Head Trauma Management in Small Animals

Traumatic brain injury (TBI) is a frequent component of head trauma in small animals. TBI is associated with high morbidity and mortality in both animals and humans. Etiologies are most commonly motor vehicle accidents in dogs and crush injuries in cats.¹ Falls from heights, gunshot wounds, bite wounds, and accidental or purposeful attacks from humans are other causes. Recovery is enhanced by early and aggressive therapy. Treatment is focused on maintaining cerebral perfusion pressure (CPP), reducing intracranial pressure (ICP), and treating secondary injury. This article reviews the pathophysiology of head trauma, patient assessment, diagnostic testing, treatment recommendations, monitoring, and prognosis.

Pathophysiology of Head Trauma Patients

Increased Intracranial Pressure

Mean arterial pressure (MAP) minus ICP is the CPP. The Monro–Kellie doctrine states that the volume of brain parenchyma, blood, and cerebrospinal fluid is constant, and any change in volume without compensation leads to an increase in ICP. Usually, there is a high intracranial compliance and a minimal effect on ICP with fluid shifts in the brain vasculature and cerebrospinal fluid.

When the volume-buffering capacity is exceeded beyond the limits of compensatory mechanisms, the ICP will increase. Increased ICP leads to a decrease in CPP, cerebral ischemia, and neuronal death. Severe increases in ICP trigger a cerebral ischemic response called the Cushing reflex (manifested as hypertension with bradycardia) in an attempt to maintain appropriate CPP. The Cushing reflex occurs with an acute and severe increase in ICP, which results in a decrease in cerebral blood flow and thus an increase in carbon dioxide. The Cushing reflex occurs in terminal stages of brain herniation and is indicative of possible life-threatening elevations in ICP; thus, aggressive treatment should be initiated. Prior to this stage, there is likely failure of other hemostatic mechanisms related to Pco₂ (partial pressure of carbon dioxide), blood pressure, cerebral metabolic rate, and pressure autoregulation.

Primary Brain Injury

Primary brain injury is the direct physical damage from the traumatic event. Injuries range from mild contusion to severe laceration of the brain parenchyma. Vasculature damage may also lead to intracranial hemorrhage, hematoma formation, and subsequent vasogenic edema. Unstable skull fractures can contribute to primary injury as well.^2-5

Secondary Brain Injury

A complex cascade of biochemical derangements causes secondary injury within minutes to days after the initial trauma. Trauma causes increased release of excitatory neurotransmitters and depletion of adenosine triphosphate. A sudden influx of sodium and calcium into cells leads to a further increase in excitatory neurotransmitters. Increases in sodium lead to cytotoxic edema along with failure of membrane pumps, whereas increases in calcium lead to neuronal damage and death. Local tissue acidosis and hypoperfusion trigger production of reactive oxygen radicals, which damage the neuronal cell membranes. TBI also causes release of inflammatory cytokines, which accumulate in tissues and worsen secondary injury by activating the arachidonic acid and coagulation cascades, thus damaging the blood–brain barrier (BBB). Inflammation leads to release of nitric oxide, which leads to excessive vasodilation and loss of pressure autoregulation. Cerebral perfusion is compromised with systemic changes such as hypotension, hypoxia, inflammation, changes in glucose concentrations, hyperthermia, electrolyte abnormalities, acid–base abnormalities, and hypercapnia or hypocapnia.^6-9

Assessment of Head Trauma Patients

Primary Assessment and Extracranial Stabilization

Life-threatening extracranial injuries are evaluated first (ABCs [airway, breathing, circulation]). An electrocardiogram and blood pressure test are part of the triage exam. If the animal is in shock, the clinician should immediately address hypotension, hypovolemia, and oxygenation/ventilation. Hypovolemia and hypoxemia strongly correlate with an increased ICP and mortality.⁶

The Animal Trauma Triage (ATT) scoring system was developed using 6 categories: perfusion, cardiac, respiratory, eye/muscle/integument, skeletal, and neurologic. Each category is scored on a scale of 0 to 3, with 0 indicating mild to no injury and 3 indicating severe injuries. The score for each category is added to give a maximum total ATT score of 18. The ATT was initially developed in 1994, and it was found that each point on the scale resulted in a 2.3 to 2.6 decreased likelihood of survival.¹⁰ Since then, several studies have validated this scoring system.^11-14

