Initial/Ongoing Management

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Before we begin;EBR on TBI secondary to ballistic wounds

appear contradictoryFollowing is based on 1. US, UK, ADF conflict stats 2. Civilian critique of research methods

by Smith et al. 3. Hellenic Military Academy – ‘unique’U.S. Civilian Forensic Experts, Texas,

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Basic background to BallisticsHi/Low Velocity RoundsBasic Wound Types Upon Presentation (What to look for)

Secondary complications/ ‘Sequelae’Initial /Ongoing Management

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KISS

No two situations are the same.However, if the victim is able to give:

1. Distance – approximate (from assailant)2. Round Type – Pistol or longarm (rifle)

Management approach can be pre-emptedBut first the basic differences in weapon

types …

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Muzzle velocity is the initial speed of the round as it exits the barrel – particular relevance to close proximity pistol round wounds

Pistol rounds (9mm) have relatively high muzzle velocity, 300 – 350m/s, with exceptional penetrating power at short distances for both soft and hard nose rounds (round = bullet)

Rapid decrease in velocity over short distance (20 - 60 metres)

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picsbox.biz/key/9mm bullet drop chart

globalsecurity/.org

Any form of deflection, obstacle has significant effect on penetrating power eg. thin, outer panel of car door (mushrooming, tumbling).

Centrefire longarms have higher muzzle velocity, 900 – 950 m/s and higher speeds over longer distances – due to design, rifling – as opposed to pistol rounds.

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guns.com

High Velocity Rounds Bone - Shattering - Non-Reparable - Complex, distal effectsHigh Velocity Rounds Flesh – Depends on round type - Tumbling - Penetrating Tumbling – Extensive, complex Penetrating – Possibility of very little damage as opposed to low velocity

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Low Velocity Rounds

Bone - Lower possibility of shattering - Significantly reduced possibility of distal effects, TBI

Flesh - Depends on round type (hollow point) - Likelihood of extensive damage,

used deliberately in CQB, by SF/SO

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Not all research papers recognise the significant difference in round velocity to distance in handgun bullet wounds

‘(In ballistic wounds) the essential condition is the distance to target’ - Alexandropoulou & Panagiotopoulos, 2012

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In summary, large calibre longarms and most pistols (9mm +) at close range significantly increase likelihood of TBI from pressure waves

Pistols at ‘most’ distances cause significant damage to flesh

Victim may be ‘lucky’ with high velocity flesh wound from a longarm*

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In addition to the penetration medium (bone, flesh or combination) three other factors affect wound type

Permanent cavity destroyed upon entry – missile morphology and velocity

Fragmentation – missile or bone – not all wounds

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Temporary cavity (5 – 12cm radius) – extension of permanent cavity by kinetic energy transported in tissues by missile

– Serious implications for surgery within the first 3 hour window in assessing tissue to be excised.

Vasospasm – approx. 3 hrs. from hi-vel. wound – colour, bleeding, contractility and consistency parameters for surgery assessment.

3 hrs. vasospasm/constriction followed by hyperaemia*

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TBI from a distal injury not to be confused with injuries from the temporary cavity.

‘Injuries from the temporary cavity are more common in closer proximity to less elastic (brain, liver spleen), fluid filled and dense tissue. Elastic tissue (skeletal muscle) and lower density (lung) are less affected.’

Snow and Bozeman, 2010

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Pressure Wave induced TBI‘ … instantaneous perturbation of dentate inter-neuronal networks by a transient pressure wave-delivered to the neocortex (2)’Results from combined human (DVBIC) USA), animal and simulated compound researchNeuron loss in the hippocampus – Hilus of the dentate gyrus due to pressure waveCells are large and not tightly packed

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Wikipedia Commons

Wikipedia Commons

TBI - Damage to the hippocampus, then damage to the hypothalamus if pressure wave strong enough

BBB - appears to open periodically within first 24 hours of TBI – allowing passage of proteins and substances otherwise excluded from the brain . Alterations to brain osmolarity and oedema formation

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Over expression of Aquaporin channels – permit movement of water into lateral ventricles > exacerbate cerebral oedema

Glutamate (excitatory neurotransmitter) causes influx of Sodium and calcium > hi intra cellular concentrations after TBI.

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Excess Calcium initially buffered by sarcoplasmic reticulum, eventually saturated, excess taken up by mitochondria acting as ‘calcium sink’ under stress situations

With other stimuli, mitochondrial permeability transition pore forms > depolarization, swell with calcium intake, leak due to intra-organelle oedema and ATP production becomes deficient. In a highly metabolically active cell > energy failure. Cytochrome C is also released which promotes apoptosis.

High IC Ca+ attacks cytoskeleton, cytosolic proteins and DNA structures

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And;

Head impact after insult – compounding factor

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A – Airway – C Spine protection/Haemorrhage controlB – BreathingC – Circulation/CompressionsD – Defib./Disability Observe for: Ecchymosis (do not confuse w/bruising) Paralysis of face muscles Declination of eyes to one side CSF liquid from ear, nose or wound One short, lucid interval followed by reduced LOC, headache, nausea and vomiting

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•Fluids

•Oxygen

•BGLs - Insulin

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Ideal state – Eu to moderate hypervolaemia

Isotonic and hypertonic fluids – essential early intervention to maintain cerebral perfusion. To be managed with delayed hyperaemia that can lead to cerebral oedema and inc. ICP

NS not Lactated Ringers/Hartmann's

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Fluids do not replace O2 carrying capacity. At some point blood will have to be given in severe cases.

