Romanian Neurosurgery  |  Volume XXXII  |  Number 1 |  2018  |  January-March 

 
Article 

 
Management and outcome of moderate head 

trauma: our experience 

 

 

Mohammed T. Alshaimaa, Mohammed A. Sultan, Wael K. Zakaria, Mohammed E. Elshehawi 
EGYPT 

 

 

 

DOI: 10.2478/romneu-2018-0016 
 



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 129 

 

 
 
 
 
 
 

DOI: 10.2478/romneu-2018-0016   

Management and outcome of moderate head trauma: our 
experience 

Mohammed T. Alshaimaa, Mohammed A. Sultan, Wael K. Zakaria, 
Mohammed E. Elshehawi 

Department of Neurosurgery, Mansoura University Hospital, Mansoura, EGYPT 

 
Abstract: Objective: The aim of this study is to follow up patients with moderate head 
trauma who were admitted to Mansoura University Hospital in the period from 1 Dec. 
2015 to 30 Jul. 2016 until discharge and determine the outcome of head trauma. Material 
and Methods: This prospective study were conducted on all patients with moderate  head 
trauma admitted to Mansoura Emergency Hospital during the period from 1 Dec. 2015 
to 30 Jul. 2016 with exclude Polytrauma, bleeding disorders, severe liver and kidney  
disease  patients. Results: In this study, we correlated different risk factors with 
management and with outcome. Management may be surgical or conservative and 
outcome may be alive or dead. We have 60 patients   with 17 cases (28.3%) were   treated 
surgically and 43 cases (71.6%) were treated conservatively. According to outcome 36 
cases (60%) were alive and 24 cases (40%) died, all cases managed in ICU. According to 
sex, 10 cases (17%) were female and 50 cases were male (83%) with statistically non-
significant effect on outcome (P = 0.7) and management (P =0.7).  road traffic  accidents  
is most common cause of injury with  33 cases (55%),  and Cause of injury had 
statistically significant effect on management (P = 0.02) and statistically non-significant 
effect on outcome (p = 0.4). GCS on admission had no statistically significant effect on 
management (P=0.8) and outcome (P=0.1) with mean of 10.1±1.2 and GCS on discharge 
had no statistically significant effect on management (P=0.6). Conclusion: There were 
significant effect of age of patients, systemic diseases (such as DM, HTN, chronic kidney 
diseases, and chronic liver diseases), type of lesions (especially SDH, SAH), and serum 
electrolytes (especially serum Sodium) on outcome which determined by GCS at 
discharge, length of hospital stay, and the state of the patient at discharge.  
Key words:  Road Traffic accident, Glasgow coma scale 

 
Introduction 

In all of the world, Traumatic brain injury 
(TBI) considered as a critical public health and 

socio-economic problem. It is considered a 
major cause of death, in young adults, and 
result in lifelong disability in those who 
recovered³²’³³. TBI looks like a silent epidemic, 



 
 
 
 
 
130 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

because unawareness of the society about the 
magnitude of this problem²⁸’⁴⁰. In Egypt, TBI 
is a serious public health problem ³⁹.  

Treating patients with TBI in USA cost 
about more than 9$ billion per year ⁴⁹. TBI has 
two peaks of high incidence: first among 
young adult male between 15 to 24 years old, 
and other among elderly people of both sex 
older than 75 years ³⁹’⁴⁰⁴¹. Incidence in male is 
about 12–16% which double females incidence 
(8%). Male have high incidence to be 
hospitalized and are nearly 3 times more to die 
from this injury ³’¹⁰. 

Most people who survived a head injury 
presented with a normal or mild deterioration 
of conscious level (Glasgow Coma Scale more 
than 12) with the majority of fatal outcomes 
happened in the moderate or severe head 
injury groups, which represent   only 5% of 
cases. We defined Head injury as any trauma 
to the head other than any superficial injuries 
to the face ³⁹’⁴⁰. It can be classified by 
mechanism of injury to closed injury or 
penetrating injury, by morphology to 
fractures, focal intracranial injury, and diffuse 
injury, or by severity of injury to mild, 
moderate, and severe. Primary brain injury 
define as   immediate brain damage happened  
upon time of impact. This includes different 
verities as  cerebral contusions, diffuse axonal 
injuries, and acute subdural or epidural 
hematomas, subarachnoid hemorrhage and 
intracerebral hemorrhage. Secondary brain 
injury include other pathology as   progressive 
cerebral oedema, ischemia, and increase size  
of cerebral contusions and the surrounding 
focal oedema, which lead to increase in 
intracranial pressure and can lead to cerebral 
herniation and death¹⁹’⁴⁰’⁴¹. 

Disabilities of TBI patients change 
according GCS: we  have 47% moderate to 
severe disabilities at 12 months and a third do 
not return to work For patients  with mild 
injuries (GCS 13–15),. For patients  with 
moderate brain  injuries (GCS 9–12), 
moderate to severe disabilities are 45% , and 
while 48% of severely injured patients have 
moderate to severe disabilities, only 14% have 
a good outcome at one  year after trauma ⁴⁹’⁵⁵. 
Pathophysiology of TBI: 

We divided traumatic brain injury into the 
primary neuronal injury which followed by 
secondary injury. The primary injury define as 
the initial injury of neuron that occurs 
immediately at time of impact. ⁴’²². While 
secondary injury occurred  minutes, hours or 
days after injury impact and lead to worsen  
the primary lesions ⁵⁷’⁵⁹. 

Secondary injury considered as cellular and 
molecular processes which started by the 
primary injury and aggravated by the cerebral 
damage as result of hypotensive or hypoxic 
events, hypoglycemia, and elevated 
intracranial pressure cause cerebral ischemia. 
Andrriesson³’⁴. Glutamate excitotoxicity, 
neuronal depolarization, disturbance of ionic 
homeostasis, nitric oxide and oxygen free 
radicals, lipid peroxidation, disruption of 
blood-brain barrier, cerebral edema and 
ischemia, mitochondrial dysfunction, axonal 
disruption and necrotic cell death considered 
as mechanisms of secondary injury  ³⁸’⁴⁵. 

TBI start a close circle of neurotoxic 
phenomena which aggravate each other and 
end finally in cell death either by apoptosis or 
cell necrosis ⁵⁹. 
Diagnosis of TBI: 

Assessing the GCS and size of pupils and 



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 131 

 

 
 
 
 
 
 

reaction to light considered as initial 
neurologic examination. Prove alcohol 
intoxication lowers initial GCS in TBI patients 
¹⁸’²⁴.  

Computed tomography (CT) of the head is 
used for both confirming TBI and follow up 
patients over time after impact. CT scan can be 
used to know the type and severity of the 
injury; with upper hand for detecting 
intracranial hematoms ³²’³³. 50% of moderate 
TBI patients have abnormal finding in CT 
scan¹⁹. 

Treatment: 
Treatment divided into: pre-hospital, 

casualty department, and other, which 
includes both surgical treatment and intensive 
care unit treatment ⁸’⁹. 
Prognosis and Outcome: 

Mortality in moderate TBI is 15 %, and 75 
% of these deaths happen in sever injured 
patients¹⁹’²⁹. More than 50% of the survivors 
after moderate TBI suffer cognitive problem 
and whose recover without significant 
disability only 20 %²¹.  

