Keywords
traumatic brain injury) - brain CT perfusion - cerebral perfusion - decompressive
surgery - Glasgow Outcome Scale-extended (GOS-E)
Introduction
Traumatic brain injury (TBI) is the leading cause of death and disability worldwide.[1] It is the leading cause of incapacitation in young people around the world, particularly
those under the age of 40.[2] In poor- and middle-income nations like India, the burden is borne by more than
90% of the population, especially the younger and more productive generations, with
significant financial ramifications.[3] Traffic-related accidents account for between 45 and 60% of brain injuries in India,
followed by falls (20–30%) with violence accounting for another 10 to 20%, depending
on the research.[4]
Because of the risk of cerebral edema and intracranial hypertension (IH) that TBI
patients face, treating them is a huge problem. A mass effect from cerebral hematomas,
concussions, diffuse brain edema, or hydrocephalus can raise intracranial pressure
(ICP) following TBI. By decreasing cerebral perfusion pressure, IH can cause brain
ischemia.[5] A higher mortality rate following TBI is linked to IH.[6] In TBI patients, refractory ICP due to post-traumatic brain edema is a critical
prognostic factor.[7] The first 48 hours of a patient's stay in the hospital are the most resource-intensive
and also the most dangerous.[8] To avoid serious morbidity, it is critical to decrease ICP as soon as possible.[9] More than half of all patients who die after a TBI do so due to high ICP.[10]
Some patients' ICP will continue to rise despite the best medical therapy, according
to the Monroe-Kelly doctrine.[9] Patients with increasing ICP fall into one of two categories from a surgical perspective:
those for whom maximal medical therapy is no longer effective, and those for whom
medical therapy must be supplemented with decompressive surgery. Early decisions should
be based on frequent and close clinical reassessment and repeat neuroimaging.
The cranial decompression is a way to transform fixed volume and limited reserve cranium
into an open system that can accommodate additional mass.[11] Most people agree that a decompressive craniectomy (DC) does not undo the effects
of a primary brain injury.[12] TBI patients' ICP has been demonstrated to decrease when DC is administered.[13]
It is widely accepted that the opening of the dura is essential. Dura excision and
duroplasty are time-consuming procedures that may have an adverse effect on the result
in critically ill patients.[14]
Therefore, to decrease ICP, decompressive surgery may be in form of like DC with duraplasty
(type I), DC without duraplasty (type II), DC with duraplasty (type III), and decompressive
craniectomy without duraplasty (type IV).
Due to cerebral edema, decreased cerebral blood flow (CBF), and metabolic dysfunction,
decompressive surgery for TBI has been associated with poor clinical results.[15] Patients having decompressive surgery have altered patterns of global and regional
CBF, but these changes are not clearly defined.[16] There is a paucity of information on the effects of decompressive surgery on microvascular
cerebral perfusion.[17] As a result of decompression surgery, further information is needed on the alterations
in cerebral hemodynamics.
Brain noncontrast computed tomography (NCCT) is the gold standard diagnostic technique
for TBI. NCCT may underestimate the magnitude of the lesion and provide little information
on secondary ischemia damage.[18] Several modalities, including single-photon emission computed tomography (SPECT),
positron emission tomography (PET), brain CT perfusion (CTP), and Xenon perfusion,
have been employed over the years to provide information about TBI patients' injuries
and prognosis.[19] CTP can be added to NCCT brain as an immediate and concurrent procedure, making
it an excellent option for TBI patients.[20] There is no doubt that CTP provides timely data on cerebral perfusion. CTP may be
useful in predicting long-term results in patients with severe TBI.[18]
A reference artery and venous region, as well as each scan pixel, are given time versus
contrast concentration curves.[21] Color-coded maps and quantification of perfusion parameters such as CBF, cerebral
blood volume (CBV), time to peak (TTP), and mean transit time (MTT) can be generated
after data processing.[22] CBV/MTT is used to compute the CBF for each location. When calculating CBF, milliliters
per 100 grams of tissue per minute is used. To find the CBV, divide the parenchymal
pixel's area under the curve by the venous pixel's area under the curve. CBV is expressed
as milliliters per 100 grams of tissue. Using the time concentration curve for each
voxel and the arterial reference region, MTT is a measure of how long it takes blood
to travel across the capillary network on average. Seconds are used to measure MTT.[21] When performing a perfusion study, the MTT, CBV, and CBF measurements for various
brain regions can be used to identify areas of ischemia and aberrant perfusion using
the CTP.