ICP to be maintained at < 20mmHg and CPP at >60mmHg (hospital based monitoring)

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O2 – caution excess

Up to 50% pre-hospital admissions, inadvertent hyperventilation leads to pCO2 < 33mmHg > incr. mortality in patients with TBI.

Hypocapnea - Implications for vasoconstriction , reduced cerebral blood flow and regional ischemia.

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O2 – Caution excess/under use

Insufficient O2 - Common problems associated with TBI are changing LOCs and transient periods of hypoxia. Hypoxic periods > bradycardia in TBI patients and exacerbate secondary brain injury

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IIT background Lantus/Levemir, medium short acting if time, circumstances permit

Glucose Constant BGL monitoringConservative control, both hyper and

hypoglycaemia can aggravate primary brain injury

Insulin – assess short, medium, long actingSerious implications for brain energy‘Meta-analysis’ – does not support IIT

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Hypothermia

Randomized trials at 37 & 30 Degrees CelsiusReduce glutamate release and free radical

production after TBI. Essential to maintain therapeutic levels for CNS signalling. Excess glutamate responsible for neurological dysfunction associated with TBI.

Glutamate levels increase by over 250% in the dentate gyrus alone in mild brain injury

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Magnesium Salts – with mannitol to improve brain bio-availability - Mg down regulates aquaporin 4 reducing cellular oedema*

MgSO4 induces smooth muscle relaxation, principally in the airway

Clinical trials stating that Mg was of no benefit – pts required intracranial brain surgery within 8 hrs or had the GCS of a rocking chair

Cyclosporine A – inhibit opening of the mitochondrial permeability transition pore.

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DVT/PE ProphylaxisCompression stockingsHold LMW heparin/low dose unfractionated

heparin until 48 – 72 hours after admission – possible risk for expansion of intracranial haemorrhage

Stress Ulcer Prophylaxis (Severe TBI)PPI infusion – most effective (Pantoprazole)H2 blockers – block histamine, reduce enteric acid

(location)Sucralfate – duodenal ulcers – specific to stress

ulcer proph.Early enteral feeding

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Avoid:

Calcium channel blockers Reduce systemic blood pressure and CPP

Corticosteroids Bleeding, hyperglycaemia, increase in

cerebral metabolic rate and fluid retention

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Principally hospital based

Prevent sequelae – ischemia, haematoma, vasospasm

Pulse OximetryIntraparenchymal Brain Catheters increasing in

use due to ease, versatility and ‘short learning curve’ (ICU)

ICP and PtiO2/PbrO2/PBTO2 determine treatment

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To determine benefits of MgCl2 over MgSO4 – possibility of reduced toxicity with MgCl2

Possible benefits of Substance P inhibitors in TBI patients

Oestrogen and Progesterone in TBI management Mg in combination with Tirilazad – nonglucocorticoid neuroprotectant

to reduce vasospasm B2 – Antioxidant, NS function Dexanabinol – anticonvulsant, neuroprotectant

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Tape paper bags to the hands of GSW victims until police swabs completed

Place any cut/discarded clothing in paper, not plastic bags due to condensation and damage to potential evidence.

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Alexandropoulou, C., & Panagiotopoulos, E. (2010). Wound Ballistics: Analysis of Blunt and Penetrating Trauma Mechanisms. Health Science Journal, 4(4), 225-236.

Courtney, A., & Courtney, M. (2007). Links between traumatic brain injury and ballistic pressure waves originating in the thoracic cavity and extremities. Brain Injury, 21(7), 657-662

Davis, D., Fakhry, S., Wang, H., Bulger, E., Domeier, R., Trask, A., & ... Robinson, L. (2007). Paramedic rapid sequence intubation for severe traumatic brain injury: perspectives from an expert panel. Prehospital Emergency Care, 11(1), 1-8.

Dr. Vincent J. M. Di Maio, Chief Medical Examiner and Director of the Regional Crime Laboratory, County of Bexar, San Antonio, Texas (from his Gunshot Wounds, CRC Press, Boca Raton, FL, 1985).

Sen, A, & Gulati, P. (2010). Use of Magnesium in Traumatic Brain Injury. Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics.

Snow, A., & Bozeman, J. (2010). Role implications for nurses caring for gunshot wound victims. Critical Care Nursing Quarterly, 33(3), 259-264

Wallace, D. (2009). Improvised explosive devices and traumatic brain injury: the military experience in Iraq and Afghanistan. Australasian Psychiatry, 17(3), 218-224.

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DVT Prophylaxishttp://www.sjtrem.com/content/20/1/12 IPBC;http://www.slideshare.net/pgpapanikolaou/08

3009papanikolaoupanagiotis439744

The Dentate Gyrus;http://www.jle.com/en/revues/bio_rech/mrh/e-

docs/00/04/11/9B/article.phtml

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