Death incidence 3.5 years after injury in  
teenagers and adults affected by moderate or 
severe TBI who were discharged from hospital 
after treatment was  more than twice 
compared to persons in the general population 
of similar age, sex, and race ³’¹⁹. 

There are many  predictors factors of 
outcome after TBI include GCS after 
resuscitation, age, pupillary reactivity, CT 
findings, and the presence of major associated  
extra-cranial injury ⁴⁵’⁵⁷. 

Material and Methods 
This prospective study, after approval by 

the local ethical committee of anesthesia & 
surgical intensive care department Mansoura 
university hospital were conducted on all 
patients with head trauma admitted to 
Mansoura Emergency Hospital during the 
period from 1 Dec. 2015 to 30 Jul. 2016. 

Inclusion criteria: 
Patients with head trauma only, different 

age group (pediatrics from 0 to 15 years, adults 
from 15 to 65 year, geriatrics more than 65 
year)., patients with moderate head injury 
GCS (9-12), patients with intracranial 
hemorrhage, patients with skull fracture 
depressed or linear, patients with cerebral 
contusions, patients treated surgically and 
treated conservative, drug abuse patients and 
alcohol drinkers, diabetic patients smokers, 
controlled hypertensive patient, patient with 
mild liver disease and mild renal disease 
controlled with treatment. 

Exclusion criteria: 
Polytrauma patients (abdominal injury, 

chest injury, fracture spine, bone fractures), 
patients with bleeding disorders, patients on 
anticoagulant therapy, severe liver disease 
patients, severe kidney disease patients, mild 
head injury GCS (13-15) and severe head 
injury GCS (8 or less). 

Results 
In this study, we correlated different risk 

factors with management and outcome. 
Management may be surgical or conservative 
and outcome may be alive or dead. We found 
that total number of cases treated surgically 
was 17 cases (28.3%) and 43 cases (71.6%) were 
treated conservatively. According to outcome 
36 cases (60%) were alive and 24 cases (40%) 



 
 
 
 
 
132 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

died, all cases managed in ICU, figures (1, 2). 
In this study, total number of cases was 

divided into 3 groups according to age: 1) 
Children: 16 cases (26.7%) with age ranging 
from 1 month to 16 years. 2) Adult: 38 cases 
(63.3%) with age ranging from 17 years to 59 
years. 3) Elderly: 6 cases (10%) with age ≥ 60 
years, table (1) and figure (3). 

According to sex, 10 cases (17%) were 
female and 50 cases were male (83%), 
according to P value sex had statistically non-
significant effect on outcome (P = 0.7) and 
management (P =0.7), table (2) and figure (4).  

According to the cause of injury, falls was 
19 cases (31.6%), road traffic accidents (RTA) 
33 cases (55%), struggle 4 cases (6.6%) and 
direct head trauma (DHT) 4 cases (6.6%). 
Cause of injury had statistically significant 
effect on management (P = 0.02) and 
statistically non-significant effect on outcome 
(p = 0.4), as shown in table (3, 4) and figure (5).  

In this study, patients who had DM 10 
cases, 9 cases had HTN, only 1 case had history 
of drug abuse and 6 cases had other medical 
disorder e.g. CLD, CKD, epilepsy, cardiac 
diseases. These cases might have only one 
disease or might have more than one systemic 
diseases, as shown in table (5). 

GCS on admission had no statistically 
significant effect on management (P value 
=0.8) and outcome (P=0.1) with mean of 
10.1±1.2 and GCS on discharge had no 
statistically significant effect on management 
(P=0.6), as shown in table (6). 

In our study, we depended on CT diagnosis 
to illustrate type of TBI and its relation to 
management and outcome. Patients who had 
EDH were13 cases, 20 cases had SDH, 8 cases 
had SAH, 18 cases had contusions, 2 cases had 

ICH, 4 cases had DAI, 12 cases had brain 
edema, 19 cases had fissure fracture, 2  cases 
had depressed fracture, 1 case had fracture 
base of skull, 5cases had pneumocephalus, 
tables (7, 8,9) and figure (6). 

According to measured data we observed 
that blood pressure had statistically significant 
effect on outcome (P value = 0.006 for systolic 
BP and P value = 0.002 for diastolic BP) and 
non-significant effect on management (P 
value=0.2 for systolic BP & P=0.1 for diastolic 
BP). Arterial Blood Gases (ABG) had 
statistically significant effect (P = 0.04) on 
management and no statistically significance 
on outcome (P=0.7). Serum sodium (Na.) 
value had statistically significant effect in 
outcome (P=0.004) while it had no statistically 
significant effect on management (P=0.5). 
Serum potassium (K.) had neither statistically 
significant effect on management (P=0.3) nor 
on outcome (P=0.2). INR in most cases was 
within normal range with mean 1.2±0.2 which 
had neither statistically significant effect on 
management (P=0.9) nor on outcome (P=0.4). 
Liver enzymes (ALT) had no statistically 
significant effect on management (P=0.08) 
while it had statistically significant effect on 
outcome (P=0.03). All cases had leukocytosis 
(normal WBCs 4000-11000) which had 
neither statistically significant effect on 
outcome (P=0.9) nor management (p=0.07).  
Hemoglobin (Hg.) had neither statistically 
significant effect on management (P=0.7) nor 
outcome (P=0.1). Platelets had neither 
statistically significant effect on management 
(P=0.6) nor outcome (P=0.3). Serum 
creatinine had statistically non-significant 
effect on management (P=0.6) while it had 
statistically significant effect on outcome 



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 133 

 

 
 
 
 
 
 

(P≤0.001). Random Blood Sugar (RBS) had no 
statistically significant effect on management 
(P=0.4) while it had statistically significant 
effect on outcome (P≤0.001), as shown in table 
(10). 

According to the duration of hospital stay, 
survived patients had longer duration of 
hospital stay than dead patients with mean 
duration of hospital stay for survived 8(4-45) 
and for dead 7(1-27), which had statistically 
non-significant effect on outcome (P =1). 
Patients treated surgically had longer duration 
of hospital stay than treated conservatively 
with mean of duration of hospital stay for 
surgical treatment 8 (2-45) and for 
conservative treatment 7.5(1-30) day which 
had no statistically significant effect on 
management (P =1), as shown in figures (7, 8). 

