electroencephalogram, circulation, and lung function after ...€¦ · all parameters were recorded...

Electroencephalogram, Circulation, and Lung Function AfterHigh-Velocity Behind Armor Blunt TraumaDan Drobin, MD, PhD, Dan Gryth, MD, Jonas K. E. Persson, MD, PhD, David Rocksen, PhD,Ulf P. Arborelius, PhD, Lars-Gunnar Olsson, RT, Jenny Bursell, BSc, and B. Thomas Kjellstrom, MD, PhD

Background: Behind armor blunttrauma (BABT) is defined as the nonpen-etrating injury resulting from a ballisticimpact on personal body armor. The pro-tective vest may impede the projectile, butsome of the kinetic energy is transferredto the body, causing internal injuries andoccasionally death. The aim in this studywas to investigate changes in electroen-cephalogram (EEG) and physiologic pa-rameters after high-velocity BABT.

Methods: Eight anesthetized pigs,wearing body armor (including a ceramic

plate) on the right side of their thorax,were shot with a 7.62-mm assault rifle (ve-locity approximately 800 m/s). The shotsdid not penetrate the armor and these an-imals were compared with control animals(n � 4), shot with blank ammunition.EEG and several physiologic parameterswere thereafter monitored during a 2-hourperiod after the shot.

Results: All animals survived duringthe experimental period. Five of the ex-posed animals showed a temporary effecton EEG. Furthermore, exposed animals

displayed decreased cardiac capacity andan impaired oxygenation of the blood.Postmortem examination revealed subcu-taneous hematomas and crush injuries tothe right lung.

Conclusion: The results in our ani-mal model indicate that high-velocityBABT induce circulatory and respiratorydysfunction, and in some cases even tran-sient cerebral functional disturbances.

Key Words: Behind armor blunttrauma, BABT, EEG, Blunt trauma, Pul-monary contusion.

J Trauma. 2007;63:405–413.

Behind armor blunt trauma (BABT) is defined as thenonpenetrating injury resulting from the rapid defor-mation of protective body armor. In recent years,

there have been unpublished reports about cases with fataloutcome after such nonpenetrating impacts. These caseshave been related to high-speed bullets (close to or over800 m/s), demonstrating the relevance of studying high-velocity BABT.

Because of rising numbers of military and civilian sur-veillance operations, there is an increasing need of sufficientpersonal body armor. In addition, high-velocity weaponshave become more widely spread.

The development of armor-penetrating ammunition andthe desire to reduce weight creates challenges during thedevelopment of new body armor.1 Hence, the level of pro-

tection requires a continuous adaptation to meet the demandsof newer projectiles and weapons.

Energy transfer to the body during BABT causes accel-eration of the thoracic wall and underlying organs, resultingin deformation and injuries.2–9 Pressure waves propagatethrough the body, which might affect the brain, even if thehead is not hit. One study in pigs showed a suppressedelectroencephalogram (EEG) pattern directly after impact,after a shot in the hind leg with a high-velocity weapon.10

Furthermore, structural damage in the central nervous systemhas been illustrated in a similar setting using electronmicroscopy.11 However, no data has been previously pub-lished concerning high-velocity BABT and brain function.During battle, even minor brain dysfunction leading to inca-pacitation could be fatal if the person cannot defend himselfor herself or escape. Such dysfunction could be observed asEEG changes in the laboratory setting.

There are several possible reasons for a direct fatal out-come from BABT: a primary crush injury that causes tissuedamage leading to (1) hemorrhage, (2) pulmonary dysfunc-tion, or (3) heart failure. Development of acute respiratorydistress syndrome (ARDS) cannot be ruled out. As a matterof fact, almost 30% of patients with a pulmonary contusiondevelop ARDS.12

Efforts have been made to understand the exact mechan-ical and biologic mechanisms behind BABT, both to improvemedical care and to develop efficient body armor. It has beensuggested that the injuries of BABT have some similarities toblunt chest trauma observed in road traffic collisions, fallsfrom high levels, and other forms of civilian blunt impact.2

However, in contrast to these examples, the impact velocity is

Submitted for publication December 29, 2005.Accepted for publication June 21, 2006.Copyright © 2007 by Lippincott Williams & WilkinsFrom the Department of Defence Medicine (D.D., D.G., J.K.E.P., D.R.,

U.P.A., J.B., B.T.K.), Swedish Defence Research Agency (FOI), Stockholm;the Department of Clinical Neurophysiology (J.K.E.P.), Karolinska Instituteat Karolinska University Hospital, Stockholm; the Department of Anaesthe-siology and Intensive Care (D.D., D.G.), Karolinska Institute at Soder Hospi-tal, Stockholm; the Department of Armor and Survivability (L.-G.O.), SwedishDefence Research Agency (FOI), Tumba, Sweden; and the Department ofSurgery (B.T.K.), Karolinska Institute at Stockholm Soder Hospital, Stockholm.

