Intracranial extradural hematoma: Spontaneous rapid decompression - not resolution.

The surgical option to evacuate an intracranial extradural hematoma (EDH) was postponed in a 2-year-old female child who appeared fully alert and active after a brief spell of unconsciousness following a fall from height. The child was received, with a swelling on and around the right parietal eminence, by the emergency staff just half an hour after the time of injury. The immediate X-ray skull and first computed tomography (CT) scan head showed a parietal bone fracture, EDH, and cephalhematoma. However, follow-up CT scan head after about 4½ h revealed the dramatic absence of EDH but increased size and bogginess of cephalhematoma. The EDH had transported into subgaleal space resulting in a decompression of intracranial compartment in <5 h, thereby preventing surgical intervention but necessitating monitoring, though there was no back flow intracranially.

Introduction

Intracranial extradural hematoma (EDH) is a neurosurgical emergency and is usually fatal in children and young adults if not treated surgically in time. However, infants and elderly patients due to the flexibility of cranial vault and less brain volume, respectively, may not show symptoms and signs of deterioration and may be managed either surgically or medically. Furthermore, the fact is that 1.5% of all patients treated for head trauma have EDHs for which surgery is needed but spontaneous resolution may also occur.[1] The present case report appears to consider the various reported claims of “spontaneous resolution of an EDH in <72 h” as debatable because the complete resolution of a hematoma needs more span-of-time than claimed.

Case Report

A 2-year-old female child was brought to the emergency room of the Department of Neurosurgery with a history of fall, just 30 min before, from a height of about 3 m followed by a brief period of unconsciousness and swelling on the right side of the head. There was no history of associated convulsions, urinary incontinence, or vomiting. The child had stable vital signs and was alert with no neurodeficit but irritable and crying and the examination revealed a right parietal cephalhematoma. All investigations such as X-ray chest, cervical spine, pelvis, and ultrasonography abdomen were normal. However, X-ray skull showed a mildly-diastatic linear fracture in the parietal region with a cephalhematoma [Figure 1]. A cranial computed tomographic (CT) scanning confirmed the findings of a right parietal diastatic fracture and cephalhematoma [Figure 2] with an additional EDH in the right parietal area just under the fracture site. The EDH was about 25 ml in volume, 13 mm in thickness at the widest point, and caused about 6 mm shift in the midline to the opposite side. There was also a mild ipsilateral ventricular compromise [Figure 3]. Since the child had recovered fully from a short spell of unconsciousness to full alertness, it was decided to investigate and prepare the child preanesthetically. During this period, the patient was monitored closely in surgical intensive care unit when it was observed that the cephalhematoma increased in size without any change in hemoglobin level. However, just before the surgical intervention for the EDH, the patient was subjected to a check CT scan head, exactly 4½ h after the first CT scan, and it revealed normal intracranial compartment with no EDH but an enlarged cephalhematoma [Figure 4]. The patient was managed conservatively and closely observed for the next 72 h and then discharged in a healthy condition.

Figure 1

X-ray skull lateral view shows a vertical, linear, and mildly-diastatic fracture in the parietal bone with a cephalhematoma

Figure 2

Plain computed tomography scan (bone-window) cranium displays a mild diastatic linear fracture in the right parietal bone with evident cephalhematoma

Figure 3

Plain computed tomography scan head 30 min after injury reveals right parietal cephalhematoma, extradural hematoma, and mild midline shift to opposite side with ipsilateral mild ventricular compromise

Figure 4

Check noncontrast computed tomography head 4.30 h after the first computed tomography scan shows increased cephalhematoma and no intracranial hematomas or midline shift

