Head trauma in dogs

Introduction

Head trauma and traumatic brain injury (TBI) are a cause of significant morbidity and mortality in small animals. One review of blunt trauma in dogs reported 25% of cases to have evidence of TBI, and these were associated with decreased survival rates 1. Causes of head trauma include blunt trauma from a moving vehicle, bite wounds, falls, crush injuries, missile injuries (e.g., gunshots), and human-inflicted trauma 2. In one study, most cases of trauma in dogs and cats were from blunt vehicular trauma and crush injuries, respectively 3. Head trauma may be self-limiting, but it can also result in significant TBI, coma, and even death, with reported mortality rates ranging from 18-24% 4. Head trauma in veterinary patients can initially appear concerning, with owners questioning the prognosis for recovery, but animals appear to be rather resilient, and many can recover with appropriate care, even if radical amounts of cerebral tissue are lost 5. This article reviews the pathophysiology, patient assessment, diagnostics, and treatment recommendations for dogs suffering from head trauma and traumatic brain injury.

Pathophysiology

Normal brain physiology

The cranium is considered a fixed space, with the Monro-Kellie doctrine (Figure 1) stating that the volume within the cranium (composed of brain parenchyma, blood, and cerebrospinal fluid) must remain constant. An increase in any of those components, or the addition of a mass-like component, causes a compensatory decrease in the other components; this is known as altered intracranial compliance. A lack of compensation will lead to increased intracranial pressure (ICP).

Intracranial pressure is the pressure exerted on the cranium by the tissues and fluids. Cerebral blood flow (CBF) provides oxygen and nutrient delivery to brain tissue and is primarily determined by cerebral perfusion pressure (CPP). This can be represented by the equation CPP = MAP – ICP, where MAP is the mean arterial pressure. The driving pressure of CBF is the CPP, as exemplified in the equation CBF = CPP/CVR, where CVR is the cerebrovascular resistance.

Autoregulation maintains the cerebral blood flow despite changes in blood pressure (MAP 50-150 mmHg) by regulating cerebral vessel size. Under normal conditions, intracranial compliance is high, such that changes in intracranial volume will minimally affect ICP. However, head trauma can lead to an increase in ICP with loss of autoregulation, resulting in pressure-dependent flow (i.e., the CBF becomes more dependent on MAP). A significant increase in ICP can ultimately lead to decreased CPP and CBF, which in turn causes ischemia and neuronal death 6.

Primary and secondary injury

Primary injury (Table 1) refers to the physical disruption of tissues within the cranium that occurs immediately at the time of the traumatic event (Figure 2). It can be classified according to the location, the type of injury, and whether it is focal or diffuse 7. Once primary injury is present it cannot be changed, but it affects and influences secondary injury, which occurs after and in reaction to the primary injury. This involves a complex series of biological events that may lead to neuronal death, involving the release and accumulation of excitatory neurotransmitters, cytotoxic edema, and activation of proteases and inflammatory mediators, as well as mitochondrial dysfunction and generation of reactive oxygen species (ROS). The brain parenchyma, with its abundance of lipid, is particularly at risk of lipid peroxidation 8, which can be exacerbated by intracranial hemorrhage and the release of iron ions. Neuronal cell destruction through these processes leads to activation of nitric oxide (NO) pathways, with consequential cerebral vasodilation and alterations in CBF and vascular permeability, contributing to the loss of autoregulation.

Table 1. Classifications of primary injury.

Other intracranial factors can also exacerbate secondary injury, including intracranial hypertension, lactic acidosis, compromise of the blood-brain barrier (BBB), vasospasm, hemorrhage, infection, mass effects, and seizure activity 9. Systemic factors can worsen secondary injury via compromise of CBF, including hypotension, hyper- or hypoglycemia, hyperthermia, hyper- or hypocapnia, hypoxia, and acid-base or electrolyte derangements.

The combination of hypertension and bradycardia in a neurological patient is known as the Cushing reflex, and it can be indicative of severe intracranial hypertension. As brain herniation may be imminent with TBI, rapid recognition and immediate intervention is required. The presence of the Cushing reflex has been shown to be specific for brain herniation in dogs, but its absence does not exclude intracranial hypertension 10 and the clinician should be aware of this; it is therefore reasonable to assume intracranial hypertension is present if the clinical findings are generally supportive.

