Journal of Emergencies, Trauma, and Shock
Home About us Editors Ahead of Print Current Issue Archives Search Instructions Subscribe Advertise Login 
Users online:2411   Print this pageEmail this pageSmall font sizeDefault font sizeIncrease font size   


 
 Table of Contents    
ORIGINAL ARTICLE  
Year : 2011  |  Volume : 4  |  Issue : 3  |  Page : 355-358
Studying patients of severe traumatic brain injury with severe abdominal injury in Japan


Department of Traumatology and Critical Care Medicine, National Defense Medical College (NDMC), Japan

Click here for correspondence address and email

Date of Submission28-Apr-2010
Date of Acceptance19-Jul-2010
Date of Web Publication16-Aug-2011
 

   Abstract 

Background : Characteristics of extracranial injury in patients with diffuse axonal injury (DAI) have not been clarified. Materials and Methods : This retrospective study reviewed medical records from January 2003 to December 2007. Subjects comprised 35 patients meeting the following criteria: 1) head injury without mass lesion; 2) Glasgow coma scale (GCS) on arrival <15; and 3) magnetic resonance imaging (MRI) examination including T2*-weighted imaging. Subjects were divided into two groups: severe traumatic brain injury (TBI) group (patients with GCS ≤8, n=19) and moderate TBI group (patients with GCS >8, n=16) Results : Shock index (heart rate/systolic blood pressure) was significantly higher in the severe TBI group than in the moderate TBI group, while base excess on arrival was significantly lower in the severe TBI group than in the moderate TBI group. The abbreviated injury scale (AIS) for the face, thorax, extremities and external structures showed no significant differences between the severe TBI group, but AIS for the abdomen and the sum of extracranial AIS was greater in the severe TBI group than in the moderate TBI group. Duration of hospitalization was longer and outcomes were worse in the severe TBI group than in the moderate TBI group. Conclusion : Because patients with severe TBI are more likely to have abdominal injury than patients with moderate TBI, physicians should be aware of the potential for such complications when treating severe TBI.

Keywords: Diffuse axonal injury, abdominal injury, abbreviated injury scale, polytrauma, outcome

How to cite this article:
Yanagawa Y. Studying patients of severe traumatic brain injury with severe abdominal injury in Japan. J Emerg Trauma Shock 2011;4:355-8

How to cite this URL:
Yanagawa Y. Studying patients of severe traumatic brain injury with severe abdominal injury in Japan. J Emerg Trauma Shock [serial online] 2011 [cited 2019 Nov 12];4:355-8. Available from: http://www.onlinejets.org/text.asp?2011/4/3/355/83863



   Introduction Top


Traumatic brain injury (TBI) caused by motor vehicle accidents, firearms, and falls are recorded as a leading cause of death and lifelong disability among young adults. [1],[2],[3],[4] The Glasgow coma scale (GCS) has been extensively studied for its ability to predict outcomes in TBI patients. [3] Lower GCS is associated with worsened outcomes. Representative TBIs that could induce unconsciousness include intracranial hematoma, cerebral contusion and axonal injury.

Patients with severe major injuries in two or more different sites, who require surgical intervention to stabilize vital signs may often experience cardiac arrest in the prehospital arena and thus display poor prognosis. [4],[5] This institute, which is a 15-year-old level 1 urban trauma center in Japan, has no record of any patients with blunt injury who were alive on arrival and required life-saving surgical operations for two different sites of injury, one of which was the head. However, patients have been encountered who showed diffuse axonal injury (DAI) and required insertion of a sensor into the intracranial space to control intracranial pressure, [6] and also underwent a major operation for injuries at other sites. No reports to date appear to have indicated characteristics of extracranial injuries in patients with DAI. The present study therefore retrospectively investigated the characteristics of extracranial injuries in patients with DAI.


   Materials and Methods Top


This retrospective study protocol was approved by the institutional review board. The study was conducted by reviewing medical records from January 2003 to December 2007. In this study, DAI was defined as present in a patient who showed no focal lesions and prolonged unconsciousness lasting ≥24 h. Accordingly, to identify DAI, the study included patients meeting the following criteria: 1) head injury without cerebral contusion >1 cm 2 on computed tomography (CT), subdural hematoma, or epidural hematoma; 2) GCS on arrival <15; and 3) magnetic resonance imaging (MRI) including T2*-weighted imaging performed during hospitalization. The study excluded patients meeting the following criteria: 1) age >60 years or 2) death due to head injury. Subjects were divided into two groups: severe TBI group (patients with GCS ≤8) and moderate TBI group (patients with GCS >8). In this study, the term TBI was used in place of DAI because some unconscious patients with TBI did not show any traumatic lesions on MRI.