 

 
Figure 1 - illustrates percentage of dead to alive 

 
Figure 2 illustrates percentage of surgical to 

conservative treatment 
 

 
Figure 3 illustrates age groups 

 

 
Figure 4 illustrates percentage of male to female 

 

 
Figure 5 illustrates cause of injury

 
Figure 6 illustrates relation between hospital stay and 

outcome 
 

 
Figure 7 illustrates relation of hospital stay to 

management 

 

 

 

 

 
 

 

 



 
 
 
 
 
134 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

TABLE I 

Correlates age groups to management and outcome 

 Management Outcome 

 Surgical 

N=17 

No (%) 

Conservative 

N=43 

No (%) 

Significance test 

 

Alive 

N=36 

No (%) 

Dead 

N=24 

No (%) 

Significance test 

Child 3(17.6) 13 (30.2) P = 0.5 MCT 

P=0.5 

15 (41.7) 1 (4.2) P = 0.003* MCT 

P=0.001* 

Adult 13(76.5) 25 (58.1) P = 0.3  20 (55.6) 18 (75) P = 0.1  

Elderly 1(5.9) 5 (11.6) P = 0.8  1 (2.8) 5 (20.8) P = 0.07  

 

TABLE II 

Correlates sex to management and outcome 

 Management Outcome 

 Surgical 

N=17 

No (%) 

Conservative 

N=43 

No (%) 

Significance test Alive 

N=36 

No (%) 

Dead 

N=24 

No (%) 

Significance test 

Age:median 

(min-max) 

25 (2 - 74) 20 (0.5 - 74) Z =0.3, P = 0.7 18.5 (0.5 - 71) 49.5 (5 -74) Z = 4.1, P ≤ 0.001* 

female 2 (11.8) 8 (18.6) FET 

P= 0.7 

7(19.4) 3(12.5) FET 

P= 0.7 

male 15 (88.2) 35 (81.4)  29(80.6) 21(87.5)  

Z of Mann-Whitney test            SD: standard deviation  
FET:  Fisher’s Exact Test           MCT: Monte Carlo Test        
P: Probability              P value is significant if ≤ 0.05, highly significant if ≤ 0.0001 
  



 
 
 
 
 

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TABLE III 

Correlates cause of injury to management and outcome 

 Management Outcome 

 Surgical 

N=17 

No (%) 

Conservative 

N=43 

No (%) 

Significance test 

 

Alive 

N=36 

No (%) 

Dead 

N=24 

No (%) 

Significance test 

falls 2(11.8) 17 (39.5) P = 0.08 MCT 

P = 0.02* 

14(38.9) 5(20.8) P = 0.2 MCT 

P = 0.4 

RTA 12(70.6) 21 (48.8) P = 0.2  17(47.2) 16(66.7) P = 0.2  

struggle 3 (17.6) 1 (2.3) P = 0.1  2(5.6) 2(8.3) P = 1  

DHT 0 (0) 4 (9.3) P = 0.5  3(8.3) 1(4.2) P = 0.9  

*There is significant correlation between cause of injury and management (P=0.02) 
 

TABLE IV 

Correlates cause of injury to age groups 

 Cause of injury Significance test 

 Falls 

n = 19 

RTA 

n =33 

Struggle 

n =4 

DHT 

n =4 

 

Age group 

Child 10 (52.6) 4 (12.1) 0 (0) 2 (50) MCT 

P = 0.001* 

Adult 4 (21.1) 28 (84.8) 4 (100) 2 (50)  

Elderly 5 (26.3) 1 (3) 0 (0) 0 (0)  

*There is statistically significant correlation between age of patient and the cause of injury (P=0.001) 
 



 
 
 
 
 
136 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

TABLE V 

Correlates systemic diseases to management and outcome 
 Management 

 
outcome 

 Surgical 
N=17 

No (%) 

Conservative 
N=43 

No (%) 

Significance test 
 

Alive 
N=36 

No (%) 

Dead 
N=24 

No (%) 

Significance test 

DM 3 (17.6) 7 (16.3) FET 
P = 1 

1(2.8) 9(37.5) FET 
P = 0.001* 

Hypertension 1 (5.9) 8 (18.6) FET 
P= 0.4 

1(2.8) 8(33.3) FET 
P= 0.002* 

Drug abuse 1 (5.9) 0 (0) FET 
P= 0.3 

1(2.8) 0(0) FET 
P= 1 

Other systemic 
diseases….. 

1 (5.9) 5 (11.6) FET 
P= 0.7 

2(5.6) 4(16.7) FET 
P= 0.2 

*There is significant correlation between DM, HTN and outcome (P=0.001), (P=0.002) respectively 
 

TABLE VI 

Correlates GCS to management and outcome 
 Management Outcome 
 Surgical 

N=17 
No (%) 

Conservative 
N=43 

No (%) 

Significance test 
 

Alive 
N=36 

No (%) 

Dead 
N=24 

No (%) 

Significance test 

Initial GCS 10.1±1.2 10.3 ± 1.2 P = 0.6 10.2778 ±1.1 10.1 ± 1.3 P = 0.6 
9.00 8 (47.1) 14 (32.6) P=0.9 MCT 

P = 0.8 
10 (27.8) 12 (50) P = 0.08 MCT 

P = 0.1 
10.00 3 (17.6) 12 (27.9) P =0.6  12(33.3) 3 (12.5) P = 0.1  
11.00 3 (17.6) 8 (18.6) P=1 

 
 8 (22.2) 3 (12.5) P = 0.5  

12.00 3 (17.6) 9 (20.9) P =1  6 (16.7) 6 (25) P = 0.4  
GCS on discharge 

14.00 2 (4.3) 7 (28.6)  
FET 

P = 0.6 

    

15.00 7 (35.7) 20 (71.4)      
 

  



 
 
 
 
 

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TABLE VII 

Correlates type of lesion to management and outcome according to CT on admission 
 Management Outcome 
 Surgical 

N=17 
No (%) 

Conservative 
N=43 

No (%) 

Significance test 
 

Alive 
N=36 

No (%) 

Dead 
N=24 

No (%) 

Significance test 
 

EDH: 
Only 

Other lesion 

 
4(44.4) 
5(55.6) 

 
1(33.3) 
3(66.7) 

FET 
P = 1 

 
5 (50) 
5 (50) 

 
0 (0) 

3 (100) 

FET 
P = 0.2 

SDH: 
Only 

And other lesion 

 
3(33.3) 
6 (66.7) 

 
5(45.5) 
6(54.5) 

FET, 
P = 0.7 

 
4 (57.1) 
3 (42.9) 

 
4(30.8) 
9 (69.2) 

FET 
P= 0.4 

SAH: 
Only 

And other lesion 

 
0(0) 
0 (0) 

 
2(12.5) 
6 (87.5) 

FET 
P = 1 

 
0 (0) 

1 (100) 

 
2 (28.6) 
5 (71.4) 

FET 
P= 1 

Contusion: 
Only 

And other lesion 

 
0 

2 (100) 

 
2(100) 

14 (87.5) 

FET 
P = 1 

 
2 (25) 
6 (75) 

 
0 (0) 

10 (100) 

FET 
P = 0.2 

ICH: 
Only 

And other lesion 

 
0(0) 
0 (0) 

 
1(50) 
1 (50) 

FET 
P = 1 

 
0 (0) 

1 (100) 

 
1 (100) 

0 (0) 

FET 
P = 1 

Fissure fracture: 
Only 

And other lesion 

 
0 

7 (100) 

 
2(16.7) 

10 (83.3) 

FET 
P = 0.5 

 
2 (18.2) 
9(81.8) 

 
0 (0) 

8 (100) 

FET 
P = 0.5 

depressed Fracture: 
Only 

And other lesion 

 
0 

1 (100) 

 
0 (0) 

1(100) 

FET 
P= 1 

 
0 (0) 

1 (100) 

 
0 (0) 

1(100) 

FET 
P=1 

Fracture base skull: 
Only 

And other lesion 

 
0 
0 

 
0 (0) 

1 (100) 

FET 
P =1 

 
0 (0) 

1 (100) 

 
0 (0) 
0 (0) 

FET 
P=1 

Brain edema: 
Only 

And other lesion 

 
0 
0 

 
4(33.3) 
8(66.7) 

FET 
P = 1 

 
3 (33.3) 
6 (66.7) 

