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Table of Contents
CASE REPORT
Year : 2019  |  Volume : 16  |  Issue : 4  |  Page : 244-246

Pericontusional penumbra in patients with traumatic brain injury


1 Department of Neurosurgery, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
2 Department of Anesthesia, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
3 Neurosurgery-Critical Care, RED LATINO, Organizacion Latinoamericana de Trauma y Cuidado Neurointensivo, Bogota, Colombia

Date of Submission10-May-2019
Date of Acceptance30-Oct-2019
Date of Web Publication12-Dec-2019

Correspondence Address:
Amit Agrawal
Department of Neurosurgery, Narayana Medical College Hospital, Chinthareddypalem, Nellore - 524 003, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/am.am_23_19

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  Abstract 


Recently, a number of studies have recognized the importance of traumatic pericontusional penumbra as a potential target for therapeutic interventions to prevent the secondary brain damage. We report an illustrative case of a 40-year-old female patient who was brought to the emergency room with the alleged history of fall from the bike. Computed tomography scan brain showed left sylvian and left temporoparietal subarachnoid hemorrhage, patchy contusion of the left frontal and temporal lobes, linear fracture of the right temporal bone with edema, mass effect, and mild midline shift. After 6 h of intensive care unit stay, the patient developed pupillary asymmetry and a repeat scan showed significant increase in the size of cerebral contusions with gross pericontusional edema, mass effect, and midline shift. The patient underwent urgent left frontotemporoparietal craniotomy and evacuation of the contused brain and hematoma. Pericontusional penumbra is increasingly recognized and strategies are being suggested to salvage the apparently hypoxic (not yet ischemic) brain to preserve the neurological functions and to improve functional outcome. In future, we need more studies to support the concept of pericontusional penumbra and further characterize the imaging findings for early clinical diagnosis and to plan early appropriate intervention.

Keywords: Cerebral contusion, penumbra, secondary brain injury, traumatic brain injury


How to cite this article:
Agrawal A, Kumar V A, Moscote-Salazar LR, Kiran Kumar V A. Pericontusional penumbra in patients with traumatic brain injury. Apollo Med 2019;16:244-6

How to cite this URL:
Agrawal A, Kumar V A, Moscote-Salazar LR, Kiran Kumar V A. Pericontusional penumbra in patients with traumatic brain injury. Apollo Med [serial online] 2019 [cited 2020 Apr 8];16:244-6. Available from: http://www.apollomedicine.org/text.asp?2019/16/4/244/272818




  Introduction Top


In patients with severe traumatic brain injury, raised intracranial pressure and cerebral ischemia is a major concern as it can lead to cerebral hypoperfusion and secondary brain injury followed by poorer irreversible neuronal damage and poorer outcome.[1],[2],[3],[4] Recently, a number of studies have recognized the importance of traumatic pericontusional penumbra as a potential target for therapeutic interventions to prevent the secondary brain damage.[4],[5] The concept of traumatic pericontusional penumbra explores the fact that the regions surrounding the contused brain can be hypoxic, but not ischemic at least in the initial phases.


  Case Report Top


A 40-year-old female patient was brought to the emergency room with the alleged history of fall from the bike (the patient was pillion rider) about 6 h of the incident. She was unconscious since the time of accident, had multiple episodes of vomiting, and right ear and nasal bleed. There was no history of seizures. On examination, her pulse rate was 116 beats/min and blood pressure was 130/80 mmHg. Her Glasgow Coma Score (GCS) was E2V2M5. Her pupils were bilateral 2 mm and reacting to light. In view of low GCS, the patient was intubated and kept on elective ventilation. After stabilizing her general condition, she was shifted for an urgent computed tomography (CT) scan of the brain. CT scan brain showed left sylvian and left temporoparietal subarachnoid hemorrhage, patchy contusion of the left frontal and temporal lobes, linear fracture of the right temporal bone with edema, mass effect, and mild midline shift [Figure 1]a, [Figure 1]b, [Figure 1]c. Blood investigation showed hemoglobin 8.8 g/dl and random blood glucose 189 mg/dl. Other blood investigations including coagulation profile were within normal range. The patient was planned for conservative treatment and kept in neurocritical unit for close monitoring. She was started on antiedema measures and antiepileptics. After 6 h of intensive care unit stay, the patient developed pupillary asymmetry (right pupil 2 mm reacting to light and left 4 mm sluggishly reacting to light). The patient was shifted for an urgent repeat CT scan of the brain. Repeat scan showed significant increase in the size of cerebral contusions with gross pericontusional edema, mass effect, and midline shift [Figure 1]d, [Figure 1]e, [Figure 1]f. The patient underwent urgent left frontotemporoparietal craniotomy and evacuation of the contused brain and hematoma. Following surgery, the brain was lax and pulsatile. The dura could be closed primarily and bone flap could be replaced. The patient was electively ventilated and continued with antiedema measures and antiepileptics. Pupillary asymmetry resolved in immediate postoperative period. Postoperative CT scan of the brain showed good evacuation of the contusion and resolution of mass effect and midline shift [Figure 1]g, [Figure 1]h, [Figure 1]i. As it was anticipated that the patient will need prolonged ventilation, she underwent tracheostomy. The patient was making a gradual recovery; however, on 5th postoperative day, she was dull and drowsy. A follow-up CT scan showed increase in cerebral edema with mass effect. To relieve the mass effect, the bone flap was removed and a lax duraplasty was performed. The patient made gradual recovery in her sensorium and could be weaned off from the ventilator and from tracheostomy.
Figure 1: (a-c) Initial computed tomography scan showing subarachnoid hemorrhage in left sylvian fissure with patchy contusion involving left frontal and temporal lobe with mild mass effect and obliteration of the basal cisterns, (d-f) follow-up computed tomography scan showing significant enlargement of frontal and temporal contusion with pericontusional edema, significant mass effect, and midline shift and (g-i) postoperative computed tomography scan showing reduction in the size of the cerebral contusions and pericontusional edema, basal cisterns opened up, ventricles are symmetrically visible, please note the increased area of normally appearing brain between frontal and temporal contusions

