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33rd Annual Scientific Meeting proceedings

Stream: SA   |   Session: Spinal Trauma II
Date/Time: 08-07-2023 (11:10 - 11:40)   |   Location: Conference Hall Complex A
Spinal Trauma - Complications
De Decker SDD
Royal Veterinary College, Hatfield, United Kingdom.

The increased demand of veterinary specialisation has resulted in more widespread availability of spinal surgery. Although this type of surgery can result in excellent outcomes, not every case will recover uneventfully. Complications can vary in severity form mild and spontaneously improving to life-changing and even life-threatening events. Prevention of complications is often easier than treatment. Adequate surgical technique and appropriate postoperative care are crucial in preventing complications.

Intra-operative complications
Intra-operative complications are rare if appropriate planning and surgical technique are maintained. Intra-operative complications include residual spinal cord compression, haemorrhage, iatrogenic damage of neural structures, vertebral fractures, hypotension, iatrogenic damage to soft-tissue structures, and cardiorespiratory arrest. Specific surgical procedures are associated with specific complications.

Non-neurological post-operative complications
Common non-neurological complications include urinary tract infections, bladder wall damage, skin lesions, and joint and muscle contractures. Structured and adequate postoperative care is crucial in preventing such complications.

The basic components of postoperative care for spinal injury patients are bladder management, analgesia, and physiotherapy. It should be assumed that an animal with severe spinal injury is unable to urinate unless proven otherwise. The bladder should be manually emptied every 4 to 6 hours until voluntary urination is witnessed. This can be done by manual bladder expression, intermittent aseptic catheterisation, or placement of an indwelling catheter with a closed collection system. Failure to provide adequate bladder management can result in urinary tract infections, urine scalding, bladder wall stretching, persistent bladder atonia, and bladder wall rupture. Animals should not be discharged from hospitalisation until voluntary urination has returned or the owners are comfortable on how to provide bladder management at home.

Non-ambulatory patients are sensitive for the development of skin problems, which can vary from skin irritation and urine scalding to decubital ulcers. The reason for this vulnerability is most likely multifactorial, including prolonged recumbency with reduced blood flow and pressure on contact points, potential incontinence and urine scalding, and ‘dragging’ of limbs over the floor. Animals should be kept on a dry and clean surface, regularly turned, kept clean, and physiotherapy should regularly be performed. Physiotherapy decreases the likelihood of decubital ulcers by promoting blood flow. Other advantages of physiotherapy and/or hydrotherapy include encouraging joint and muscle health, thereby preventing development of joint and muscle contractures.

Neurological post-operative complications
Early postoperative neurological deterioration
is characterised by neurological deterioration within the first 10 days after surgery. Although it is not uncommon for a successfully treated animal to demonstrate a more severe neurological status immediately after surgery compared to before surgery, further neurological deterioration during hospitalisation should raise suspicion of a complication. The most common causes for early postoperative neurological deterioration are progressive myelomalacia and further extrusion of calcified material through the operated intervertebral disc space. Other causes of early postoperative neurological deterioration are epidural haemorrhage/hematoma formation, infection and reaction to material placed over the hemilaminectomy site.

Although fenestration of the operated intervertebral disc is aimed at decreasing the likelihood of further extrusion of calcified nucleus pulposus, it does not completely exclude the possibility of this complication.  

Progressive myelomalacia is a devastating complication characterised by progressive haemorrhagic necrosis and lysis of the spinal cord. This cascade of necrosis moves in a cranial and caudal direction until the complete spinal cord has lost its physical integrity. The underlying aetiology of this phenomenon is currently unknown. It occurs in approximately 10% of dogs that present with paraplegia and absent deep pain sensation (a higher prevalence of 33% has been reported in French bulldogs). Progressive myelomalacia develops typically within 5 days of onset of paraplegia and can therefore develops after spinal surgery has already been performed. This complication is associated with specific clinical characteristics and a presumptive diagnosis can be based on results of serial neurological examinations:

  • The cutaneus trunci reflex moves progressively cranial.
  • Dogs can have a ‘frightened expression’ and feel uncomfortable.
  • Loss of spinal reflexes in the pelvic (and in the later stages also the thoracic) limbs.
  • The abdomen becomes atonic and flaccid.
  • In the later stages, the thoracic limbs will also become affected, and dogs will develop respiratory compromise.
  • Most affected dogs will die from suffocation.

Progressive myelomalacia is also associated with specific MRI (and myelographic) abnormalities. Prognosis is grave and euthanasia should be considered.

Late onset neurological deterioration is most often caused by IVDE at a different or distant intervertebral disc space. Recurrence rates are variable and range from 2% to 51%. Risk factors for recurrent IVDE at a distant site include breed and prophylactic fenestration. Reported recurrence rates are substantially higher in specific breeds, such as miniature dachshunds and French bulldogs. Late-onset of recurrence of clinical signs occurs in 25% and 51% of miniature dachshunds and French bulldogs, respectively. Although prophylactic fenestration is associated with a significantly lower risk of recurrence, this surgical approach is associated with extensive epaxial muscle dissection and longer anaesthesia times. Other causes of late onset neurological deterioration are infection, soft tissue encroachment into the surgical site, laminectomy membrane formation, implant failure, subarachnoid diverticulum formation, and development of spinal conditions unrelated to the previous surgery.





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