The authors Dan Drobin, MD, PhD, and Dan Gryth, MD contributedequally to the present study.

Supported by the Swedish Armed Forces.Address for reprints: Dan Gryth, MD, Department of Defence Medicine,

FOI/Karolinska Institutet, Retzius Vag 8, B1:5; SE 171 77 Stockholm, Sweden;email: [email protected].

DOI: 10.1097/01.ta.0000236015.68105.48

The Journal of TRAUMA� Injury, Infection, and Critical Care

Volume 63 • Number 2 405

much larger in BABT and covers a smaller surface area,although the peak velocity of the thoracic wall should not beconsidered equal to bullet velocity.

The aim of the present study was to investigate thepathophysiologic changes in brain function, circulation, andrespiration that may arise after BABT caused by a high-velocity projectile. Our results demonstrate that high-velocityBABT induce circulatory and respiratory disturbances and insome cases even EEG changes.

MATERIALS AND METHODSMeasurement of Back Face Deformation

These tests were performed before animal experiments toevaluate the deformation of the body armor, measured asimpression in ballistic plasticine (National Institute of Justice[NIJ] Standard 0101.04). The body armor was a speciallymanufactured vest segment, corresponding to the SwedishArmed Forces standard issue, Mark m/94 (Åkers KrutbrukProtection AB, Åkers Styckebruk, Sweden), size 255 � 300mm, consisting of a ceramic plate and 14 underlying layers ofaramid fabric. A layer of cotton fabric was placed betweenthe block of plasticine and the armor to simulate a field shirt.Four body armors were used for the back face deformationtest and only one shot was fired at each.

A standard assault rifle (Swedish Armed Forces MarkAK4) equipped with a laser-aiming device (Diode laser typeS 1889, Melles Griot, Taby, Sweden) was used throughoutthe experiments. The weapon was fixed to a small gun car-riage and placed 10 m in front of the target. All ammunitionwas of Danish issue, NATO type, 7.62 � 51 mm; (M/94,Ammunitions-arsenalet, Frederikshavn, Denmark). Projectilevelocity was measured with an optical shutter device (Chro-nograph Beta model, Shooting Chrony, Inc. Mississauga,Ontario, Canada).

Mean bullet impact velocity was 802 (799 – 806) m/sand mean impression in plasticine was 28 (24 –31) mm. Inthe subsequent animal experiments, the eight exposed pigswere protected by an equivalent body armor as the oneduring the impression depth measurements.

Animal ExperimentsAn ethics committee (Permit A1-2000, Umeå, Sweden)

approved the investigation. All animal studies were performedaccording to the Guide for the Care and Use of LaboratoryAnimals.13

Animals were accommodated in an accredited animalfacility at least 2 days before the experiment and fed astandard diet with free access to tap water. Ambient roomtemperature was maintained at 21°C to 22°C with a photo-period of 12 hours of light and 12 hours of darkness. TwelveSwedish landrace pigs (females or castrated males) with amean body mass of 63 (50–91) kg were used. Eight were shotwith live ammunition and four were used as controls (shotwith blank ammunition).

Animal Preparation, Blood Sampling, Recording ofCirculatory and Respiratory Parameters

The experimental setting is displayed in Figure 1. Theanesthesia was performed with infusion of ketamine hydro-chloride 50 mg/mL (Ketalar, Parke-Davis, Pontypool, Gwent,Great Britain) and pethidin hydrochloride 50 mg/mL (Petidin,Pharmacia-Upjohn, Stockholm, Sweden). Tracheotomieswere performed and the animals were mechanically venti-lated in a volume-controlled mode with room air (SiemensServo Ventilator 900C, Siemens-Elema, Solna, Sweden) at arate of 20 breaths/min and the tidal volume was adjusted toachieve normoventilation.

