Abstract
A combination of multiple injury types are typically involved in combat-related head injuries. Innovations in firearms, has led to new types of brain injuries from which we are able to learn much about how the brain responds to trauma. Traumatic brain injury is physical injury to brain tissue that temporarily or permanently impairs brain function. Initial treatment consists of ensuring a reliable airway and maintaining adequate ventilation, oxygenation, and blood pressure. Neurosurgical damage control includes early intracranial pressure control; cerebral blood flow preservation; and prevention of secondary cerebral injury from hypoxia, hypotension, and hyperthemia. Evacuation to the nearest neurosurgeon, avoiding diagnostic delays, and initiating cerebral resuscitation allow for the best chance for ultimate functional recovery.
Key Words: Traumatic brain injury, Intracranial pressure, Combat head injury, Primary brain injury, Secondary brain injury
Introduction
Head injury usually refers to traumatic brain injury (TBI), but is a broader category because it can involve damage to structures other than the brain, such as the scalp and skull. The incidence of fatal head wounds has remained similar throughout history in spite of modern Kevlar helmets. The “Decade of the Brain” saw advances made in brain research and formulation of standardized guidelines for treatment of TBI [1, 2].
Definition
Traumatic brain injury is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile [3, 4, 5]. The terms head injury and brain injury are often used interchangeably [6, 7].
Pathophysiology
Intracranial pressure (ICP) is the normally positive pressure present in the cranial cavity ranging from 5 mm Hg in an infant to 15 mm Hg in an adult. Cerebral perfusion pressure (CPP) equals mean blood pressure (BP) minus ICP. CPP should be maintained at higher than 70 mm Hg in adults and at higher than 60 mm Hg in children [8, 9].
Cerebral blood flow is kept stable under normal conditions due to linear changes in cerebrovascular resistance. This phenomenon is called cerebral autoregulation and means that changes in CPP between 50 mm Hg and 150 mm Hg do not cause significant changes in the cerebral blood flow. However, under traumatic conditions, autoregulation is lost, resulting in a linear relationship of BP to cerebral blood flow. Therefore, maintenance of adequate BP is of vital importance for brain survival.
Because the cranium is a closed space, the sum of the intracranial volumes of brain, blood, cerebrospinal fluid (CSF), and other components (e.g., hematomas, mass lesions) are constant. This is called the Kellie-Monro principle and implies that changes in one of the intracranial components will result in compensatory alteration in the others. Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected [10]. Symptoms are also dependent on the injury's severity.
Traditional Classification of Head Injuries
Open injuries: are the most commonly encountered brain injuries in combat.
Closed injuries: seen more often in civilian settings, may have a higher frequency in military operations other than war.
Scalp injuries: may be closed (contusion) or open (puncture, laceration, or avulsion).
Skull fractures: may be open or closed, and are described as linear, comminuted, or depressed. Skull fractures are usually associated with some degree of brain injury, varying from mild concussion, to devastating diffuse brain injury, to intracranial hematomas.
Combat head injuries
A combination of multiple injury types are typically involved in combat-related brain injuries. Those injuries generally involve the face, neck, and orbit; entry wounds may be through the upper neck, face, orbit, or temple.
Types of Combat Head Injury
-
a
Blunt: (closed head injury).
-
b
Penetrating: these may be (i) Penetrating with retained fragments, (ii) Perforating, (iii) Guttering (grooving the skull), (iv) Tangential, (v) Cranial facial degloving (lateral temple, bifrontal).
-
c
Blast over-pressure CNS injuries:
A force transmitted by the great vessels of the chest to the brain; associated with unconsciousness, confusion, headache, tinnitus, dizziness, tremors, increased startle response, and occasionally (in the most severe forms) increased ICP. Bleeding may occur from multiple orifices including ears, nose, and mouth.
Mechanisms of Injury
Primary brain injury: is caused at the time of impact and is a function of the energy transmitted to the brain by the offending agent. Types of primary brain injury are: (a) Diffuse axonal injury: results from shearing of grey-white matter interface (b) Cerebral concussion: defined by a period of amnesia, (c) Cerebral contusion and (d) Laceration.
Very little can be done by healthcare providers to influence the primary injury. Enforcement of personal protective measures (helmet) by the command is essential prevention [8].
Secondary brain injury results from disturbance of brain and systemic physiology by the traumatic event. It is defined as subsequent or progressive brain damage arising from events developing as a result of the primary brain injury. Hypotension and hypoxia are the two most acute and easily treatable mechanisms of secondary injury [8].
Types of secondary brain injury are: (a) Intra cranial hematomas, (b) Cerebral edema, (c) Ischemia, (d) Infection, (e) Epilepsy/seizures and (f) Metabolic/endocrine disturbances.
Management
The management of head injuries is aimed at preventing secondary injury [12, 13]. The management includes pre-hospital care and triage, initial management at combat sector hospital and finally evacuation for definitive management at tertiary care hospital.
