Canine Traumatic Injury Study Guide

Overview and Clinical Importance

Traumatic brain injury (TBI) and spinal cord injury (SCI) are common neurological emergencies in canine patients. TBI occurs in approximately 25% of dogs presenting with blunt trauma, with motor vehicle accidents being the most common cause. Spinal cord injuries frequently result from vertebral fractures, luxations, or intervertebral disc extrusion. Both conditions require rapid assessment and aggressive management to minimize secondary injury and optimize patient outcomes. Understanding the pathophysiology of primary and secondary injury is essential for effective treatment.

Part 1: Traumatic Brain Injury (TBI)

Etiology and Epidemiology

Common causes of TBI in dogs include motor vehicle accidents (most common), falls from heights, bite wounds, blunt trauma, and gunshot wounds. In military working dogs, head injury accounts for 21% of traumatic deaths. Dogs spending time outdoors are at higher risk. Notably, canine skulls are relatively thicker than human skulls, providing some protective advantage, though severe trauma easily overcomes this protection.

Pathophysiology: Primary vs. Secondary Injury

Primary Brain Injury

Primary injury occurs immediately at the time of trauma and results from direct mechanical forces (acceleration, deceleration, torsion) applied to the cranium. Types include: parenchymal tears, vascular tearing and hemorrhage (epidural, subdural, intraparenchymal hematomas), cerebral contusions, diffuse axonal injury (most common), and skull fractures with parenchymal compression. Primary injury is largely irreversible, and treatment focuses on preventing secondary damage.

Secondary Brain Injury

Secondary injury develops in the minutes to hours following trauma due to a cascade of physical and biochemical changes. Key mechanisms include: cerebral edema, intracranial hypertension, ischemia from reduced cerebral blood flow, excitotoxicity from glutamate release, free radical formation and lipid peroxidation, inflammatory cascade activation, and electrolyte disturbances. Medical management is directed primarily at minimizing secondary injury.

Cerebral Perfusion Pressure (CPP)

CPP = MAP - ICP (where MAP = mean arterial pressure, ICP = intracranial pressure). Normal ICP in dogs ranges from 0-10 mmHg. In healthy animals, autoregulatory mechanisms maintain constant cerebral blood flow (CBF) over a wide range of MAPs (50-150 mmHg). After TBI, autoregulation is often impaired, making CBF directly dependent on blood pressure. The goal is to maintain MAP greater than 80-90 mmHg to ensure adequate CPP.

The Cushing Reflex (Cushing's Triad)

The Cushing reflex is a physiological response to acute, severe increases in ICP causing brainstem hypoxia. It represents a last-ditch effort to maintain cerebral perfusion and consists of: systemic hypertension (widened pulse pressure), reflex bradycardia, and irregular respirations. This triad indicates impending brain herniation and is a terminal sign requiring immediate, aggressive intervention.

Clinical Assessment of TBI

Initial Stabilization: The ABCDs

Always address life-threatening extracranial issues first: Airway (ensure patency), Breathing (assess ventilation and oxygenation), Circulation (address hemorrhage and shock), Disability (neurological assessment). Hypoxemia and hypotension are the two most detrimental secondary insults and must be corrected immediately.

Neurological Examination

Key elements include: level of consciousness (most reliable indicator of cerebral function), pupillary light response (cranial nerves II and III), physiologic nystagmus (vestibulo-ocular reflex), motor activity and posture, and systemic signs. Clinical signs suggesting cerebral injury include circling, ataxia, blindness, altered mentation, loss of consciousness, seizures, and abnormal breathing patterns (Cheyne-Stokes respirations).

Modified Glasgow Coma Scale (MGCS)

The MGCS is an objective scoring system adapted from human medicine for veterinary patients. It evaluates three categories: motor activity, brainstem reflexes, and level of consciousness. Each category receives a score from 1-6, with a total score ranging from 3 (grave prognosis) to 18 (normal). The MGCS predicts probability of survival in the first 48 hours after head trauma.

Abnormal Postures in TBI

Diagnostics for TBI

Minimum Database

Essential initial diagnostics include: PCV/TS (assess for hemorrhage, performed in greater than 95% of cases), blood glucose (hyperglycemia correlates with injury severity and worse prognosis in dogs), blood pressure (maintain systolic greater than 100 mmHg, MAP greater than 80-90 mmHg), venous or arterial blood gas (assess ventilation, oxygenation, acid-base status), electrolytes, and lactate. ECG monitoring is indicated for traumatic arrhythmias.