Fig. 1. Experimental set-up in the animal facility.


406 August 2007

Through a cervical cut-down, the left carotid artery wascannulated with a polyethylene catheter (Portex Ltd., Kent,England) to measure systolic, diastolic, and mean arterialblood pressure (MAP).

An optical pulmonary thermodilution catheter (Opticath,Abbot, 7 French Critical Care Systems, AJ Zwolle, Nether-lands) was inserted into the right external jugular vein, formeasurements of central venous pressure (CVP), mean pul-monary artery pressure (MPAP), cardiac output (CO), mixedvenous saturation (SvO2), and body core temperature. Afterthe preparation was completed, animals were allowed 30minutes rest to achieve steady state.

Electrocardiogram (ECG), MAP, CVP, and MPAP weremeasured and monitored with a Sirecust 960 (Siemens Med-ical Electronics, Danvers, MA).

Blood samples were obtained from the arterial line foranalysis of arterial blood saturation (SaO2), PO2, PCO2, Na�, K�,Ca��, pH, base excess (GEM Premier Plus analyzer, Instru-mentation Laboratories, Milano, Italy), lactate (Miniphotometer,8, DR Lange GmbH, Berlin, Germany), whole blood hemoglo-bin (Hb) (Hemoglobin Photometer Electrolux, Mecatronic AB,Helsingborg, Sweden), and blood glucose (B-Glucose analyzer,Hemocue AB, Angelholm, Sweden).

All parameters were recorded at baseline, 1, 5, 10, and 15minutes after impact, and thereafter every 15 minutes untilthe end of the experiment at 120 minutes.

In addition to the directly measured physiologic vari-ables, a number of variables were calculated according to theformulas in Table 1.

Recording of ElectroencephalogramElectrical activity from the brain cortex was registered

by bipolar electroencephalogram (EEG) in seven of theeight experimental animals and in the four controls. In theexposed group, EEG recording was not performed in oneof the pigs because of technical problems. Registration ofthe EEG signal was performed with five electrodesscrewed into the outer part of the skull bone in the midlineover the frontal and parietal lobes, bilaterally over thetemporal lobes and at the vertex. The registration wasmade with a mobile eight-channel EEG recorder (ModelNo. EEG-7209, Nihon Kohden Corporation, Tokyo, Japan).Two ground electrodes were placed subcutaneously in the

neck. An equilibration time of 30 minutes was allowed beforestarting of the EEG recording.

The EEG recording started 5 minutes before the firingof the weapon, to get a baseline pattern, and was continueduntil 15 minutes after the impact followed by 2-minuterecordings every 15 minutes. This recording protocol con-tinued until the animal was killed at 120 minutes. Anexperienced specialist in clinical neurophysiology manu-ally analyzed the EEG sheets.

The EEG pattern was graded into one of five differentlevels according to the estimated change in frequency andamplitude over time: (1) slight to moderate reduction infrequencies, i.e., a reduction of the fast frequency band (slow-ing in frequency range); (2) pronounced reduction in frequen-cies, i.e. a dominance of the slow frequency band (markedslowing in frequency range); (3) overall reduction in ampli-tudes of 50% or more (depression pattern); (4) short bursts ofslow activity with an otherwise global suppression of allcortical activity (burst-suppression pattern); (5) a totally sup-pressed EEG pattern (isoelectric pattern). An illustration ofthe EEG levels is outlined in Figure 2A.

This grading was based on earlier observed changes in EEGpattern after experimental concussion in awake animals,14 whichin its turn was graded according to a previous established stagingsystem for concussion in humans.15 The pre-exposure baselinepattern was graded as zero.

Armor and Shooting ProcedureThe armor was firmly attached to the right side of the

thorax with two 3-cm broad girdles.Twelve animals were randomized, immediately before

the shooting with live ammunition (8 in the exposed group) orblank ammunition (4 in the control group). The firing of thegun was synchronized to the endpoint of the inspiratoryphase.

The control animals were subjected to gun shot with thesame weapon but using blank ammunition. The amount ofgunpowder in the blanks was adjusted to produce a similarsound level as the live ammunition.

