Managing Disorders of the Canine Front Limb

Original Editor - Ansi Van Der Walt Top Contributors - Jess Bell, Tarina van der Stockt and Kim Jackson

This article or area is currently under construction and may only be partially complete. Please come back soon to see the finished work! (17/02/2021)

Introduction

Forelimb lameness in dogs is very common, but it can be difficult to determine the exact cause of lameness. This page discusses some of the more common types of forelimb lameness in the canine patient.

Shoulder

The shoulder joint in canine patients is the most mobile of all limb joints. Motion at the shoulder includes abduction, adduction, internal rotation, external rotation, but the primary movement is in the sagittal plane. Stability of the canine shoulder is maintained by the joint capsule, the medial and lateral glenohumeral ligaments, as well as large tendons located inside or just outside the joint.

Osteochondrosis

The most common cause of shoulder lameness is osteochondrosis (OCD). This condition occurs when cartilage grows at a faster rate than the underlying bone, which causes areas of cartilage thickening. The thickened cartilage becomes prone to shearing forces and may detach from the subchondral bone. Once there is detachment, the synovial fluid comes into direct contact with the subchondral bone, which causes inflammation. At this stage in the disease process, the syndrome becomes known as osteochondrosis dissecans and has an inflammatory component.

Early diagnosis is important as it can influence recovery rate and may prevent degenerative changes from occurring.

Key features

• Dogs are aged between 6 and 9 months of age (although it can present up until 12 months of age)
• Affects medium to large breed dogs more than small-breed dogs
• Around one third of dogs are affected bilaterally
• The shoulder joint is most often affected, but it can occur in other joints and dogs can have multiple joints affected
• There will usually be a history of intermittent lameness, that may occur from around 6 months of age. There will usually be some shoulder muscle atrophy. Pain is provoked with passive shoulder extension and flexion, as well as with digital pressure over the humeral head
• It can be imaged with x-ray, ultrasound, CT and MRI

Management

Ideally, the OCD lesion will be surgically removed. Once the cartilage flap is removed, the area will fill with connective tissue. If this flap is not removed, there will be ongoing joint irritation, which will cause long-term deficits and degeneration of the joint cartilage (i.e. there is a high risk of osteoarthritis). Young dogs aged between 6 and 10 months have the best outcomes following surgical interventions.

Rehabilitation

There are few evidence-based recommendations for rehabilitation following the surgical removal of an OCD lesion. Some studies recommend between 4 and 12 weeks of complete non weight bearing, which usually means 4-12 weeks of cage rest.

Physiotherapy in the initial phase aims to:

• Restore full passive range of motion (ROM)
• Reduce joint swelling
• Introduce static strengthening exercises
• Gradually introduce non-weight bearing exercises through range (e.g. swimming)

In order to progress to weight bearing exercises, the dog needs to have:

• No pain or swelling in the joint
• Full passive ROM
• Radiographic evidence that the OCD lesion is healing / filling

After 4 to 6 months, the dog may be allowed to start with progressive cardiovascular exercises - i.e. longer walks, straight-line running. They must be on their leash so that they do not twist / turn and strain the joint surface. A dog can only start more strenuous activities (i.e. sudden turning, spinning, sudden stops, acceleration) 6 months after surgery, if they have no recurrence of pain or joint effusion.

Supraspinatus Tendinopathy

Supraspinatus tendinopathy usually occurs in working / performance dogs. Canapp and colleagues found that there is no specific age, sex, or breed predisposition to developing this condition. It is believed that supraspinatus tendinopathy is caused by overuse (i.e. chronic, repetitive activities) and a failure for adequate remodelling in the tendon. Inflammation may be present in the early stages, but it is not typically involved in the later stages of the disease process.