Patient assessment

Patient assessment should encompass a brief primary survey evaluating the ABCs (airway, breathing, and circulation) followed by a more thorough secondary survey. Hypoxemia, changes to ventilation, and hypotension contribute to secondary brain injury and require rapid recognition and treatment. Respiratory assessment should minimally include evaluation of the airway, respiratory rate and effort, SpO₂, and thoracic point-of-care ultrasound (POCUS). Cardiovascular evaluation should minimally include mucous membrane color, capillary refill time, heart and pulse rate, pulse quality, blood lactate, distal extremity palpation for relative temperature, and blood pressure. With severe head trauma, deranged cerebral autoregulation makes CBF and CPP more dependent on MAP, which makes maintaining blood pressure essential when managing such patients.

Neurological assessment

Neurological assessment should ideally be performed before administrating analgesics and after adequate resuscitation if possible. This should focus on the animal’s level of consciousness, posture and brainstem reflexes. Dogs with head trauma and TBI may demonstrate either a decerebrate or decerebellate posture, although normal posturing does not rule out TBI (Figure 3 and 4). A decerebrate patient may be identified by extension of the head and neck (opisthotonos) as well as all four limbs; decerebellate posturing is characterized by opisthotonos and extension of the forelimbs, with normal to flexed pelvic limbs. In both situations mentation is also often affected, as these patients can have significant intracranial disease. When assessing brainstem reflexes, pupil size, pupillary light reflexes, and physiologic nystagmus should be evaluated (Figure 5). Since cervical trauma can occur concurrently with head trauma, it is also beneficial to evaluate motor and sensory function.

The Modified Glasgow Coma Scale (MGCS) has been validated in dogs (and cats) 11 to assess the severity of neurological deficits (Box 1). This scale scores three categories – motor activity, brainstem reflexes, and level of consciousness – from one to six, with one study showing an MGCS score of 8 on admission to be consistent with a 50% probability of survival in the first 48 hours of hospitalization 11. Serial MGCS measurements (e.g., performed every 30-60 minutes after the initial presentation) can help monitor response to therapy. Other scoring systems, such as the Animal Trauma Triage (ATT) score have also been validated.

Box 1. Modified Glasgow Coma Scale (MGCS).

Diagnostic imaging

Imaging can involve both extracranial and intracranial imaging. Extracranial imaging includes radiography of the thorax, abdomen and any affected limbs to evaluate for comorbidities (e.g., rib fractures, pulmonary contusions, pneumothorax, abdominal free fluid, diaphragmatic herniation, luxations, long bone fractures). POCUS may be more sensitive in detecting pulmonary contusions and small amounts of thoracic or abdominal free fluid 12. Where available, whole body computed tomography (CT) scans can have the advantage of quickly obtaining a vast amount of information with minimal sedation and manipulation of the patient.

Intracranial imaging is warranted in patients not responsive to medical therapy, those that deteriorate after an initial response to medical therapy, and patients with focal or asymmetric neurological disease 13. Skull radiographs are insensitive and are not recommended 8. CT (Figure 6) is preferred over MRI in the emergency setting since it does not require general anesthesia, is typically faster to perform, and is more sensitive for detecting fractures and areas of acute hemorrhage or edema 4,8. However, MRI may provide prognostic value and can aid prediction of developing post-traumatic epilepsy (Figure 7) 14.

Intracranial disease treatment

Head elevation

Elevation of the head at an angle of 15-30^o may decrease intracranial pressure by promoting venous drainage without compromising CBF 15. A stiff board or plank should be used to support either the entire animal (Figure 8) or at minimum from the shoulder and above, to reduce the risk of compressing or distorting the neck that could occlude venous drainage.

Oxygen therapy and ventilation

The goal of oxygen supplementation is to maintain normoxemia. Routine oxygen supplementation should be avoided, as hyperoxemia can worsen reperfusion injury. If oxygen supplementation is needed, flow-by oxygen may be considered until further stabilization is performed. Nasal cannulae should be used cautiously, as fractures may alter the normal anatomy, and in extreme circumstances may cause communication into the cranium. High flow oxygen therapy has the benefits of increased comfort by providing warmed and moistened oxygen, but sneezing from nasal irritation can lead to increased ICP. Oxygen cages may be less stressful, and some allow climate control, but have the disadvantage of creating a barrier between the patient and care team, which can compromise the intensive care and monitoring often needed.