Postmortal ExaminationAfter 2 hours observation time, the animals were killed

with pentobarbital 60 mg/mL, 70 mL or more intravenously

Table 1 Abbreviations and Calculations for Variables Used in the Present Study

Abbreviation Variable Source Unit

SV Stroke volume CO/HR mL/strokeSVR Systemic vascular resistance 80 � (MAP � CVP)/CO mm Hg/L/minSvO2 O2 saturation, mixed venous Pulse oximetry (a. pulmonalis) %SaO2 O2 saturation Pulse oximetry (a. carotis) %VO2 Oxygen uptake CO � 0.0139 � Hb � (SaO2 � SvO2) mL/minDO2 Oxygen delivery CO � (0.0139 � Hb � SaO2) mL/minO2ER Oxygen extraction ratio VO2/DO2 � 100 %

EEG and Physiologic Parameters After BABT


until the ECG became isoelectric. An autopsy was performedon all 12 animals directly after the euthanasia and they wereexamined for gross pathologic findings. The thorax wall, thelungs, the heart, the liver, and the bowels of the upper part ofthe abdomen were examined.

Statistical MethodsThe experimental design was two groups followed over

time. Measurements were performed at 12 predefined timepoints. Because some data were missing at the late phase ofthe experimental period, we used a linear mixed-effectsmodel for the statistical analysis.16 PROC MIXED in thestatistical package SAS (SAS Institute, Inc., Cary, NC) wasused for the analysis. In the diagrams, the least square meansare depicted inside 95% confidence intervals. p values of 0.05or less were considered significant.

RESULTSAnimal Experiments

Body mass in the exposed group was 62 (50–91) kg, andin the control group 66 (58–72) kg. In four of the eightexposed animals, bullet velocity was recorded and found to

be 802 (797–811) m/s, which is in agreement with the resultsfrom the back face deformation study.

All animals in the two groups survived the whole obser-vation period of 120 minutes postinsult. No hemoptysis wasobserved.

EEGThere were no differences in the baseline EEG pattern

between exposed and control animals or between the individ-ual animals in the experimental and control groups, respec-tively. In five of the seven EEG-monitored exposed animalsthere was a change in the EEG pattern within 20 seconds afterthe trauma (Fig. 2B). The observed changes were light tomoderate reductions in frequencies, which were seen bilater-ally over the hemispheres without any obvious side differ-ences. In all of these animals, there were gradual returns tothe baseline pattern within 2 minutes after exposure. Theseanimals remained at baseline during the rest of the observa-tion period. In the two remaining exposed animals, there wereno changes in EEG activity during the observation period. Inall four control animals the EEG activity was unchangedcompared with baseline throughout the experimental course.

Fig. 2. (A) Grading of EEG-changes. Recorded EEG in an exposed animal is outlined. EEG levels 0 (baseline)–5 (isoelectric EEG) aredepicted. (B) EEG-changes 1 minute after impact. Decrease in EEG activity is shown for 7 of 8 exposed animals.


408 August 2007

Circulatory EffectsIn the exposed group, blood pressure expressed as MAP

dropped from 116 mm Hg (baseline) to 91 mm Hg during thefirst minute (Fig. 3A). This change was significant comparedwith baseline (p � 0.05), but there was no significant differ-ence compared with the control group at this time. Exposedanimals demonstrated a fast recovery of MAP in this study.We observed baseline values of MAP as early as 5 minutesafter the shot.

CO in exposed animals demonstrated a marked dropfrom 5.5 L/min to 4.2 L/min during the first minute after theshot (Fig. 3B). The difference between the groups was sig-nificant at 1 to 10 minutes postimpact (p � 0.05), followedby a gradual recovery in exposed animals. Control animals(shot with blank ammunition) demonstrated a gradual de-crease of CO during the experimental course. We did notobserve any significant overall differences in CO betweencontrol and exposed animals.

The difference in stroke volume (SV) between thegroups was significant at 1, 5, and 10 minutes after impact(p � 0.05). We observed a marked drop of 25% in strokevolume (SV) during the first minute (Fig. 3C). At 15 minutesafter impact, exposed animals had recovered to a certain degree,followed by a gradual decrease. Control animals demonstrated agradual decrease of SV during the experimental course. We didnot observe any significant overall differences of SV betweencontrol and exposed animals (p � 0.074).

Respiratory EffectsWe observed a decline of SaO2 immediately after impact

and a continued decrease during the first 30 minutes (Fig.4A). The lowest value for SaO2 was recorded at 30 minutesafter impact followed by a gradual recovery. We did notobserve any significant overall differences between controland exposed animals.

