Late Onset of Post Traumatic Brain Oedema/A Case Report

Dr. Abdulrahim Zwayed^1*,  Dr. Sreenivas A.V. ², Dr. Balola Miraghani ³, Dr.Ammar Salim Al Zadjali ⁴, Dr.Sultan Rashid Al Matrushi⁵, Dr. Yasser Abdul Raziek ⁶ , Dr Halima Mohammed Al Amri⁷, Dr.Faisal Khalfan Al Balushi ⁸,  Dr.Hetal Chokshi⁹, Dr. Abdulrazak Ahmed¹⁰

1,2,3. Department of Neurosurgery, Sohar Hospital, Sohar, Sultanate of Oman.

4,5 Paediatrics   Intensive care unit, Sohar Hospital, Sohar, Sultanate of Oman.

6,7 Radiology, Sohar Hospital, Sohar, Sultanate of Oman.

8,9,10 Anesthesia, Sohar Hospital, Sohar, Sultanate of Oman.

*Correspondence to: Dr. Abdulrahim-Rahim H. Zwayed (Ph.D.) Department of Neurosurgery, Sohar Hospital, Sohar, Sultanate of Oman.

Copyright

© 2024 Dr. Abdulrahim-Rahim H. Zwayed., This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: 25 March 2024

Published: 03 April 2024

DOI: https://doi.org/10.5281/zenodo.10910840

Introduction

Post traumatic cerebral edema is a multiplex process. Mainly two types of cerebral edema occurred after traumatic brain injury-vasogenic edema and cytotoxic edema.

Management is mainly divided into two part- medical and surgical. Medical management includes management of increased intracranial pressure and later blocking of the pathways involved in the formation and progression of cerebral edema.

In refractory cases, surgical decompression plays a role in controlling the intracranial pressure due to cerebral edema. Here we report a case of   Late onset of post traumatic brain oedema, We discuss the clinical picture, radiological findings and surgical procedure.

Keywords: traumatic brain injury; late onset, Cerebral oedema

The case

This is a 3 years old female involved in road traffic accident with family. She was conscious, alert, active, pupils equally reacting to light. Her first CT on arrival to the emergency unit was un remarkable.

First CT on admission was normal

As a routine work to keep such young patients under observation, On the 3rd day post trauma and after around 70 hours from the accident, the patient developed recurrent attacks of convulsions followed by loss of consciousness, so intubation done and connected to ventilator. The patient also developed un equality of pupils of size and reaction to light, and right sided weakness. A new head CT done which showed massive brain oedema with midline shift of about 6 mm

Fig 1: 2nd Head  CT scan after 72 hours, massive brain oedema &mass effect

Then an urgent operation done as left parietal decompressive craniectomy where removal of the bone done with release of the dura

Fig 2: Left parietal decompressive craniectomy

The bone flap was kept in the anterior abdominal wall for further cranioplasty later on.

The patient was extubated on the 3rd postoperative day and discharged on 10th postoperative day after stiches removal and advice for follow up in the neurosurgical outpatient clinic or consult on need to the emergency unit.

After 8 weeks the patient re- admitted for cranioplasty as replacement of the bone flap to the defect skull region

She stayed in the hospital for about 7 days where stiches removal done and advice for physiotherapy as she has right hemiparesis and follow up

After about 6 months the patient seen in the neurosurgical outpatient clinic and she was active with no neurological deficits 

 Discussion

Post traumatic cerebral edema is a multiplex process(3,5). Mainly two types of cerebral edema occurred after traumatic brain injury-vasogenic edema and cytotoxic edema. Cytotoxic cerebral edema is due to accumulation of water in the intercellular space. Mitochondria mainly cause cytotoxic edema due to the involvement of oxidative metabolism. edema develops due to disruption of blood-brain barrier or altered permeability of blood-brain barrier so correlate with the level of impact and or activation of molecular pathways related with neuroinflammation (1,3,5).

Management is mainly divided into two part- medical and surgical. Medical management (osmotic diuresis or hyperosmolar therapy) is the initial step to control the edema and ICP. (2)

In refractory cases, surgical intervention (decompressive craniectomy) has shown superior control of intra cranial pressure (ICP) includes management of increased intracranial pressure (ICP) and later blocking of the pathways involved in the formation and progression of cerebral edema. In refractory cases, surgical decompression plays a role in controlling the intracranial pressure due to cerebral edema (4,13).