The following variables were analyzed between the severe TBI group: sex, age, mechanism of injury, incidence of skull fracture, GCS on arrival, systolic blood pressure, shock index (i.e., heart rate/systolic blood pressure), [7] status of light reflex, abbreviated injury scale (AIS) [8] of the extracranial regions (face, thorax, abdomen, extremities and external structures), sum of extracranial AIS scores, value of arterial base excess (base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO 2 of 40 mmHg) as measured by blood gas analysis on arrival; presence of traumatic microbleeds detected by T2*-weighted imaging, duration of hospitalization, and Glasgow outcome score at 3 months after admission. The AIS is an anatomical scoring system in which injuries are ranked on a scale of 1-6 (1, minor; 2, moderate; 3, serious; 4, severe; 5, critical; 6, unsurvivable injury). T2*-weighted imaging was performed in the axial plane using the following parameters: repetition time, 900 ms; echo time, 30 ms; excitations, 2; flip angle, 200°; matrix, 256 Χ 192; section thickness, 5 mm with a 2.5-mm gap, and imaging time, 2 min 56 s. All foci >1 mm in diameter showing signal hypointensity on T2*-weighted imaging were defined as traumatic microbleeds.

Statistical analyses were performed using the unpaired Student's t-test and the χ2 test. Values of P<0.05 were considered indicative of a statistically significant difference.


   Results Top


A total of 469 patients with head injury were admitted during the investigation period. Of these, 138 patients >60 years old, 53 patients with cerebral herniation, and 100 patients with intracranial mass lesions due to cerebral contusion and/or intracranial hematoma were excluded. Of the remaining 178 patients, 113 were alert on arrival and were excluded. Thirty-five of the remaining 65 patients showed persistent disturbance of consciousness for ≥24 h after admission and underwent MRI, and were thus defined as subjects in this study (the severe TBI group, n=19; the moderate TBI group, n=16).

No significant differences were apparent between the two groups with regard to sex, age, mechanism of injury or incidence of skull fracture [Table 1].
Table 1: Subject background data


Click here to view


Shock index was significantly higher in the severe TBI group than in the moderate TBI group, while base excess on arrival was lower in the severe TBI group than in the moderate TBI group [Table 2].
Table 2: Physiological data and AIS on arrival


Click here to view


AIS of the face, thorax, extremities and external structures showed no significant differences between the two groups, but AIS of the abdomen and the sum of extracranial AIS scores were higher in the severe TBI group than in the moderate TBI group [Table 3]. Four patients in the severe TBI group showed abdominal injury requiring surgery (diaphragmatic rupture, n=2; splenic rupture, n=1; bladder rupture, n=1), but the moderate TBI group included no such cases (P=0.1). In addition, the severe TBI group included four patients with pelvic fractures, whereas the moderate TBI group had no such cases (P=0.1).

The number of traumatic microbleeds detected by MRI was higher in the severe TBI group than in the moderate TBI group [Table 4].
Table 3: AIS for extracranial injury on arrival


Click here to view
Table 4: Results of MRI


Click here to view


Duration of hospitalization was longer and outcomes were worse in the severe TBI group than in the moderate TBI group [Table 5]. All subjects in both the severe TBI groups survived.
Table 5: Outcomes


Click here to view


None of the remaining 434 patients with blunt trauma who were excluded from the study and were alive on arrival required life-saving surgery for two different sites of injury, one of which was the head. Only one of the patients excluded from the study showed DAI and acute subdural hematoma requiring surgery, and underwent delayed repair for diaphragmatic rupture. [9]


   Discussion Top


This study demonstrated that patients with severe TBI were more likely to have abdominal injury than patients with moderate TBI, representing the first investigation to report such a relationship. The combination of head and abdominal injuries is usually rare, [10],[11] maybe because the abdomen is relatively far from the head compared to other regions, and is protected by the bony thorax and pelvis. As a result, the abdomen and head might rarely receive the same high-energy impact at the same time. DAI forms when axons undergo rapid stretching as a result of angular acceleration, damaging the axonal cytoskeleton and resulting in a loss of elasticity and impairment of axoplasmic transport. [12],[13],[14],[15] Subsequent swelling of the axon occurs with discrete bulb formations or elongated varicosities that accumulate transported proteins. These swollen axons may become disconnected and contribute to additional neuropathological changes in brain tissue, resulting in the formation of DAI. DAI can occur without direct impact to the head. [15] DAI occurs more frequently with force applied in the coronal plane, rather than in the sagittal or axial planes. [15],[16],[17],[18] The severity of DAI depends on the energy of the impact. [19] Two cases in the severe TBI group showed diaphragmatic rupture, induced when the body quickly decelerated while the organs continued to move downward or forward at a much higher velocity, tearing vessels and tissues from the normal points of attachment. [20] Rapid changes in acceleration or deceleration to the head and abdomen, such as moving rapidly and then suddenly hitting the ground in a traffic accident or fall, could be associated with a rare combination of injuries to the head and abdomen.