A newer veterinary trauma score, VetCOT (Veterinary Committee on Trauma), has been developed that uses 4 predictive variables: blood ionized calcium and plasma lactate concentration within 6 hours of admission, and presence or absence of head and/or spinal trauma. However, further validation studies are needed for this scoring system.¹⁵

Neurogenic pulmonary edema can develop rapidly following a TBI, causing dyspnea, hypoxemia, and hypercapnia, and therefore potentially increased ICP. The pathophysiology is not well understood, but it is thought to be due to a marked peripheral vasoconstriction secondary to an increase in sympathoadrenal activity. The vasoconstriction is then thought to lead to systemic hypertension and pulmonary capillary hypertension with subsequent edema. Neurogenic pulmonary edema is typically self-limiting and resolves within hours to days. Early intervention and aggressive supportive therapy are important. This consists of employing therapies that improve oxygenation and support of respiratory function (e.g., oxygen mask, oxygen cage, oxygen via nasal catheter), minimizing stress with use of light sedation as needed, and administering diuretics (furosemide 2 to 4 mg/kg IV q4h to q12h) in the acute phase. Intubation and positive-pressure ventilation are recommended for critically dyspneic animals.^16-19

Hyperthermia may be noted as a result of trauma to the thermoregulatory center, iatrogenic causes, stress, seizures, or pain. Hyperthermia should be addressed immediately as it increases cellular metabolism and vasodilation, which may lead to an increase in ICP.²⁰

After addressing life-threatening injuries, the patient should be fully evaluated for other injuries (e.g., fractures, thoracic or abdominal injuries).

Neurologic Assessment and Intracranial Stabilization

A full neurologic exam and a Small Animal Coma Scale (SACS) evaluation, also known as the modified Glasgow Coma Scale (MGCS), should be performed next (FIGURE 1).²¹ The SACS evaluates motor activity, brainstem reflexes, and level of consciousness, with a total score of 18. A lower score is associated with a poorer prognosis. The idea of a SACS was derived from the work of Teasdale and Jennett, who developed the Glasgow Coma Scale (GCS) in humans. Although much of the GCS relies on verbal responses in humans, the SACS delivers scores based on physical and neurologic responses that are evaluated or observed. The result is an objective measurement of the patient’s status. SACS assessment helps the clinician assess severity of neurologic status and initial prognosis; it also allows the clinician to perform serial SACS scores to monitor for improvements or deteriorations.²

Figure 1. Small Animal Coma Scale. Evaluations are made of each category and the composite score can be used to estimate patient outcome.

Hyperosmolar therapy (mannitol, hypertonic saline) is the treatment of choice for reducing ICP in patients with TBI. Hypertonic saline may be favored over mannitol because it significantly decreases ICP to a greater degree and for a longer duration compared with mannitol²²; however, the Brain Trauma Foundation guidelines in human medicine still consider mannitol as first-line treatment in patients with TBI if the patients are euvolemic and preferably normotensive.²³ Hypertonic saline may also be a better choice for hypovolemic patients, although hypernatremia is a contraindication for use. Dose recommendations for hypertonic saline are 3 to 4 mL/kg (7.5% sodium chloride [NaCl]) and 5.3 mL/kg (3% NaCl). The dose recommendation for mannitol is 0.5 to 1.5 g/kg as a bolus over 15 to 20 minutes; however, one study in humans showed that a higher dose (1.4 g/kg) showed significantly better outcomes when compared to a lower dose (0.7 g/kg).²⁴ The lower concentration of hypertonic saline (3%) is preferred when using a peripheral vein because the higher concentration (7.5%) usually causes a severe vasculitis.

In addition to hyperosmolar therapy, elevating the head at a 15° to 30° angle with the head and neck extended helps reduce cerebral blood volume by increasing venous drainage from the brain. This helps decrease the ICP and increase the CPP. Care must be taken to avoid compression of the jugular veins, which leads to an increase in ICP.^2,25

If the patient is actively having seizures, diazepam or midazolam is the first-line treatment for rescue (diazepam 0.5 to 1 mg/kg IV or midazolam 0.3 to 0.5 mg/kg IV or intranasally). The dose can be repeated up to 4 times in an hour. For prevention of further seizure activity, a maintenance anticonvulsant medication should be started after a seizure. Levetiracetam is a good option. It has low sedative properties and is less likely to interfere with serial neurologic assessments. The loading dose of levetiracetam is 60 mg/kg IV, followed by 30 mg/kg IV q8h. Levetiracetam should be administered diluted as per the package insert and given slowly over 15 minutes to avoid possible severe and life-threatening adverse reactions.²⁶ Prolonged seizure activity can cause hypoxemia secondary to noncardiogenic pulmonary edema or aspiration pneumonia.¹⁹ It can also cause cerebral edema and hyperthermia. Prompt and aggressive treatment of seizures is very important.

