Head and Spinal trauma:
The skull is a closed cavity, consisting of several fused bones. Externally it is covered by muscle tissue, connective tissue, and a highly vascular scalp. Internally lies the brain, which is surrounded by the dura mater, which is continuous with the skull, the arachnoid layer, and the pia mater which adheres to the brain. Cerebrospinal fluid is produced in the ventricles of the brain and fills the space between the arachnoid and pia layers. Several veins and arteries pass through the arachnoid layer to reach the brain.
The skull itself forms a vault that is generally very strong but does have thinner areas in the temporal regions, and the base of the skull (Cribiform plate). The brain floats in CSF, and is anchored at the brainstem, which means it moves with a degree of freedom as the ead changes position. CSP provides some protection against trauma, however a significant impact can cause the brain to strike the interior surface of the skull.
The cranial vault itself has a finite volume, that is completely accounted for by the brain, CSF, and blood volume in the intracerebral vessels. If there is any increase in space taken up by one of the 3, the other 2 pay the price. If for example there is a bleed into the subdural space, there is less volume for CSF and cerebral tissue. In response the body reduces the CSF volume. This is temporary and will eventually become insufficient. This leads to an increase in intracranial pressure (ICP).
Perfusion of the brain is dependent upon maintaining CPP (cerebral perfusion pressure. CPP itself is a function of the relationship between MAP and ICP.
Remember:
MAP = DBP x 1/3 (SBP – DBP)
CPP = MAP – ICP
When the ICP rises above 15mmHg we begin to see signs of cognitive deterioration. If ICP rises > 25mmHg the patient will be in critical danger of developing cerebral herniation syndrome. In this situation the pressure in the skull has risen to the point that the brain no longer has sufficient volume to occupy in the cranial vault. The only direction the brain can go is down, through the foramen magnum at the base of the skull. This causes compression of the brainstem (Pons and medulla) which is the control centre for the vital functions in the body (respiration, heart rate, etc).
Cerebral herniation syndrome: This typically presents with aniscoria, unilateral paralysis, and posturing. Additionally the signs of Cushing's Triad may be present 1) Bradycardia, 2) Hypertension with wide pulse pressure, and 3) Irregular respirations. There are various surgical and medical interventions, from the use of osmotic diuretics such as Mannitol, to neurosugrical intervention. In the prehospital environment we generally attempt to address elevated ICP by managing the patient's ETCO2. This is because CO2 is a potent vasodilator. By ventilating the patient to an ETCO2 of 30-35mmHg it is believed that we can reduce vasodilation in cerebral vessels, and limit pressure in the cranial cavity. This buys the patient time to get to a surgeon.
Head injuries: Trauma to the head can occur from blunt or penetrating forces, with a variety of mechanisms.
Fractures of the skull itself can be open, closed, linear, or depressed. With the latter being of particular concern regarding damage to the underlying structures.
Scalp lacerations: These tend to bleed profusely due to the highly vascular nature of the scalp itself. Holding pressure is generally effective. Adult patient's generally do not have a high risk of shock with these injuries, however children are at a greater risk.
Facial fractures:
The most well known classification of facial fractures is the LeFort system. Lefort 1 fractures involve the maxilla. LeFort 2 fractures involve the maxilla and nasal bones. LeFort 3 fractures involve everything from the brow ridge down.
These patients are at high risk for fractures of the basal skull. At the rear of the sinus cavity is the Cribiform plate. This is a thin area of bone, through which the olfactory nerve inters the sinuses. A fracture of this bone provides an opening into the cranial cavity, that presents a risk of cerebral damage if nasal airways are used. Signs of basal skull fracture include: Ottorrhea, Rhinorrhea, Periorbital ecchymosis and Mastoid bruising (Battle Signs).
The major risk with facial fractures or hemorrhages is airway obstruction.
Brain injuries:
Concussion: A concussion is a transient disruption to neurological function that occurs following impact of the brain against the skull. Concussions vary in severity, but generally do not represent contusion or hemorrhage within the brain itself. They usually present immediately after blunt impact, with confusion, ALOC, and a combination of Anterograde and Retrograde Amnesia.
Cerebral contusion: This is actual bruising that occurs from tearing of intracerebral blood vessels. These patients usually undergo a period of prolonged unconsciousness or coma following a blunt trauma. Focal neurological signs, confusion, and amnesia are common, as is combative behaviour.
