related to disseminated intravascular clotting and fibrinolysis in head injury. Neurosurgery 1980;7:445-9. [11] Courville CB. Effects of closed cranial injuries on the midbrain and upper pons. Res Publ Nerv Ment Dis Proc 1945; 24:131-50.
Atluru et al: Delayed Intracerebral Hemorrhage
301
A
Atluru V, Epstein LG, Zilka A. Delayed traumatic intracerebral hemorrhage in children. Pediatr Neurol 1986;2:297-301.
Introduction Delayed traumatic intracerebral hemorrhage (DTICH) was described initially by Bollinger [1] using clinical criteria: the absence of pre-existing vascular disease, a definite history of trauma, an asymptomatic interval, and a subsequent apoplectiform episode. This entity is rare, especially in children, with only 18 cases recorded [2-5]. In one-half of these patients, the diagnosis was made at surgery or at autopsy; more recently reported cases were diagnosed by computed tomography (CT) as in our series. The "interval" between the traumatic episode and the onset of hemorrhage in previous reports ranged from two days to three weeks [3]. It is difficult to be certain that a preexisting hematoma with subsequent swelling or extension did not account for the delayed deterioration. All prior studies have been hampered by limited diagnostic means to evaluate intracerebral hematoma. The advent of CT has been a major asset in this regard. We report five children with DTICH who had CT scans preceding and following delayed hemorrhage.
From the *Division of Pediatric Neurology and ~Division of Neuroradiology; Nassau County Medical Center; East Meadow, New York; and the ~Departments of Neurosciences and Pediatrics; University of Medicine and Dentistry of New Jersey; Newark, New Jersey.
Figure 1. (A) Patient 1. Initial CT scan is normal. (B) CT scan 35 days later reveals an intracerebral hematoma in the right temporal /obe.
Case Reports Patient 1. This 6-year-old boy fell from a pick-up truck. He was unconscious for several minutes, but was able to respond purposefully to verbal stimuli on arrival at the hospital. Skull x-rays and cranial CT (Fig 1A) were normal. The child was discharged after three days of observation without neurologic deficit. He remained well until three weeks later when he developed a right-sided headache, with vomiting and drowsiness. Neurologic examination revealed a lethargic child with a left Babinski sign as the only focal finding. A repeat CT scan demonstrated a large intracerebral hematoma in the right temporal
Communications should be addressed to: Dr. Atluru; Nassau County Medical Center; 2201 Hempstead Turnpike; East Meadow, NY 11554. Received April 25, 1986; accepted May 7, 1986.
Atluru et al: Delayed Intracerebral Hemorrhage
297
A
B
Figure 2. (.4) Patient 2. CT scan demonstrates a cerebral contusion in the left p a m t a l lobe. (B) CT scan three days later depicts two hematomas 2 em in length and several small blood densities in the left hemisphere. t
region (Fig 1B). The hematoma was surrounded by a hypodense region indicating cerebral edema, and was associated with a slight right-to-left shift of midline structures. Prothrombin and partial thmmboplastin times were normal. Cerebral angiography demonstrared an avascular mass corresponding to the right temporal hematoma, but no evidence of an aneurysm or arretiovenous malformation. Neurosurgical consultation was obtained; it was decided to manage the patient conservatively with steroids and osmotic diuretics. The child demonstrated no further deterioration and gradually improved over two weeks. Three serial follow-up CT scans revealed a gradual decrease in the size of the hematoma. A C T scan performed four months later documented complete resolution of the hematoma with a small residual hypodense area remaining. Nenmlogic examination eight months following discharge was normal. Patient 2. This 14-year-old boy was struck in the left parietal region. CT scan on admission was interpreted as normal, but rermspectively may have revealed a cerebral contusion in the left parietal lobe (Fig 2A). The child was minimally lethargic, but was oriented and had no focal neurologic deficit. Three days later he developed severe headaches, appeared confused, and was mildly dysphasic. On examination he had a moderate tight hemiparesis. Repeat CT scan demonstrated two adjacent 2 cm hematomas in the left hemisphere (Fig 2B). Coagulation studies were normal. He was treated conservatively with steroids. He gradually improved over two weeks and was transferred to an intermediate care facility for rehabilitation and was discharged after five weeks. At that time he had a normal mental status examination, normal speech, and a mild right hemiparesis. Patient 3. This infant girl was born by spontaneous, breech, vaginal delivery after a 36-week uncomplicated gestation, weighing 1,890 grams. Apgar scores were 4,7, and 9 at 1,5, and 10 minutes, respectively, and she required supplemental oxygen for one hour after birth. After discharge she was readmitted to the hospital four weeks later with diarrhea diagnosed as milk intolerance. The child was afebrile and not dehydrated. Laboratory studies, including electrolytes, BUN, creatinine, and glucose were normal. Three weeks later the baby was found by the nursing staff to have a large left subgaleal hematoma. The precise mechanism of trauma was never ascertained.