IH has been linked to decreased CBF in patients with severe TBI. Loss of cerebral
autoregulation and abnormalities in CPP were shown to be associated with abnormalities
on the CTP.[23] Mild and severe TBI patients' functional prognosis can be predicted using CTP.[18]
[24]
Hemodynamic alterations in the acute phases of head TBI are well-known. CTP can aid
in the clarification of these changes and the determination of whether or not they
have any predictive value for patients with TBI. Reduced CBF and CBV upon admission
have been demonstrated in previous research to be predictive of outcome in severe
brain injury when compared to the Glasgow Outcome Scale (GOS) at 3 months.[25]
CTP's usefulness in the treatment of TBI is still being investigated. Comparative
research of CTP in the various modalities of cranial decompression has not yet been
reported to our knowledge. Patients with TBI who underwent decompression surgery were
studied using pre- and postoperative CTP.
It was our intention to see if using CTP to the decompressive surgery of TBI patients
could turn it into something more than just an academic exercise. CTP scanning may
also be useful in the management of TBI patients with respect to various decompressive
surgical techniques.
Our study's goal is to compare CTP with various decompressive surgery procedures for
TBI.
Materials and Methods
Study Design
An independent, prospective cohort study was conducted at Sawai Man Singh Medical
College Jaipur and received ethics permission from the Ethics Committee (227/MC/EC/2021).
The study was conducted between 2019 and 2021. The patient was enrolled in the study
after receiving informed written agreement from a close relative or attendant.
Patients' Inclusion Criteria
All patients with head injuries who were scheduled to undergo decompressive surgery,
were included in this study.
Patients' Exclusion Criteria
Pregnancy, a history of craniotomy or any serious chronic illness, respiratory or
circulatory failures, any extracranial injury that could affect the outcome, diffuse
axonal injury without the presence of intracranial hematoma, the absence of brain
stem reflexes, hemodynamically instable, and any known contraindication to CT contrast
agents (such as an allergy or anaphylactic reaction) were all considered exclusion
criteria for this study.
Surgical Procedures
Based on the patient's clinical condition, radiographic evidence of midline shift
on CT scan and/or increased ICP, and signs or symptoms of a refractory IH despite
acceptable medical therapy, surgeons decided to proceed with decompressive surgery.
Type of the decompressive surgery was decided on the basis of intraoperative findings.
Postoperative patients were managed in the neurosurgical intensive care unit.
Radiological Evaluation
To carry out the CTP, a written informed permission was obtained following the decision
to proceed with decompressive surgery. CTP imaging was conducted before surgery and
5 days (to evaluate the impact of cranial decompression on brain perfusion) after
decompressive surgery to assess cerebral perfusion ([Fig. 1]).
Fig. 1 Upper part of figure is preoperative computed tomography perfusion (CTP) and lower
part of figure is postoperative day 5 CTP photo.
The CT scanner used was the Philips Ingenuity 128 slice CT scanner. NCCT brain was
performed on all patients at 120 kV, 300 mA, and 5 mm per layer with a 5 mm layer
gap as a baseline. A 30 mm section of brain parenchyma was sampled for the purpose
of performing brain CTP on a specific area of interest. It was done at a voltage of
120 kV, an amperage according to body to body's weight and 1.25 mm thickness per slice.
Injection of a nonionic contrast medium (iohexol 755 mg/mL, equivalent to 350 mg/L
of iodine) was performed with a high-pressure syringe through the cubital vein (18G
IV cannula) at a flow rate of 4.0 mL/s and dose of 100 mL using a power injector before
the scan began. A saline flush (total 30 mL) was then performed at a rate of 3.0 mL/sec.
After performing CTP, perfusion software was used to produce parametric maps from
CTP raw data on a workstation. To record CBF, CBV, MTT, and TTP parameters, each region
of interest (ROI) was inserted in the perilesional brain parenchymal area close to
a contusion, subdural hemorrhage (SDH), or ICH or potential surgical side.
Postoperative CTP was done using the same technique and ROI pattern as the preoperative
CTP. A comparison and correlation of the two CTP values was then performed, as well
as surgical outcomes and an GOS-extended (GOS-E). For reasons like death before postoperative
CTP or hypotension or renal insufficiency, some individuals were omitted from the
study. As a result, there were 75 patients who participated in the research.
Statistical Analysis
Data was entered in Excel spreadsheets. Shapiro–Wilk test (p > 0.05) was used to check normality of data. Normal data was expressed in form of
mean and standard deviation and was analyzed using Student's t-test and one-way analysis of variance test. Non-normal data was expressed in form
of median and interquartile range and analyzed using Wilcoxon and Kruskal–Wallis test.
