Help! My Patient Sustained Head Trauma!
Traumatic brain injury (TBI) in dogs and cats is a dynamic process. The outcome depends not only on the severity of the primary injury, but also on the resulting secondary effects. Primary injury is defined as injury that occurs at the moment of impact and results in physical disruption of tissues (fracture, etc.). Secondary injury is defined as the physiologic alterations that occur hours to days after the primary injury. Medical therapy is aimed at affecting secondary injury. Animals with TBI frequently have serious injuries elsewhere and shock, hemorrhage, airway obstruction, pneumothorax, and traumatic cardiac arrhythmias should be detected and treated timely.
Pathophysiology
Following TBI local vascular disruption can cause hemorrhage, which results in deposition of iron, free radical formation and mass effect. The effects on the vascular system contribute to vasogenic edema. Cytotoxic edema is the other type of edema that can occur in head trauma. Cytotoxic edema forms when excessive neurotransmitters are released by surrounding cells, which cause overstimulation of neurotransmitter-dependent channels, causing excessive intracellular accumulation of sodium and calcium. Increased intracellular sodium results in an osmotic draw of water into the cell, causing swelling and possibly apoptosis.
Cerebral Perfusion and the Cushing's Reflex
Cerebral perfusion is the driving force behind cerebral blood flow and cerebral blood flow is reduced in the first 24 hours following traumatic brain injury. Reductions in cerebral blood flow can result in poor delivery of oxygen and metabolic substrates and inadequate removal of waste and CO2. CO2 is a potent vasodilator, therefore excessive local CO2 may result in local (or global if severe enough) vasodilation. Maintaining cerebral perfusion, and therefore cerebral blood flow is critical in the head injured patient. There are several equations that are commonly used in TBI and they include:
CPP = MAP – ICP1
CBF = CPP/CVR
CPP = cerebral perfusion pressureCBF = cerebral blood flowMAP = mean arterial blood pressureCVR = cerebral vascular resistanceICP = intracranial pressure
Animals with TBI may develop focal or global increases in CO2 as cerebral blood flow decreases, which result in vasodilation and therefore causes worsening CBF. Following TBI, the brain’s intrinsic ability to manage cerebral blood flow and perfusion pressure becomes altered. Vasomotor centers in the brain may detect increased CO2 and attempt to vasoconstrict through increase in sympathetic function. Systemic hypertension then occurs, which is noted clinically as an increase in MAP. This increase is detected by baroreceptors and a reflexive bradycardia ensues. Animals with decreased mentation, hypertension and bradycardia are at increased risk of having or eminently developing increased ICP. This triad of abnormalities (bradycardia, hypertension and altered mentation) in a post-traumatic patient is called the Cushing’s reflex. The end result of excessive increased ICP is brain herniation.
Management of the Head Trauma Patient
1) Get oxygen to the brain: A clear airway must be established, oxygen and CO2 status should be determined. If oxygen supplementation is required, an oxygen cage or mask may be used. Remember to avoid nasal canula as sneezing can increase ICP. Also, oxygen supplementation will correct hypoxemia, but will not prevent hypercarbia in a hypoventilating animal. Tracheal intubation and mechanical ventilation is indicated in animals that are apneic or hypoventilating.
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2) Monitor blood pressure and heart rate: Head-injured patients require maintenance of systemic and cerebral hemodynamics. The two most important goals are preservation of CPP and maintenance of systemic oxygen availability. Ideally mean arterial blood should be constantly monitored in these patients. Hemodynamic goals include a MAP>80-90 mm Hg and <115-120 mm Hg. Fluid restriction is NOT encouraged in the post-traumatic patient because of the risks to systemic health and the minimal benefit to reducing cerebral edema. Colloidal support may improve blood flow (and perfusion) however, the 2007 SAFE study in human TBI demonstrated an increased mortality in patients receiving albumin compared to those receiving saline rehydration. It remains unknown if all colloidal support would have the same outcome.3
3) Manage Increasing intracranial pressure: Mannitol (1 gm/kg slow IV over 20-30 minutes) has become a cornerstone in the management of increased ICP. There are several proposed mechanisms of action by which mannitol decreases ICP. 1) It expands circulating volume, decreases blood viscosity and therefore increases cerebral blood flow and cerebral oxygen delivery. 2) Reduction of CSF production 3) free radical scavenger 4) Delayed effect: osmotic action: transfer of extravascular edema fluid (in neurons) into the intravascular space: occurs 15-30 minutes after administration when gradients are established between plasma and cells. The effects of mannitol persist for a variable period ranging from 1 to 3 hours depending on clinical conditions. Mannitol can be administered as repeated boluses, or continuous infusion. Due to a rebound effect, risk of hypernatremia and hyperosmolarity, mannitol should not be administered more often than 3 times over a 24 hour period. Dangers of repeated dosage are related to effects on blood volume and electrolytes rather than specific toxicity and the patient's blood volume status should be closely observed. Hypertonic saline may also be used instead of mannitol and is considered equivalent by most neurologists for most patients. Hypertonic saline (4 mL/kg of 7.5% or 5.4 mL/kg of 3%) has the added advantage of rapidly restoring volume by causing an osmotic shift from extracellular to intravascular space. Due to the high sodium level, salt toxicity is possible therefore; serum sodium levels should be frequently monitored. The exception may be patients that are volume depleted; these patients may benefit from hypertonic saline more than mannitol. For a favorable prognosis, a response to medical therapy should be seen within 4 to 6 hours following commencement of treatment. An animal should be assessed every 30 minutes until stabilized.