 
1 (33.3) 
2 (66.7) 

FET 
P=0.4 

DAI: 
Only DAI 

DAI and other lesion 

 
0 (0) 
0(0) 

 
4 (100) 

0 

FET 
P = 1 

 
4 (100) 

0 (0) 

 
0 (0) 
0 (0) 

FET 
P = 0.1 

Pneumocephalus: 
Only 

And other lesion 

 
0 (0) 

2 (100) 

 
0 (0) 

3 (100) 

FET 
P = 1 

 
0 (0) 

5 (100) 

 
0  (0) 
0 (0) 

FET 
P = 0.07 

 

  



 
 
 
 
 
138 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

TABLE VIII 

Correlates type of lesion to outcome 

 Outcome Significance test 

 Alive 

n = 36 

Dead 

n = 24 

 

 No (%) No (%)  

EDH 10 (27.8) 3 (12.5) 1.9=2א 

P = 0.2 

SDH 7 (19.4) 13 (54.2) 7.8 = 2א 

P = 0.005* 

SAH 1 (2.8) 7 (29.2) FET 

P = 0.005* 

Contusion 8 (22.2) 10 (41.7) 2.6 = 2א 

P = 0.1 

ICH 1 (2.8) 1 (4.2) FET 

P = 1 

Fissure fracture 11 (30.6) 8 (33.3) 0.05= 2א 

P = 0.8 

Fracture depressed 1 (2.8) 1 (4.2) FET 

P = 1 

Fracture base of the skull 1 (2.8) 0 (0) FET 

P = 1 

Brain edema 9 (25) 3 (12.5) FET 

P = 0.3 

DAI 4 (11.1) 0 (0) FET 

P = 0.1 

Pneumocephalus 5 (13.9) 0 (0) FET 

P = 0.08 
*There is significant correlation between SDH, SAH and outcome (P=0.005), (P=0.005) respectively. 



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 139 

 

 
 
 
 
 
 

TABLE IX 

Correlates age with type of lesion 

 Child 

n=16 

No (%) 

Adult 

n=38 

No (%) 

Elderly 

n=6 

No (%) 

Significance test 

EDH 3(18.8) 9(25) 1(12.5) MCT 

P = 0.7 

SDH 1(6.3) 15(41.7)* 4(50) MCT 

P= 0.03* 

SAH 1(6.3) 5(13.9) 2(25) MCT 

P = 0.5 

Contusion 5(31.3) 10(27.8) 3(37.5) MCT 

P = 0.9 

ICH 0(0) 1(2.8) 1(12.5) MCT 

P = 0.3 

Fracture: fissure 9(56.3) 10(27.8)* 0(0) MCT 

P = 0.02* 

Fracture: depressed 0(0) 2(5.6) 0(0) MCT 

P= 0.7 

Fracture base skull 1(6.3) 0(0) 0(0) MCT 

P= 0.4 

Brain edema 5(31.3) 7(19.4) 0(0) MCT 

P= 0.2 

DAI 1(6.3) 3(8.3) 0(0) MCT 

P= 0.8 

Pneumocephalus 2(12.5) 3(8.3) 0(0) MCT 

P= 0.7 
*There is significant correlation between age of patients and type of lesion SDH, fissure fracture (P=0.03), 

(P=0.02) respectively. 
  



 
 
 
 
 
140 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

TABLE X 

Correlates lab. Data to management and outcome 

*There is significant correlation between PH and management (P=0.04), Sr. Na and outcome (P=0.004), ALT and 
outcome (P=0.03), Sr. creatinine and outcome (P≤0.001). 

 

Discussion 
We discussed in this study different risk 

factors which affect management and outcome 
of TBI patients. These risk factors include age, 
sex, cause of injury, systemic diseases, drug 
abuse, GCS on admission, and type of lesion. 

In the present study we found that children 

and adults had better outcome than elderly 
who had poor outcome. There is significant 
correlation between age and outcome 
(P=0.001), especially child group and outcome 
(P= 0.003). Some studies found that increasing 
age is a strong independent factor in prognosis 
of TBI, with a significant increase in fair  
outcome in patients older than 60 years of age, 

Parameter Management Outcome 
 Surgical       n= 

17 
Mean ± SD 

Conservative     
n=43 

Mean ± SD 

Significance 
test 

Alive 
N=36 

Mean ± SD 

Dead 
N=24 

Mean ± SD 

Significance 
test 

Systolic Bl.\P 118.3 ±18.6 127.1 ± 25.8 P = 0.2 116.9 ± 17.5 135.8 ± 28.1 P = 0.006* 
Diastolic Bl.\P 73.9 ± 6.9 78.1 ±14.2 P = 0.1 72.8 

±10.03 
82.9±13.7 P = 0.002* 

INR 1.2 ± 0.1 1.2405± 0.2 P = 0.9 1.2 ± 0.2 1.3 ± 0.2 P = 0.4 
ABGPH 7.29 ± 0.1 7.34 ± 0.07 P = 0.04* 7.3 ± 0.1 7.3 ± 0.07 P = 0.7 

ABG.PCO2 37.7 ± 11.1 35.5 ± 8.8 P = 0.4 36.4± 9.1 35.7± 10.3 P = 0.8 
ABG.HCO3 20.7 ± 3.2 20.1 ± 4.2 P = 0.6 20.5 ± 3.8 20.01 ± 4.2 P = 0.7 

ABG: Na 147.1 ± 8.3 148.8 ± 8.1 P = 0.5 145.9 ± 7.3 151.9 ± 8.04 P = 0.004* 
ABG.K 3.4 ± 0.5 3.3 ± 0.5 P = 0.3 3.4 ± 0.5 3.2 ± 0.6 P = 0.2 

ALT: median(min-max) 20 (13 - 50) 25 (13 - 196) Z = 1.7, P = 
0.08 

22 (13 - 196) 26 (16 - 92) Z = 2.1, P = 0.03* 

WBCs 19370.6 ± 
3954.1 

16786.1±5172.9 t= 1.9,P = 0.07 17530.6 ± 
5464.99612 

 

17500 ± 
4222.50698 

t= 0.02,P = 0.9 

HB 11.3±1.6 11.5±2.2 t= 0.3,P= 0.7 11.1 ±2.3 
 

11.9 ±1.5 t= 1.7,P= 0.1 

Platelets 248823.5 
±72919.7 

233253.5 
±101687.2 

t=0.6,P = 0.6 249083.3 ± 
100879.7 

220537.5 ±
81934.09 

t=1.2,P = 0.3 

RBS 171.9 ±63.9 157.1 ±55.1 t=0.9,P = 0.4 135.7 ±34.4 
 

199.8 ±64.2 t=4.5,P≤0.001* 

Sr. creatinine 0.9 ±0 .2 0.8 ±0.3 t=0.5,P= 0.6 0.7 ± 0.3 
 

1.02 ± 0.3 t=3.7,P≤0.001* 

Duration of hospital stay: 
median(min-max) 

8 (2 - 45) 7.5 (1 - 30) Z = 0, P = 1 8 (4 - 45) 7 (1 - 27) Z = 0.9,  P= 1 



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 141 

 

 
 
 
 
 
 

that's due to a higher rate of co-medication 
and anticoagulants administration which 
increase the extent of intracerebral bleeding⁸’⁹. 
Xueyan et al. ⁵⁷, illustrated in his study, several 
factors were found to contribute to the poor 
outcome in elderly patients, including lower 
Glasgow Coma Scale scores, existing systemic 
diseases as hypertension, systemic 
complications, midline shift, and inefficient 
intensive care unit. 