Carbon dioxide plays a significant role in CBF. Hypercapnia causes vasodilation and increased ICP, whilst hypocapnia causes vasoconstriction and decreased ICP. While hyperventilation was previously recommended, this can be detrimental; even small amounts of hypocapnia (PaCO₂ < 34%) can cause excessive vasoconstriction with decreased CBF, ischemia, and neuronal death 16.

Intravenous fluid therapy

Intravenous (IV) fluid therapy is a mainstay of shock treatment, but controversy remains as to the most appropriate fluids to administer for head trauma, and a consensus has not been reached. Fluid therapy should be directed towards resolving hypovolemia, preventing hypotension, and maintaining CBF. Patients with head trauma commonly present in varying degrees of hypovolemic shock, and maintaining systolic blood pressure > 90 mmHg is recommended 4. A human study showed a 150% increase in mortality in patients that had even a single episode of hypotension with systolic blood pressure < 90 mmHg 17.

Due to the potential for breakdown of the blood-brain barrier (BBB) in patients with TBI, fluid therapy may contribute to continued damage of the brain parenchyma via vasogenic edema, cytotoxic edema, and fluid shifts. However, maintaining an adequate CPP is vital since autoregulation is frequently compromised and dependent on blood pressure. The fluid plan must be selected, frequently monitored, and adjusted as needed for each patient.

Isotonic crystalloids

High amounts of intravenous free water may contribute to cerebral edema due to the loss of cellular tight junctions in the damaged brain parenchyma, so 0.9% NaCl, which contains the least amount of free water, is a potential choice. However, due to the higher amounts of chloride and the lack of a buffer, it is also an acidifying solution that may worsen any pre-existing acid-base derangements, and it is associated with acute kidney injury 18. Buffered isotonic crystalloids are a reasonable and justifiable choice. Regardless of the crystalloid selected, therapy should be directed at correcting the derangements noted above (e.g., shock). The authors recommend 10-20 mL/kg given over 10-15 minutes to effect.

Colloids

Colloid solutions are designed to be plasma expanders, as they increase oncotic pressures to retain volume within the intravascular space. As such, they may be an attractive tool in the resuscitation of the hypovolemic or hypotensive head trauma patient. There is a concern that oncotic particles might leak into a traumatized brain due to disruption in the BBB, but no veterinary randomized trials have been performed to test the effects of colloids in TBI cases. However, post-hoc evaluation of a study in human TBI patients comparing resuscitation with saline versus albumin 19 did find a significantly increased risk of death associated with albumin. Until definitive studies show a clear benefit of colloids over crystalloids, the authors do not recommend the use of colloids in TBI.

Hypertonic saline

Hypertonic saline has several attributes that make it an attractive treatment in patients with TBI. It creates an osmotic potential for cellular shifts of water from the intracellular and interstitial spaces into the intravascular space to increase intravascular volume. In doing so, it also increases cardiac output. It also provides intravascular volume expansion greater than its own volume. With these properties, it is particularly effective for hypotensive TBI patients, but as a crystalloid it will rapidly redistribute into the interstitial space, so its IV volume expansion properties only last 45-75 minutes. Other benefits of hypertonic saline are discussed below.

Hyperosmolar fluids

Either mannitol or hypertonic saline can be beneficial due to their hyperosmolar properties. Mannitol is an osmotic diuretic that also has free radical scavenging properties 13 and additionally reduces blood viscosity and improves microcirculatory blood flow. Vasoconstriction of the pial arterioles also decreases cerebral blood volume and ICP 20,21. The recommended dose is 0.5-1.5 g/kg IV over 15-20 minutes 7,8,21, and it can reduce intracranial pressure for 2-5 hours 21, but since it causes diuresis, patients should be volume-resuscitated before administration and euvolemia maintained.

Hypertonic saline is a volume expander via its osmolar effects, but it has other additional benefits. These include reduced endothelial swelling and improved regional blood flow, rheologic properties that decrease blood viscosity and improve perfusion, decreased brain excitotoxicity by promoting reuptake of excitatory neurotransmitters such as glutamate, and immunomodulatory effects 4,7,13. Hypertonic saline may be superior to mannitol in reducing intracranial hypertension 7, but it should always be followed by isotonic crystalloids to maintain adequate hydration, and caution must be taken if used in dysnatremic cases. The recommended dose is 4 mL/kg of 7.5% or 5.4 mL/kg of 3% saline IV over 15-20 minutes.

