Managing head trauma (Proceedings) - Veterinary Healthcare
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Managing head trauma (Proceedings)


CVC IN WASHINGTON, D.C. PROCEEDINGS


Mechanisms

Primary injury is a direct result of the initial insult, is complete at the time of presentation and cannot be altered. Secondary brain injury is an alteration of brain tissue, either anatomical or physiological, which occurs after the primary injury, and can be prevented or ameliorated with optimal supportive care. Secondary injury includes bleeds, cerebral edema, vasospasms, and elevations in intracranial pressure (ICP). The intracranial contents are enclosed in a non-distensible protective bone and consist of brain tissue (80%), cerebrospinal fluid (CSF) (10%), and blood (10 %). An increase in one component will result in a decrease in volume, increase in pressure. Initially, CSF fluid is displaced into the subarachnoid space, then cerebral blood flow is displaced into the jugular vessels. Subsequent very small increases in intracranial volume results in marked increase in ICP. A brain shift or herniation can result. Contusions, hematomas, intracranial bleeds, edema, and tumors are the most common findings that lead to pressure-volume decompensation. A slow, progressive rise is better tolerated than a small acute increase in ICP.

During hypoxia or ischemia, the brain cannot meet the energy demands causing a mismatching of oxygen supply and tissue demand. Cerebral blood flow (CBF) is regulated by: neuronal stimulation, PaO2, PaCO2 , and pressure autoregulation. The brain is very sensitive to changes in PaCO2 , with a 1 mmHg change resulting in a 3-4% change in CBF and cerebral blood volume. CBF is maintained over a range of mean arterial pressures of 50-150 mmHg. The true driving force of CBF is cerebral perfusion pressure (CPP), and when ICP is elevated, CPP equals MAP - ICP. Injured areas of the brain lose the ability to autoregulate, with regional blood flow becoming ldependent upon mean arterial pressure (MAP) and ICP.

There is a flow-metabolism coupling, with the cerebral metabolic rate (CMRO2 ) dependent upon the CBF. Local CMRO2 increases with neuronal activity, such as seizures or fever, and decreases with decreased activity as with hypothermia and anesthetic agents. When CBF decreases below autoregulation, oxygen extraction increases to maintain CMRO2 until a further decline in CBF causes compensatory mechanisms to be exhausted.

Two of the most dramatic causes of secondary injury to the brain is hypotension and hypoxemia, capable of downgrading the outcome. In man, elevation in ICP is a critical secondary insult and the single major contributor to the mortality rate encountered in TBI in humans. Any cause of increased ICP must be sought out and effectively treated.

Physical and neurologic examination

It is important to look for external and internal evidence of trauma. Evidence of hypoxia or cyanosis, echymosis or petechiation, or cardiac or respiratory insufficiency warrants investigation for metabolic etiologies. Retinal exam findings of hemorrhage or distended vessels suggests hypertension or coagulopathy; papilledema suggests cerebral edema; retinal detachment suggests infectious, neoplastic or hypertensive causes. Bradycardia reflects midbrain, pontine or medullary pathology. Evidence of blood around the ears, eyes and nose can reflect trauma severe enough to cause intracranial bleeding. Palpation of the skull can reveal compression fractures that require surgical decompression. When trauma is the cause, careful examination is necessary to detect life-threatening pneumothorax, hemothorax, pulmonary contusions, cardiac arrhythmias, internal bleeding, external bleeding, fractures, and shock. Rapid, irregular breathing patterns with or without cyanosis can suggest respiratory compromise or thromboembolic disease and hypoxemia.

The clinical signs of head injury are related to the degree of secondary brain injury. Neurologic signs localized to a focal area are more typical of intracranial bleeds, herniation or focal vasospasms. Generalized neurologic deficits are more likely to be due to cerebral edema . Secondary brain injury is often initiated at the scene of the trauma when there is hypotension and hypoxia associated with blood loss and shock. Trauma induced brain injury can worsen dramatically during resuscitative efforts due to hypertension and intracranial bleeds. The brain has high oxygen and glucose requirements, minimal storage of oxygen, few recruitable capillaries, and consumes oxygen at a constant rate - setting the stage for hypoxic injury. Fever, seizures or thrashing and afferent stimuli increase the cerebral metabolic rate of oxygen consumption. These conditions should be avoided.

A decline in the level of consciousness implies progression of secondary brain injury due to intracranial bleeding, herniation or cerebral edema.

Whether or not the animal had seizure activity aids in localizing the brain lesion to the cerebral cortex or diencephalon. Traumatic etiologies are associated with secondary brain injury from either bleeding or cerebral edema.

Brain injury affecting any portion of the ascending reticular activating system (ARAS: reticular formation with pathways to the thalamus and cerebral cortex), can alter the level of consciousness in the small animal patient. The levels of consciousness range from awake to mental depression, then delirium, to stupor, and then coma. Stupor is defined as unconscious but responsive to noxious stimuli. Coma implies unresponsive loss of consciousness.

The goal of the neurologic exam is to detect the level of severity and guide the intensity of therapeutics by determining whether the lesion is focal or diffuse and localizing the lesion [to either the cerebral cortical or subcortical area (better prognosis), the midbrain, or the brainstem (grave prognosis)]. The neurolotic examination should determine the level of consciousness and whether or not animal is arousable..

Abnormal respiratory patterns can help localize CNS lesions. Cerebral and diencephalic lesions may produce Cheyne Stokes respiratory patterns, typically seen as a rhythmic waxing and waning in ventilatory rate and depth. In the dog and cat, there has to be diffuse, severe cortical damage for this to be seen. Hyperventilation can be seen with lesions of the midbrain or pons, though metabolic acidosis, respiratory alkalosis, and pain must be ruled out. Irregular respirations (apneustic breathing) can be associated with toxicity or suppression of the brain stem respiratory centers.Detection of severe bradycardia or arrhythmias can be suggestive of brainstem problems.

Localization of brain injury can be done by assessing the function of the cranial nerves: normal cranial nerve exam with cerebral and diencephalic pathology; CNIII deficits reflect midbrain pathology; any deficit of CN V-XII reflects pontine and medullary pathology. Pupillary light reflexes are evaluated: normal responsive pupils or small but reactive pupils indicate cerebral or diencephalic lesion; dilated unresponsive pupils (unilateral or bilateral) or midpoint fixed unresponsive pupils reflect midbrain lesions; mid position unresponsive suggests pons; mid position or normal suggests medulla oblongata. The eye position can reflect regions of the brain that are affected: ventrolateral strabismus reflects midbrain pathology. The oculocephalic reflex is done(if etiology allows cervical manipulation): loss of vestibular nystagmus reflects midbrain or brainstem pathology.

Postural changes are imortant: decerebrate rigidity is a result of midbrain pathology. Midbrain and brainstem signs can result from bleeds, thrombosis, trauma, progression of cerebral edema, and brain herniation, most commonly. Brain edema, herniation, hemorrhage, laceration, contusion, hematomas, or skull fracture are some of the possibilities.


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Source: CVC IN WASHINGTON, D.C. PROCEEDINGS,
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