Approach to head trauma (Proceedings)


The treatment of head trauma is a controversial topic in veterinary medicine. Unfortunately, there does not appear to be a generalized consensus as to the approach to treating head trauma.

The treatment of head trauma is a controversial topic in veterinary medicine. Unfortunately, there does not appear to be a generalized consensus as to the approach to treating head trauma. In general, most veterinarians will agree that the main goal of treating head trauma is to the restore oxygen delivery to the brain and to reduce cerebral edema and intracranial pressure. The controversial part is how to achieve these goals. The only treatments in head trauma that appear to be agreed upon are treatment of shock, oxygen therapy, and head elevation.

During head trauma, pathophysiologically there is primary brain injury and secondary brain injury. Primary brain injury is the injury that occurs at the time of the trauma. This includes the direct injury to the parenchyma and blood vessels in the brain. There generally is nothing that can be done to help the primary injury except for tincture of time. Secondary brain injury is the injury that occurs as a result of inflammation, edema, vasculitis, and increased intracranial pressure. Depletion of ATP in the brain (which is exacerbated by hypoxemia and hypovolemia), increased release of excitatory neurotransmitters (especially glutamate), hyperglycemia, and oxygen free radicals in the brain all contribute to secondary brain injury. It is the secondary brain injury that can be helped with appropriate treatment.

The first step is to normalize blood pressure. In order to maximize oxygen delivery to the brain, cerebral perfusion pressure needs to be maintained. Cerebral perfusion pressure (CPP) is a reflection of mean arterial pressure (MAP) minus intracranial pressure (ICP). If the patient is in shock and is hypotensive, the animal's blood pressure needs to be normalized in order to maintain CPP and hence oxygen delivery to the brain. Normalizing the mean arterial pressure also decreases ICP, since low blood pressure causes cerebral vasodilation; therefore, normalizing the blood pressure will aid in reversal of cerebral vasodilation. In addition, the normal cerebral vasculature autoregulation that occurs with changes in blood pressure is frequently ineffective in the low blood pressure ranges in the head trauma patient. Since the cranial vault tends to be a finite space and the main structures in the cranial vault are parenchyma, blood vessels, and CSF, attempts to prevent cerebral vasodilation are necessary, especially if there is presence of cerebral edema or hemorrhage, which is competing for space in the cranial vault. In addition to normalizing blood pressure, maintaining a normal arterial partial pressure of carbon dioxide is also important, as hypercarbia will cause cerebral vasodilation. Avoiding anesthesia or excessive sedation will help prevent hypoventilation. Buprenorphine or butorphanol may be better analgesic choices than pure opioids (i.e. morphine, hydromorphone) if hypoventilation is of concern.

The concept of normalizing blood pressure leads to the controversial subject of which fluid resuscitation is best for head trauma patients. In other words, which fluid will raise blood pressure quickly, but will not contribute significantly to secondary brain injury and edema? In general, if the amount of crystalloids that are administered can be reduced, it will decrease the progression of cerebral edema. Hetastarch alone as a resuscitation fluid (5-10 ml/kg IV bolus over 10-15 minutes), or a combination of hetastarch/hypertonic saline or dextrans/hypertonic saline (3-5 mls/kg IV bolus over 10-15 minutes of a combination of 2/3 colloid and 1/3 21% hypertonic saline) is currently thought to be the best resuscitation fluid to reduce secondary brain injury in head trauma. In fact, the mere use of colloids, regardless of the amount of crystalloids given, has been shown to be beneficial in head trauma. Crystalloids can still be used judiciously and should not be withheld in the shock patient if colloids are not immediately available (starting with a ¼ shock dose over 10-15 minutes is generally safe, as long as the fluid is titrated to effect – the ¼ shock dose is approximately 15 ml/kg IV in the cat and 22 ml/kg IV in the dog). There is some evidence that in neonates, Lactated Ringers is the best crystalloid choice because neonates utilize lactate more efficiently as an energy source in the brain compared with glucose. It is important to note that hypertonic saline alone has not been shown to be helpful in head trauma patients and in fact may worsen outcome. Targeting a MAP of 80 mmHg should be the resuscitation goal.

Once the animal is properly resuscitated for shock, then the second step is to attempt to decrease intracranial pressure. As previously discussed, normalizing MAP will help decrease ICP by decreasing cerebral vasodilation. Secondly, oxygen supplementation may decrease ICP because during hypoxemia the brain vasculature vasodilates in an attempt to maintain oxygen delivery to the brain. The third treatment of choice for elevated ICP is 15 to 30 degree head elevation. This will help to decrease intracranial pressure by potentially decreasing intracranial blood volume. In addition, avoiding pressure on the jugular veins and avoiding making the animal cough (an important thing to keep in mind if you have to intubate the animal) will help prevent unnecessary increases in ICP.

The fourth treatment of choice for elevated ICP is mannitol administration. Administering mannitol to the head trauma patient is controversial. Mannitol is an osmotic diuretic, which in theory will decrease blood volume and can decrease cerebral edema. In addition, it is a free-radical scavenger and will decrease blood viscosity which may help with micro-perfusion. The argument against mannitol is that if there is an active bleed in the brain, it could leak out with the hemorrhage, causing a hyperosmolar environment and potentially pull more fluid into the area of hemorrhage. Another argument against mannitol use is that it can transiently cause increased intravascular volume, which could transiently increase intracranial pressure. Despite concerns over mannitol use, in the author's experience, it seems that the majority of head trauma cases in veterinary medicine respond favorably to mannitol and rarely decline after mannitol use. This may be because subdural hematomas appear to be fairly uncommon in veterinary patients, although this may simply be a reflection of the fact that we advanced imaging (i.e. CT) to diagnose intracranial bleeding is rarely performed in these patients. Giving 0.5 to 1 g/kg of mannitol IV over 20-30 minutes is generally the protocol. If there is concern about intracranial hemorrhage, giving 0.5 g/kg initially and then observing for improvement or decline in mental status may be useful. If the signs improve or remain unchanged after the 0.5 g/kg, then the dose can be repeated. Do not exceed 3 g/kg total dose in a 24 hours time period.

