Translational Surgery

ORIGINAL ARTICLE
Year
: 2017  |  Volume : 2  |  Issue : 4  |  Page : 81--84

Large decompressive craniectomy combined with vascular reconstruction in patients with severe craniocerebral injury


Xipeng Wang1, Feng Ruan2, Ping Liu2,  
1 Department of Orthopaedic Surgery, Hospital of Kanazawa Medical University, 1-1 Daigaku, Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan
2 Department of Orthopaedic Surgery, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei, China

Correspondence Address:
Ping Liu
Department of Orthopaedic Surgery, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430077, Hubei
China

Abstract

Aim: This study aims to compare the effect of large decompressive craniectomy combined with vascular reconstruction and traditional decompressive craniectomy in the treatment of severe craniocerebral injury. Methods: Forty-eight cases of severe craniocerebral injury were collected from March 2012 to March 2015 in Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology. Patients undergoing large decompressive craniectomy combined with vascular reconstruction or traditional decompressive craniectomy were randomly divided into two groups: the experimental group and the control group. The hemodynamic changes were observed by computed tomography perfusion, and the postoperative Glasgow Outcome Score (GOS) was analyzed. Results: The cerebral blood flow (CBF) and cerebral blood volume (CBV) scores in experimental group were higher than that in the control group at 1 week and 1 month after the operation (P < 0.05). The mean transit time (MTT) and time to peak (TTP) scores in experimental group were lower than that in the control group at 1 week and 1 month after the operation (P < 0.05). The relative CBF and relative CBV values of the control group in 1 week were higher than that in 1 month, while the relative MTT and relative TTP values in 1 week were lower than that in 1 month. The rate of good recovery (including good and residual cases) in experimental group was higher than that in the control group whereas the rate of poor recovery (including severe disability, vegetative state, and death) in experimental group was lower than that in the control group (P < 0.05). Conclusion: The large decompressive craniectomy combined with vascular reconstruction can not only decrease intracranial pressure but also recover the blood supply of the brain. It deserves the clinical promotion.



How to cite this article:
Wang X, Ruan F, Liu P. Large decompressive craniectomy combined with vascular reconstruction in patients with severe craniocerebral injury.Transl Surg 2017;2:81-84


How to cite this URL:
Wang X, Ruan F, Liu P. Large decompressive craniectomy combined with vascular reconstruction in patients with severe craniocerebral injury. Transl Surg [serial online] 2017 [cited 2018 Aug 18 ];2:81-84
Available from: http://www.translsurg.com/text.asp?2017/2/4/81/221877


Full Text

 Introduction



Severe craniocerebral injury carries high mortality and morbidity. The literature-reported fatality rate was about 35%.[1] In patients with severe frontal–temporal lobe brain contusion complicated by intracranial hematoma, cerebral edema, cerebral infarction, and cerebral hernia, the prognosis is poor.[2],[3] The present treatment utilizes the emergency standard big bone flap decompression and removal of intracranial hematoma.[4] However, due to brain damage, small blood vessels and normal blood circulation and blood-brain barrier are destroyed which needs time to establish a new blood supply. Postoperative use of vasodilators to remove blood stasis treatment is less effective, and the utility of simple bone disc decompression surgery for local blood circulation obstacle is not obvious. Cerebral revascularization for the treatment of cerebral ischemic diseases using the middle meningeal artery and the temporal artery as a blood donor improves the ischemic symptoms of Moyamoya disease.[5],[6] This study used bone disc decompression with indirect blood vessel revascularization therapy in patients with frontal–temporal lobe brain contusion of severe head injury. As postoperative analyses, computed tomography perfusion (CTP) imaging was used to evaluate the cerebral hemodynamic changes, and the Glasgow Outcome Scale (GOS) was used 6 months after surgery to assess the outcome of patients with severe craniocerebral injury who received the clinical treatment.[7]

 Methods



Clinical data

Forty-eight patients were admitted in Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology from March 2012 to March 2015 with frontal–temporal lobe brain contusion were enrolled in the study, and among which 23 cases were male and 25 were female with an age range of 52–75 years (average: 59.3 years) and a GCS score of 3–8 points. The etiology of the injury was the following: traffic injury in 25 cases, fall in 13 cases, mixed injury in 8 cases, and other injury in 2 cases [Table 1]. All patients had indications for craniotomy decompression surgery. According to admission time sorting by odd or even, the patients were divided into control group (standard big bone flap decompression) and experimental group (big bone flap decompression with dura mater blood vessel revascularization), with 24 cases in each group. Inclusion criteria for entry into the study were the following: (1) Clear history of trauma, with priority to severe head injury involving the frontal–temporal lobe brain; (2) clinical manifestations of coma, hemiplegia, aphasia, limb paralysis, or vital sign change; (3) dilated pupil or pupils; (4) CT examination showed supratentorial lesions, one side of the frontal–temporal lobe brain contusion, and subdural hematoma; (5) hematoma >60 mL, ventricle narrowed or closed, midline structure shift >5 mm; and (6) patients' age of 18–68 years. Exclusion criteria were: (1) Primary brain stem injury, uncontrolled hemorrhagic shock, respiratory system failure, or abnormal blood coagulation function; (2) the suspicion of cerebrovascular diseases such as hypertension and frequent headaches; (3) and a brain tumor.{Table 1}

