Patients are commonly presented to small animal clinicians with head trauma. Successful management requires an understanding of brain injury, patient stabilisation and flat-bone fracture repair.

A forceful impact to the head large enough to cause fractures may also cause primary brain injury; contusions, lacerations, intracranial haemorrhage and continued trauma from unstable skull fragments.¹ Secondary brain injury is caused by continuing haemorrhage, oedema, and activation of biochemical pathways which perpetuate the primary brain injury and increase intracranial pressure. Hypotension and hypoxaemia further encourage this perpetuation of inflammatory events, the result being a rise in intracranial pressure.¹ Clinicians have the opportunity to exert a therapeutic effect on secondary brain injury.

In the normal patient, two processes occur to prevent inappropriate intracranial pressure.¹ Pressure autoregulation keeps intracranial pressure constant despite changes in blood pressure. Chemical autoregulation is the process where changes in arterial carbon dioxide levels cause a change in brain perfusion. The brain has an additional protective mechanism called intracranial compliance whereby brain vasculature and cerebrospinal fluid volume can decrease in response to increasing intracranial haemorrhage volume and brain oedema. These compensatory mechanisms have a limit, and when exceeded, intracranial pressure increases, perfusion pressure decreases and ischaemia and neuronal cell death occurs. If systemic hypotension occurs, cerebral vasodilation increases intracranial pressure without a corresponding increase in cerebral perfusion, further adding to the secondary brain injury. Therefore, the priority in emergency management of trauma patients is correction of systemic physiological abnormalities.

After the ABC (airway, breathing, circulation) is evaluated and normalised, a primary survey of the patient is performed to evaluate the four priority patient systems (respiratory, cardiovascular, neurological and urinary). Any abnormality in these systems (e.g., suspected pneumothorax) is promptly managed before diagnostic imaging, which may include a spinal series of radiographs to assess for spinal trauma, or assessment for thoracic and abdominal pathology (e.g., bladder rupture). Full clinical examination, neurological examination and baseline serum biochemistry and haematology is warranted. Imaging of the head is best performed with computed tomography due to the difficulty in making confident conclusions from radiographs of the head due to superimposition.

Shock is to be aggressively managed; prompt correction of hypotension, hypovolaemia, hypoxaemia and respiratory dysfunction (thoracic pain, pleural space disease). A therapeutic plan which under-corrects hypotension out of concern for aggravating brain oedema is contraindicated.¹ Hypotension encourages further brain injury and its aggressive and prompt correction is paramount. Hypertonic saline and colloid boluses may have advantages over crystalloid fluid therapy because of their ability to pull fluid from the interstitium into the vascular compartment. Blood products are useful if the patient is anaemic, the rule of thumb being 1 ml/kg of packed red blood cells or 2 ml/kg of whole blood increase the PCV by 1%. The end-point of fluid resuscitation is correction of systolic blood pressure to greater than 90mmHg and normalisation of perfusion parameters (mental state, mucus membrane colour, capillary refill time, heart rate, pulse quality and temperature of the extremities).

Oxygen supplementation is standard care for neurological trauma patients. A nasal oxygen catheter, placed to the level of the medial canthus of the eye, provides ease of management and delivers a 40% inspired oxygen concentration if given at 100 ml/kg/min.¹ End-tidal carbon dioxide measurement can be used as monitoring tool to ensure ventilation is administered at a rate where arterial carbon dioxide is normalised.

The head can be kept elevated, without impeding jugular flow, to assist with decreasing intracranial pressure. Mannitol may decrease ICP for 2–5 hours due to its ability to pull fluid into the vascular compartment combined with its diuretic action. The initial bolus is thought to cause cerebral vasoconstriction by decreasing blood viscosity, yet cerebral perfusion is improved by the osmotic effects of increasing blood volume (similar to giving a synthetic colloid).¹ A concern that mannitol may increase the volume of cerebral haemorrhage is not supported by the literature or by clinical experience.¹ Furosemide is not currently recommended because it is not thought to reduce cerebral oedema but does reduce intravascular volume.¹

High dose methylprednisolone increases mortality in humans with head trauma² and causes immunosuppression and gastrointestinal and renal complications. Systemic corticosteroids are not indicated for managing patients with brain or spinal trauma.