Diagnostic Testing for Head Trauma Patients

During triage, emergency diagnostic testing should include blood pressure, packed cell volume, total protein, blood glucose, electrolytes, coagulation screening, and urine specific gravity. Point-of-care thoracic ultrasound is recommended to identify pleural effusion, pneumothorax, and pulmonary contusions. After life-threatening abnormalities are addressed, a full complete blood count, chemistry panel, and thoracic and abdominal radiographs are indicated. If available, a full-body computed tomography (CT) scan can be considered in lieu of other imaging modalities for evaluating limbs, the vertebral column, and thoracic and abdominal cavities.^1,2,27-29

When evaluating head injury, noncontrast CT is the gold standard diagnostic test in humans because it helps clinicians identify fractures, damage to brain parenchyma, hemorrhage/hematomas, and signs of brain herniation.³ A helpful feature of CT is 3-dimensional reconstruction, which helps with visualization of the extent of the fracture and aids in surgical planning (FIGURE 2). A magnetic resonance imaging (MRI) scan is typically more sensitive for subtle lesions, but it requires general anesthesia, images bone poorly, and is often not available in general practices.³⁰ CT is faster, less expensive, and better at visualizing fractures and peracute hemorrhage; in addition, it requires sedation rather than anesthesia.⁴ Chai et al developed the Koret CT score (KCTS), which is a 7-point prognostic scale using CT scan findings. The score includes points for hemorrhage, midline shift or lateral ventricle asymmetry, cranial vault fracture, depressed fracture (1 point each), and infratentorial lesion (3 points).³¹ If advanced imaging of the head is not available, skull radiographs may be helpful in identifying skull fractures, but they are not helpful in evaluating the brain parenchyma.²

Figure 2. Noncontrast computed tomography (CT) images of a 2-year-old spayed female miniature pinscher with a history of head trauma. There are multiple fractures of the right aspect of the calvarium, including comminuted fractures of the right parietal bone, right temporal bone, and right occipital bone. Most of these fracture fragments are displaced outwardly from the brain; however, there is slight depression of one of the caudodorsal fragments of the parietal bone. Variable swelling of the subcutaneous tissues at the fracture is heterogeneous and contains multiple patchy regions of fluid-dense material. There is a large amount of hypodense tissue within the brain deep to the right calvarial fractures. The hypodense regions within the brain may be hemorrhage of various stages and/or edema, causing a mass effect. (A) Transverse soft-tissue window of the skull and brain showing the hypodense area representing hemorrhage and edema and creating a mass effect (asterisk).

Figure 2B. (B AND C) 3-dimensional reconstructions of the CT scan showing the extent of the fractures.

Figure 2C. (B AND C) 3-dimensional reconstructions of the CT scan showing the extent of the fractures.

Figure 2D. (D AND E) Dorsal and transverse soft-tissue window CT images showing the depressed/overlapping caudodorsal fragment of the parietal bone (arrows).

Figure 2E. (D AND E) Dorsal and transverse soft-tissue window CT images showing the depressed/overlapping caudodorsal fragment of the parietal bone (arrows).

Treatment of Head Trauma Patients

Medical Therapy

Intravenous Fluid Therapy

The main goal of fluid therapy is to promptly correct hypovolemia and/or hypotension to maintain adequate CPP. Aggressive fluid therapy was once thought to worsen brain edema; however, it is now contraindicated to volume-limit TBI patients. Hypotension is a negative outcome predictor causing increased ICP and mortality in humans. A human study showed that 1 episode of hypotension in patients with a systolic blood pressure of <90 mm Hg was linked to a 150% increase in mortality.³²

Although no specific guidelines for the type of fluids used in patients with TBI exist, there are several options, including isotonic crystalloids, hypertonic crystalloids, artificial colloids, and blood products. In a healthy animal, the BBB is permeable to water, but almost impermeable to ions and colloids due to tight intercellular junctions. However, after injury, the BBB may be disrupted, which may result in increased nonselective permeability to ions and colloidal particles.³³ Overly aggressive fluid resuscitation may increase cerebral edema; however, a more important concern is restoring and maintaining CPP.