Surgical method

In the control group, traditional standard big bone flap decompression surgery were employed. Following steps were taken: A frontotemporal large arc incision was started near the center line, 2-3 cm within the hairline, parallel to the superior sagittal sinus, and was extended backward to the top nodules. Then it was curved downward to the temple, straight down to the ear, ended in the front of the tragus 1 cm to the zygomatic arch. The scalp incision was made to the skull with the formation of a myocutaneous flap. It was turned forward and downward (namely the frontotemporal), exposing the skull of frontotemporal area. About 5–6 burr holes were made, and craniotomy was performed with the bone saw and rongeurs creating a defect of about 12 cm × 14 cm, including the frontal and temporal bone scales and parietal large free bone flap. Epidural and subdural hematoma, necrotic tissue because of brain contusion were then removed. The dura mater was suspended, and an indwelling drainage tube was placed. After that a bonnet aponeurosis layer and scalp were closed.

In the experimental group, the procedure was basically the same as in control group, but care was taken to avoid damage to the temporal artery when the scalp incision was made. When the temporalis was stripped, care was also taken to retain the full deep temporal artery network, and a free bone flap including the preserved middle meningeal artery was made. The removal of subdural hematoma and necrotic of the brain tissue was then undertaken. The trunk and main branches of middle meningeal artery were cut open on both sides of the dura mater, with a width of 0.5–1.0 cm. The remaining parts of the dura mater were incised in a radial fashion. Then the temporalis muscle on the side of the head, through the opening in the skull, is placed onto the surface of the brain. Or the STA-MCA (superficial temporal artery to middle cerebral artery) bypass was done. The bone flap was removed, with an epidural drainage tube placed. Then bonnet aponeurosis layers and scalp were closed.

Evaluation index

On the seventh day and thirtieth day after surgery, we used a Philips Light Speed 256 CTP CT scanner to evaluate the patients. We used VPCT Neuro analysis software to get the value of cerebral blood flow (CBF), cerebral blood volume (CBV), mean through time, transit time (MTT), and time to peak (TTP) figure of perfusion parameters. We chose the frontal–temporal lobe brain contusion as the most serious part of the area (region of interest [ROI]), and the system automatically selected the contralateral mirror ROIs, perfusion parameters of each ROI, namely, CBF, CBV, MTT, and TTP values. As each patient, the ROI parameter of with average absolute CBF, CBV, MTT and TTP values, with operation side and the ratio of the contralateral to calculate the relative perfusion parameters, namely, relative CBF (rCBF) and relative CBV (rCBV), relative MTT (rMTT), and relative TTP (rTTP). We compared the two groups of operation parameters as to absolute value, the evaluation of the treatment group and control group in postoperative 1 week and 1 month after the differences in blood perfusion; 6 months after surgery, the two groups of patients were compared using the GOS score.

Statistical analysis

Statistical analysis was performed by SPSS software version 20.0 (Made in Netherlands), measurement data to x_ ± s, it is compared between group by t-test, expressed as a percentage of count data. Chi-square test was used to compare the groups. P < 0.05 was considered statistically significant.

 Results



In the experimental group, the 1 week and 1 month postoperative CBF and CBV values were significantly higher than that of the control group. The MTT and TTP values were significantly lower than that of the control group. The difference was statistically significant (P < 0.05). In the experimental group, the 1 week and 1 month CBF and CBV values, MTT, and TTP differences had no statistical significance (P > 0.05), and the control group 1 month CBF, CBV below the level 1 week, determined by MTT, TTP is higher than 1 week (P < 0.05); experimental postoperative week and 1 month of rCBF, rCBV, rMTT, rTTP comparison difference has no statistical significance (P > 0.05), and compared with postoperative 1 week, while the control group after 1 month of rCBF, significantly lower rCBV, rMTT, rTTP increased significantly, the difference was statistically significant (P < 0.05), the experimental group 1 week and 1 month rCBF, rCBV, rMTT, rTTP differences had no statistical significance (P > 0.05), control group 1 month rCBF and rCBV below the level 1 week, rMTT, rTTP above 1 week (P < 0.05,) [Table 2].{Table 2}

At 6 months after surgery, according to GOS score in the experimental group, 17 cases did well, 3 cases were of residue, heavy residue, and vegetative state, and one case died. In the control group, 9 cases did well, 4 cases were of residue, 5 cases were of heavy residue, 4 cases were of vegetative state, and 2 cases died. The experimental group had a good recovery (including the good and the residue) in a total of 20 cases and was higher than that of control group (13 cases). The proportion of the difference was statistically signifcant (Chi-square = 2.11, P < 0.05), and poor recovery (including heavy residue, vegetative state, death) the proportion of lower is than the control group (11 cases). It was difference of statistically signifcant (Chi-square = 2.40, P < 0.05).