Discussion

Since a potential communication existed in the form of a mildly-diastatic linear fracture in the right parietal bone, in the present case, the under-pressure EDH in the completely-occupied (with brain, cerebrospinal fluid, and blood) cranial cavity oozed out in the subgaleal space which subsequently enlarged in size. The fracture-line, as potential communication, is not the only and single factor responsible for the decompression of hematoma. However, the difference between the pressures of extracranial and intracranial spaces also has to play a significant role in forcing the hematomas outside or inside. The intracranial pressure variations occur due to physiological, degenerative, and pathological causes in different age groups. Reversely, an intracranial hematoma should increase in size if more space is available in case of an elderly patient with brain atrophy. Similarly, extracranial soft tissue spaces also exhibit interstitial pressures, which are liable to changes from atmospheric pressures, thickness, and turgor of the soft tissue coverings, posttraumatic open wounds, pressure dressings, and bandages. This may explain the exploitation of a diastatic fracture-line by the existing EDH to leak out of intracranial space. Thus, rather than resolution of hematoma in a given period of time, the process of disappearance of hematoma from extradural space appears merely to be the transportation of a hematoma or else the resolution should occur simultaneously in both the extradural, as well as in subgaleal spaces. Nevertheless, on the contrary, in the present case, the volume of extracranial space (cephalhematoma) increased in size. It is reported that EDH is a serious complication of head injury, which requires rapid diagnosis and early surgical evacuation as a standard management.[23] However, conservative follow-up has also been reported in the literature.[245] Many reported cases of spontaneous rapid resolution encourage the opinion of conservative follow-up.[6] Various theories have been proposed to explain the underlying mechanism of these cases.[3678] The conservative management may be encouraged and facilitated nowadays by the increase in the number of intensive care units, which enhances the close monitoring and follow-up of these patients, the availability of the neurosurgeons in health care centers and easy access to increasingly available CT machines, essential in the diagnosis and follow-up of such patients. The rapid spontaneous resolution of epidural hematoma has been reported in children, as well as in adults. The search in the available literature reveals that 8 cases of EDH hematoma in the pediatric population have been reported to have spontaneously resolved.[7] Similarly, 5 cases of “spontaneous EDH resolution” were seen and reported in the adult population.[8] The oldest patient reported in the literature was 65 years old.[9] Among various theories that have been proposed to explain the underlying mechanisms of rapid spontaneous resolution is the existence of potential communication with a fracture between intracranial and extracranial spaces.[710] The increased intracranial pressure creates a pressure-gradient between EDH and extracranial soft tissue spaces so that hematoma is forced out of extradural space through fracture-line. The reported literature points out the second probable mechanism in spontaneous resolution as the pressure-induced re-distribution of the EDH secondary to brain swelling along the inner table of the cranial vault.[11] However, dissipation of the hematoma seems harder due to tenacious adhesions between the dura matter and skull.[91213] Another theory emphasizes that the extra-cranial blood may be pushed into the extradural space through a fracture-line, due to an increased extracranial subgaleal interstitial pressure and the pressure-gradient after injury. Hence, as the subgaleal interstitial pressure decreases, the blood from intracranial extradural space leaks back. However the process takes about 18 h to complete.[13] Because of this fallacy, the theory is insufficient to explain the underlying mechanism for all the cases, especially for those where hematoma resolved in <18 h. Looking at the resolution-times in pediatric cases, the longest period of time for the resolution was 72 h,[6] and the shortest time period was only 1-h.[11] Bullock et al. reported that epidural hematoma <30 cm in volume, <15 mm in thickness, and leading to <5 mm midline shift in patients with a Glasgow Coma Scale score of more than 8 without any focal neurodeficit could be managed conservatively. These patients need serial CT scans and close monitoring and observation in a neurosurgical center.[14] Eventually, in such situations there is a need for the individualization in the management of each case differently depending on the condition of the patient, imaging and neurosurgical team.

Conclusion

There is a rare chance for some patients with cranial EDHs to be managed conservatively due to a spontaneous reduction in the size of hematoma irrespective of the mechanism involved but not always in most.

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Conflicts of interest

There are no conflicts of interest.