Diffuse Axonal injury: This occurs when an insult to the brain is severe enough to produce cerebral edema, and increased ICP. Generally these patients present with coma.
Intracranial hemorrhage: Bleeding in the brain is classified based upon where it occurs. -Epidural bleeds: Generally these follow a fracture of the temporal bone, and subsequent severing of the middle meningeal artery. Blood pools between the skull and the dura, compressing the brain. These patients usually present with LOC, followed by a brief lucid peiod that rapidly deteriorates back into coma. Cushing's triad may be present and cerebral hemorrhage is a likely outcome. -Subdural bleeds: This results from disruption of the bridging veins that travel between the dura and the arachnoid layers. The bleeding is slower than that of an epidural bleed and may go unnoticed for hours to days. Patients usually develop headache, followed by gradual deterioration of LOA, until coma eventually occurs. -Subarachnoid hemorrhage: These bleeds are also generally slow and may present with stroke-like symptoms. -Intra-cerebral bleeds: Typically are the result of a ruptured cerebral aneurysm, and present as a hemorrhagic stroke.
Coup-Contra-coup injuries: This occurs with rapid deceleration injuries, which cause the brain to strike the front of the skull and then the back.
Primary brain injury: This is the actual injury at the site of initial trauma.
Secondary brain injury: This is injury that occurs due to swelling and ischemia following a primary brain injury.
Spinal Cord Injuries:
The spine is composed of the spinal column, a hollow tube consisting of 33 vertebrae, separated by fibrous discs, and the spinal cord, which is a nervous structure that is an extension of the brain stem. Various nerves branch out of the cord at different levels, innervating body regions and organs.
Mechanisms of spinal injury:
Hyperextension injuries: This is posterior extension of the spine that exceeds structural capability. The result is fracture of vertebrae. Displacement of these fractures may disrupt the spinal cord itself.
Hyperflexion injuries: This is anterior flexion of the spine beyond its acceptable range of motion.
Compression: This is the placement of an axial load on the spine, that exceeds compressive integrity.
Rotation: This is circular movement of the spine.
Lateral Stress: This involves force applied horizontally across the spine.
Distraction: This is the opposite of compression and involves forces that pull the vertebrae apart vertically (as in hangings).
Spinal cord injuries will present differently depending upon the affected area. Injuries above C5 are typically fatal as the innervation for the diaphragm comes from above this level. Common presentation of spinal cord injury include:
Neck or back pain.
Paralysis or paresthesia
Incontinence
Priapism
obvious deformity
Shock
In general if the mechanism is severe, we want to assume potential spinal injury and take action to implement spinal motion restriction. Gone are the days of backboarding every patient, as this has been proven to be more harmful than helpful. Typically the majority of the spinal column is kept stable by the muscles, tendons, and ligaments that surround it. The primary concern is the cervical spine, which we want to immobilize with a rigid collar until imaging can be don in the ED.
Neurogenic shock: Neurogenic shock is a form of distributive shock that occurs when vessels below the level of injury are cut off from sympathetic innervation. Without the ability to trigger catecholamine release, these vessels dilate, blood pools, and preload to the heart drops. This is life threatening and needs to be dealt with through fluid resuscitation.
Autonomic dysreflexia:
This is a potentially dangerous situation that occurs in patients with a spinal cord injury at T6 or above. It is usually initiated by signals from the bladder (indwelling catheter patients), or the bowel. What happens is the bladder, for example, becomes full and sends a sympathetic signal to the spinal cord to notify the brain. This impulse cannot cross the point of injury, and so the spine triggers a sympathetic NS response below the injury site. This means vasoconstriction, among other things. The result is of course, systemic HTN develops. The carotid baroreceptors pick this HTN up and say “hold up, this is a problem”, and they stimulate the vagus nerve to drop heart rate in an effort to reduce BP. The result of this is bradycardia, and a parasympathetic response above the level of the spinal cord injury.
Symptoms include:
HTN
Bradycardia
Flushing of the face (due to parasympathetic stimulation of cranial nerve VII)
Sweating above the injury site and dry skin below it.
Headache
This needs to be treated in hospital and transport is needed.
This is far from an exhaustive review of potential head and spinal trauma, however my goal is to identify commonly encountered problems that we run into in the field.
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