In the present study, we found that 
incidence of TBI in male was higher than 
female with a ratio of (5:1) respectively which 
indicates that male gender was a risk factor for 
TBI due to the higher incidence of RTA which 
affects mainly males who are the main workers 
and drivers in Egypt although sex did not 
affect outcome of TBI. This finding was in 
agreement with Taha᾽s (2015) results of his 
study which was about closed severe traumatic 
brain injury and was done in Egypt. He found 
that out of 80 cases, 71 male (88.8%), and the 
rest are female (11.2%) with mean age of 
27.45± 16.46 year.  

Brock᾽s et al. ¹⁰ also reported that the 
incidence of TBI in male was 12–16% and 8% 
in females so men were more likely to be 
admitted in hospital and are nearly three times 
more likely to die after TBI. Albrecht et al. ² 
found that same mortality following isolated 
TBI among older adults in both sex. 

 In the present study, we found that the 
most frequent causes of TBI were road traffic 
accident, falling from height, struggle and 
direct head trauma (DHT) respectively. There 
is statistically significant correlation between 
age of patient and the cause of injury (P value 
=0.001). Falls represented the most common 

cause of traumatic brain injury in extremes of 
age group while RTA and struggle were the 
most common causes in adult group.  

This finding was in agreement with Taha᾽s 
(2015) results of his study which was done in 
Egypt, as he reported that RTA was the most 
important cause of head injury in 52 (65%) of 
patients with severe TBI followed by falls in 12 
(15%) of those patients.  

Tagliaferri and his collagues ⁵²and Raja et 
al. ⁴⁷considered road traffic accidents is the 
commonest causes of head injury in adults 
(40%) and falls (37%). The commonest cause 
of injury was pedestrian (36%), and falls (24%) 
In children.  

Maas et.al. ³² illustrated in his study that the 
incidence of TBI was increasing due to the 
increased use of motor vehicles especially in 
middle and low income countries but in high 
income countries which have traffic safety 
regulations result in decline in traffic-related 
TBI. Vulnerable road users (pedestrians, 
cyclists, etc.) were particularly at risk. 

According to systemic diseases and 
substance abuse we found that patients with 
systemic diseases had poor prognosis and 
worse outcome than other patients who did 
not have systemic diseases. There is significant 
correlation between DM, HTN and outcome 
(P=0.001), (P=0.002) respectively. 
Lustenberger et. al. ³¹ found that TBI 
associated with diabetes mellitus have an 
almost 1.5 fold increased mortality when 
compared to patients with isolated TBI. They 
reported significantly increased in-hospital 
mortality in patients with vs without DM 
(22.6% vs. 16.8%. p=0.002). 



 
 
 
 
 
142 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

Timur et. al. ⁵⁴ reported in his result that 
patients with TBI and pre-hospital HTN 
showed significantly higher mortality than 
TBI patients with normotensive blood 
pressure (13.5% vs. 25.3%, p<0.001). Changes 
in blood pressure during the pre-hospital 
period, also resulted in higher hospital 
mortality.  

Rixen et.al. ⁴⁸ illustrated the mechanism by 
which HTN increase morbidity and mortality 
through elevating cerebral perfusion pressure, 
which leads to enforced dilatation of cerebral 
arterioles and rise in cerebral blood volume 
with elevating intra-cerebral pressure. This in 
turn leads to deterioration of the blood brain 
barrier with inversion of the hydrostatic 
gradients and finally to the formation of 
cerebral edema and/or hemorrhage.  

In our study, we found that there is 
significant correlation between ALT and 
outcome (P = 0.03). Lustenberger et.al. ³⁰, 
illustrated that TBI with liver disease was 
associated with two-fold increased mortality. 

In our study, we found a significant effect 
of chronic kidney diseases on outcome (p ≤ 
0.001) and this finding was in agreement with 
Liao et. al. ²⁹results as they found a significant 
difference between TBI with end stage renal 
disease patients and patients without renal 
disease on mortality (P ≤ 0.0001). This is due 
to a greater number of comorbidities, such as 
diabetes mellitus, stroke, systemic 
hypertension, and heart disease in those 
patients than non-ESRD patients admitted to 
the ICU.  

In the present study, we found that only 
one case of drug abuse which had good 
outcome, may be other cases of drug abuse 

were missed, this was due to lack of screening 
tests for substance abuse to patients with TBI 
in our hospital. O᾽Phelan et.al. ⁴³unexpectedly 
found that alcohol intake to be associated with 
decreased mortality. Mathias and Osborn 
(2016) found that alcohol had either 
deleterious or protective effects on the brain 
after a TBI and pre-injury alcohol abuse only 
had a very limited impact on the cognitive 
outcomes of their intoxicated mild TBI 
sample. 

Alternatively, Dinh et. al. (2014) found that 
alcohol consumption may lead to more serious 
injuries which, in turn, may contribute to 
poorer cognitive outcomes. Intoxicated 
patients affecting GCS through decreasing it 
by 2–3 points are challenging to classify and 
should be treated with higher attention (Harry 
et.al. 2007). 

According to GCS at time of admission as 
a risk factor that affect outcome we found that 
cases with GCS 9 had worse outcome than 
cases with GCS 12. So the lower GCS, the more 
chance for surgical treatment and the worst 
outcome. Perel et al. (2008) and Agrawal et al. 
(2012) considered that GCS after full 
resuscitation was one of the most important 
predictor factor of outcome after TBI. Baum J. 
et.al. (2016) illustrated that every 1-point 
decline in initial GCS at hospital presentation 
was associated with a 14% increased risk for 
fair outcome. Osler et.al. (2016) considered 
that GCS was an important predictor of 
mortality in both TBI and non-TBI patients 
but GCS is a more stronger predictor of death 
in TBI patients and patients with lower GCS 
have poor outcome than others.  



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 143 

 

 
 
 
 
 
 

In the present study, most patients who 
survived had GCS 15 on discharge and good 
outcome and mostly managed conservatively. 
We determined outcome of patients at 
hospital discharge. We did not evaluate long 
term outcomes because difficulty in follow-up 
of many patients after discharge. Maas et.al. 
(2008) suggested that outcome after head 
injury is better to be assessed at 6 months after 
injury, as experience showed that about 85% of 
recovery happened within this time period, 
but further improvement could occur later. 

According to type of lesion, Baum et. al. 
(2016) found that TBI outcome is more 
dependent on the severity of the brain injury 
and less so on extra cranial injuries. In the 
present study, we found that most common 
type of hemorrhage was SDH, its incidence 
was 33% of cases of the study which was in 
agreement with Mackenzie (2000) result who 
found that acute SDH was the commonest type 
of traumatic intracranial hematoma.  

In the present study, acute EDH incidence 
was 22% of cases of moderate head trauma and 
was common in adult group 9 cases versus 3 
children and 1 elderly. Bullock et. al. (2006) 
illustrated that EDH is rare in the elderly 
group, due to dura adherent to the skull. EDH 
generally had good outcome 27% of patients 
were alive but if associated with intracranial 
lesions outcome become poor (12% died).  