The mixed venous oxygen saturation (SvO2) displayed asomewhat different pattern. We observed a gradual decreaseuntil 15 minutes after the shot and low remaining valuesduring the rest of the experiment (Fig. 4B). The overalldifference between the groups was significant (p � 0.05).

Oxygen Transport EffectsOxygen delivery (DO2) and oxygen extraction (O2ER)

are calculated values influenced by both reduction of CO andsaturation of the arterial blood (Table 1). For DO2, we ob-served a significant difference between exposed and controlanimals 1, 5, 10, and 30 minutes after impact (p � 0.05) (Fig.5A). We did not observe any significant overall differencesbetween control and exposed animals (p � 0.076). The re-duction in DO2 was compensated by an increased O2ER,which was enhanced as early as 1 minute after the impact(Fig. 5B). The difference in O2ER between groups was sig-nificant at 5 and 15 minutes (p � 0.05). We did not observeany significant overall differences of O2ER between controland exposed animals (p � 0.066).

Blood AnalysisLactate showed a significant overall difference between

exposed and control animals (p � 0.05). The blood levels oflactate increased over time in exposed animals but seemed tostabilize at the later phase of the observation period (Fig. 6).Control animals were unchanged during the whole experi-ment. Na�, K�, Ca��, pH, base excess, hemoglobin, blood

Fig. 3. The circulatory parameters mean arterial pressure(MAP) (A), cardiac output (CO) (B), and stroke volume (SV) (C)in pigs exposed to high-velocity BABT (F), compared with controlanimals (�).



glucose, and the temperature did not show any significantdifference (data not shown).

Postmortem ExaminationBeneath the body armor point of impact, an almost cir-

cular skin lesion consisting of cutaneous abrasion with asubcutaneous hematoma were evident in all exposed animalsbut there was no laceration of the skin. The mean diameter ofthe skin lesion was 6 (4.5–8) cm. In four exposed animals,fractures of one or two ribs were found beneath the skinabrasions. Lacerations and hemorrhage in the intercostalmusculature were noted.

All exposed animals exhibited a hematoma in the lunglobe underlying the impact area (most often the middle lobeof the right lung). In two animals, a small laceration of lungtissue was also demonstrated. There was no hemothorax orpneumothorax. The examination of the left lung, heart, liver,and bowels did not show any macroscopic injuries. No grosspathologic finding was demonstrated in the control animalsexcept for blue discoloring of the dorsal parts of the lung.

DISCUSSIONIt is evident that the BABT exists as the injury that can

be induced by the impact of a bullet into body armor.2,3 Thereis unpublished information, from military channels, about

Fig. 4. The arterial saturation (SaO2) (A) and mixed venous satu-ration (SvO2) (B) in animals exposed to high-velocity BABT (F),compared with control animals (�).

Fig. 5. Oxygen delivery (DO2) (A) and oxygen extraction (O2ER)(B) in animals exposed to high-velocity BABT (F), compared withcontrol animals (�).

Fig. 6. Lactate production in pigs exposed to high-velocity BABT(F), compared with control animals (�).


410 August 2007

fatal incidents after nonpenetrating impacts. However, aproblem in the study of BABT is the lack of epidemiologicdata. It is also impracticable to perform experiments on livinghumans. Human corpses can provide some information aboutstructural injuries, like fractures,17 but not on pathophysio-logic events in vivo over time, which are possible to monitorduring animal experiments. Simulation models have beenused, but the models are no better than their input data, andit is obvious that the existing knowledge about the mecha-nisms is too weak to permit reliable descriptions of therelationship between applied violence and resulting injury.Information about the consequences of BABT is importantfor development of protective equipment, for militarytactics,18 and for medical planning. The experimental setup inour study, with a shot from a military rifle fired at the rightthorax side, is the standard proposed by the North AtlanticTreaty Organisation (NATO) Task Group on BABT (TG-BABT � TG HFM-001).19 It gives a maximal exposure ofthe lung and a lesser exposure of the heart. If the target hadbeen over the heart, or in full expiration, the physiologicresponse could have been different. Some previous studieshave been performed on impacts against other anatomicpoints of the chest using different experimental models.6,20–22

In one study, when the strikes were against the mid-sternumthey observed sternal fractures, cardiac contusion, and dys-rhythmias such as ventricular fibrillation.22 Disrupted aorticvalves were observed in one animal model using goats andtargeting the “cardiac window”.20 None of these cardiac in-juries or arrhythmia were observed in our study. In thosecases where the impacts were over the lung parenchyma, theinjuries were similar to ours.20,22

The AK-47 assault rifle (Kalashnikov), with a peak ve-locity of approximately 700 m/s, was the most commonlyused weapon of the native Somalia troops,23 demonstratingthe relevance of using high velocity weapons in BABT stud-ies. In our study, the bullet weight of 9.5 g with a velocity of802 m/s led to a kinetic energy of 3.06 kJ, which was reducedto 0 in about 25 microseconds after impact.