Advanced Imaging

CT scan is preferred for acute evaluation of skull fractures and intracranial hemorrhage. MRI provides better assessment of parenchymal injury and has prognostic value. Dogs with lesions affecting the caudal fossa (brainstem/cerebellum) or both rostral and caudal fossa typically have poorer outcomes. Advanced imaging is indicated when patients fail to respond to aggressive medical therapy or deteriorate after initial response.

Treatment of TBI

Goals of Therapy

The primary goals are to: maintain adequate cerebral perfusion pressure, ensure adequate oxygenation (SpO2 greater than or equal to 95%), reduce intracranial pressure, and prevent secondary injury. Target values include: MAP greater than 80-90 mmHg, systolic BP greater than 100 mmHg, PaCO2 30-40 mmHg, and normoglycemia.

Medical Management

Part 2: Spinal Cord Injury (SCI)

Etiology

Common causes of traumatic SCI include: vertebral fractures and luxations (motor vehicle accidents, falls, bite wounds), acute intervertebral disc extrusion (IVDE - most common cause of SCI in dogs), gunshot wounds, and crush injuries. The thoracolumbar region (T3-L3) is most commonly affected (50-60% of cases). Approximately 20% of patients with spinal trauma have multiple vertebral fractures/luxations.

Pathophysiology of SCI

Primary Injury

Primary injury results from direct mechanical damage including: concussion, contusion, laceration, compression, and transection. The amount of neural tissue injury depends on the rapidity and severity of insult and the duration of compression.

Secondary Injury

Secondary injury occurs through: vascular changes (ischemia, hemorrhage), excitotoxicity, free radical formation, inflammatory response, apoptosis, and glial scar formation. Secondary injury can extend the lesion cranially and caudally beyond the original injury site.

Neuroanatomic Localization

Schiff-Sherrington Posture

Schiff-Sherrington posture is characterized by hyperextension of the thoracic limbs with paralysis of the pelvic limbs. It results from acute, severe thoracolumbar spinal cord injury (T2-L4) that interrupts the ascending inhibitory influence of border cells (located in L1-L7) on thoracic limb extensor motor neurons.

Neurological Grading for SCI

Cutaneous Trunci (Panniculus) Reflex

The cutaneous trunci reflex helps localize thoracolumbar lesions. Stimulate the skin along the dorsum and observe for skin twitch. The reflex is absent caudal to the lesion. The cutoff level is typically 1-2 vertebrae caudal to the actual lesion site. This is useful for planning imaging and surgery.

Progressive Myelomalacia (PMM)

PMM is a uniformly fatal complication of severe SCI characterized by progressive hemorrhagic necrosis that spreads cranially and caudally from the initial lesion site. It typically develops within 24 hours to 14 days after injury. Clinical signs include: progressive loss of pelvic limb reflexes and tone, cranial migration of the cutaneous trunci cutoff, loss of anal tone and perineal reflex, respiratory failure (when ascending myelomalacia reaches C5), and ultimately death. French Bulldogs are at particularly high risk (up to 33% in deep pain negative patients).

Diagnostics for SCI

Radiography: Has limited sensitivity (72% for fractures, 77.5% for luxations). Useful for initial screening but may miss articular process fractures and underestimate instability. Obtain orthogonal views with patient in lateral recumbency using horizontal beam technique. CT scan: Superior for detecting osseous lesions, fracture morphology, and vertebral canal fragments. MRI: Best for assessing spinal cord injury, soft tissue damage, and prognosis. Shows cord edema, hemorrhage, and compression.

Treatment of SCI

Initial Stabilization

Immobilize the patient on a rigid board to prevent further spinal displacement. Avoid flexion, extension, and rotation of the spine during handling. Address systemic injuries and shock. Provide analgesia (opioids preferred).

Conservative vs. Surgical Management

Prognosis Summary

Memory Aids

TBI Management: 'CHOMP' C - CPP maintenance (MAP greater than 80-90) H - Head elevation (15-30 degrees) O - Oxygen supplementation (SpO2 greater than 95%) M - Mannitol or hypertonic saline for elevated ICP P - Pain control with opioids

Cushing Reflex: 'Hyper-Brady-Irregular' Hypertension + Bradycardia + Irregular respirations = Brain herniation imminent!

Deep Pain Testing: 'Conscious Response Counts' Apply hemostats to toe bone - look for CONSCIOUS response (vocalization, head turn) Withdrawal alone = spinal reflex only, does NOT indicate intact nociception