JOURNAL OF NEUROSCIENCE AND NEUROSURGERY (ISSN:2517-7400)

Brain Stem Contusion (BSC); RTA (Road traffic accident); Brainstem; Intensive Care Unit (I.C.U); Quality of Life (QOL)

Traumatic Brain Injury (TBI) constitutes a wide spectrum of clinic-radiological events, ranging from EDH (Extra dural hematoma), ASDH (Acute Subdural Hematoma), contusion or DAI (Diffuse Axonal Injury). TBI present to Emergency Department (ED) either due to RTA (Road Traffic Accident), an assault or a fall from height. They result in closed type or open type of head injury. Brain stem is the part of brain more over injured by severe collisional impact to the skull causing alteration in microstructural organization inside the brain. Patients usually present with altered sensorium. The impact of trauma may be either localized or distributed all over. Here we present an uncommon case of traumatic “Brain Stem Contusion” (BSC), its presentation & management in an acute setting.

Pulse rate was 62 per min, blood pressure 140/80 mm of Hg. Respiration was abdominothoracic type, 18 per minute; left pupil dilated but sluggishly reacting to light, right side normally reacting to light. There was right side weakness (Figure 1a) of both the limbs. Noncontrast CT scan of the brain revealed brain stem contusion (BSC), in the midbrain area on the right side with DAI (Figure 2).

All routine blood investigations, liver function test, coagulation profile, renal function test, cardiological evaluation, Chest X Ray (CXR) and Ultrasonogram (USG) of abdomen and pelvis were within normal limit. The plantar reflex was up going, suggesting an UMN (Upper Motor Neuron) type of involvement.

The BSC started resolving & in the second NCCT brain, it has vanished; but DAI was persisting (Figure 3). The Marshall CT grade was 2 .The patient underwent tracheostomy on post trauma day-3; for the need of proper ventilation (reduction of the anatomical dead space). The respiration remained regular and abdomino-thoracic type, since the day of admission.

The patient had unequal pupils; being dilated on left size, with sluggish reaction to light. The pupil size was measured with a pupilometer, by the ophthalmologist of our hospital. Patient was monitored regularly on daily basis: for, temperature, BP, PR, Respiratory rate and pupil size followed by the neurological assessment of motor system (Chart-1).

On post trauma day 4, we started giving adequate nutrition to the patient through the nasogastric tube. Relatives were counseled and taught about the conservative patient care. After day 20, the patient was discharged with medications. The neurological status improved, the pupils became equal with normal reaction to light; but isolated left side hemiparesis persisted. The patient is on follow up after that, on monthly basis for last 3 months. Barring left hemiparesis of MRC grade-2/5, he has fully recovered neurologically. CT scan of brain had no evidence of BSC on day-20 (Figure 4).

The most frequent site of haemorrhage is the midline rostral brainstem. When associated with Space Occupying Lesion (SOL) and increase in ICP, it’s called Duret haemorrhage. In case of Diffuse Axonal Injury (DAI), dorso-lateral quadrant is the site of lesion. Diffuse vascular injury results in BSL in the periventricular areas.

BSC portend an ominous outcome with a poor prognosis. The severity of outcome depends on the contusion size (hematoma volume ≥ 6 ml); its site- midbrain, pons, medulla, or in toto; intraventricular extension; hydrocephalus. No definitive management protocol exists till now. Associated pathology may be dealt with, depending on the hematoma size; with presence or absence of mass effect. In our report, the patient had midbrain bleed, not involving the ventricle, and there was no associated hydrocephalus.

Hemiparesis is due to involvement of the corticospinal tracts and the left sided pupillary dilation can be explained as local pathology involving the long cilliary nerve [1].

Commichau et al. (2003) described that rise in temperature of body manifesting from a central cause leads to rise in morbidity and mortality rate, among patients with TBI. Greer et al. (2008) showed that, as an independent variable fever is consistently associated with worse outcome in patients with TBI. Deogaonkar (2005) illustrated that, the severity of fever caused by massive volume intracerebral hematoma is attributed to direct compression of brainstem and hypothalamic thermoregulatory centers. Wijdicks and St Louis (1997), in a retrospective study correlated mortality rate in patients associated with low GCS < 8, absent brainstem reflex like oculocephalic reflex or poor motor response in brainstem hemorrhage [2].

Tintore M et al. concluded that infratentorial lesions increases the disability rate [3]. Today, though multimodal investigation facility is available still CT remains the reliable immediate imaging modality of choice for any TBI, the diagnostic features being contusion, obliteration of basal cistern, blood in prepontine or perimesencephalic cistern [4-6].

Biomechanics of BSC are: damage by direct impact, flexion and distortion and vascular involvement or hyperextension. Primary brainstem lesion (contusion or laceration) is due to movement of the brain along the sharp tentorial edges [7]. According to Cooper et al. acute flexion is the main recognized factor for BSC, contrary to hyperextension [8].

Usually, BSC patients present with low GCS, making ICU care with ventillator support, the need of the hour. Prompt care by neurosurgeons, nursing care and last, but not the least patient’s own attendants’ care are the pillars upon which this arduous task rests on. Attitude towards the “conservative” patient, matters the most. In resource poor public hospitals, these are the group of patients prone to the most neglect. Systemic changes like pulmonary complications, cardiological changes must be monitored, apart from the vital parameters. Associated injury to abdomen, thorax or any bony or soft tissue must involve general surgeon and orthopedicians. Of course spinal injury must be ruled out after deliberation on the brain lesion [9].

Mohapatra et al. reported survival in more than 50% of such cases. In their 70 patients study, 38 patients survived and 22 had a good recovery. Age, associated skull fracture and other associated injury continue to be the determinant of survival. Young patients have a good outcome Kim et al. [4] in their study on brainstem haemorrhage showed long term survival in these patients [10].

Hashimoto et al. [11] have described 21 brainstem lesions out of a study of 239 traumatic brain injury cases, out of which 5 were ‘pure brainstem lesions’. How these cases were managed has not been enumerated (with respect to intensive care management), although an unfavorable outcome of all these brainstem cases, particularly when more than one in number has been mentioned.

In another Tunisian study by Bahloul M et al. [12] 40 cases had normal CT scans & 50 (EDH, n=30; SDH, n=6; lobectomy, n=3; depressed skull #, n=10 & DC, n=1) required surgical intervention, out of 276 child victims of traumatic brain injury. Though all the patients were treated in intensive care set up, data regarding primary brain stem lesions managed is lacking. 

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