A Rare Case Report of the Coexistence of Ipsilateral Burst Frontal Lobe, Acute-on-Chronic Subdural Hematoma, and Extradural Hematoma: Rarest in Occurrence

Abstract

Burst frontal lobe or frontal lobe contusion is commonly seen in road traffic accidents (RTA) or assault. Chronic subdural hematomas are seen in elderly patients with history of nonsteroidal anti-inflammatory drugs use, chronic alcohol intake, and antithrombotic and/or anticoagulant therapy. Extradural and acute subdural hematomas are often seen in young patients following RTA or trauma. The coexistence of all the above-mentioned conditions, that is, lobar contusion, acute-on-chronic subdural hematoma (SDH), and acute extradural hematoma (EDH), in a patient is rare. Based on the Glasgow Coma Scale and imaging findings, early surgical intervention was planned in our patient. Early surgical evacuation of contusion, acute-on-chronic SDH, and EDH, as was done in our patient, will lead to early recovery. Avoiding alcohol intake and use of helmets while riding motorcycles will lead to reduction of such RTA in future.

Keywords

lobar contusion - subdural hematoma - burst frontal lobe - extradural hematoma - sphenopalatine vein

Introduction

Road traffic accident (RTA) is the most common cause of traumatic brain injury among adolescents and adults, often leading to acute subdural hematoma (SDH) and extradural hematoma (EDH). Burst lobe or contusion of the cortex is an indirect indication of the severity of the injury. Chronic SDH is more common in elderly individuals with history of nonsteroidal anti-inflammatory drugs (NSAIDs), antithrombotic medications, and trivial trauma or frequent fall. The coexistence of burst lobe, acute-on-chronic SDH, and EDH on the same side is very rare, and no literature has been found on this condition. Hence, we are reporting one such rare case.

Case Report

Case Illustration

A 61-year-old male resident of Bangalore with no known comorbidities and not on any medication presented to the emergency room with the history of a slip and fall at home and was in altered sensorium since then. At the time of admission, his Glasgow Coma Scale (GCS) score was E1V2M4. His pupils were bilaterally sluggishly reactive, with right upper and lower limb power of grade 3/5 according to the British Medical Research Council (MRC) scale and the rest were moving against gravity. He had multiple abrasions on the face and on the right shoulder and right knee. His blood pressure was 118/66 mm Hg and the pulse rate was 56 beats per minute. The patient was resuscitated in the emergency room and all routine investigations were done.

Computed tomography (CT) scan of the head showed left-sided frontal lobe contusion, left-sided frontotemporoparietal (FTP) acute-on-chronic SDH and left-sided parietal EDH ([Figs. 1] [2] [3]). There were no previous similar complaints in the past and no history of drug intake/alcohol intake or trauma. There was no history of surgery.

Fig. 1 Computed tomography scan of the brain showing left burst frontal lobe with acute-on-chronic subdural hematoma (SDH).

Fig. 2 Computed tomography scan showing left parietal region extradural hematoma (EDH) in sagittal view.

Fig. 3 Evacuated left frontal burst lobe and acute-on-chronic subdural hematoma (SDH).

Following poor neurological status, emergency surgery was planned. Preoperative routine investigations along with coagulation profile were found to be normal. The patient was taken to the emergency operating room where left-sided FTP craniotomy was done ([Fig. 3]). EDH was evacuated first and then the dura was opened and acute-on-chronic SDH was also evacuated. The left-sided burst frontal lobe was opened and contusion was also evacuated. Postevacuation the brain was lax and pulsatile; hence, bone was replaced. Postoperative scans showed an evacuated state of EDH and acute-on-chronic SDH and contusion was also removed. Reduced midline shift and mass effect were observed ([Fig. 4]). The patient was observed in the critical care unit for 24 hours. He improved neurologically in the postoperative period and was discharged on fourth day with a GCS score of 15 (E4V5M6) with residual weakness of MRC grade 4 +/5 in the right upper and lower limb, with no other fresh neurological deficit.

Fig. 4 Evacuated left parietal extradural hematoma (EDH).

Discussion

EDH occurs mostly following trauma. EDH has high success rates in terms of quality of life and years preserved[1] when done at the earliest with patients fitting into the surgery criteria. When compared with EDH, patients with SDH have worse prognosis even with advances in modern head trauma management, with mortality rates reaching as high as 60%.[2]

The mechanisms of traumatic EDH and SDH formation are different. EDH occurs in the temporal or temporoparietal region when anterior or posterior divisions of the middle meningeal arteries are damaged. Many times, EDH at the temporal pole occurs due to a rupture of the sphenopalatine vein. The blood in the extradural space starts to strip the dura and after some time produces mass effect and brainstem compression. In case of acute SDH, fracture or underlying damaged brain parenchyma or the bridging vein gets torn and causes SDH. As it increases, it also produces brainstem compression. Nearly half of these patients will have traumatic brain injury in the form of contusions, hematomas, or lacerations.

Many trials have proven beyond doubt that the underlying brain injury determines the outcome of these patients.[3] In our case, the CT at admission showed left burst frontal lobe with acute-on-chronic SDH and left parietal EDH. All these were producing mass effect and midline shift toward the right side with no bone fracture noted.

Intra-Op

A left question mark flap was marked and left-sided large FTP craniotomy was done. After removing the bone flap, on the parietal region, extradural hematoma was seen, which was evacuated. The dura was bluish and tense, and it was opened in the C shape with the sphenoid ridge as the base. On opening the dura, a gush of dark, machine-colored fluid mixed with fresh blood was found. On SDH evacuation, left frontal region contusion with contusion connecting with the SDH was noted, and it was also evacuated. Postevacuation, the brain was lax and pulsatile and no fresh bleed was noted; hence, the bone flap was re-placed. Post-op CT scan showed complete evacuation of SDH and EDH with a small lining of contusion left behind. There was significant reduction of the mass effect and midline shift; no fresh bleed or hematoma was noted. The postoperative period was uneventful with good improvement and weakness improved from 3/5 to 4 +/5 at the time of discharge. He was advised regular physical therapy and counseled for alcohol intake. He came for follow-up after 2 weeks with no residual weakness, and the surgical wound had also healed with an acceptable scar.

Conclusion

Trauma is the leading cause of head injury. We reported this case as it was rare and unique to have contusion, acute-on-chronic SDH, and EDH on the ipsilateral side, and the patient recovered completely without residual weakness and no signs of lobar dysfunction. Timely intervention and adequate care can lead to improvements and sometimes full recovery as seen in our case.

Conflict of Interest

None declared.

• References

• 1 Pickard JD, Bailey S, Sanderson H, Rees M, Garfield JS. Steps towards cost-benefit analysis of regional neurosurgical care. BMJ 1990; 301 (6753) 629-635
• 2 Massaro F, Lanotte M, Faccani G, Triolo C. One hundred and twenty-seven cases of acute subdural haematoma operated on. Correlation between CT scan findings and outcome. Acta Neurochir (Wien) 1996; 138 (02) 185-191
• 3 Kapsalaki EZ, Machinis TG, Robinson III JS, Newman B, Grigorian AA, Fountas KN. Spontaneous resolution of acute cranial subdural hematomas. Clin Neurol Neurosurg 2007; 109 (03) 287-291

Publication History

Article published online:
10 February 2025