298
PEDIATRIC NEUROLOGY
Vol. 2 No. 5
The baby was alert and feeding well. A skull x-ray demonstrated a diastatic fracture in the left parietal region extending to the right parietal and occipital bones. A C T scan revealed a hypodense area underlying the fracture and a small (1 cm) hyperdense lesion of blood density (Fig 3A). The neurologic examination remained normal until two days later when she developed right partial motor seizures with secondary generalization. These episodes were controlled with intravenous phenobarbital and phenytoin The following morning she remained lethargic and unwilling to eat. A repeat CT scan depicted a large left hemispheral intracerebral hematoma i n v o l ~ the basal ganglia with rupture into the left lateral ventricle (Fig 3B), The neurologic examination was normal except for lethargy and a tense anterior fontanel which improved over the next two days. Coagulation studies were normal. A repeat CT scan after eight weeks demonstrated resolution of the intracerebral hematoma, but revealed porencephalic and leptomeningeal cysts. The child was discharged from the hospital after surgical repair of the leptomeningeal cysts. She had a mild right hemiparesis. She has remained seizure-free on a modest dose of phenobarbital The child was re-evaluated periodically and at 16 months of age had considerable developmental delay. Gross motor development was assessed at a 5-month le*el, and fine motor and adaptive functions at a 10-month level. Neurologic examination revealed marked right hemiparesis and secondary microcephaly. Patient 4. This 12-year-old boy was struck by an automobile. Minutes later, when examined in the emergency room, he exhibited weak withdrawal of all his extremities to noxious stimuli. Both pupils were fully dilated and unresponsive to light. Cold caloric stimulation of each side produced only abduction of the ipsilateral eye. Corneal reaction was positive in both eyes. Deep tendon reflexes were 2 + to 3 + and plantar responses were extensor. The child had sustained multiple fractures of the lower extremities. ACT scan revealed partial obliteration of the quadrigeminal cistern, suggesring midbrain swelling and small lateral ventricles (Fig 4A). He was treated with steroids and osmotic diuretics. An intracranial pressure monitor was not required. On the second hospital day, the patient exhibited purposeful withdrawal to noxious stimuli of all extremities, with no change in the rest of the neurologic examination. Coagulation studies were normal. On the seventh hospital day the patient developed
A
B
Figure 3. (A) Patient 3. CT scan demonstrates a left parietal diastatic fracture with an underlying cerebral contusion and a small hyperdense area of blood density. (t3) CT scan three days later reveals a large left hemisp heral intracerebral hematoma. hypertension with a blood pressure in the range of 150-220 systolic and 100-130 diastolic. A repeat CT scan that day demonstrated a discrete hemorrhage in the paramedian midbrain tegmentum (Fig 4B). The hypertension persisted for several days in spite of therapy with multiple antihypertensive medications, with no deterioration of the patient's neurologic examination. The patient continued to improve. After four weeks, he was aroused easily, responding to his name by opening his right eye. A repeat CT scan demonstrated mild cerebral atrophy with complete resolution of the midbrain hemorrhage. By five weeks he was following commands. He remained mute, with only an occasional outburst of speech when upset. His speech improved gradually, and after nine weeks he was fairly fluent. The patient was walking with assistance. Six months after his ac-
A
cident, the patient was attending school on a regular basis. Psychometric testing showed his performance to be at, or slightly below, his grade level in all areas. He had residual bilateral third nerve palsies with mild bilateral hemiparesis, slightly more severe on the right. Patient 5. This 10-year-old boy was struck by an automobile. He was unconscious and exhibited decerebrate posturing on the right and decorticate posturing on the left to noxious stimuli. A right third nerve paresis was present. He had multiple pelvic and right femoral fractures. Skull x-ray revealed a right parietal fracture and two basal fractures. CT scan demonstrated a right temporal contusion with compression of the right lateral ventricle (Fig 5A). The patient was treated with steroids and osmotic diuretics in the intensive care unit.
B
Figure 4. (A) Patient 4. CT scan demonstrates partial obliteration of the quadrigeminal cistern. (t3) Enhanced CT scan six days later depicts a discrete hyperdense lesion in the paramedian midbrain tegmentum.