If the pig had been shot without the armor, it wouldhave led to immediate death. During this study, none of theexposed animals died, but on the contrary, no animal wasunaffected. Half of the shot animals (4 of 8) had rib fracturesand all had a lung contusion. This contusion with the accom-panying lung hemorrhage was the most serious gross injury inexposed animals. A similar BABT-induced contusion hasbeen described previously by several authors.3,4,7,24–26

The most prominent disturbances of physiologic param-eters in the present study were the changes in brain activity,circulation, and oxygenation. The initial drop in CO, whichseems to be most related to a drop in SV resulting from thefact that heart rate was nearly unaffected, resulted in a tem-porary drop in systemic blood pressure (MAP). The arterialsaturation was deteriorated and this, together with the re-duced CO, led to a marked drop in DO2. An increased O2ERcompensated for the reduced DO2, but this compensation did

not seem to be sufficient, since the blood lactate level in-creased as a sign of peripheral anaerobic metabolism. It isunlikely that this reduction in oxygenation should be causedonly by the primary lung contusion. Other effects, such asintrapulmonary shunt, with a similar pathophysiology as pul-monary embolism, may lead to excessive capillary flow innontraumatized lung areas. These lung areas might normallybe less ventilated leading to decreased capacity of bloodoxygenation. Furthermore, hemorrhage inside the lung result-ing in occluded alveoli, or production of inflammatory me-diators leading to decreased respiratory function in both lungsmust be taken into account.27,28 The hypothesis that differ-ence in saturation between the groups in our study is causedby lung edema declivis is not likely, because the unexposedcontrol animals also were maintained in a supine positionduring the experimental course. However, it should be men-tioned that the control animals demonstrated a slightly de-creased saturation, which might be caused by edema declivis.

EEG changes were one of the most interesting findingsin this study. This is, to our knowledge, the first study todemonstrate that high-velocity BABT induce EEG changes,which may be an indicator of brain dysfunction. The rapidlyoccurring generally transient changes in the EEG pattern,which was demonstrated in five of the seven exposed ani-mals, were different from the baseline patterns recorded inthe control animals, indicating that the trauma almost in-stantly elicited a global cerebral dysfunction.

The EEG showed within 20 seconds a pattern similar tothe one observed in animals subjected to experimental headconcussion.29 Similar factors responsible for producing ex-perimental concussion in animals seem responsible for EEGchanges after head injury in humans.30,31 An immediate slow-ing of the EEG activity has been previously described in pigsafter high energy missile trauma in the hind limb.10 It has alsobeen shown that pressure waves generated by high-energymissile impact in the thigh can be recorded in the abdomen aswell as within the brain.32

The EEG pattern is registered from the brain cortex, butbecause the cortical activity is dependent on input from sub-cortical brain structures, the observed changes could reflect adirect effect on vital centers in the brain stem such as thecenter for wakefulness. Also, the fact that the EEG changeswere general could be an indication that the signals wereelicited from deep brain structures, and consequently werenot signs of local processes from more superficial structuresof the hemispheres.

The lack of EEG changes in two of the recordedexposed pigs might be a result of a more profound anesthesia,because anesthesia is known to stabilize neuronal membranefunction.33 However, ketamine (10.0 mg/kg) has previouslybeen shown to increase the spectral amplitudes of low- andintermediate-frequency EEG components and decrease high-frequency voltage in pigs.34 Although our experimental pro-tocol is standardized, small differences in body weight orwhere the impact was on the torso must be taken into account.



Biologic variation in sensitivity to trauma might also causesome deviation in our results.