Discrete data was summarized in form of proportions and difference in proportion was
analyzed using chi-squared test. All statistical analyses were conducted with a 95%
threshold of significance.
Results
In our study, half of the participants 37 (49.33%) were of the 20 to 34 years age
group and least 3 (4%) were of 5 to 19 years and 65 to 79 years age group. Mean age
of the participants was 38.62 ± 14.75 years. Most 63(84%) of the participants were
male. Road traffic accident was the most common (78.67%, 59/75) cause of injury. Around
half of the participants (37; 49.33%) had undergone type I surgery, followed by type
III surgery (21; 28%), type II surgery (10; 13.33%) and least 7 (9.33%) participants
undergone type IV surgery. Maximum 27 (36%) of the participants had SDH and contusion
both, followed by contusion (18; 24%) and SDH (12; 16%).
Among participants who had undergone type I surgery, CBV and CBF improved postoperatively
and improvement in CBF in affected area was statistically significant (p < 0.05). However, MTT and TTP decreased postoperatively and change in MTT and TTP
postoperatively in affected area was statistically significant (p < 0.05). There was found to be statistically significant improvement in postoperative
median Glasgow Coma Scale (GCS [motor]) from preoperative (p < 0.05; [Table 1]) median.
Table 1
Difference in pre- and postoperative CBV, CBF, MTT, TTP, GCS (motor) among patients
undergone type I surgery
|
Type I (n = 37)
|
|
|
Variable
|
Pre
|
Post
|
p-Value
|
|
CBV
|
3.88 ± 1.75
|
3.92 ± 1.31
|
t = −0.116, Df = 36, p-value = 0.909
|
|
CBF
|
32.75 ± 12.92
|
44.12 ± 16.55
|
t = −4.378, Df = 36, p-value < 0.001
|
|
MTT
|
7.49 ± 2.64
|
6.03 ± 2.81
|
t = 3.507, Df = 36, p-value = 0.001
|
|
TTP
|
31.45 ± 6.23
|
25.35 ± 5.05
|
t = 5.819, Df = 36, p-value < 0.001
|
|
GCS (motor)
|
5(6-5)
|
6(6-6)
|
Z value= 4.025, p-value < 0.001
|
Abbreviations: CBF, cerebral blood flow; CBV, cerebral blood volume; GCS, Glasgow
Coma Score; MTT, mean transit time; TTP, time to peak.
Among participants who had undergone type II surgery, CBV and CBF in affected area
improved significantly postoperatively (p < 0.05). However, MTT and TTP decreased postoperatively and change in MTT and TTP
postoperatively in affected area was statistically not significant (p > 0.05). Preoperative GCS (motor) among participants was 5 (5.25–5) and it increased
to 5.5 (6–5) postoperatively, although this improvement in GCS (motor) was statistically
not significant (p > 0.05; [Table 2]).
Table 2
Difference in pre- and postoperative CBV, CBF, MTT, TTP, GCS (motor) among patients
undergone type II surgery
|
Type II (n =10)
|
|
|
Variable
|
Pre
|
Post
|
p-Value
|
|
CBV
|
2.34 ± 0.66
|
2.95 ± 0.85
|
t = −3.34, Df = 9, p-value = 0.009
|
|
CBF
|
20.81 ± 10.37
|
29.39 ± 13.29
|
t = −3.56, Df = 9, p-value = 0.006
|
|
MTT
|
9.84 ± 9.19
|
6.97 ± 3.07
|
t = 1.4, Df = 9, p-value = 0.195
|
|
TTP
|
36.89 ± 6.63
|
33.36 ± 9.39
|
t = 1.415, Df = 9, p-value = 0.191
|
|
GCS (motor)
|
5(5.25-5)
|
5.5(6-5)
|
Z value= 1.890, p-value = 0.059
|
Abbreviations: CBF, cerebral blood flow; CBV, cerebral blood volume; GCS, Glasgow
Coma Score; MTT, mean transit time; TTP, time to peak.
Among participants who had undergone type III surgery, CBV and CBF improved postoperatively
and improvement in CBV in affected area was statistically significant (p-value < 0.05). However, postoperative MTT and TTP in affected area decreased significantly
from preoperative values (p < 0.05). Preoperative GCS (motor) among participants was 5 (5-4) and it increased
to 5 (6-5) postoperatively, and improvement in GCS (motor) was statistically significant
(p < 0.05; [Table 3]).
