Emergency approach to head trauma (Proceedings)

Article

Traumatic brain injury in the small animal patient may be the result of a variety of traumatic events.

Pathophysiology of Traumatic Brain Injury (TBI):

TBI in the small animal patient may be the result of a variety of traumatic events. Primary brain injury results from a variety of forces (acceleration, deceleration, torsion, etc.) imparted on the cranium and its contents and may range from mass-lesions caused by vascular disruption (epidural hematoma, subdural hematoma, intraparenchymal hemorrhage) to contusions and diffuse axonal injury (most common). Excluding the surgical management of mass lesions (hemorrhage) and depressed skull fractures; there is little that we as veterinarians can do about the primary injury. However, minimizing the incidence or impact of secondary brain injury is the focus of the emergency medical management of the small animal TBI patient.

Secondary brain injury refers to a variety of pathophysiologic processes that culminate in progressive neuronal damage at sites both local and distant from the primary injury. Of greatest importance of the mechanisms of secondary brain injury and that to which therapy can most easily and practically be directed against is decreased global oxygen delivery (DO2). Oxygen delivery to any tissue in the body is dependent on blood flow (Cardiac Output (CO)) and oxygen content of the arterial blood (CaO2). Cardiac output is equal to the product of stroke volume and heart rate. Stroke volume can be depleted in the trauma patient secondary to blood loss, restricted fluid administration, and the administration of diuretics. Blood oxygen content is defined by the following equation: CaO2 = (Hemoglobin X 1.34 X SaO2) + (.003 X PaO2). According to the equation, CaO2 can be depleted through alterations in blood hemoglobin concentration (hemorrhage) and oxygen saturation (pulmonary contusion, pleural space diseases, etc). Insufficient oxygen delivery to neuronal tissue will accentuate the already depleted ATP levels and predispose to the accumulation of lactic acid through anaerobic glycolysis. Aggressive resuscitation of the trauma patient will minimize the occurrence of secondary brain injury from decreased DO2.

Clinical Approach to the Head Trauma Patient:

The approach to the small animal TBI patient should initially address the three major body systems (cardiovascular, respiratory, and CNS) in an effort to identify and institute treatment for immediately life threatening problems. Treatment for problems identified based on the examination of the cardiovascular and respiratory systems should be instituted immediately such that delivery of oxygen to the brain can be maximized. A rapid history including the time of the trauma, clinical signs immediately after the trauma and progression until the present time, medications administered, and previous pertinent medical history should be sought out soon after presentation.

Clinical manifestations and physical and neurologic examination findings in the small animal patient that has suffered TBI may include an altered level of consciousness (agitation/delirium, depression, stupor, coma), seizures, ataxia, proprioceptive deficits, and various cranial nerve deficits including but not limited to head tilt, circling, and nystagmus. The veterinarian may observe obvious wounds to the head and / or neck region, episcleral hemorrhage, hyphema, epistaxis, oral trauma (broken teeth, jaw), blood in the ears, and fractures on palpation of the bones of the head. Inappropriate bradycardia should alert the clinician to the possibility of severely increased intracranial pressure. Identification of any of the aforementioned injuries should prompt the clinician to consider the possibility of a significant intracranial injury and further diagnostic options. Immobilization of the small animal with suspected TBI is important due to the possibility of concurrent cervical spinal injury.

A resurgence of attention is being paid to grading the severity of TBI according to the Modified Glasgow Coma Score (MGCS). The MGCS was developed in 1983 by Shores in an effort to grade the severity of neurologic injury, allow for comparison to that baseline over time, and finally to predict prognosis. The scale was proposed as follows:1

Motor activity

Normal gait, normal spinal reflexes 6

Hemiparesis, tetraparesis, or decerebrate activity 5

Recumbent, intermittent extensor rigidity 4

Recumbent, constant extensor rigidity 3

Recumbent, constant extensor rigidity with opisthotonus 2

Recumbent, hypotonia of mm, depressed or absent spinal reflexes 1

Brain stem reflexes

Normal PLR and oculocephalic (OC) reflexes (OCR) 6

Slow PLR and normal to reduced OCR 5

Bilateral unresponsive meiosis with normal to reduced OCR 4

Pinpoint pupils with reduced to absent OCR 3

Unilateral, unresponsive mydriasis with reduced to absent OCR 2

Bilateral, unresponsive mydriasis with reduced to absent OCR 1

Level of consciousness

Occasional periods of alertness and responsive to environment 6

Depression or delirium, responds but response may be inappropriate 5

Semicomatose, responsive to visual stimuli 4

Semicomatose, responsive to auditory stimuli 3

Semicomatose, responsive only to repeated noxious stimuli 2

Comatose, unresponsive to repeated noxious stimuli 1

A score is given in each of the categories above (motor activity, brain stem reflexes, and level of consciousness) and then the scores are totaled. It has been proposed that a score of 3-8 suggests a grave prognosis, 9-14 suggests a guarded prognosis, and 15-18 suggests a good prognosis.1 Retrospective evaluation of a series of 38 dogs with head trauma correlated the probability of survival within the first 48 hours with MGCS.2 A prospective evaluation of 24 dogs with head trauma showed that MGCS predicted length of stay, cost of care, and thus severity of injury but concluded that further studies will be necessary to determine if MGCS is a good predictor of outcome.3 Future studies will also be necessary to determine if MGCS will be a useful predictor of the necessity for CT scan after head trauma in dogs.