Seizures can occur secondary to head trauma and therapy is indicated. Short-term prophylactic therapy can also be considered supported by data in humans.³ Options include diazepam, propofol and barbiturates.⁴

Pre-operative management also includes monitoring and treating electrolyte and coagulation abnormalities, sepsis and wounds. Surgical management may be indicated to treat continuing intracranial haemorrhage, skull fractures causing deteriorating neurological function, or to remove foreign material. Decompressive craniotomy is controversial in humans and animals. Craniotomy combined with durotomy does decrease intracranial pressure⁵ although the therapeutic benefit is unclear. Surgical intervention should be considered in head traumatised dogs and cats that are deteriorating neurologically despite aggressive medical therapy in which compressive lesions secondary to haemorrhage has been documented with advanced imaging.¹

Prognosis for severely brain-injured pets is generally guarded to poor but some animals may miraculously improve with medical management. A patient presenting as comatose with absent brainstem reflexes has a poorer prognosis than patient that presents with reasonable neurological function.¹ The Modified Glasgow Coma scale can be a useful monitoring tool with limited survival prediction in the first 48 hrs.⁶ It provides a score based on patient motor activity, brainstem reflexes and level of consciousness.

Maxillofacial healing is more rapid (compared to the mandible) because of the large surface area, which allows for increased vascular supply. The maxilla is broadly attached to the skull, which distributes forces over a much larger area, and surgical fixation is less commonly required than with fractures of the mandible.

Despite the maxilla being non-load bearing, fracture fixation may be considered where there is a significant structural or functional deformity, or a fracture traverses the dental arcade causing malocclusion.⁷ In this case a miniplate can be applied adjacent to the alveolar border, again avoiding the tooth roots. If a fracture is causing a defect of the facial frame, plates can be applied generally along what is known at the 'buttresses' of the face, which has thicker bone for implants. The lateral buttress courses from just under the orbit in the direction of the carnassial tooth, the medial buttress runs in a paramedian direction from the orbit to the incisors.⁷ Access is from the dorsal midline or lateral to the alveolar margin. Zygomatic fractures causing deviation of the globe can be approached and reduced directly.

Use of wiring in the maxilla is less often required because the forces in the maxilla are spread over a much wider area, the lever arm of the mandible or the weight bearing forces of the spine and long bones are not present. However, maxillary fracture fragment wiring may be useful. Because the maxillary bone is thin, overriding can occur. Techniques to overcome this overriding include combining orthopaedic wire with Kirschner wires used as 'skewers' or 'splints'.⁷

External skeletal fixators are often not indicated for maxillary fractures because the thin bone does not allow for adequate pin purchase;⁷ however, they have been previously used successfully.⁸

Malocclusion secondary to maxillary fractures can sometimes be corrected by realigning the mandibular symphysis to better suit the maxillary abnormalities with an intentional symphyseal shift.⁹

References

1.  Dewey CW, Fletcher DJ. Medical and surgical management of the brain injured pet. In: Tobias, Johnston, eds. Veterinary Surgery Small Animal. Saunders; 2012:504–510.

2.  Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet. 2005;365:1957.

3.  Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev. 2001;(4):CD000173.

4.  Vite CH, Long SN. Neurological emergencies. In: BSAVA Manual of Canine and Feline Emergency and Critical Care. 2nd ed. BSAVA; 2007.

5.  Bagley RS, Harrington ML, Pluhar GE, et al. Effect of craniectomy/durotomy alone and in combination with hyperventilation, diuretics, and corticosteroids on intracranial pressure in clinically normal dogs. Am J Vet Res. 1996;57:116.

6.  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;15:581.

7.  Boudrieau RJ. Mandibular and maxillofacial fractures. In: Tobias, Johnston, eds. Veterinary Surgery Small Animal. Saunders; 2012:1054–1077.

8.  Stambaugh JE, Nunamaker VMD. External skeletal fixation of comminuted maxillary fractures in dogs. Veterinary Surgery. 1982;11(2):72–76.

9.  Buchet M, Boudrieau RJ. Correction of malocclusion secondary to maxillary impaction fractures using a mandibular symphyseal realignment in eight cats. J Am Anim Hosp Assoc. 1999;35(1):68–76.