Atluru et al: Delayed Intracerebral Hemorrhage
299
A
t/
FigureS. (A) Patient S. A CT scan reveals a contusion in the right temporM lobe. (B) CT scan eight days later depicts a discrete 1.8 cm hematoma in the rtght tempora/ lobe.
On the second hospital day he had some spontaneous movement of his extremities bilaterally, alternating on the left with spontaneous decorticate posturing. On admission, prothrombin time was 11 / 10 sec, partial thromboplastin time 27.2/30 sec, and on the following day they were 14/11 and 75/35 sec, respectively. Platelet count dropped from 275,000 to 75,000/ram3. The patient was treated with a transfusion of blood and fresh frozen plasma. During the first week he demonstrated no further improvement. The right third nerve dysfunction persisted and a left hemiparesis became more apparent, A repeat CT scan revealed a 1.8 cm discrete hematoma deep in the right temporal lobe adjacent to the area of contusion noted on the initial scan (Fig 5B). The intracranial pressure monitor, in place from the day of admission, documented no significant rise in pressure, nor was there any abrupt deterioration in clinical status. The child improved gradually over the next seven weeks. He was discharged eight weeks after admission with a right third nerve paresis and a mild left hemiparesis. Six months later he was attending regular school and his neurologic examination was normal with the exception of a partial right third nerve paresis.
Discl188ion Although delayed traumatic intracerebral h e m a t o m a s are said to be rare, particularly in children, the true incidence is not known. In a review o f the literature through 1970, Morin and Pitts [2] cited only four cases occurring in patients less than 20 years o f age and added two additional cases. Batatham and Dennyson [3] reported the largest series, with 21 patients, o f w h o m 3 were below age 20 years. The details of the clinical presentation are not described. In these nine childhood cases, the definitive diagnosis of intra. cerebral h e m a t o m a was m a d e at the time o f surgery or by autopsy. Nine other childhood cases of D T I C H were reported that were d o c u m e n t e d by CT scans [4,5]. On clinical grounds, the incidence could either be overestimated by including patients with a significant h e m a t o m a at the time of initial injury and subsequent deterioration due to e d e m a or extension o f the
300
PEDIATRICNEUROLOGY
Vol. 2 No. 5
hemorrhage, or be underestimated in earlier reported series of intracerebral h e m a t o m a s when serial CT scans were not obtained. The five patients reported here had initial scans which did not demonstrate a significant intracerebral h e m a t o m a . Following clinical deterioration, a repeat CT scan demonstrated delayed hemorrhage. Currently serial CT scans provide the best documentation of this p h e n o m e n o n m children. Larger studies utilizing CT scans will more accurately determ i n e the incidence of D T I C H in all age groups. Although the present study confirms the occurrence of D T I C H , the pathogenesis remains undetermined. Bollinger [1], in his original paper, hypothesized that hemorrhage was a result of direct damage to an arterial vessel wall with necrosis later leading to rupture. Alternatively, Baratham and Dennyson [3] proposed that local changes in blood flow or vessel wall integrity caused a gradual diapedesis and oozing which accumulated and coalesced to form a larger hemorrhage. They reviewed the prior autopsy studies by Evans and Scheinker [6] revealing "vasoparalysis" and the more recent data from experimental animal models d e m o n . strating local increase in cerebral blood flow following trauma [7], and speculated that a loss of local autoregulation would allow an increase in systemic blood pressure to be transmitted to small veins, facilitating diapedesis. In addition, hypertension, hypoxia, carbon dioxide retention, or any factor resulting in an elevation o f venous pressure, would exacerbate this tendency [5]. In some cases D T I C H may be due to gradual bleeding into a previously unrecognized area o f brain contusion. Delayed intracerebral hematom_as have been discovered after evacuation of traumatic extracerebral h e m a t o m a s [10], suggesting that such bleeding may be