Imaging studies (CT or MRI) of the intracranial structures should be considered in any patient with focal clinical signs, moderate to severe clinical signs of TBI on presentation, failure of clinical signs to improve within hours of initiation of treatment, or deterioration in clinical signs. Imaging will allow the clinician to rule in or out a significant mass lesion (epidural, subdural, or intraparenchymal hemorrhage) or depressed skull fractures as contributory to the clinical signs. Mass lesions and depressed skull fractures in patients with moderate to severe trauma and static or progressive clinical signs should be approached surgically. Imaging studies will also allow the clinician a better appreciation for the other injuries (contusion, edema) often present in the head trauma patient.

Treatment of Head Trauma:

The following will discuss the pros, cons, indications, and contraindications for the various treatment options for the veterinary patient with TBI. Until controlled, prospective studies can be performed in clinical small animal patients with naturally occurring TBI, medical treatment recommendations for small animals must be made based on knowledge gained through human medical research as well as experimental models of head trauma in animals. The limitations of cross-species application of these recommendations must also be noted.

Fluid Therapy: Fluid therapy for the dog or cat that has sustained TBI should be directed towards rapid restoration of intravascular volume and support of CPP through support of MAP. Bouts of hypoxemia or hypotension have been implicated as predictors of poor neurologic outcome in human patients that have suffered head trauma.4 Fluid therapy should never be restricted in the head trauma patient as dehydration will only result in slight decreases in ICP.5 At the same time, fluid restriction may jeopardize the MAP and thus CPP. Options for fluid resuscitation of the head trauma patient include:

Isotonic Crystalloid Fluids: Isotonic crystalloid solutions (Normosol-R, .9% Saline) are reasonable resuscitation fluids for the patient that has sustained TBI. If isotonic crystalloid solutions are chosen for resuscitation, only that volume necessary to restore euvolemia, provide maintenance, and balance out ongoing losses should be administered. Hypo / under-resuscitation should be avoided. Similarly, over-resuscitation may predispose to worsening cellular edema and increased intracranial pressure and should also be avoided. Hypotonic fluids should not be administered to the head trauma patient (unless critical to the maintenance of electrolyte homeostasis) because they can easily cross into the interstitium and equilibrate with the intracellular space thus perpetuating cellular edema.

Hypertonic Saline: Hypertonic saline resuscitation has the advantages of smaller volume resuscitation, rapid restoration of intravascular volume thus improving CPP, improved contractility, and its osmotic effect at the level of the brain thus lowering ICP. Disadvantages include perpetuation of hypernatremia and the pulmonary vagal reflex that can result in bradycardia during administration. There is some evidence that hypertonic saline may disrupt the blood brain barrier and thus nullify some of its beneficial effects.6 Hypertonic saline may be administered at a dose of 4ml/kg of a 7.5% solution by slow IV infusion. Diligent monitoring of serum sodium concentration is critical after administration especially with concurrent administration of other hypertonics such as mannitol. The effects of hypertonic saline may be short lived, but may be extended by concurrent administration of a colloidal solution (Hetastarch or Dextran). Concurrent isotonic crystalloid administration for maintenance purposes and provision for ongoing losses will be required.

Colloidal Solutions: Colloid solutions are considered by some to be the resuscitation fluid of choice in the patient that has sustained TBI. Benefits include a smaller volume necessary for resuscitation (when compared to crystalloid solutions), persistence in the vascular system (long half-life) and thus support of CPP, potential for minimizing vascular leakage, and prolonging the intravascular effects of hypertonic solutions such as mannitol and hypertonic saline. Hetastarch (6%) (5-10ml/kg IV) is probably the most readily available colloid for resuscitation of the canine patient with TBI. In cats, the bolus (2.5-5ml/Kg) must be given over 20-30minutes.

Blood Products: Blood products are a very desirable resuscitation fluid in the patient with concurrent injuries resulting in hemorrhage and hypovolemia. Packed red blood cells, fresh whole blood, and fresh frozen plasma are all acceptable options. The use of hemoglobin based oxygen carriers (HBOCs) in head trauma requires further investigation.