Shock index was higher in the severe TBI group than in the moderate TBI group in the current series, while base excess on arrival was lower in the severe TBI group than in the moderate TBI group. Generally, isolated head injury without cerebral herniation rarely induces hypotension. [5] In addition, no correlation has been observed between base excess and severity of head injury. [21] Hemorrhaging from extracranial injuries in a patient with severe TBI tends to result in hemorrhagic shock following a reduction in base excess due to hypoperfusion of tissues, as severe TBI is obviously associated with more severe extracranial injuries than moderate TBI. [22] Such hypotension could induce a second brain insult to the head injury, [23] so hypotension may affect the outcomes in severe TBI.

The association seen between the number of traumatic microbleeds detected on MRI and outcomes has also been reported in several previous studies. [6],[24]

TBI itself does not necessarily represent a medical emergency requiring treatment; immediate concerns are amnesia (a mild form of DAI) and damage to the brainstem (a severe form of DAI). Both these possibilities may be excluded in the present case, as we selected surviving patients with prolonged unconsciousness. Clinically, patients with amnesia could still complain of pain induced by any concomitant organ injury, so there is little chance of overlooking hidden injuries. In contrast, severe brainstem injuries can easily prove lethal by causing malfunctions in respiration and circulation. Patients with such injuries tend to present in a deeply comatose state, and thus may be more likely to have abdominal injuries in comparison with patients with severe TBI, as more severe unconsciousness was associated with a greater risk of the presence of abdominal injury according to the present results.

Patients with severe TBI were more likely to have abdominal injuries when compared with patients showing moderate TBI. Hidden organ injuries could be missed because unconscious patients are unable to complain about injuries. From this retrospective study, it appears that physicians should be aware of the possibility of such co-morbidities when treating severe DAI.


   Conclusion Top


Patients with severe TBI are more likely to have abdominal injury than patients with moderate TBI. Physicians should thus be aware of the possibility of such complications when treating severe TBI.

 
   References Top

1.Probst C, Zelle BA, Sittaro NA, Lohse R, Krettek C, Pape HC. Late death after multiple severe trauma: when does it occur and what are the causes? J Trauma 2009;66:1212-7.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Dereeper E, Ciardelli R, Vincent JL. Fatal outcome after polytrauma: multiple organ failure or cerebral damage? Resuscitation 1998;36:15-8.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.McNett M. A review of the predictive ability of Glasgow Coma Scale scores in head-injured patients. J Neurosci Nurs 2007;39:68-75.  Back to cited text no. 3
[PUBMED]    
4.Yanagawa Y, Saitoh D, Takasu A, Kaneko N, Sakamoto T, Okada Y. Experience of treatment for blunt traumatic out-of-hospital cardiopulmonary arrest patients over 24 years: head injury v.s. non-head injury. No Shinkei Geka 2004;32:231-5.  Back to cited text no. 4
    
5.Yanagawa Y, Sakamoto T, Saitoh D, Terai C, Okada Y, Nawashiro H, et al. Significance of shock in head-injured patients with skull fracture. Neurol Med Chir 2000;40:133-8.  Back to cited text no. 5
    
6.Yanagawa Y, Sakamoto T, Takasu A, Okada Y. Relationship between maximum intracranial pressure and traumatic lesions detected by T2*-weighted imaging in diffuse axonal injury. J Trauma 2009;66:162-5.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Rady MY, Smithline HA, Blake H, Nowak R, Rivers E. A comparison of the shock index and conventional vital signs to identify acute, critical illness in the emergency department. Ann Emerg Med 1994;24:685-90.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Association for the advancement of automotive medicine. The abbreviated injury scale: 1990 revision. Association for the advancement of automotive medicine, Des Plaines; 1990.  Back to cited text no. 8
    
9.Kaneko N, Yanagawa Y. Delayed diagnosis of a traumatic diaphragmatic rupture in a patient requiring mechanical ventilation: Utilization of Coronal and 3-Dimensional Computed Tomography. JJAAM 2008;19:119-24.  Back to cited text no. 9
    