Table 3
Difference in pre- and postoperative CBV, CBF, MTT, TTP, GCS (motor) among patients
undergone type III surgery
|
Type III (n = 21)
|
|
|
Variable
|
Pre
|
Post
|
p-Value
|
|
CBV
|
3.43 ± 1.78
|
3.86 ± 1.45
|
t = −1.576, Df = 20, p-value = 0.131
|
|
CBF
|
26.0 ± 11.29
|
38.27 ± 14.52
|
t = −5.377, Df = 20, p-value < 0.001
|
|
MTT
|
8.26 ± 3.45
|
6.41 ± 2.12
|
t = 2.476, Df = 20, p-value = 0.022
|
|
TTP
|
34.67 ± 6.28
|
28.41 ± 8.51
|
t = 3.164, Df = 20, p-value = 0.005
|
|
GCS (motor)
|
5(5-4)
|
5(6-5)
|
Z value= 2.486, p-value = 0.013
|
Abbreviations: CBF, cerebral blood flow; CBV, cerebral blood volume; GCS, Glasgow
Coma Score; MTT, mean transit time; TTP, time to peak.
Participants who had undergone type IV surgery showed improvement in CBV and CBF postoperatively,
although this improvement in affected area was statistically not significant (p > 0.05). However, MTT and TTP decreased postoperatively and change in MTT and TTP
in affected area was also not significant statistically (p > 0.05). Improvement in median GCS (motor) was also statistically not significant
(p > 0.05; [Table 4]).
Table 4
Difference in pre- and postoperative CBV, CBF, MTT, TTP, GCS (motor) among patients
undergone type IV surgery
|
Type IV (n = 7)
|
|
|
Variable
|
Pre
|
Post
|
p-Value
|
|
CBV
|
2.5 ± 0.70
|
3.09 ± 1.12
|
t = −2.251, Df = 6, p-value = 0.065
|
|
CBF
|
18.34 ± 11.2
|
30.93 ± 21.95
|
t = −2.338, Df = 6, p-value = 0.058
|
|
MTT
|
11.9 ± 10.6
|
8.49 ± 5.96
|
t = 1.867, Df = 6, p-value = 0.111
|
|
TTP
|
35.16 ± 6.8
|
30.41 ± 10.16
|
t = 1.596, Df = 6, p-value = 0.161
|
|
GCS (motor)
|
5(5-2)
|
5(6-3)
|
Z value= 1.890, p-value = 0.059
|
Abbreviations: CBF, cerebral blood flow; CBV, cerebral blood volume; GCS, Glasgow
Coma Score; MTT, mean transit time; TTP, time to peak.
Among participants who had both SDH and contusion, maximum (40.74%, 11/27) participants
had undergone type I surgery, followed by type III surgery (22.22%, 6/27), type II
and type IV surgery each in (18.52%, 5/27) participants. Among participants who had
contusion, two-third (66.67%, 12/18) of participants had undergone type I surgery
and none of them undergone type II surgery. Association of type of injury with the
surgery participants had undergone was statistically significant (p-value <0.05).
Among participants who had undergone type I, II, III, and IV surgery, median GOS-E
score at 3 months after surgery was 7 (7-6), 5 (6-1.5), 3 (6-3), and 4 (5.5-2), respectively.
And difference in GOS-E score with type of surgeries participants had undergone was
statistically significant (Kruskal–Wallis test 24.191, Df = 3, p-value < 0.001). Among participants who undergone type I surgery, most 22(59.5) of
the participants had 7-8 GOS-E, none had 1-2 GOS-E at 3 months after the surgery.
Among participants who undergone type III surgery, most 9(42.9) of the participants
had 3-4 GOS-E and only 3(14.3) participants had 7-8 GOS-E. Association between type
of surgery and GOS-E after 3 months was found to be statistically significant (X2 = 27.116,
Df = 9, p-value= 0.001).
Maximum improvement in CBV was seen in cases of type II and least in cases of type
IV surgery. Improvement in CBF was maximum among participants of type III surgery,
while least among participants of type IV surgery. Improvement in GCS motor was maximum
among type IV surgery participants. Association between type of surgery with improvement
in CBV, CBF, MTT, TTP, and trauma to operation time was found to be statistically
insignificant (p-value > 0.05) and association of GCS motor change with type of surgery was statistically
significant (p-value < 0.05; [Table 5]).