Lasix therapy has been advocated for use to decrease intracranial pressure in conjunction with mannitol therapy. Some neurologists feel that lasix in addition to mannitol enhances the diuretic effect and more significantly reduces ICP. There appears to be controversy as to when the lasix should be administered (either 15-20 minutes prior to or after the mannitol). The dose is typically 1-2 mg/kg IV.

Steroid use in head trauma remains controversial, but currently is out of favor in the emergency and critical care specialty. Steroids have not been shown to improve outcome and have worsened outcome in some human studies. There is no clear-cut reason for the worse outcome with steroid use, but it may be associated with hyperglycemia (see below). The only time steroids in head trauma have been shown to be helpful is PRIOR to the head trauma incident!

Hyperglycemia in head trauma has become a hot topic. In people, the degree of hyperglycemia on presentation is associated with the severity of the head trauma and outcome. A study in dogs and cats by Dr. Rebecca Syring out of the University of Pennsylvania confirmed that hyperglycemia correlates with the severity of head trauma, but is not correlated with outcome. It is unclear why hyperglycemia is present in severe head trauma, although the leading theory is that the amount of catecholamine release (and hence the severity of trauma) is associated with the severity of hyperglycemia. It is also unclear whether or not the hyperglycemia in and of itself contributes to secondary brain injury and cerebral edema. Some people believe the hyperglycemia may be detrimental if brain oxygen delivery is reduced. This is because glucose metabolism in the brain during anaerobic metabolism will potentially increase brain lactate levels, which may lead to cellular acidosis and increased brain cell death. To date, there is not data as to whether veterinarians should be controlling hyperglycemia associated with head trauma or not.

Future considerations for treatment of secondary head trauma may eventually focus on attempting to decrease brain cell death by controlling glutamate levels in the brain and decreasing calcium build up in the cells. This may be achieved by blocking NMDA receptors, which release glutamate, and by administering calcium channel blockers. There have been no studies to date regarding these techniques and currently cannot be recommended clinically.

Once the head trauma patient is stabilized, the animal must be continually reassessed neurologically. Neurologic status is extremely difficult to assess in a patient that is in shock, as the shock state in and of itself may cause decreased mentation. In general, animals appear to recover very quickly from head trauma. It is the author's recommendation to at least give head trauma patients 24-48 hours of time before making a final decision as to which direction a patient may go regarding recovery. However, a patient that is comatose for >48 hours likely has a grave prognosis. Keep in mind that some neurologic injuries take months to fully recover. The nice thing about the veterinary patient is that higher cognitive function is not necessary to function on a daily basis. If the animal can eat, drink, eliminate, interact appropriately, and sleep, and an owner is willing to nurse the animal along, time may be all that is needed to make a full recovery with minimal residual side effects. In fact, many head trauma patients will continue eating and drinking despite being in an obtunded state (i.e. depressed mentation with a decreased response to stimuli and environment). It is clearly important to ensure that the animal has a gag reflex prior to offering food or water.

The Modified Glasgow Coma Scale may help determine prognosis. A score of 3-8 is considered Grave, 9-14 is considered guarded, and 15-18 is considered to be good.

In conclusion, head trauma is treated somewhat differently than other types of traumatic injuries. Focusing on maintaining mean arterial pressure, volume resuscitation with colloids, reducing intracranial pressure, providing oxygen for 12-24 hours, elevating the head, and tincture of time are all important concepts in treating head trauma. Making decisions about neurologic status too early may result in inappropriate assessment of long term prognosis. Many animals do remarkably well after head trauma and should be given the opportunity to recover for a period of time prior to making an ultimate prognosis as to recovery.

References/suggested reading

Dewey CW. Brain Trauma. In: Wingfield WE, Raffe MR, editors. The Veterinary ICU Book. Jackson Hole, WY: Teton New Media Press; 2002. pp. 911-920.

Dewey CW, Emergency Treatment of Head/Spinal Trauma, 11th Annual IVECCS Proc., 2005, pp 493-497.

Syring, R. S. Hyperglycemia in dogs and cats with head trauma: 122 cases (1997-1999). Journal of the American Veterinary Medical Association 218 (7), 2001, p.1124-1129.

McMichael, M. and Dhupa, N. Pediatric critical care medicine: physiologic considerations. Compendium on Continuing Education for the Practicing Veterinarian 22(3), 2000, p.206-215.

McMichael, M. and Dhupa, N. Pediatric critical care medicine: specific syndromes. Compendium on Continuing Education for the Practicing Veterinarian 22(4), 2000, p.353-360.

Platt, S.R., Radaelli S.T., and McDonnell J.J. The prognostic value of the modified Glasgow Coma Scale in head trauma in dogs. Journal of Veterinary Internal Medicine 15(6), 2001, p. 581-584.

Matthews KA. Veterinary emergency and Critical Care Manual – Suggested Reading.

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