Key Features

• Canine patients with this condition usually present with varying degrees of lameness. This lameness increases with activity, and is usually not very responsive to conservative treatment
• Weight-bearing lameness is often worse with activity
• There may be atrophy of the supraspinatus muscle
• There is usually pain on direct palpation of the supraspinatus tendon and with shoulder flexion
• There is often concurrent elbow dysplasia and or other pathological changes in the shoulder
• After function returns, dogs have a lifelong increased susceptibility to re-injury because the fibrotic scar tissue has reduced strength when compared to the original tendon

Management

The medical management usually involves non-steroidal anti-inflammatories (NSAIDs) and controlled activity for a period of time alongside physiotherapy management. Other treatments may include: acupuncture, deep cross-friction massage, heat, ultrasound, range of motion exercises / stretching, therapeutic laser extracorporeal shockwave therapy, regenerative medicine therapy and  ultrasound-guided injections of platelet-rich plasma.

Canapp found that 74.6 percent of canine patients do not respond well to NSAID therapy and 40.8 percent do not respond to rehabilitation therapy. However, surgical options tend to have low efficacy and lameness tends to persist.

Physiotherapy Management

In 2009, Cook and Purdam proposed the continuum model for tendinopathies. They divide tendinopathy into three phases:

1. Reactive tendinopathy
2. Tendon dysrepair
3. Degenerative tendinopathy

In the reactive stage, there is diffuse increased cellularity and ground substance. This is followed in the second phase by the appearance of focal areas of collagen disorganisation and neurovascular ingrowth. Finally, this progresses to a morphology with discrete areas of degenerative tendinopathy. However, as Cook and colleagues note, the relationship between structure, pain and function in tendons is not yet fully understood and this contributes in part to the complexities surrounding the management of tendinopathy.

Phase One

As in human patients, the first phase of rehabilitation in canine patients focuses on:

• Reducing pain
• Avoiding activities that cause compression of the tendon (for supraspinatus this means avoiding activities that occur in full shoulder flexion)
• Avoiding the Stretch-Shortening-Cycle. Swimming is NOT an appropriate choice for this reason
• Introducing isometric exercises in a mid-range position to avoid excessive strain on the tendon. In highly irritable tendons, bilateral exercises with shorter holding times and fewer repetitions may be indicated.

Other modalities that may be useful, include ice, TENS and LASER.

Once the dog’s pain is controlled, it has good static stability of its limb, and it can achieve an isometric static contraction without an increase in symptoms, it is possible to move into phase two of tendon rehabilitation.

Phase Two

Phase two focuses on strengthening. The aim is to gradually increase the tendon’s ability to produce force and manage load.

• Repetitive loading such as running / walking are unlikely to stimulate significant adaptive changes
• The focus is rather on heavier loads that can promote change in muscle and tendon and improve their load capacity

Exercise prescription must be tailored to the patient in terms of:

• Pain level
• Specific weakness
• Patient goals
• Requirements of sport / work

Tendinopathy loading programmes generally fall into three categories:

1. Eccentric loading
2. Heavy slow resistance training
3. Combined approach

Eccentric exercises have been the mainstay of tendinopathy treatment for many years. More recently, however, research has highlighted the benefit of also focusing on the concentric phase of exercises with heavy slow resistance training

The aim in phase two is to continue to achieve strength changes in the mid-range position and to avoid tendon compression. It is also important to avoid rapid cycling of the tendon. Exercises should be slow, deliberate and against some resistance.

NB:

• Tendon rehabilitation tends to take time
• For the first 24 to 36 hours after loading, there is a net loss of collagen production - this means there must be adequate time for recovery to allow any strain to the tendon to recover. A fatigued tendon will be at greater risk of regressing.

Phase Three

It is possible to progress to phase three (i.e. functional rehabilitation) when the patient has good neuromuscular control, relatively even muscle development, no recurrence of pain and swelling or any regression in function. For sporting / working dogs, it is particularly important to include functional rehabilitation. Functional rehabilitation falls into three categories:

1. Exercises that are specific to the functional requirements of the affected muscle and tendon
2. Improving load capacity of the entire kinetic chain
3. Addressing movement dysfunctions that could cause recurrence of the tendinopathy

It is also important to achieve neuroplastic training of the tendon. There are significant neuromotor changes in tendinopathy that affect the descending control of the neuromuscular junction where there is pain and swelling in a tendon. It is, therefore, important to restore optimal communication between the central nervous system and the tendon to ensure it can function under high loads. This can be achieved by the use of an external marker. In dogs, this can be achieved by ensuring that a dog does an activity in response to a verbal cue for a reward (e.g. treat).