Table 5
Association of improvement in variable with the type of surgery patients undergone
|
Variable
|
I (n = 37)
|
II (n = 10)
|
III (n = 21)
|
IV (n = 21)
|
Test of significance
|
|
Improvement in CBV
|
0.34(0.7–0.04)
|
0.50 (0.63-0.24)
|
0.31 (1.29-0.18)
|
0.27 (1.14-0.1)
|
p-Value= 0.712
|
|
Improvement in CBF
|
10.73(15.64–4.42)
|
6.06 (11.07-3.38)
|
11.14 (22.52-5.28)
|
4.53 (22.81-2.92)
|
p-Value = 0.677
|
|
Improvement in MTT
|
−1.12(−0.46–2.56)
|
−0.84 (−0.15–2.18)
|
−1.83 (−0.39–3.41)
|
−1.84 (−0.58–3.68)
|
p-Value= 0.833
|
|
Improvement in TTP
|
−6.05(−2.15–9.41)
|
−6.21 (3.64–10.01)
|
−5.68 (−3.36–8.1)
|
−6.64 (−4.24–8.36)
|
p-Value= 0.968
|
|
Improvement in GCS motor
|
0(1-0)
|
0 (1-0)
|
0 (1-0)
|
1 (1-0)
|
p-Value= 0.002
|
|
Trauma to operation time
|
43.32 ± 40.48
|
47.60 ± 68.76
|
25.67 ± 32.61
|
26.71 ± 21.77
|
F= 1.136, Df = 3, p-value = 0.341
|
Abbreviations: CBF, cerebral blood flow; CBV, cerebral blood volume; GCS, Glasgow
Coma Score; MTT, mean transit time; TTP, time to peak.
There was positive correlation of GOS-E at 3 months with preoperative CBV (ρ = 0.423),
preoperative CBF (ρ = 0.531) and this correlation was statistically significant (p-value < 0.05).
There was negative correlation of GOS-E at 3 months with preoperative MTT (ρ = −0.155)
and preoperative TTP (ρ = −0.234), and correlation with preoperative TTP was significant
(p-value < 0.05) and with preoperative MTT correlation was statistically insignificant
(p-value > 0.05)
Discussion
CTP research in people with TBI has been ongoing for more than a decade; however,
there are still few trials with sufficiently large sample sizes. Many researchers
have examined the potential of CTP in assessing TBI's aberrant cerebral perfusion[26] as well as changes after treatment[27] and prognostication.[24] We wanted to see if there was any association between preoperative and postoperative
CTP findings in different types of decompressive surgery. Our attempt was to reliably
identify who will be vegetative versus who will be high functioning on the basis of
preoperative CTP for better outcome for surgery in TBI patients.
In our study, road traffic accident (78.67%) was the most frequent reason, similar
to the prior batch of reports (India).[28] Type I was performed most commonly (49.33%) followed by type III (28%). In our patients,
most common finding on the NCCT was combined SDH and contusions (36%). Sinha et al
found in their study that intracerebral contusions (65%) and SDHs (almost as common)
were the most common radiological findings in TBI (63%).[28]
CBV and CBF values improved, whereas MTT and TTP values dropped in all types of surgeries,
indicating an improvement in cerebral perfusion in all types of procedures. TBI patients
with refractory high ICP have showed significant increases in CBF velocity after DC,
indicating postdecompression CBF rise.[29] TBI patient after undergoing DC showed an approximately threefold increase in cerebral
microvascular blood flow in contrast ultrasonography (USG).[30] There was transitory localized hyper perfusion in the decompressed brain that lasted
at least 1 week after DC in five individuals studied by Yamakami and Yamaura.[31]
Heppner et al[30] conducted a pilot study on microvascular cerebral perfusion following DC using contrast
USG, which included six patients. They reported increase in CBF and CBV 48 hours after
surgery. Several investigations employing transcranial Doppler to quantify macrovascular
flow have demonstrated increased flow velocities in both hemispheres.[29]
Soustiel et al[32] reported a considerable rise of roughly 4 mL/100 g/min in CBF in seven patients
following DC. Daboussi et al[29] reported that CBF velocities in patients after DC were increased immediately and
symmetrically.
Researchers observed that predecompression MTTs were about 8.2 seconds in both cerebral
hemispheres, indicating that brain was in distress before the procedure. To minimize
MTT in the cerebral hemispheres, doctors performed a craniectomy.[27] Yamakami and Yamaura showed an increase in CBF after DC using PET in patients with
ischemic stroke.[31]
Jaeger et al[33] stated an increase in oxygenation levels ipsilateral to the area of ischemia following
DC. These researchers discovered a strong link between MTT and oxygenation levels
in the brain. DC also resulted changes in cerebral perfusion pressure due to changes
in ICP.[34] MTT and CBF were shown to be the (Perfusion Computed Tomography) (PCT) measures
most responsive to even small changes in cerebral perfusion pressure.[35]
Type I and type IV had statistically insignificant improvements in CBV and changes
in MTT and TTP postoperatively, suggesting cerebral perfusion autoregulation failure.