1. Pre-Hospital care
Pre-hospital care is as per ATLS guidelines. The GCS will classify head injury victims as: Minor-GCS 13-15, Moderate-GCS 9-12 and Severe- GCS 3-8.
Triage decisions in the patient with cranio cerebral trauma should be made based on admission GCS score. GCS < 5 indicates a dismal prognosis despite aggressive comprehensive treatment and the casualty should be considered expectant. GCS > 8 indicates that a casualty may do well if managed appropriately. GCS 6-8 can be the most reversible with forward neurosurgical management involving control of ICP and preservation of CBF.
However, the GCS grading system has limited ability to predict outcomes. A current model developed by the Department of Defense and Department of Veterans Affairs uses all three criteria of GCS after resuscitation, duration of post-traumatic amnesia (PTA), and loss of consciousness (LOC) [11]. It also has been proposed to use changes which are visible on neuroimaging, such as swelling, focal lesions, or diffuse injury as method of classification [3]. Grading scales also exist to classify the severity of mild TBI, commonly called concussion; these use duration of LOC, PTA, and other concussion symptoms [12].
Secondary evaluation
CT is the definitive radiographic study in the evaluation of head injury, and should be employed liberally as it greatly improves diagnostic accuracy and facilitates management. CT is useful in evaluating casualties with a high suspicion for spinal injury. Skull radiographs still have a place in the evaluation of head injury (especially penetrating trauma). In the absence of CT capability, AP and lateral skull radiographs help to localize foreign bodies in cases of penetrating injuries and can also demonstrate skull fractures. Standard AP, lateral, and open-mouth radiographs can be obtained to exclude cervical spine injury.
Exploratory burr holes have a definitive role in the absence of imaging services. Classical six burr holes in the absence of localizing signs in an unconscious patient is the signature tool in the hands of a peripheral surgeon.
2. Management at the forward surgical centre
There should only be 3 reasons for keeping patients with head injuries in forward areas: (a) severe shock, (b) immediate surgery required due to active intracranial bleeding or extracranial injuries, and (c) no reasonable chance of reaching a specialized center within 48-72 hours [13].
Goals: prevent infection, treat shock and relieve/prevent intracranial hypertension.
Criteria for exploratory burr holes are: (a) No CT scan facilities are immediately available, (b) No neurosurgical referral center is immediately available (c) The patient is deteriorating rapidly, with one pupil fixed and dilated (d) The patient is dying from brain stem herniation.
Place burr holes along the possible line of a trauma craniotomy and on the side of the dilating pupil or the pupil that dilated first (if known). Start just in front of the ear (1-1.5 cm) and above the zygomatic arch. If no hematoma is encountered, consider opening the dura, especially if a bluish discoloration suggests a subdural hematoma. Burr holes alone are inadequate to treat acute hematomas. Approach to penetrating injury with neurologic changes is aimed at removal of devitalized brain and easily accessible foreign bodies. Tension-free scalp closure is also essential, but replacement of multiple skull fragments in an attempt to reconstruct the skull defect is not appropriate in the battlefield setting. If severe brain swelling precludes replacement of the bone flap it can be discarded or preserved in an abdominal-wall pocket. Evacuate the patient to the nearest neurosurgical centre but transport only patients who can be expected to survive 12–24 hour movements.
3. Management at tertiary care centre
The fundamental goals of resuscitation of the head-injured patient are the restoration of circulating volume, blood pressure, oxygenation, and ventilation.
-
a)
Restoration of blood pressure and oxygenation: Hypotension (SBP < 90 mmHg) or hypoxia (apnea, cyanosis or SaO2 < 90%) must be avoided and scrupulously avoided, if possible, or corrected immediately in severe TBI patients. The MAP should be maintained above 90 mmHg through the infusion of fluids throughout the patient's course to attempt to maintain CPP > 70 mmHg. Patients with GCS < 9 who are unable to maintain their airway or who remain hypoxemic despite supplemental O2 require endotracheal intubation. PaO2 should be kept at a minimum of 100 mm Hg. PCO2 is maintained between 35 and 40 mm Hg.
-
b)
Indications for intracranial pressure monitoring: Comatose head injury patients (GCS 3-8) with abnormal CT scans should undergo ICP monitoring. Comatose patients with normal CT scans have a much lower incidence of intracranial hypertension unless they have two or more of the following features at admission: age over 40, unilateral or bilateral motor posturing, or a systolic blood pressure of less than 90 mm Hg. ICP monitoring in patients with a normal CT scan with two or more of these risk factors is suggested as a guideline. Routine ICP monitoring is not indicated in patients with mild or moderate head injury.