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  Discussion Top


It has been found that following primary brain injury, the brain lesions may progressively expand centrifugally, leading to progressive necrosis which can increase by 130-400% of the primary lesions.[6] This led to the concept of traumatic pericontusional penumbra in literature and it has been suggested that this penumbra contain potentially salvageable neural tissue.[7],[8],[9] Ischemia in the pericontusional region can lead to neuronal damage by various mechanisms including oxidative stress, neuronal, mitochondrial dysfunction, excitotoxicity, and neuronal inflammation.[10],[11],[12],[13] The formation and expansion of pericontusional penumbra can be followed by impairment of blood flow to the area, edema, compromised metabolism, and neurological deterioration, and if left untreated, permanent neurological dysfunction persists.[4],[9],[13],[14] CT scan is widely available modality of investigation to follow the progression or resolution of traumatic intracranial mass lesions. The role of advanced MR imaging, i.e., diffusion tensor imaging and positron emission tomography, has been explored to further characterize and understand the pathophysiology pericontusional penumbra.[5] On diffusion tensor imaging, these lesions are characterized by a core area with raised ADC values (suggests vasogenic edema) and surrounding thin hypointense rim with decreased ADC values (suggests cytotoxic edema).[4]


  Conclusion Top


Pericontusional penumbra is increasingly recognized and strategies are being suggested to salvage the apparently hypoxic (not yes ischemic) brain to preserve the neurological functions and to improve functional outcome. In future, we need more studies to support the concept of pericontusional penumbra and further characterize the imaging findings for early clinical diagnosis and to plan early appropriate intervention.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Vespa PM. Brain hypoxia and ischemia after traumatic brain injury: Is oxygen the right metabolic target? JAMA Neurol 2016;73:504-5.  Back to cited text no. 1
    
2.
McLaughlin MR, Marion DW. Cerebral blood flow and vasoresponsivity within and around cerebral contusions. J Neurosurg 1996;85:871-6.  Back to cited text no. 2
    
3.
Schröder ML, Muizelaar JP, Bullock MR, Salvant JB, Povlishock JT. Focal ischemia due to traumatic contusions documented by stable xenon-CT and ultrastructural studies. J Neurosurg 1995;82:966-71.  Back to cited text no. 3
    
4.
Newcombe VF, Williams GB, Outtrim JG, Chatfield D, Gulia Abate M, Geeraerts T, et al. Microstructural basis of contusion expansion in traumatic brain injury: Insights from diffusion tensor imaging. J Cereb Blood Flow Metab 2013;33:855-62.  Back to cited text no. 4
    
5.
Wang K, Liu B, Ma J. Research progress in traumatic brain penumbra. Chin Med J (Engl) 2014;127:1964-8.  Back to cited text no. 5
    
6.
Stoffel M, Rinecker M, Graf R, Baethmann A, Plesnila N. Nitric oxide in the penumbra of a focal cortical necrosis in rats. Neurosci Lett 2002;324:201-4.  Back to cited text no. 6
    
7.
Harish G, Mahadevan A, Pruthi N, Sreenivasamurthy SK, Puttamallesh VN, Keshava Prasad TS, et al. Characterization of traumatic brain injury in human brains reveals distinct cellular and molecular changes in contusion and pericontusion. J Neurochem 2015;134:156-72.  Back to cited text no. 7
    
8.
Stoffel M, Eriskat J, Plesnila M, Aggarwal N, Baethmann A. The penumbra zone of a traumatic cortical lesion: A microdialysis study of excitatory amino acid release. Acta Neurochir Suppl 1997;70:91-3.  Back to cited text no. 8
    
9.
Wu HM, Huang SC, Vespa P, Hovda DA, Bergsneider M. Redefining the pericontusional penumbra following traumatic brain injury: Evidence of deteriorating metabolic derangements based on positron emission tomography. J Neurotrauma 2013;30:352-60.  Back to cited text no. 9
    
10.
Regner A, da Silva Meirelles L, Simon D. Traumatic Penumbra: Opportunities for neuroprotective and neurorestorative processes. Traumatic Brain Injury-Pathobiology, Advanced Diagnostics and Acute Management. Rijeka: IntechOpen; 2017.  Back to cited text no. 10
    
11.
Ding K, Wang H, Wu Y, Zhang L, Xu J, Li T, et al. Rapamycin protects against apoptotic neuronal death and improves neurologic function after traumatic brain injury in mice via modulation of the mTOR-p53-bax axis. J Surg Res 2015;194:239-47.  Back to cited text no. 11
    
12.
Rosenfeld JV, Maas AI, Bragge P, Morganti-Kossmann MC, Manley GT, Gruen RL. Early management of severe traumatic brain injury. Lancet 2012;380:1088-98.  Back to cited text no. 12
    
13.
Sheriff FG, Hinson HE. Pathophysiology and clinical management of moderate and severe traumatic brain injury in the ICU. Semin Neurol 2015;35:42-9.  Back to cited text no. 13
    
14.
Sun GZ, Gao FF, Zhao ZM, Sun H, Xu W, Wu LW, et al. Endoplasmic reticulum stress-induced apoptosis in the penumbra aggravates secondary damage in rats with traumatic brain injury. Neural Regen Res 2016;11:1260-6.  Back to cited text no. 14
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