 Discussion



Severe craniocerebral injury condition is complex, often complicated by traumatic cerebral edema and cerebral infarction.[8] Traumatic brain edema and cerebral infarction are often associated with the following: brain tissue, vascular damage, cause vascular intima damage or bleeding and formation of vascular thrombosis or occlusion; It was cerebral vasospasm after subarachnoid hemorrhage and cerebral vasospasm. It is able to lead to cerebral infarction and cerebral vasospasm after a head injury, and also it can produce similar results. For 9-11 Due to brain injury, edema and swelling of the brain tissue displacement. It caused vascular displacement and pressure and weave and twist and blood retention.[12] Traumatic brain edema and posttraumatic cerebral infarction can lead to increased intracranial pressure and brain shift, and cerebral hernia is one of the leading causes of death and disability. In the late 1980s, some scholars advocated big bone flap using standard craniotomy treatment of severe head injury, and this has a wide clinical application.[13] A large number of studies [14],[15],[16] have shown that the traditional standard big bone flap decompression can significantly reduce the intracranial pressure, but the brain–blood supply reconstruction effect is still poor. This research adopted the standard big bone flap decompression with cerebral dura mater-muscle blood vessel revascularization therapy in severe craniocerebral injury to improve the blood supply of brain tissue in patients with intracranial pressure.

The study found that the experimental group at postoperative 1 week and 1 month after the CBF, CBV is significantly higher than the control group, determined by MTT, TTP, significantly lower than the control group. Compared with conventional surgery, this research adopted the joint operation of the dura mater with blood vessels and blood vessels of the temporal muscle directly applied on the surface of the brain that is damaged. The temporal muscle, blood vessels dura mater of blood vessels and blood vessels on the surface of the brain were using the proliferation of capillary directly improve the damaged parts of the brain blood circulation. Them can be able effective to reduce intracranial pressure restore damaged parts on the basis of the blood supply of brain tissue and led to the greatest extent of brain tissue rehabilitation.[17],[18] Group of postoperative 1 week and 1 month after rCBF and rCBV there were no statistically signifcant difference. The rMTT, rTTP comparison, and the control group at postoperative 1 week of rCBF, rCBV values are higher than 1 months postoperatively which is rMTT, rTTP <1 months after surgery.[19] This is mainly due to the high degree of microvascular occlusion in the control group, with microcirculation dysfunction over time, increased risk of cerebral infarction, and the experimental group to rebuild blood supply after brain organization microcirculation change smaller.[20] Good recovery in the experimental group (including the strong and the residual) was higher than that of control group. The proportion of the poor recovery (including heavy residue, vegetative state, and death) was lower than the control group, which further confirmed that the clinical effect of combined operation is superior to the traditional standard operation. The joint procedure reduces the intracranial pressure to improve the brain contusion ischemia oxygen deficit, reduces brain edema, reduces the incidence of cerebral infarction, restores brain function to get the maximum prognosis, and improves the quality of life of patients.[21]