The mechanisms behind the depressed brain activity remainunclear. The changes may occur as a result of a direct cerebralreaction to the transmitted shock wave,11 a sensory signal trans-mitted via the peripheral nervous system, hemodynamic effectsof circulatory disturbances, and hypoxia, or a combined effect.The assumption that the EEG changes in our study would besecondary to hypoxia caused by transient apnea is not likelybecause all animals were mechanically ventilated.

Irrespective of the pathophysiologic mechanisms behindthese EEG changes, the suppression most likely indicate atransient cerebral functional disturbance. These resultsclearly demonstrate the importance of studying a possibleinfluence on the cerebral function in trauma not directed tothe head. It would be of interest to investigate if the diffusebrain influence observed in our model would give features asS-100 leaking from the brain,35,36 or other markers of braininjury possible to detect with immunocytochemical staining,as have been shown in other trauma models.37

In the future, it would be desirable to have a protectionthat could defeat realistic threats (like 7.62-mm rifle rounds)without any injuries or negative effects on the performance ofthe bearer. One obvious wish is to make the body armorslighter, because combatants already carry or wear as much as45 kg (100 lb) of equipment into combat.38 Another attributeto strive for is increased protection level, to meet projectilesthat are heavier, with higher speed and that are more pene-trative. Given these facts, it seems reasonable that the BABTproblems will increase and it is therefore desirable that thepathophysiologic effects of BABT are further investigated.Spontaneously breathing exposed animals and the effects ofapnea on EEG activity should be addressed in future studies.

ACKNOWLEDGMENTSThis work was supported by the Swedish Armed Forces. We thank

Dr Peter Juel Thiis Knudsen, Department of Forensic Medicine, Univer-sity of Southern Denmark, Odense, for valuable advice; Magnus Back-heden for excellent statistical analysis; and Elisabeth Malm for skillfultechnical assistance.

REFERENCES1. Knudsen PT. NATO Specialist team on body armor. PASS Symp.

1996:213–217.2. Cannon L. Behind armour blunt trauma—an emerging problem.

J R Army Med Corps. 2001;147:87–96.3. Carroll AW, Soderstrom CA. A new nonpenetrating ballistic injury.

Ann Surg. 1978;188:753–757.4. Liden E, Berlin R, Janzon B, et al. Some observations relating to

behind-body armour blunt trauma effects caused by ballistic impact.J Trauma. 1988;27:145–148.

5. Missliwetz J, Denk W, Wieser I. Study on the wound ballisticsof fragmentation protective vests following penetration by handgun andassault rifle bullets. J Forensic Sci. 1995;40:582–584.

6. Cooper GJ, Taylor DE. Biophysics of impact injury to the chest andabdomen. J R Army Med Corps. 1989;135:58–67.

7. Hinsley DE, Tam W, Evision D. Behind armour blunt trauma to thethorax—physical and biological models. PASS Symp. 2002;103–111.

8. van Bree JL, van der Heiden N. Behind armour blunt trauma:analysis of compressions waves. PASS Symp. 1998;433–440.

9. van Bree JL, Gotts PH. The ‘twin peaks’ of BABT. PASS Symp.2000;371–380.

10. Goransson AM, Ingvar DH, Kutyna F. Remote cerebral effects onEEG in high-energy missile trauma. J Trauma. 1988;28:204–205.

11. Suneson A, Hansson H-A, Seeman T. Pressure wave injuries tothe nervous system caused by high-energy missile extremityimpact. Part II. Distant effects on the central nervous system—alight and electron microscopic study on pigs. J Trauma. 1990;30:295–306.

12. Maunder RJ, Hudson LD. Clinical risks associated with the adultrespiratory distress syndrome. In: Zapol WM, Lemaire F, eds. AdultRespiratory Distress Syndrome. Marcel Dekker, Inc.: New York -Basel - Hong Kong; 1991;1–21.

13. Guide for the Care and Use of Laboratory Animals. Bethesda, MD:NIH; 1996. Publication No. 86-23.

14. West M, Parkinson D, Havlicek V. Spectral analysis of theelectroencephalographic response in experimental concussion inthe rat. Electroencephalogr Clin Neurophysiol. 1982;53:192–200.

15. Parkinson D, West M, Pathiraja T. Concussion: comparison ofhuman and rats. Neurosurgery. 1978;3:176–180.

16. Brown H, Prescott R. Applied Mixed Models in Medicine.Chichester, West Sussex, England: John Wiley & sons; 1996.

17. Bass CR, Salzar R, Davis M, et al. Injury risk in behind armor bluntthoracic trauma. PASS Symp. 2004;115–120.

18. Butler F. Tactical combat casualty care: combining good medicinewith good tactics. J Trauma. 2003;5(Suppl 2–3):S2–S3.