Antiepileptic therapy

Seizures can cause further secondary injury via increased ICP, increased oxygen demand within the brain, and decreased CBF. Human TBI patients have increased rates of seizures as high as 12% 20, whilst one study showed a rate of 6.8% of canine patients developed post-traumatic seizures 22. Prophylactic antiepileptic drugs may be considered, but no evidence-based recommendations can be made. Benzodiazepines are recommended in the emergent setting followed by initiation of a continued antiepileptic medication, such as levetiracetam or phenobarbital.

Corticosteroids

Steroids are not recommended; whilst they are potent anti-inflammatory agents historically used to manage TBI patients, a large human clinical trial showed an increased risk of death at two and six weeks 23, and the Brain Trauma Foundation does not recommend their use 20.

Hypothermia

As TBI is associated with increased metabolic demands, hypothermia may help mitigate those demands and decrease secondary brain injury. There is currently conflicting data in human medicine about the benefit of therapeutic hypothermia via barbiturate-induced coma, with no recommendations made 20, and there is a paucity of evidence in veterinary medicine on this subject. The authors recommend allowing any hypothermic patients to warm passively, with temperature monitoring in all TBI patients to avoid hyperthermia and excessive hypothermia.

Systemic management treatments

Analgesia

Adequate analgesia cannot be understated for the head trauma patient. Opioids are a reasonable first-line, as they provide good analgesia and are generally cardiovascularly safe, but multimodal analgesia is strongly recommended once the patient has been sufficiently stabilized and evaluated.

Lidocaine is a sodium channel blocker that can be used systemically as an analgesic. Aside from providing mild to moderate analgesia, it has been shown to scavenge ROS and lipid peroxidation 21.

Ketamine is a dissociative anesthetic and an antagonist of N-methyl-D-aspartate (NMDA) receptors which may be particularly useful in TBI patients. While some previous studies suggested that it may increase ICP, new data indicate that its properties of glutamate activation inhibition, neuroprotective effects, NO synthase inhibition, and vasoconstriction all might help improve systemic blood pressure and CBF, minimize secondary brain injury, and decrease ICP 24.

Sedatives

Alpha-2 agonists such as dexmedetomidine are reliable sedatives with mild analgesic properties. Studies in humans and case reports in veterinary patients are mixed in terms of support for or against use in TBI patients, and no randomized, prospective studies have been performed in veterinary TBI patients to date, so until further data is available it is recommended this class of drug is used sparingly for cases of TBI 4.

Benzodiazepines work by modulation of gamma-amino-butyric acid (GABA) to provide sedation and anxiolysis 21, which – coupled with their concurrent anticonvulsant properties and minimal cardiovascular and respiratory effects – make for an attractive management tool.

Phenothiazines (e.g., acepromazine) work via non-specific antagonism of alpha-1 and alpha-2 receptors to provide sedation and anxiolysis 21, and although they were originally thought to lower the seizure threshold in epileptics, this has since been re-evaluated 21. At low doses, they appear to be relatively cardiovascularly safe, but at higher doses they cause vasodilation, which can lead to hypotension. Additionally, they are not reversible and provide less reliable sedation and anxiolysis.

Propofol is a short-acting hypnotic that has been used in cases of refractory status epilepticus 21. It may have neuroprotective effects via its modulation of GABA, but it also can cause hypotension, negative inotropy, and profound respiratory depression.

Miscellaneous therapies

Hyperglycemia is a relatively common finding in both human and animal TBI patients, and in the latter, it has been shown to correlate with the severity of TBI, but not with outcome 3, so the use of insulin for glycemic control is not recommended 13.

Parenteral nutrition can be considered for patients deemed at-risk of aspiration. In people, TBI is also associated with gastric ulceration and bleeding 7, and the use of prophylactic antacids, such as proton pump inhibitors (e.g., omeprazole, pantoprazole) or H₂-blockers (e.g., famotidine) can be considered. Surgical treatments warrant further research before recommendations can be made.

A summary of drugs commonly used for dogs with head injury is given in Table 2.

Table 2. Drugs commonly employed in treating head injuries in dogs.

Conclusion

Dogs that have suffered a traumatic brain injury (TBI) can be a challenge to assess and treat, yet with appropriate intervention many will show significant improvement and often appear to be able to compensate for any remaining neurologic deficits. It is, however, difficult to predict the prognosis after a TBI, as this is dependent on the severity of injury and the timing and efficacy of treatment. Serial evaluation using the coma score can be used to assess prognosis for recovery in individual cases, and owners should be informed their pet may have residual neurological deficits, including (but not limited to) seizures.