In conclusion, the standard big bone flap decompression joint cerebral dura mater-muscle blood vessel revascularization in reducing severe craniocerebral injury in patients with intracranial pressure can effectively improve the flow of blood to the damaged brain tissue. At the same time, the curative effect is distinct with a high degree of brain functional recovery, good prognosis, and is worth of clinical application and promotion.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Nemetz PN, Leibson C, Naessens JM, Beard M, Kokmen E, Annegers JF, Kurland LT. Traumatic brain injury and time to onset of Alzheimer's disease: A population-based study. Am J Epidemiol 1999;149 (1):32-40.
2Magone MT, Kwon E, Shin SY. Chronic visual dysfunction after blast-induced mild traumatic brain injury. J Rehabil Res Dev 2014;51 (1):71-80.
3Asha'Ari ZA, Ahmad R, Rahman J, Kamarudin N, Ishlah LW. Contrecoup injury in patients with traumatic temporal bone fracture. J Laryngol Otol 2011;125 (8):781-5.
4Bian AM. Experience of decompressive craniectomy. Pract J Cardiac Cereb Pneumal Vasc Dis 2003;11 (5):319-20.
5Neuss M, Kaneko H, Tambor G, Hoelschermann F, Butter C. Fatal thrombotic occlusion of left main trunk due to huge thrombus on prosthetic aortic valve after transcatheter aortic valve replacement. JACC Cardiovasc Interv 2016;9 (21):2257-8.
6Croce AC, Ferrigno A, Bertone V, Piccolini VM, Berardo C, Di Pasqua LG, Rizzo V, Bottiroli G, Vairetti M. Fatty liver oxidative events monitored by autofluorescence optical diagnosis: Comparison between subnormothermic machine perfusion and conventional cold storage preservation. Hepatol Res 2016. Doi: 10.1111/hepr. 12779.
7Kilbaugh TJ, Karlsson M, Byro M, Bebee A, Ralston J, Sullivan S, Duhaime AC, Hansson MJ, Elmér E, Margulies SS. Mitochondrial bioenergetic alterations after focal traumatic brain injury in the immature brain. Exp Neurol 2015;271:136-44.
8Mioni G, Rendell PG, Terrett G, Stablum F. Prospective memory performance in traumatic brain injury patients: A study of implementation intentions. J Int Neuropsychol Soc 2015;21 (4):305-13.
9Daradkeh G, Essa MM, Al-Adawi SS, Subash S, Mahmood L, Kumar PR. Nutritional status, assessment, requirements and adequacy of traumatic brain injury patients. Pak J Biol Sci 2014;17 (10):1089-97.
10Lequerica A, Jasey N, Portelli Tremont JN, Chiaravalloti ND. Pilot study on the effect of ramelteon on sleep disturbance after traumatic brain injury (TBI): Preliminary evidence from a clinical trial. Arch Phys Med Rehabil 2015;96 (10):1802-9.
11Yang J, Korley FK, Dai M, Everett AD. Serum neurogranin measurement as a biomarker of acute traumatic brain injury. Clin Biochem 2015;48 (13-14):843-8.
12Sakowitz OW, Harting I, Kohlhof P, Unterberg AW, Steiner HH. Acute haemorrhage into a microcystic meningioma leading to cerebral herniation. Br J Neurosurg 2005;19 (3):260-4.
13Jiang JR. Introduction of a US clinical commonly used standard large trauma craniotomy. Chin J Neurosurg 1998;14 (6):58.
14Bowers CA, Riva-Cambrin J, Hertzler DA 2nd, Walker ML. Risk factors and rates of bone flap resorption in pediatric patients after decompressive craniectomy for traumatic brain injury. J Neurosurg Pediatr 2013;11 (5):526-32.
15Sadowski C, Lübbeke A, Saudan M, Riand N, Stern R, Hoffmeyer P. Treatment of reverse oblique and transverse intertrochanteric fractures with use of an intramedullary nail or a 95 degrees screw-plate: A prospective, randomized study. J Bone Joint Surg Am 2002;84-A (3):372-81.
16Jasielski P, Glowacki M, Czernicki Z. Decompressive craniectomy in trauma: When to perform, what can be achieved. Acta Neurochir Suppl 2013;118:125-8.
17Ho KM, Honeybul S, Yip CB, Silbert BI. Prognostic significance of blood-brain barrier disruption in patients with severe nonpenetrating traumatic brain injury requiring decompressive craniectomy. J Neurosurg 2014;121 (3):674-9.
18Grigoriadis NG, Grigoriadis IG, Markoula S, Paschopoulos M, Zikopoulos K, Apostolakopoulos PG, Vizirianakis IS, Georgiou I. Pharmacological preconditioning for short-term ex vivo expansion of human umbilical cord blood hematopoietic stem cells by filgrastim. Am J Stem Cells 2016;5 (1):29-38.
19Mohamadnejad M, Vosough M, Moossavi S, Nikfam S, Mardpour S, Akhlaghpoor S, Ashrafi M, Azimian V, Jarughi N, Hosseini SE, Moeininia F, Bagheri M, Sharafkhah M, Aghdami N, Malekzadeh R, Baharvand H. Intraportal infusion of bone marrow mononuclear or CD133+cells in patients with decompensated cirrhosis: A double-blind randomized controlled trial. Stem Cells Transl Med 2016;5 (1):87-94.
20Krahulik D, Aleksijevic D, Smolka V, Klaskova E, Venhacova P, Vaverka M, Mihal V, Zapletalova J. Prospective study of hypothalamo-hypophyseal dysfunction in children and adolescents following traumatic brain injury. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2016. Doi: 10.5507/bp. 2016.047.
21Oshorov AV, Popugaev KA, Savin IA, Potapov AA. Russian. Simultaneous measurement of intraventricular and parenchymal intracranial pressure in patients with severe trauma brain injury. Anesteziol Reanimatol 2016;61 (1):37-9.