Posttraumatic cerebral edema is a complex process. In 1905, Reichardt coined the word “brain edema” and described the difference from “brain swelling. (7) The incidence is around 60% in trauma-related hematoma or mass lesion and around 15% without mass lesions. (9) Pappius and McCann (11] described cerebral edema as a special condition of the brain with excessive tissue volume due to the increase water content in the brain. The excessive tissue volume leads to increase in intracranial pressure (ICP) and decrease cerebral perfusion pressure (CPP), which eventually increases the mortality after traumatic brain injury (TBI). Cerebral edema is an independent predictor of increased mortality and morbidity after TBI (14). In one study, the presence of cerebral edema was associated with in-hospital mortality rate of 63.8%. In the same study, the cerebral edema itself caused an eight-fold increase in mortality among all severity of TBI and a five-fold increase in mortality in mild TBI group.[6]

In cases of TBI, early removal of contused brain tissue or hematoma reduces cerebral edema as the presence of contusion or hematoma releases various mediators of cerebral edema (7,11,12)

Diverse pathways are involved in the development of cerebral edema after brain injury. Mainly two types cerebral edema occur after TBI-vasogenic edema and cytotoxic edema. Vasogenic edema is the fluid accumulation in interstitial space, and cytotoxic edema is swelling of the cells. Cytotoxic edema occurs due to the involvement of different pathways or ionic channels and correlates with the secondary type of brain injury.[8,10] Vasogenic edema develops due to disruption of the blood-brain barrier (BBB) or altered permeability of BBB and correlates with the level of impact and activation of molecular pathways related with neuroinflammation.

Here in our case report the brain oedema developed after about 70 hours and actually what usually done in pediatric head injury with normal head CT that to discharge the patient after 24 hours and advice for follow up in the neurosurgical outpatient clinic or consult on need to the emergency unit but fortunately, we kept the patient under close observation in spite of unremarkable first head CT, plus in  usual post trauma cases that brain oedema developed in the first few hours of accident and making the patient drowsy or not fully conscious but  development of brain oedema after theses many  hours is something  rare .

Reference

 1/ Aarabi B, Hesdorffer DC, Ahn ES, Aresco C, Scalea TM, Eisenberg HM, et al Outcome following decompressive craniectomy for malignant swelling due to severe head injury J Neurosurg. 2006; 104:469–79.

2/Catrambone JE, He W, Prestigiacomo CJ, McIntosh TK, Carmel PW, Maniker A. The use of hypertonic saline in the treatment of post-traumatic cerebral edema: A review Eur J trauma Emerg Surg. 2008; 34:397–409

3/Chodobski A, Zink BJ, Szmydynger-Chodobska J. Blood-brain barrier pathophysiology in traumatic brain injury Transl Stroke Res. 2011;2:492–516

4/ Hudak AM, Peng L, Marquez de la Plata C, Thottakara J, Moore C, Harper C, et al Cytotoxic and vasogenic cerebral oedema in traumatic brain injury: Assessment with FLAIR and DWI imaging Brain Inj. 2014;28:1602–97.

5/ Iffland PH, Grant GA, Janigro D. Mechanisms of Cerebral Edema Leading to Early Seizures After Traumatic Brain Injury New York: Springer Series in Translational Stroke Research;. 2013

6/ Jha RM, Kochanek Unterberg AW, Stover J, Kress B, Kiening KL. Edema and brain trauma Neuroscience. 2004; 129:1021–9

7/Kochanek PM, Bramlett HM, Dixon CE, Dietrich WD, Mondello S, Wang KKW, et al Operation brain trauma therapy: 2016 Update Mil Med. 2018;183:303–12

8/Liu YL, Yuan F, Yang DX, Xu ZM, Jing Y, Yang GY, et al Adjudin attenuates cerebral edema and improves neurological function in mice with experimental traumatic brain injury J Neurotrauma. 2018;35:2850–60

9/Marmarou A, Barzo P, Fatouros P, Yamamoto T, Bullock R, Young H, et al Traumatic brain swelling in head injured patients: Brain edema or vascular engorgement Acta Neurochir Suppl. 1997;70:68–70

10/Nujaimin U, Saufi A, Rahman AG, Badrisyah I, Sani S, Zamzuri I, et al

 Post traumatic cerebral oedema in severe head injury is related to intracranial pressure and cerebral perfusion pressure but not to cerebral compliance Asian J Surg. 2009;32:157–62

11/Qiu W, Guo C, Shen H, Chen K, Wen L, Huang H, et al Effects of unilateral decompressive craniectomy on patients with unilateral acute post-traumatic brain swelling after severe traumatic brain injury Crit Care. 2009;13:R185

12/Schneider GH, Bardt T, Lanksch WR, Unterberg A. Decompressive craniectomy following traumatic brain injury: ICP, CPP and neurological outcome Acta Neurochir Suppl. 2002;81:77–92.

13/ Tucker B, Aston J, Dines M, Caraman E, Yacyshyn M, McCarthy M, et al Early brain edema is a predictor of in-hospital mortality in traumatic brain injury J Emerg Med. 2017;53:18–29

14/ Winkler EA, Minter D, Yue JK, Manley GT. Cerebral edema in traumatic brain injury: Pathophysiology and prospective therapeutic targets Neurosurg Clin N Am. 2016;27:473–88.