-
c)
Intracranial pressure treatment threshold: An absolute ICP threshold that is uniformly applicable is unlikely to exist. Current data, however, support 20-25 mm Hg as an upper threshold above which treatment to lower ICP should generally be initiated. Mannitol is effective for control of raised ICP after severe TBI. Effective doses range from 0.25 to 1g/kg/body weight. Indications to its use prior to ICP monitoring are signs of transtentorial herniation or neurological worsening not attributable to extracranial explanations. Hypovolemia should be avoided by fluid replacement.
-
d)
Use of barbiturates in the control of intracranial hypertension: High-dose barbiturate therapy is efficacious in lowering ICP and decreasing mortality in the setting of uncontrollable ICP refractory to all other conventional medical and surgical ICP-lowering treatments, in salvageable TBI patients. Utilization of barbiturates for the prophylactic treatment of ICP is not indicated.
-
e)
Role of steroids: The majority of available evidence indicates that steroids do not improve outcome or lower ICP in severely head-injured patients.
-
f)
Role of antiseizure prophylaxis following head injury: Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate, is not recommended for preventing late posttraumatic seizures. Anti -convulsants may be used to prevent early PTS in patients at risk. Routine seizure prophylaxis later than 1 week following head injury is not recommended.
-
g)
Nutrition: Replace 140% of resting metabolism expenditure in nonparalyzed patients and 100% in paralyzed patients using enteral or parenteral formulas containing at least 15% of calories as protein by day 7 after injury.
-
h)
Antibiotics: Broad-spectrum antibiotics should be administered to patients with penetrating injuries.
-
i)
Surgical: Prevent infection and relieve/prevent intracranial hypertension. ICP monitoring devices placement and relief of ICP with hemicraniectomy, duraplasty or ventriculostomy.
Conclusion
No medication exists to halt the progression of secondary injury, but the variety of pathological events presents opportunities to find treatments that interfere with the damage processes. Neuroprotection, methods to halt or mitigate secondary injury, have been the subject of great interest for their ability to limit the damage that follows TBI. However, clinical trials to test agents that could halt these cellular mechanisms have largely met with failure.
Immediate intubation with adequate ventilation is the most critical first line of treatment for a severely head-injured patient. Neurosurgical damage control includes early intracranial pressure (ICP) control; cerebral blood flow (CBF) preservation; and prevention of secondary cerebral injury from hypoxia, hypotension, and hyperthemia.
Evacuation to the nearest neurosurgeon, avoiding diagnostic delays, and initiating cerebral resuscitation allow for the best chance for ultimate functional recovery.
Conflicts of Interest
None identified
References
- 1.Marshall LF. Head injury: Recent past, present, and future. Neurosurgery. 2000;47:546–561. doi: 10.1097/00006123-200009000-00002. [DOI] [PubMed] [Google Scholar]
- 2.Bush GHW. Project on the Decade of the Brain. 1990. Presidential proclamation 6158. [Google Scholar]
- 3.Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurology. 2008;7:728–741. doi: 10.1016/S1474-4422(08)70164-9. [DOI] [PubMed] [Google Scholar]
- 4.Parikh S, Koch M, Narayan RK. Traumatic brain injury. International Anesthesiology Clinics. 2007;45:119–135. doi: 10.1097/AIA.0b013e318078cfe7. [DOI] [PubMed] [Google Scholar]
- 5.Collins C, Dean J. Occupational Therapy and Physical Dysfunction: Principles, Skills and Practice. Churchill Livingstone; Edinburgh: 2002. Acquired brain injury; pp. 395–396. [Google Scholar]
- 6.Hannay HJ, Howieson DB, Loring DW, Fischer IS, Lezak M. Neuropsychological Assessment. Oxford University Press; Oxford [Oxfordshire]: 2004. Neuropathology for neumpsychologists; pp. 158–162. [Google Scholar]
- 7.McCaffrey RJ. The Practice of Forensic Neuropsychology: Meeting Challenges in the Courtroom. Plenum Press; New York: 1997. Special issues in the evaluation of mild traumatic brain injury; pp. 71–75. [Google Scholar]
- 8.Arlinghaus KA, Shoaib AM, Price TRP. Textbook of Traumatic Brain Injury. American Psychiatric Association; Washington, DC: 2005. Neuropsychiatric assessment; pp. 63–65. [Google Scholar]
- 9.NINDS Traumatic Brain Injury Information Page. National Institute of Neurological Disorders and Stroke Retrived 2010-05-15.
- 10.Guidelines for Severe Head Injury Management. J Neurotramna. 2000;17:471–478. [Google Scholar]
- 11.EBIC Guidelines for Management of Severe Head Injury in Adults. Acta Neumchir (Wien) 1997;139:286–294. doi: 10.1007/BF01808823. [DOI] [PubMed] [Google Scholar]
- 12.Traumatic Brain Injury Task Force. 2008. Department of Defense and Department of Veterans Affairs. [Google Scholar]
- 13.Ascroft PB. Treatment of head wounds due to missiles. Lancet. 1943;2:211–218. [Google Scholar]