10.Probst C, Pape HC, Hildebrand F, Regel G, Mahlke L, Giannoudis P, et al. 30 years of polytrauma care: An analysis of the change in strategies and results of 4849 cases treated at a single institution. Injury 2009;40:77-83.  Back to cited text no. 10
[PUBMED]  [FULLTEXT]  
11.Yanagawa Y, Sakamoto T. Characteristics of pediatric trauma in an urban city in Japan. Pediatr Emerg Care 2009;25:572-4.  Back to cited text no. 11
[PUBMED]  [FULLTEXT]  
12.Smith DH, Meaney DF, Shull WH. Diffuse axonal injury in head trauma. J Head Trauma Rehabil 2003;18:307-16.  Back to cited text no. 12
[PUBMED]  [FULLTEXT]  
13.Adams JH, Graham DI, Murray LS, Scott G. Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. Ann Neurol 1982;12:557-63.  Back to cited text no. 13
[PUBMED]    
14.Imajo T, Roessman U. Diffuse axonal injury. Am J Forensic Med Pathol 1984;5:217-22.  Back to cited text no. 14
[PUBMED]    
15.Yoganandan N, Gennarelli TA, Zhang J, Pintar FA, Takhounts E, Ridella SA. Association of contact loading in diffuse axonal injuries from motor vehicle crashes. J Trauma 2009;66:309-15.  Back to cited text no. 15
[PUBMED]  [FULLTEXT]  
16.Imajo T. Diffuse axonal injury: its mechanism in an assault case. Am J Forensic Med Pathol 1996;17:324-6.  Back to cited text no. 16
[PUBMED]  [FULLTEXT]  
17.Graham DI, Raghupathi R, Saatman KE, Meaney D, McIntosh TK. Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury. Acta Neuropathol 2000;99:117-24.  Back to cited text no. 17
[PUBMED]  [FULLTEXT]  
18.Fijalkowski RJ, Stemper BD, Pintar FA, Yoganandan N, Crowe MJ, Gennarelli TA. New rat model for diffuse brain injury using coronal plane angular acceleration. J Neurotrauma 2007;24:1387-98.  Back to cited text no. 18
[PUBMED]  [FULLTEXT]  
19.Kallakuri S, Cavanaugh JM, Ozaktay AC, Takebayashi T. The effect of varying impact energy on diffuse axonal injury in the rat brain: a preliminary study. Exp Brain Res 2003;148:419-24.  Back to cited text no. 19
    
20.Seleem MI, Al-Hashemy AM. Delayed presentation of traumatic rupture of the diaphragm. Saudi Med J 2001;22:714-7.  Back to cited text no. 20
[PUBMED]    
21.Pfenninger EG, Lindner KH. Arterial blood gases in patients with acute head injury at the accident site and upon hospital admission. Acta Anaesthesiol Scand 1991;35:148-52.  Back to cited text no. 21
[PUBMED]    
22.Calvete JO, Schonhorst L, Moura DM, Friedman G. Acid-base disarrangement and gastric intramucosal acidosis predict outcome from major trauma. Rev Assoc Med Bras 2008;54:116-21.  Back to cited text no. 22
[PUBMED]  [FULLTEXT]  
23.Butcher I, Maas AI, Lu J, Marmarou A, Murray GD, Mushkudiani NA, et al. Prognostic value of admission blood pressure in traumatic brain injury: results from the IMPACT study. J Neurotrauma 2007;24:294-302.  Back to cited text no. 23
[PUBMED]  [FULLTEXT]  
24.Tong KA, Ashwal S, Holshouser BA, Nickerson JP, Wall CJ, Shutter LA, et al. Diffuse axonal injury in children: clinical correlation with hemorrhagic lesions. Ann Neurol 2004;56:36-50.  Back to cited text no. 24
[PUBMED]  [FULLTEXT]  

Top
Correspondence Address:
Youichi Yanagawa
Department of Traumatology and Critical Care Medicine, National Defense Medical College (NDMC)
Japan
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2700.83863

Rights and Permissions



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

This article has been cited by
1 Surgical management in parenchymatous organ injuries due to blunt and penetrating abdominal traumas - The authorsæ experience
Hady, H.R. and Ɓuba, M. and Myƛliwiec, P. and Trochimowicz, L. and Ɓukaszewicz, J. and Zurawska, J. and Ɓadny, J.R. and Dadan, J.
Advances in Clinical and Experimental Medicine. 2012; 21(2): 193-200
[Pubmed]



 

Top
  
 
  Search
 
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
   Introduction
    Materials and Me...
   Results
   Discussion
   Conclusion
    References
    Article Tables

 Article Access Statistics
    Viewed2158    
    Printed150    
    Emailed1    
    PDF Downloaded16    
    Comments [Add]    
    Cited by others 1    

Recommend this journal