19. Sarron J-C, Destombe C, Gøtse H, Mayorga M. Physiological resultsof NATO BABT experiments. PASS Symp. 2000;381–384.

20. Goldfarb MA, Ciurey TF, Weinstein MA, et al. A method for softbody armor evaluation: medical assessment. Edgewood Arsenal,Aberdeen Proving Ground, Unclassified Report EB-TR-74073. Jan1975.

21. Soderstrom CA, Carroll AW, Hawkins CE. The medicalassessment of a new soft body armor. Chemical SystemsLaboratory, Aberdeen Proving Ground, Report UnclassifiedARCSL-TR-77057. Jan 1978.

22. Cooper GJ, Pearce BP, Stainer MC, et al. The biomechanicalresponse of the thorax to nonpenetrating impact with particularreference to cardiac injuries. J Trauma. 1982;22:994 –1008.

23. Mabry RL, Holcomb JB, Baker AM, et al. United States armyrangers in Somalia: an analysis of combat casualties on an urbanbattlefield. J Trauma. 2000;49:515–528.

24. Knudsen PT, Gøtze H. Behind armour blunt trauma, biomedicalexperiments. PASS Symp. 2000;417–421.

25. Stuhmiller JH, Shen W, Niu E. Modeling for Military OperationalMedicine Scientific and Technical Objectives. Internal annual report.San Diego, CA: Jaycor; 2003.

26. Sarron JC, Destombe C, Lonjon T, et al. Review of behind armor blunttrauma studies since 1999. Presented at RTO Specialist’s meetings(RSM); coorganized by the Applied Vehicle Technology Panel andHuman Factors and Medicine Panel. Kolbe, Germany; May 19–23, 2003.

27. Marino PL. Hypoxemia and hypercapnia. The ICU Book. 2nd ed.Baltimore, MD: Williams & Wilkins. 1998;339–354.

28. Melton SM, Davis KA, Moomey CB, et al. Mediator-dependentsecondary injury after unilateral blunt thoracic trauma. Shock. 1999;11:396–402.

29. William D, Denny-Brown D. Cerebral electrical changes inexperimental concussion. Brain. 1941;64:223–238.

30. Denny-Brown D, Russell WR. Experimental cerebral concussion.Brain. 1941;64:93–164.

31. Dow RS, Ulett G, Raaf J. Electroencephalographic studiesimmediately following head injury. Am J Psychiatry. 1944;101:174–183.


412 August 2007

32. Suneson A, Hansson H-A, Seeman T. Peripheral high-energymissile hits cause pressure changes and damage to the nervoussystem: experimental studies on pigs. J Trauma. 1987;27:782–789.

33. Black S, Cucchiara RF. Neurologic monitoring. In: Miller RD, ed.Anesthesia. 3rd ed. New York, NY: Churchill Livingstone; 1990;1188–1191.

34. Åkeson J, Bjorkman S, Messeter K, et al. Cerebralpharmacodynamics of anaesthetic and subanaesthetic doses ofketamine in the normoventilated pig. Acta Anaesthesiol Scand. 1993;37:211–218.

35. Risling M, Skold M, Larson I, et al. Leakage of S-100 protein afterhigh velocity penetration injury to the brain. In: Seventh

International Neurotrauma Symposium, Adelaide, Australia; 2004;119–124.

36. Ingebrigtsen T, Waterloo K, Jacobsen EA, et al. Traumatic braindamage in minor head injury: relation of serum S-100 proteinmeasurements to magnetic resonance imaging and neurobehavioraloutcome. Neurosurgery. 1999;45:468–476.

37. Marmarou CR, Walker SA, Davis CL, Povlishock JT.Quantitative analysis of the relationship between intra-axonalneurofilament compaction and impaired axonal transportfollowing diffuse traumatic brain injury. J Neurotrauma. 2005;22:1066 –1080.

38. Champion HR, Bellamy RF, Roberts P, et al. A profile of combatinjury. J Trauma. 2003;54:S13–19.



electroencephalogram, circulation, and lung function after ...€¦ · all parameters were recorded...

Documents