Researchers observed that CBV is more closely linked to vasoconstriction and vasodilatation
than other measures of cerebral autoregulation.[36] To understand why individuals with severe infarction may be less responsive to acute
alterations following surgery, it is necessary to look at how their autoregulation
is affected.[37]
But preoperative median GCS (motor) among all type of surgeries was improved postoperatively
but statistically significant (p-value < 0.05) in type I and III and statistically not significant (p-value > 0.05) in type II and IV. Wintermark et al originally reported on the use
of CTP in severe TBI patients that a normal brain perfusion and high CBV were related
with a favorable outcome in a manner comparable to this.[18]
Our study revealed that most of patients had SDH with underlying contusion and only
contusion undergone commonly type I and type III (statistically significant, p-value <0.05).
When comparing different types of surgery for improving cerebral perfusion, no statistically
significant difference was found. This could be because cerebral perfusion is not
solely dependent on surgery type, but also on other factors such as brain parenchyma
injury, external trauma type, time from trauma to operation date, age, and many more.
This may be why improvements in cerebral perfusion have been observed in all types
of surgery. In other words, it shows that surgery does not repair the initial brain
parenchyma damage. Findings like this were previously discovered in other studies,
such as Wilberger et al[38] claimed that surgery did not affect fundamental brain damage, but can lessen major
downstream effects, such as elevated ICP and cerebral displacements or distortions,
by reducing the severity of these secondary lesions Previous research have sought
to explain variations in CBV, which appear to be connected to the outcome, but this
parameter is difficult to assess.[36]
[39] According to one study, the patterns of cerebral perfusion following DC did not
improve in all individuals after a stroke in a uniform manner[40] and worse functional outcome in elderly patients.[41]
Association between type of surgery and GCS motor change was also found to be statistically
significant (p-value < 0.05), when comparison done among types of surgeries. Amorim et al[27] and Martin et al[42] noted that CBF and BV rise does not necessarily mean improved hemodynamics because
these increases can be induced by vasospasm or hyperemia, which can have detrimental
effects on the brain.
Among participants who had undergone type I, II, III, and IV surgery, median GOS-E
score at 3 months after surgery was 7 (7-6), 5(6-1.5), 3(6-3), and 4(5.5-2), respectively.
Association between type of surgery and GOS-E after 3 months was found to be statistically
significant (X2 = 27.116, Df = 9, p-value= 0.001).
Most (59.5%) patients who undergone type I surgery showed good recovery, that is,
7-8 GOS-E score. It reflects that type I surgery generally performed in the patients
in which relatively less injured brain parenchyma was found. Patients who undergone
type III and IV surgery were end up in the severe disability, persistent vegetative
state or death. These findings also supported by previous studies like, Metting et
al[43] suggested that a lower GOS was associated with decreased frontal lobe CBF and CBV.
After a 6-month delay, the score is now extended. In SPECT, severe hypoperfusion was
found to be related with a negative result, regardless of any other confounding circumstances.[44]
The single-center and nonrandomized study design of this study constituted a drawback
of the current investigation. Many surgeons (of varying experience) have operated
on the patients in this study. As a tertiary care referral hospital, the length of
time after the injury occurred had a significant impact on our decision-making. Because
the research was limited to a single facility, it is possible that the findings cannot
be extrapolated to other settings. The study only followed up for 3 months, which
may have been a restriction of our study, as a longer follow-up could have revealed
changes in our findings and GOS-E. Another important limitation of our study is only
one postoperative CTP (which was done on postoperative day 5); further studies may
hope to remove these limitations.
Conclusion
Our findings imply that incorporating CTP data into the existing outcome predictors
enhances the prognostic model's accuracy when used in conjunction with surgical treatments
for TBI. Treatment decisions and therapeutic actions can be made based on the usage
of these modalities. Patient outcome after TBI can be better predicted with CTP. Better
prognostication may be possible if neurosurgeons are able to accurately distinguish
patients who will go into vegetative and those who will go into high functioning.
In TBI patients receiving decompressive surgery, CTP may be a useful predictive and
prognostic tool.