Endpoints of resuscitation include normalization of lactic acidosis and base-excess, return of normal or slightly increased arterial blood pressure, physical examination parameters consistent with resuscitation (pink mucous membranes, normal capillary refill time, normal heart-rate, strong pulses), and normal urine output.

Glucocorticoids: The question of glucocorticoid usage is always up for debate with regard to utility in the management of TBI. Examination of the literature finds no consistent advantage to the utilization of glucocorticoids in head injured patients and potentially some disadvantages. Glucocorticoids, through their counter-regulatory hormone mechanisms can potentiate hyperglycemia. Hyperglycemia can result in the provision of additional substrate for anaerobic metabolism and thus the production of lactic acid. Intracellular acidosis may result in ongoing cellular injury. In a study of veterinary head trauma patients, degree of hyperglycemia was correlated with severity of head trauma.7 According to the Brain Trauma Foundation, "The use of glucocorticoids is not recommended for improving outcome or reducing intracranial pressure (ICP) in patients with severe head injury".8 Some advocate the use of insulin to maintain blood glucose concentrations between70-200mg/dL.

Mannitol: Mannitol is a sugar with a strong osmotic effect that has been shown to decrease both ICP and cerebral edema after traumatic brain injury. Mannitol exerts its advantageous effects through intravascular volume expansion, reflex cerebral vasoconstriction (decreased CBV) secondary to decreased blood viscosity, osmotic effects, and possibly through its free-radical scavenging effects.5-6 Undesirable effects of mannitol include its diuretic effect that could predispose to decreases in intravascular volume and subsequent decreases in DO2 to the brain. Free water losses at the kidney may also result in hypernatremia after mannitol therapy. Close monitoring of electrolytes (primarily sodium) is critical to the management of patients who have received mannitol. Concern has traditionally existed over the use of mannitol in the patient with possible intracranial hemorrhage because of the potential for mannitol to reach the extravascular space and exert its osmotic effect there, thus increasing ICP. However, current thinking is centered around the belief that the advantageous effects of mannitol on a global level are more significant than the negative effects that could result on a local level. Mannitol should not be withheld from the severe head trauma patient in the face of deteriorating neurologic status or documented increased ICP. There is no "Standard" recommendation from the Brain Trauma Foundation regarding mannitol usage. Guidelines state that "Mannitol is effective for control of raised ICP after severe head injury." Dosage ranges from 0.25 – 1g/Kg IV.8 Intermittent bolus therapy may be superior to CRI and may avoid the reverse osmotic shift phenomena in which brain concentrations of mannitol exceed blood concentrations thus perpetuating cerebral edema. As a general guideline, no more than three doses of mannitol should be administered within a 24-hour period.

Hyperventilation in Head Trauma: Hyperventilation (decreased PaCO2) results in decreased ICP through vasoconstriction of cerebral vasculature. Vasoconstriction, however, will result in decreased cerebral blood flow and thus decreased oxygen delivery to neurons (cerebral ischemia). Prolonged hyperventilation has been associated with inferior neurologic outcomes in people with severe injury when compared to those in which hyperventilation was avoided.11 Hyperventilation is only recommended as an emergency and transient effort to lower ICP. TBI patients undergoing anesthesia for diagnostic or therapeutic procedures should have PaCO2 kept in the 35mmHg range. The advantage of positive pressure ventilatory support is that both oxygenation and ventilation can be controlled and episodes of desaturation of hemoglobin can be minimized. According to the Brain Trauma Foundation, Standard Recommendations state that "in the absence of increased ICP, chronic prolonged hyperventilation therapy (PaCO2 ( 25mmHg) should be avoided after severe traumatic brain injury" and Guidelines state that "the use of prophylactic hyperventilation (PaCO2 ( 35mmHg) therapy during the first 24 hours after severe TBI should be avoided because it can compromise cerebral perfusion during a time when cerebral blood flow is reduced".8 Transient hyperventilation may be necessary for treatment of the acutely deteriorating patient with head trauma.

Elevation of the Head: Placing the patient on a board such that the head is approximately 20-30 degrees above the pelvis may improve cerebral venous drainage. Excessive elevation may decrease CPP and elevation of just the head may result in compression of the jugular veins and thus decreased venous drainage (and secondarily increased ICP). Jugular vein phlebotomy and catheterization is avoided for similar purposes (decreased venous drainage).

Oxygen Therapy: Oxygen therapy should me administered to maximize oxygen saturation of hemoglobin as measured by pulse oximetry at the bedside. When providing oxygen to the head trauma patient, we should strive to make oxygen saturation approach 99%. Oxygen can be administered by cage, mask, hood, nasal cannulae, or transtracheal delivery methods. Those methods that cause coughing or sneezing should be avoided if at all possible as these effects may transiently increase ICP. If oxygenation cannot be maintained without FiO2> 0.6 (60%), positive pressure ventilation is indicated.