Grandhi et al. (2014) showed that ASDH 
compared with EDH had worst outcome due 
to severity of underlying brain damage 
associated with ASDH, and the rate of 
mortality are greater especially in elderly 
patients group with poor initial GCS, and 
other systemic injuries  

In the present study, SAH was a common 
intra-cerebral lesion, its incidence was 13% of 
moderate head trauma. It had worst outcome 
especially if associated with other lesion and 
mostly treated conservatively if not associated 
with other intra-cerebral lesions. Borczuk et. 
al. (2013) found that patients with isolated 
traumatic SAH were at lower risk of 
deterioration in comparison with patients 
having other intracranial injuries. Gaetani et 
al. (1995) considered that SAH was a negative 
prognostic factor in traumatic head injuries 
especially if there was an associated intra-
cerebral hematoma. Quigley et al. (2013) 
illustrated that management of traumatic SAH 
was usually conservative in isolated traumatic 
SAH without other intracranial lesions. 

In the present study, cerebral contusions 
were a common lesion, its incidence was 30% 
of moderate head trauma patients and its 
management was mainly conservative. 
Generally CC had poor outcome especially if 
associated with other intra-cerebral lesions. 
This was in agreement with Houseman et. al. 
(2012), Soustiel et. al. (2008) and Maas (2016)  
results who found cerebral contusions were 
one of the most common traumatic findings 
and it presented in more than 50% of patients 
of moderate and severe TBI. Saeed et al. (2014) 
result reported not all patients with CC require 
surgical intervention, 56% of patients can 
manage conservative and the remaining 44% 
need surgical evacuation, surgery was done for 
other intracranial lesions. Chieragato et al. 
(2005) study showed intracranial lesions 
which increase the chances of a bad 
neurological outcome were (cerebral 



 
 
 
 
 
144 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

contusions, subdural hematoma and 
subarachnoid hemorrhage).  

In the present study, we found that fissure 
fracture was the most common type of 
fracture, it had good outcome and was treated 
conservatively especially if not associated with 
other lesions. Raja et. al. (2013) had confirmed 
this findings in his study as the dominant type 
of skull fracture was linear (fissured) fracture 
in 50% of cases followed by depressed fracture 
in 30%, comminuted fracture in 20%.  

 In the present study, we found only one 
case of fracture base of the skull that 
documented on CT scan of the head. Actually 
there were 15 cases of TBI presented with 
periorbital hematoma, CSF rhinorrhea and\or 
CSF otorrhea, bleeding per nose and\or per 
ear. This finding was explained in Chawla et.al. 
(2105) study, as to detect a fracture on a CT 
scan there must be discontinuity of the skull. A 
linear fracture that comes in the same plane of 
a CT slice may not be visualised. Linear 
fractures in the base of the skull were difficult 
to be identified by CT scan unless depressed or 
separated.  

In the present study, we found 4 cases of 
DAI and their CT scan was normal presented 
by disturbed conscious level only and not 
associated with other injuries and all were 
treated conservative and had good outcome. 
Yuh EL (2013) suggested that up to one third 
of patients presented with mild traumatic 
brain injury (GCS 13-15) and a normal CT 
scan upon presentation will demonstrate 
structural abnormalities on later MR imaging. 
Joshue et. al. (2013) unexpectedly found that 
diffuse axonal injury was rarely fatal but was 
associated with increased possibilities of a 

poor functional recovery, prognosis was 
generally considered poor.  

In the present study, we found that brain 
edema was considered a secondary lesion 
which mostly occurred associated with other 
lesions and it was present in 20% of all 
moderate TBI patients. Adults were more 
susceptible to brain edema than children. It 
was mostly treated conservatively and 
generally had good outcome. Makarenko et. al. 
(2016) found that secondary brain injury cause 
a significant morbidity and mortality partly 
due to brain edema which reduces intracranial 
compliance and may cause a dangerous rise in 
intracranial pressure which leads to reduced 
cerebral blood flow and cerebral perfusion. 

 In the present study, the incidence of 
pneumocephalus was 8.3% of moderate head 
trauma, occurring in adult more than in 
children. It always occurred associated with 
other lesions, treated conservatively and had 
good outcome. 

In the present study, we found that 
incidence of moderate traumatic brain injury 
in children was 26.6%, the most common 
hemorrhages in this group were contusion 
(31%), EDH (19%), SDH (6.3%), and SAH 
(6.3%) respectively. Fissure fracture was 
common in child group (56%).  

We found that adult group were more 
prone to injury than any age group due to 
increased incidence of RTA in our country, 
common hemorrhages in these group were 
ASDH (41.7%), contusion (27.8), EDH (25%), 
SAH (13.9%) respectively. The common 
fracture in this group was fissure (27.8%), 
depressed (5.6%).  



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 145 

 

 
 
 
 
 
 

Bullock et. al. (2006) found that elderly 
population is more liable to hge due to 
increased fragility of blood vessel walls and 
increasing antithrombotic and anticoagulant 
drugs usage. Also we found that the most 
common hemorrhages in elderly were SDH 
(50%) contusion (37.5%), SAH (25%), EDH 
(12.5%), and ICH (12.5%) respectively. 

In the present study, we found that Serum 
Na had significant effect on outcome 
(P=0.004). Hypernatremia may be attributed 
to the use of normal saline (0.9%) for the first 
24 hours, the use of hyperosmolar diuretics 
(mannitol) and loop diuretics (furosemides) 
and its allowed to have high serum Na till 160 
-170 mmol\l in such patients. This cause 
hyperosmolarity of blood which withdraws 
water from brain cells and decreasing brain 
edema. 

Our results was in agreement with 
Maggiore and Picetti (2009) results, they 
reported the incidence of hypernatremia was 
significantly related with increased patients 
mortality (P = 0.003).  This is due to the 
coexistence of precipitating factors such as 
impaired sensorium, altered thirst, central 
diabetes insipidus, and increased insensible 
losses. Also, these patients often receive 
dehydrating measures to reduce cerebral 
edema and controlling intracranial pressure.  

Bradshaw and Smith (2008) and Xing et.al. 
(2015)  illustrated that electrolyte disorder was 
a common problem in TBI patients who are at 
a high risk for the development of 
hypokalemia, hypernatremia. Hypernatremia 
occurs in TBI patients less commonly than 
hyponatremia. Hypernatremia is often an 
indicator of the severity of the underlying 

disease. Hypokalemia is a common electrolyte 
disorder in hospitalized patients, with a 
prevalence of 21% and according the severity 
of post-traumatic hypokalemia, the severity of 
head injury can be assisted. 

Conclusion 
The most common cause of injury is road 

traffic accidents with Cause of injury had 
statistically significant effect on management 
and statistically non-significant effect on 
outcome. Patient gender had no effect on 
management and outcome. We found 
significant effect of age of patients, systemic 
diseases (such as DM, HTN, chronic kidney 
diseases, and chronic liver diseases), type of 
lesions (especially SDH, SAH), and serum 
electrolytes (especially serum Sodium) on 
outcome which determined by GCS at 
discharge, length of hospital stay, and the state 
of the patient at discharge.  