Dose recommendations for fluid therapy include quarter shock doses (based on a shock volume of 90 mL/kg in dogs and 60 mL/kg in cats) given rapidly for isotonic crystalloids (e.g., lactated Ringer solution, 0.9% saline). Synthetic colloids can be used at 10 to 20 mL/kg in dogs (max 40 mL/kg/hr) rapidly or 5 mL/kg in cats slowly over 5 to 10 minutes. Fluid therapy should be continued until adequate tissue perfusion is reached (i.e., normal heart rate, blood pressure, pulse quality, mucous membrane color, capillary refill time).

Hypertonic saline (4 mL/kg [7.5% NaCl] and 5.3 mL/kg [3% NaCl]) is another option for correcting hypovolemic/hypotensive shock, but the duration of action is only 15 to 75 minutes. Hypertonic saline boluses should always be followed with at least a maintenance rate of isotonic crystalloids.

Oxygenation and Ventilation

Decreased cerebral oxygen delivery is the main perpetrator of secondary brain injury. Pulse oximetry is a good way of determining oxygenation status; however, blood gas analysis is ideal. An oxygen saturation (Spo₂) ≥95% is normal and reflects an arterial partial pressure of oxygen (Pao₂) of ≥80 mm Hg. An Spo₂ of <89% is indicative of severe hypoxemia and reflects a Pao₂ of <60 mm Hg. When blood gas analysis is available, the Pao₂ should be maintained at ≥90 mm Hg. Oxygen supplementation is often necessary.^34,35

Anticonvulsants

Seizures are common in humans after a TBI, with an incidence of 54%.³⁶ In veterinary patients, the incidence is thought to be lower, at 6% to 36%, depending on the study.^23,37,38 Seizures after a TBI can be immediate (within 24 hours of TBI), early (24 hours to 7 days after TBI), and later (>7 days after TBI). In human patients, prophylactic administration of some antiseizure medications (e.g., phenytoin, valproate) reduces the risk of immediate and early seizures; however, these medications are not used in veterinary patients due to their very short half-life.^19,39,40 Although levetiracetam does not have enough evidence to support its efficacy for preventing immediate and early posttraumatic seizures in humans, it may be indicated for use in veterinary patients for at least 7 days after a TBI because it is relatively safe and nonsedating.⁴⁰

Corticosteroids

Corticosteroids are contraindicated in patients with a TBI because it has been proven that they increase mortality in humans.⁴¹

Pain Management and Sedation

Adequate pain control is important for patient comfort and to avoid an increase in ICP secondary to increased cerebral metabolic rate. Opioids are commonly used, have minimal cardiovascular effects, and are easily reversed. A constant rate infusion of a full µ-agonist (e.g., fentanyl) is recommended because it provides a more consistent analgesia level. The recommended dose for fentanyl is 2 to 6 µg/kg/hr. Naloxone can be used as a reversal agent if needed.

Benzodiazepines are a great choice for the use of sedation and/or anxiolytics, as they have a minimal effect on ICP and the cardiovascular/respiratory system. α₂ Agonists, such as dexmedetomidine, are a potential choice that provides excellent sedation, anxiolysis, and analgesia without causing respiratory depression and is reversible. However, the use of dexmedetomidine in head trauma is controversial because, although it may have neuroprotective properties, it can be associated with more hypotension in human patients.^42,43

Nutritional Support

Patients with a TBI have a high rate of metabolism and catabolism. Early nutritional support is important as it helps maintain the integrity of the gastrointestinal mucosa, improves immune function, and lessens the metabolic response to stress.⁴⁴ Early (within 5 to 7 days) nutritional support in humans after a TBI is associated with a reduced mortality rate.⁴⁵ The caloric need ranges from 87% to 200% above normal in TBI patients.⁴⁶ Enteral nutrition (nasogastric or esophagostomy tubes) is used in veterinary patients if they are unable to consume sufficient calories. Prokinetic medications should be used concurrently as patients with TBI often have delayed gastric emptying.

Antibiotics

Antibiotics are indicated in the presence of shock, open wounds, open fractures of the calvarium (especially basilar or sinus fractures), and foreign material embedded into the brain parenchyma. Antibiotics should be lipid soluble to facilitate crossing the BBB and have bactericidal properties.²

Surgical Therapy

A recent study in humans with TBI showed that patients who underwent a decompressive craniotomy had a lower mortality rate than patients who received standard medical care.⁴⁷ Indications for craniotomy in veterinary patients with TBI include removal of epidural or subdural hematomas, decompression of skull fractures, removal of foreign materials lodged into the brain parenchyma, achieving hemostasis, and decompression for progressive neurologic deterioration.