Seizure Prophylaxis: The incidence of early and late post-traumatic seizures in the veterinary head trauma patient is currently unknown. At the present time, in human medicine, routine seizure prophylaxis for late onset seizures is not a standard recommendation.8 Anticonvulsants are recommended for early posttraumatic seizures.8 In veterinary medicine, benzodiazepines (for the actively seizing patient) and barbiturates (phenobarbital) are the most readily available drugs for this purpose. The author frequently utilizes phenobarbital for the prevention of early post-traumatic seizures in patients that demonstrate seizure activity for a minimum of 2 months in patients with moderate to severe TBI.

Sedation / anesthesia in the small animal with TBI: Cardiovascular and respiratory sparing sedation protocols are optimal in TBI (oxybarbiturates, narcotic / benzodiazepine combinations). ETCO2 and oxygen saturation (SpO2) should be monitored to avoid episodes of hypoventilation and hypoxemia. Blood pressure should be monitored closely and hypotension should be avoided. Ketamine at the present time is not recommended due to increases in ICP that result after administration, however usage of ketamine in the head trauma patient is presently being reinvestigated.

Monitoring of the Head Trauma Patient:

Monitoring of the veterinary head trauma patient should focus on the three major body systems. Blood pressure (oscillometric, Doppler, or direct arterial blood pressure) should be monitored every 1-2 hours or more frequently as deemed necessary. Systolic blood pressure should ALWAYS be greater than 120mmHg recognizing that in the absence of pressure autoregulation, cerebral blood flow may be reduced even at this pressure. A goal of MAP 80-120mmHg is reasonable. ECG monitoring on a continuous basis is excellent for assessment of heart rate and rhythm. Bradycardia may be a sign of severe increases in ICP (see cerebral ischemic response). Continuous pulse oximetry allows the veterinarian to monitor for bouts of arterial desaturation (commonly associated with secondary brain injury). SpO2 should approach 99%. Arterial blood gas analysis and / or end-tidal capnography will allow the clinician to assess PaCO2 levels and possibly avoid bouts of hypoventilation (>40mmHg). Much of the monitoring equipment available today has functions for preset alarms. Utilization of these alarms to sound upon desaturation, bradycardia, hypotension, etc. is useful. If mannitol or hypertonic saline are being utilized, frequent assessment of electrolytes (at least twice daily) is critical to avoid hypernatremia or a host of other electrolyte abnormalities. Electrolytes, acid/base status, and blood glucose should always be assessed at least once daily in the critically ill patient and fluid therapy adjusted to maintain electrolytes within normal limits. Normalization of blood glucose may be beneficial to the patient that has suffered head trauma. Measurement of urine output via urethral catheterization will facilitate calculation of fluid ins-and-outs such that fluid therapy can be tailored to help maintain euvolemia and hydration. Frequent neurologic examinations focused on MGCS can help identify both progressive intracranial conditions and clinical improvement. Any negative changes in physiologic parameters or physical exam parameters should instigate rapid diagnostic and therapeutic responses on the part of the clinician.

Conclusion

TBI is a common cause of morbidity and mortality in the small animal trauma patient. Veterinarians should work initially to identify and correct major body systems abnormalities. By doing so, secondary brain injury will be attenuated and a greater likelihood of a positive outcome will be achieved.

References

Shores A. Craniocerebral Trauma. In Kirk RW ed. Current Veterinary Therapy X. Philadelphia: WB Saunders Co., 1983: 847-854.

Platt SR, Radaelli ST, McDonnelll JJ. The prognostic value of the modified Glasgow coma scale in head trauma in dogs. J Vet Intern Med 2001;15: 581-584.

Streeter EM, McDonnell JJ, O'Toole TE et al. Prospective evaluation of head trauma in 24 dogs: modified Glasgow coma scale, animal trauma triage score, computed tomography findings and outcome, in Proceedings. 9th International Veterinary Emergency and Critical Care Symposium 2003; 774.

Chestnut RM, Marshall LF, Klauber MR et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34: 216-222.

Proulx J, Dhupa N. Severe Brain Injury. Part II. Therapy. Comp Cont Ed Pract Vet 1998;20: 993-1005.

Dewey CW. Emergency management of the head trauma patient. Vet Clin North Am Small Anim Pract 2000;30: 207-223.

Syring RS, Otto CM, Drobatz KJ. Hyperglycemia in dogs and cats with head trauma: 122 Cases (1997 – 1999). J Am Vet Med Assoc 2001;218: 1124-1129.

The Brain Trauma Foundation, The American Association of Neurological Surgeons, The Joint Section on Neurotrama and Critical Care. Guidelines for the management of severe head injury. 1995.

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