References 
1-Agrawal D, Joshua SP, Gupta D, Sinha S, Satyarthee 
GD. (2012). Can Glasgow coma score at discharge 
represent final outcome in severe head injury? J Emerg 
Trauma Shock 5(3):217–9. 
2-Albrecht JS, Mc-Cunn M, Stein DM, Simoni-Wastila L, 
Smith GS. (2016). Sex differences in mortality following 
isolated traumatic brain injury among older adults. The 
Journal of Trauma and Acute Care Surgery. 81(3):486-
492. 
3-Andriessen TM, Horn J, Franschman G, van der Naalt 
J, Haitsma I, Jacobs B, et al. (2011). Epidemiology, 
severity classification, and outcome of moderate and 
severe traumatic brain injury: a prospective multicenter 
study. J Neurotrauma. 28:2019–31. 
4-Andriessen TM, Jacobs B, Vos PE. (2010). Clinical 
characteristics and pathophysiological mechanisms of 
focal and diffuse traumatic brain injury. J Cell Mol Med. 
14(10):2381–2392. 



 
 
 
 
 
146 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

5-Baum J, Entezami P, Shah K, Medhkour A. (2016). 
Predictors of Outcomes in Traumatic Brain Injury. 
World Neurosurg. 
6- Borczuk P, Penn J, Peak D, Chang Y. (2013). Patients 
with traumatic subarachnoid hemorrhage are at low risk 
for deterioration or neurosurgical intervention. J Trauma 
Acute Care Surg 74:1504-1509. 
7-Bradshaw K and Smith M. (2008). Disorders of sodium 
balance after brain injury Critical Care & Pain | Volume 
8 Number 4. 
8-Brain Trauma Foundation (BTF), American 
Association of Neurological Surgeons, Congress of 
Neurological Surgeons, Joint Section on Neurotrauma 
and Critical Care. (2007). Guidelines for the management 
of severe traumatic brain injury. Journal of Neurotrauma. 
24 Supplement 1:S1-S95. 
9-Brain Trauma Foundation (BTF). (2000). Early 
indicators of prognosis in severe traumatic brain injury. J 
Neurotrauma 17:535–627. 
10-Brock F.R. Thomas J. Farrer, Mark Primosch, Dawson 
W. Hedges. (2013). Prevalence of Traumatic Brain Injury 
in the General Adult Population: A Meta-Analysis. 
Neuroepidemiology, 40:154–159. 
11- Bullock M.R., Chesnut R., Ghajar J., Gordon D., Hartl 
R., Newell D.W. et al. (2006). Surgical Management of 
acute epidural haematomas. Neurosurgery vol. 58 :( 
Supplement) 52-7. 
12-Bullock M.R.,  Chesnut R, Ghajar J, Gordon D, Hartl 
R, Newell DW, Servadei F, Walters BC, Wilberger JE. 
(2006). Surgical Management of Acute Subdural 
Hematomas. Neurosurgery 58:S2-16-S2-24. 
13-Bullock MR, Chesnut R, Ghajar J, et al. (2006). 
Surgical management of depressed cranial fractures. 
Neurosurgery, 58:S56. 
14- Bullock RM, Chesnut R, Ghajar J, Gordon D, Hartl R, 
Newell DW, et al. (2006). Surgical management of 
traumatic parenchymal lesions. Neurosurgery. 58:S2-25–
46. 
15-Chavli K. H., Sharma B. R., Harish D., Anup Sharma. 
(2006) Head injury: The principal killer in road traffic 
accidents. JIAFM, 28(4) ISSN: 0971-0973. 
16-Chawla H.,  Yadav KR,  Griwan SM,   Malhotra R,  and  
Paliwal KP. (2015).     Sensitivity and specificity of CT scan 
in revealing skull fracture in medico-legal head injury 
victims. Australas Med J. 8(7): 235–238. 
17-Chieragato A, Fainardi E, Morselli-Labate AM, 
Antonelli V, Compagnone C, Targa L, Kraus J, Servadei 

F. (2005). Factors associated with neurological outcome 
and lesion progression in traumatic subarachnoid 
hemorrhage patients. Neurosurgery. 56:671–680. 
18-Christopher Wood G. and Bradley A. Boucher. (2011). 
Management of Acute Traumatic Brain Injury. PSAP-
VII.  Neurology and Psychiatry. 
19-Compagnone  C., d’Avella D., Servadei F., Angileri 
F.F., Brambilla G., Conti C., et al. (2009). Patients with 
moderate head injury: a prospective multicenter study of 
315 patients. Neurosurgery, 64:690–697. 
20-Daniel Agustın Godoy, Andre´s Rubiano, Alejandro 
A. Rabinstein, Ross Bullock. Juan Sahuquillo. (2016). 
Moderate Traumatic Brain Injury: The Grey Zone of 
Neurotrauma. Neurocrit care, page 4. 
21-Fabbri A, Servadei F, Marchesini G, Stein SC, Vandelli 
A. (2008). Early predictors of unfavourable outcome in 
subjects with moderate head injury in the emergency 
department. J Neurol Neurosurg Psychiatry, 79:567–73 
22-Frattalone AR, Ling GSF. (2013). moderate and severe 
traumatic brain injury: pathophysiology and 
management. Neurosurg Clin N Am. 24(3):309-319. 
23- Gaetani P, Tancioni F, Tartara F, Carnevale L, 
Brambilla G, Mille T, et al. (1995). Prognostic value of the 
amount of posttraumatic subarachnoid haemorrhage in a 
six month follow up period. J Neurol Neurosurg 
Psychiatry; 59:635—7. 
24-Grandhi R, Bonfield CM, Newman WC, Okonkwo 
DO. (2014). surgical management of traumatic brain 
injury: a review of guidelines, pathophysiology, 
neurophysiology, outcomes, and controversies. J 
Neurosurg Sci. 58:249–59. 
25-Harry McNaughton, Michael Ardagh, Andrew 
Beattie. (2007). Traumatic Brain Injury: Diagnosis, Acute 
Management and Rehabilitation ACC2404. New Zealand 
guidelines group for ACC.p.4. 
26-Houseman C, Belverud S, Narayan R. Closed Head 
Injury. In: Ellenbogen R, Abdulrauf S, editors. (2012). 
Principels of neurological surgery, Philadelphia: Saunders 
Elsevier; pp. 325–47. 
27- Joshua M. Levine and Monisha A. Kumar. (2013). 
Traumatic Brain Injury. Neurocritical Care Society 
Practice Update.P6. 
28-Langlios J.A. & Sattin, R.W. (2005). Traumatic brain 
injury in United States: Emergency Department Visits, 
Hospitalizations, and Deaths research and programs of 
the Centers for Disease Control and Prevention (CDC). 
J.Head Trauma Rehabil. 20,187-188. 



