Keywords
infarct - traumatic - computed tomographic scan - modified Rankin scale - rehabilitation
Introduction
Intracranial hematomas, contusions are common after traumatic brain injury (TBI) in
children and young population. However, cerebral infarction after traumatic head injury
is a rare entity with frequency ranging from 1.9 to 10.4%.[1]
[2]
[3]
[4]
[5]
[6] Diagnosis of this pathology in the pediatric population is usually difficult.[7]
[8] Such pathologies can be associated with hematologic alterations and vascular lesions.[9] Here, we present a case of boy who suffered from a right anterior cerebral artery
(ACA) and parts of middle cerebral artery (MCA) territory infarction after moderate
TBI. Possible mechanism for development of infarction is right internal carotid artery
(ICA) dissection by fractured bone fragments and/or thrombosis. This case highlights
importance of delayed computed tomographic (CT) scan in detecting developing infarcts
after head injury as well as importance of rigorous rehabilitation for clinical improvement.
Case Report
A 14-year-old boy presented to emergency department due to head trauma after road
traffic accident, a pedestrian hit by a tractor. The patient presented with the complaint
of loss of consciousness for 2 hours, one episode of vomiting, and left ear bleed.
On examination, he was in altered sensorium with Glasgow coma scale (GCS) score 9
(E2M5V2), right pupil was not reacting and larger than left, left-sided paucity of
movements, and he was hemodynamically stable. CT scan of the brain was performed 3.5
hours after injury showed specks of pneumocephalus in the sellar and suprasellar region
with right sphenoid wing fracture and right orbital roof fracture ([Fig. 1A], [1B]).
Fig. 1 (A) CT brain plain 3.5 hours after trauma. (B) CT brain plain 3.5 hours after trauma (bone window). CT, computed tomography.
The patient was managed on antiedema measures, and CT scan repeated 12 hours after
trauma ([Fig. 2A], [2B]) showed right ACA territory hypodensities. CT scan performed 3 days after trauma
showed right ACA and parts of right MCA territory infarcts. Left-sided limb weakness
progressed to hemiplegia. Magnetic resonance imaging (MRI, fluid attenuation inversion
recovery [FLAIR], diffusion-weighted imaging [DWI] sequences) with contrast done 4
days after trauma showed well-developed infarcts in the right ACA territory as well
as right MCA territory supplying basal ganglia and frontal lobe regions with edema
and midline shift to left approximately 7 mm ([Fig. 3A]). Magnetic resonance angiography (MRA) with time-of-flight (TOF) sequence showed
nonvisualization of the right ICA, right ACA, and right MCA ([Fig. 3B]). Collaterals from right posterior cerebral artery (PCA) and posterior communicating
artery (PCOM) were seen supplying right MCA territory.
Fig. 2 (A) Right ACA territory infarct. (B) Right MCA supplying basal ganglion region infarcts. ACA, anterior cerebral artery;
MCA, middle cerebral artery.
Fig. 3 (A) Magnetic resonance imaging (diffusion-weighted image) with contrast done 4 days
after trauma showed well-developed infarcts in right ACA territory as well as right
MCA territory supplying basal ganglia and frontal lobe regions. (B) MRA showing nonvisualization of the right ICA, right ACA, and right MCA. ACA, anterior
cerebral artery; ICA, internal carotid artery; MCA, middle cerebral artery.
The patient was put on intracranial pressure (ICP) monitory through external ventricular
drain. ICP was raised. The patient underwent right fronto-temporo-parieto craniotomy
and decompression fifth day after trauma. Intraoperatively diseased brain was pale
and bulging with edema present, diseased tissue sent for histopathologic analysis,
and bone flap was loosely replaced to counteract raised ICP. Postoperative CT scan
showed well-developed right ACA and part of MCA territory infarct. The patient was
put in intensive care unit (ICU) for elective ventilation. He was gradually weaned
off and extubated on ninth postoperative day. Histopathology report of surgical specimen
was suggestive of cerebral infarct with hemorrhage without any evidence of thrombosed
veins. At discharge, the patient had GCS of 8T (E3M5VT) and left hemiplegia. He was
advised to undergo regular physiotherapy and general nursing care. At follow-up, 10
months after injury, the patient's left-sided weakness improved (mRS score 3), and
he was able to lift left upper limb and lower limb against gravity.
Discussion
The secondary effects of TBI might be more critical than the primary injuries. Cerebral
infarction after brain trauma has also been recognized as a potential secondary injury
though less common than other secondary injuries such as cerebral edema, posttraumatic
hydrocephalus, and vasospasms. In this case, we tried to highlight clinical presentation;
importance of CT scan specifically delayed CT and need of rehabilitation in posttraumatic
cerebral infarct.
Most patients suffering from mild head injuries achieved good recovery and needed
supportive care. However, a small number of these patients underwent subsequent neurologic
impairment due to raised ICP due to edema or by the presence of an intracranial expansive
mass such as developing intracranial hematoma. Therefore, the patient must stay in
the hospital approximately 6 hours to be clinically monitored.[10] Patients with moderate head injury defined as GCS less than 13 require more meticulous
observation. Bae et al suggested that increasing age, GCS at admission, and brain
herniation were risk factors for posttraumatic cerebral infarction (PTCI).[11] Early recognition of these factors and prompt treatment may prevent PTCI, or at
least minimize fatal consequences.[11]
Various mechanisms for development of PTCI are described in literature such as mechanical
shift and subsequent transtentorial or subfalcine herniation and development of infarction,
blunt vascular injury, and vascular injury by bony fracture fragment especially skull
base fractures.[1]
[4] CT scan plays a vital role in detecting herniation, skull base fractures, and developing
infarcts. In this case, the young male patient developed right ACA territory and part
of MCA territory infarct after a road traffic accident. Delayed CT scan showed developing
infarct correlating with the patient's left-sided weakness. Clinical presentation,
serial CT scans, MRI, and MRA of the brain showed right ACA and part of right MCA
territory infarction. Mechanism of injury can be posttraumatic right ICA dissection
and/or thromboses. The patient was operated on with craniotomy and biopsy of lesion
with loosely replacing bone flaps. He underwent physiotherapy and rehabilitation.
During follow-up, his left-sided hemiplegia improved. Hence, meticulous observation
for neurologic deterioration, serial CT scans, diagnosis, and management of raised
ICP as well as long-term rehabilitation therapy are vital in a case of PTCI.