Glucocorticoids are contraindicated in TBI due to the exacerbation of hyperglycemia. The majority of available evidence indicate that glucocorticoids do not lower ICP, or improve outcome in severely head-injured patients.
Monitoring of TBI patients
1) respiratory status, pupil size (and PLR) and level of mentation. In a very simplistic sense, inspiration and expiration are initiated in the medulla, and the rate and pattern is driven from the midbrain/pontine centers. Feedback loops, largely responsive to blood levels of CO and oxygen are present in the prosencephalon as well. Damage to specific areas of the brain will result in specific respiratory patterns.
2) Monitoring pupil size can help with formulating a prognosis (see below) and aid in initial lesion localization. Sympathetic function to the eye originates in the thalamus, descends through all parts of the brainstem and exits the spinal cord T1-T3. Damage to this tract will result in an inability to dilate the eye, or miosis. This most often occurs with damage to the thalamus (prosencephalon) or medulla. Parasympathetic innervation to the eye starts in the midbrain and goes to the eye by traveling along with the somatic fibers of cranial nerve 3. Damage to the midbrain would result in an inability to constrict the eye, or a dilated fixed pupil. If both the sympathetic and parasympathetic fibers are damaged the eye will appear fixed and midrange.
3) Monitor mentation changes are described as obtunded, stupor or coma. Obtunded animals have diminished responsiveness to the environment but will respond to tactile, visual or verbal stimuli. Animals with stupor will only respond to firm tactile stimuli (not visual or verbal) and animals in a coma will not respond to sharp tactile stimuli such as pinching with a hemostat. Body posture can also help one lesion localize the problem. Decerebrate rigidity occurs with damage to the descending corticospinal tracts, usually at the level of the midbrain. Animals have increased extensor tone to all limbs and severely decreased mentation, usually coma. This indicates a poor prognosis. Decerebellate posture occurs with damage to the cerebellar peduncles and typically has a fair to good prognosis. Patients demonstrate forelimb extension, variable pelvic limb positioning and normal mental awareness.
Prognosis
Both the modified Glasgow coma scale (MGCS) and animal trauma triage (ATT) score have been used to provide estimated, objective assessments for prognostication in animals. For the MGCS, motor activity, brainstem function and level of consciousness are scored and then compared to a graph to determine the relative survival probability.5 For the MGCS, the LOWER the number, the LOWER the probability of survival. Remember to perform 2-3 GCS before considering the number reliable if the animal is in the immediate post-traumatic period. This scale is useful for adjusting the prognosis on a daily basis, as the patient progresses through treatment.
Unlike the MGCS, the animal trauma triage score accounts for more than just intracranial trauma. Scores are summed for each of the following six categories: perfusion, cardiac, respiratory, eye/muscle/integument, skeletal and neurological. Scores are 0-3 for each category resulting in a maximum score of 18. The LOWER the number the HIGHER the probability of survival. 6 For each increase in 1 point, there is a 2-2.6x decrease in survival.7 One recent study compared the two scoring systems for animals with head trauma and identified the ATT as a more predictive and reliable scoring system.7
References:
1. Kuo KW, Bacek LM, Taylor AR. Head Trauma. Vet Clin NA Small Anim Pract. 2018;48(1):111-128.
2. Van Beek J, Mushkudiani N, Steyerber E, et al. Prognostic value of admission laboratory parameters in traumatic brain injury: Results from the IMPACT study. J Neurotrauma. 2007;24(2):315-328.
3. SAFE study I, Australian and New Zealand Intensive Care Society Clinical Trials G, Australian Red Cross Blood S, George Institute for International H, Myburg J, Cooper D. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007;357(9):874-884.
4. Hayes GM. Severe seizures associated with traumatic brain injury managed by controlled hypothermia, pharmacologic coma, and mechanical ventilation in a dog: Case report. J Vet Emerg Crit Care. 2009;19(6):629-634.
5. Platt SR, Radaelli ST, McDonnell JJ. The prognostic value of the modified Glasgow Coma scale in head trauma in dogs. J Vet Intern Med. 2001;15(6):581-584.
6. Rockar RA, Drobatz KS, Shofer FS. Development of a scoring system for the veterinary trauma patient. J Vet Emerg Crit Care. 1994;4(2):77-83.
7. Ash K, Hayes GM, Goggs R, Sumner JP. Performance evaluation and validation of the animal trauma triage score and modified Glasgow Coma Scale with suggested category adjustment in dogs: A VetCOT registry study. J Vet Emerg Crit Care. 2018;28(3):192-200.
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