accelerated by the removal of other intracranial mass lesions which initially may tamponade intraparenchymal hemorrhage. Seven of the nine cases of CT-documented DTICH in children were recognized following extracerebral hematoma decompression [4,5]; however, none of our patients had extracerebral hematomas. Disseminated intravascular coagulation and fibrinolysis (DICF) has been reported following head injury in children [9,10]. DICF after head trauma is probably caused by the release of thromboplastic substances (e.g., phospholipoprotein membranes) from injured meninges and brain tissue into the circulation. Kaufman et al. [10] reported 12 patients with DTICH, 11 of whom had clotting abnormalities. The authors raised the intriguing possibility that DTICH may occur predominantly in head trauma victims with coagulopathy. Alternatively, DICF may be an epiphenomenon because it also occurs in patients with significant head injury, without discrete hemorrhage. In the present series only one of five patients had a clotting abnormality, and none had received aspirin; three patients were treated with osmotic diuretics that may cause a mild anticoagulant effect. Prospective studies will be necessary to determine if coagulation abnormalities are important in the development of DTICH. Four patients in this report had cerebral contusions in the area of subsequent intracerebral hematoma. These cases support the theory of prior damage to brain parenchyma, affecting blood vessel integrity and/or autoregulation, setting the stage for delayed hemorrhage. In these cases, the delayed hemorrhage occurred consistently after the second day of the head injury. It is difficult to assess whether the hypertension experienced by Patient 4 was a result of, or contributed to the midbrain hemorrhage. The facts that the oculomotor findings preceded the onset of the hypertension by several days and demonstrated no clinical worsening at the time the hypertension was identified argues against the hemorrhage resulting from hypertension. Hypertension is a frequent clinical correlate of primary midbrain hemorrhage [11]. It is possible, however, that the hypertension caused extension of smaller hemorrhages not detectable by CT scan in an area of recent contusion. Elevated intracranial pressure may have contributed to the hemorrhage, but unfortunately pressure was not monitored. Generally, the initial presentation, clinical course, and CT scan findings are most consistent with primary brainstem contusion with delayed hemorrhage. In the one child with an initially normal CT scan, the
delayed hemorrhage occurred approximately five weeks after injury. Cerebral angiography failed to reveal any evidence suggestive of carotid artery disease or preexisting arteriovenous malformation. This child's course is likely the result of a different mechanism that is similar to Bollinger's suggestion of a more discrete injury to a small cerebral blood vessel. All of the five patients survived. Of these, one recovered completely, and three recovered with mild deficits. One patient, the only infant in the series, recovered but was left with a significant motor deficit and overall delayed development. All patients recovered without the need for surgical evacuation of their hematomas. It has been suggested that the intracranial pressure monitoring may be a useful adjunct in deciding which patients with intracerebral hematomas are candidates for surgical intervention [8]. It is likely that the availability of CT scans will demonstrate that DTICH is more common than previously reported in both adults and children. Sydney Louis, MD reviewed the manuscript and Christine Kolsch provided secretarial assistance. References 11] Bollinger O. Veber traumatische span-apoplexie ein beitrag zur lehre yon der hirnershutterung. Internationale beitrage zur wissenschaftlichen medicin. Festschrift. Rudolf Virchow. Berlin: A Hirshwald, 1881;2:457-70. [2] Morin MA, Pitts FW. Delayed apoplexy following head injury (' 'Traumatische Span -Apoplexie' '). J Neurosurg 1970; 33: 542 -7. [3] Baratham G, Dennyson W. Delayed traumatic intracerebral hemorrhage. J Neurol Neurosurg Psychiatry 1972; 35:698-706. [4] Gudeman SK, Kishore PRS, Miller JD, Girevendulis AK, Lipper MH, Becker DP. The genesis and significance of delayed traumatic intracerebral hematoma. Neurosurgery 1979; 5: 309-13. [5] Ninchoji T, Uemura K, Shimoyama I, Hinokuma K, Bun T, Nakajima S. Traumatic intracerebral haematomas of delayed onset. Acta Neurochir 1984;71:69-90. [6] Evans Jp, Scheinker IM. I. Histologic studies of the brain following head trauma. If. Post-traumatic petechial and massive intracerebral hemorrhage. J Neurosurg 1946;3:101 - 13. [7] Brock M. Experimental "luxury perfusion" in the cerebral cortex of the cat. Prog Brain Res 1968;30:125. 18] Jennett B, Teasdale G. Management of head injuries. Philadelphia: FA Davis, 1981;157:172-4. [9] Miner ME, Kaufman HH, Graham SH, Haar FH, Gildenberg PL. Disseminated intravascular coagulation fibrinolytic syndrome following head injury in children: Frequency and prognostic implications. J Pediatr 1982 ; 100:687-91. [10] Kaufman HM, Moake JL, Olson JD, et al. Delayed and recurrent intracerebral hematomas related to disseminated intravascular clotting and fibrinolysis in head injury. Neurosurgery 1980;7:445-9. [11] Courville CB. Effects of closed cranial injuries on the midbrain and upper pons. Res Publ Nerv Ment Dis Proc 1945; 24:131-50.
Atluru et al: Delayed Intracerebral Hemorrhage
301