 
 
 
 
 

Romanian Neurosurgery (2018) XXXII 1: 129 - 148 | 147 

 

 
 
 
 
 
 

29-Liao JC, Ho CH,  Liang FW, Wang JJ, Lin KC, Chio 
CC, Kuo JR. (2014). One-Year Mortality Associations in 
Hemodialysis Patients after Traumatic Brain Injury. An 
Eight-Year Population-Based Study.  PLoS ONE 9(4). 
30-Lustenberger T, Talving P, Lam L, Inaba K, Branco 
BC, Plurad D, Demetriades D. (2011). Liver cirrhosis and 
traumatic brain injury: a fatal combination based on 
National Trauma Databank analysis.  Am Surg. Mar; 
77(3):311-4. 
31-Lustenberger T1, Talving P, Lam L, Inaba K, Bass M, 
Plurad D, Demetriades D. (2013). Effect of diabetes 
mellitus on outcome in patients with traumatic brain 
injury: a national trauma databank analysis. Brain Inj. 
27(3):281-5. 
32-Maas A. (2016). Traumatic brain injury: Changing 
concepts and approaches, Chinese Journal of 
Traumatology xxx 1-4. 
33-Maas A., Stocchetti N., Bullock R. (2008). Moderate 
and severe traumatic brain injury in adults. Lancet 
Neurol. 7: 728–41. 
34-Maas Al, Hukkelhoven CW, Marshall LF, Steyerberg 
EW. (2005). Prediction of outcome in traumatic brain 
injury with computed tomographic characteristics: a 
comparison between the computed tomographic 
classification and combinations of computed 
tomographic predictors. Neurosurgery J. 57:1173. 
35-MacKenzie EJ. (2000). Epidemiology of injuries: 
current trends and future       challenges. Epidemiol Rev. 
22:112-119. 
36-  Maggiore U., Picetti E., Antonucci E., Parenti E., 
Regolisti G., Mergoni        M., Vezzani A., Cabassi A. and 
Fiaccadori E. (2009). The relation     between the incidence 
of hypernatremia and mortality in patients with severe 
traumatic brain injury. Critical Care,13:R110. 
37-Makarenko S, Griesdale E. D., Gooderham P., Sekhon 
M.S. (2016). Multimodal neuromonitoring for traumatic 
brain injury: A shift towards individualized therapy. 
Journal of Clinical Neuroscience 26, 8–13. 
38-Mathias J. L. and Osborn A. J. (2016). Impact of day-
of-injury alcohol consumption on outcomes after 
traumatic brain injury: A meta-analysis. 
Neuropsychological Rehabilitation. 
39-McHugh GS, Engel DC, Butcher I, et al. (2007). 
Prognostic value of secondary insults in traumatic brain 
injury: results from the IMPACT study. J Neurotrauma; 
24:287. 

40- Montaser, Ahmed Hassan, Ahmed Ibrahim. (2013). 
Epidemiology of moderate and severe traumatic brain 
injury in Cairo University Hospital in 2010.Scandinavian 
Journal of Trauma, Resuscitation and Emergency 
Medicine.21, Suppl 2. 
41-National Institute for Health and Clinical Excellence 
(NICE). (2014). Head injury Triage, assessment, 
investigation and early management of head injury in 
children, young people and adults. Clinical guideline 
Published: 22 January. 
42- National Institute of Neurological Disorders and 
Stroke. (2002). Traumatic Brain Injury: Hope through 
Research. 
43-National Institute of Neurological Disorders and 
Stroke. NINDS. (2015). Common Data Elements: 
Traumatic Brain Injury. August 12. 
44-O'Phelan, Kristine, McArthur, David L. Chang, 
Cherylee W. J. Green, Deborah, Hovda, David A. (2008). 
The Impact of Substance Abuse on Mortality in Patients 
with Severe Traumatic Brain Injury. Journal of Trauma-
Injury Infection & Critical Care: September - Volume 65 
- Issue 3 - pp 674-677. 
45-Osler T., Cook A., Glance L.G., Lecky F., Bouamra O., 
Garrett M.,  Buzas J. S., Hosmer W. D. (2016). The 
differential mortality of Glasgow Coma Score in patients 
with and without head injury. Injury, Int. J. Care Injured 
47, 1879–1885. 
46-Perel P, Arango M, Clayton T, et al. (2008). MRC 
CRASH Trial Collaborators. Predicting outcome after 
traumatic brain injury: practical prognostic models based 
on large cohort of international patients. BMJ. 
336(7641):425–429. 
47-Quigley MR, Chew BG, Swartz CE, Wilberger JE. 
(2013). the clinical significance of isolated traumatic 
subarachnoid hemorrhage. J Trauma Acute Care Surg 
74:581-584. 
48-Raja R, Verma A, Rathore S. (2013). Pattern of Skull 
Fractures in Cases of Head Injury by Blunt Force. J Indian 
Acad Forensic Med. October-December, Vol. 35, No. 4 
(0971-0973) 
49-Rixen D, Steinhausen E, Dahmen J, Bouillon B, 
German Society of Trauma Surgery (DGU). (2012). [S3 
guideline on treatment of polytrauma/severe injuries. 
Initial surgical phase: significance--possibilities--
difficulties?]. Unfallchirurg. Jan; 115(1):22-9. 



 
 
 
 
 
148 | Alshaimaa et al - Moderate head trauma 

 

 
 
 
 
 
 

50-Rutland B.W., Langlois JA, Thomas KE, Xi YL. (2006). 
Incidence of traumatic brain injury in the United States, 
2003. J Head Trauma Rehabil. 21:544-548 
51-Saeed M., Ahmed S., Ali A. (2014). Current 
Consideration Regarding Operative Versus Non-
Operative Outcome of Brain Contusion Patients. 
Pakistan Journal of Medicine and Dentistry. Vol.3 (01). 
52-Soustiel JF, Mahamid E, Goldsher D, Zaaroor M. 
(2008). Perfusion-CT for early assessment of traumatic 
cerebral contusions. Neuroradiology.50:189–96. 
53- Tagliaferri F, Compagnone C, Korsic M, Servadei, 
Kraus J. (2006). Asystematic review of brain injury 
epidemiology in Europe. Acta Neurochir (Wien) 
148:255–68. 
54-Timmons SD. (2008). Extra-axial hematomas. In: 
Loftus CM, editor. Neurosurgical Emergencies. 2nd ed: 
Thieme Medical Publishers. p. 53-67. 
55- Timur S., Miersch D., Kienbaum P., Flohé S.,  
Johannes S.,  Lefering R., and Trauma Registry DGU. 
(2012). the Impact of Arterial Hypertension on 
Polytrauma and Traumatic Brain Injury. Dtsch Arztebl 
Int. Dec; 109(49): 849–856. 

56-Tsang KKT, Whitfield PC. (2012). Traumatic brain 
injury: review of current management strategies. British 
Journal of Oral and Maxillofacial Surgery 50; 298–308. 
57-Xing W., Xin L., Xiangqiong L., Jian Y., Sun Y., 
Zhuoying D., Xuehai W., Ying M., Liangfu Z., Sirong W., 
Jin H. (2015). Prevalence of severe hypokalaemia in 
patients with traumatic brain injury. Injury, Int. J. Care 
Injured 46, 35–41. 
58-Xueyan W., Shengwen L., Wang S., Zhang S., Yang H., 
Ou Y., Min Z.,  James L., Shu K., Chen J., Lei T.  (2016). 
Elderly Patients with Severe Traumatic Brain Injury 
Could Benefit from Surgical Treatment. World 
Neurosurg. 89:147-152. 
59- Yuh EL, Mukherjee P, Lingsma HF, et al. 2013. 
Magnetic resonance imaging improves 3-month outcome 
prediction in mild traumatic brain injury. Ann Neurol. 
73: 224-235. 
60-Zammit C, Knight WA. (2013). Severe traumatic brain 
injury in adults. Emerg Med Pract.15:1–28. 
 

 
 


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