Monitoring of Head Trauma Patients

Physical examinations (including vital signs and perfusion parameters) and neurologic assessments (including serial SACS scores) should be performed frequently, with a gradual taper as the patient stabilizes. In general, veterinary patients in critical condition should be monitored every 15 to 60 minutes, those in serious condition every 30 to 90 minutes, those in fair condition every 2 to 4 hours, and those in good condition every 4 to 6 hours.²

The electrocardiogram is monitored initially in patients with thoracic trauma as arrhythmias are a common cause of traumatic myocarditis in trauma patients.⁴⁸

Blood pressure should be monitored closely and maintained at a minimum of 100 mm Hg systolic pressure to maintain adequate CPP. Additionally, blood pressure should always be evaluated in the face of bradycardia to evaluate for the Cushing reflex.

ICP monitoring is the gold standard in the treatment of human patients with TBI. However, the high cost, technical challenges, and invasiveness limit its use in veterinary patients.^2,49-51

Prognosis for Head Trauma Patients

TBI can be associated with several complications, including coagulopathies, pneumonia, sepsis, generalized hypothalamic-pituitary dysfunction (including transient or permanent diabetes insipidus), and seizures.^52,53 Patients with severe head trauma have a guarded to poor prognosis with lower SACS scores (<8). Dogs and cats can have a great recuperative ability after a TBI and can have successful outcomes with aggressive and appropriate therapy.⁵⁴ One of the best indicators of prognosis is serial SACS scores. It is important to note that even if the initial SACS score is low (e.g., a grave prognosis), if SACS scores improve with time, a more favorable outcome can be predicted.² In one study, the probability of death or permanent, severe disability in a dog following TBI was >90% with a SACS score of ≤8 and <10% in patients with a SACS score of ≥10 on initial evaluation.²¹

In addition to serial clinical and neurologic evaluation, KCTS may also be a helpful prognostic indicator, with a score of ≤3 points being associated with survival with 85% sensitivity and 100% specificity in one study.⁵⁵ A different study found that post-TBI CT findings may have a limited prognostic significance but that CT is still a valuable tool in identifying structural abnormalities.⁴⁰ MRI is useful in predicting prognosis when evaluating MRI grade (1 for normal parenchyma and 5 for bilateral brainstem lesions with or without other lesions). One study found a negative correlation between MRI grade and prognosis. In dogs, injuries of the caudal fossa or caudal and rostral fossa had worse outcomes.⁵⁶ In cats, this location was not statistically significantly associated with a worse outcome.⁵⁷

A high lactate concentration has been shown to be a negative prognostic indicator in some studies, but conflicting results were found in other studies.^12,15,58 Ionized hypocalcemia is a negative prognostic indicator.¹⁵ In humans, hyperglycemia is a negative prognostic indicator because of the acceleration of secondary brain injury.^29,59 In veterinary patients, those with severe TBI may have hyperglycemia, although it has not always been a proven prognostic indicator.¹ More recent data suggest that a higher glucose concentration on admission is a negative prognostic indicator in dogs but not in cats.⁶⁰

In humans with TBI, presence of coagulopathy is associated with an increase in morbidity and mortality.⁶¹ In veterinary patients, an increase in partial thromboplastin time/prothrombin time is correlated with a lower MGCS score and thus may be a prognostic indicator.⁶²

Maintaining adequate CPP is one of the most important factors in the treatment of patients with TBI, and hypotension with a MAP <100 mm Hg is a negative prognostic indicator.⁶³

Severe concurrent injuries noted by a high ATT score, poor perfusion, and requirement for administration of hypertonic saline or endotracheal intubation are poor prognostic indicators.¹⁴

Summary

TBI is a frequent component of head trauma in small animals, and prognosis can be good with expedient and aggressive treatment. Treatment is aimed at maintaining normal CPP and reducing ICP, as well as supportive care and frequent monitoring. In some cases, surgery may be warranted. Maintaining a MAP ≥90 mm Hg with a systolic ≥100 mm Hg and an Spo₂ ≥95% is very important. Performing serial SACS scores is the best way to estimate prognosis.