VSR-511 Class 10 and 11

Septic arthritis

• Infection of joint by pathogenic bacteria

• Etiology

                               o    Partial/Complte failure  of passive transfer of immunoglobulin from dam/colostrums-            decreased acidity of stomach leading to systemic infection.

• Traumatic injury
• Haematogenous spread of bacteria –Actinobacillosis,E.coli,Streptococcus, staphylococcus,salmonella.
• Navel cord infection-E.coli,streptococci.
• Unhygienic condition –Iatrogenic by joint aspiration/injection/arthrotomy.

·         Pathophysiology:

o    Bacterial proliferation causes synovitis and necrosis –increased lysosomal enzymes(Proteases-Decrease proteoglycans and Glycosaminoglycans, and Collagenases decrease collagen formation).Both leading to weak cartilage formation, which is  easily affected by trauma.

• Clinical signs
• Pain
• Open wound with discharge
• Swelling
• Joint effusion
• lameness
• Diagnosis
• Clinical signs and history
• Radiography
• Ultrasonography
• Synovial fluid evaluation
• Arthroscopy
• Treatment
• Systemic  antibiotic treatments
• Through  lavage of joints
• Slow release intra articular antibiotic therapy

OSTEOCHONDRITIS DISSECANS

·  Failure of endochondral ossification and persistant hypertrophied cartilage.

·  Developmental joint disease of rapidly growing animal of articular surfaces in joints.

·  Growth cartilage focal damage during endochondral ossification.

·  Common sites are femoro-patellar, tibiotarsal and shoulder joints.

• Etiology
• Overfeeding of grains- Excess digestible energy
• Mineral imbalance of calcium and phosphorous
• Toxicity
• Deficiency in copper
• Hormonal imbalance
• Decreased Vit D
• Increased Glucocorticoids 
• Heredity/ genetic predisposition
• Rough exercise
• Clinical signs
• Effusion of affected joint
• Mild to moderate lameness  
• Muscle wasting
• Diagnosis
• Clinical signs and history
• Radiography
• Neurological examination 
• Treatment
• Restriction of exercise
• Correction of minearals and vitamin deficiency
• Restriction of excessive grain feeding
• Hyaluronic acid with polysulphated glycosaminoglycal treatment
• Arthroscopic surgical treatment

DEGENERATIVE JOINT DISEASE (Osteo arthritis) Progressive deterioration of articular cartilage, bone and soft tissues in joints. Split cartilage,synovitis and joint effusions are seen commonly. Etiology Ostochondritis dissecans Intra-articular fractures Chronic low grade trauma Septic arthritis Poor confirmation  Pathology Loss of cartilage elasticity Decrease in content of PSGAGS and hyaluronic acid Liberation of degradative enzymes which results in damage to articular surface Clinical signs Soft tissue swelling around joint Low grade chronic lameness Joint effusion  Diagnosis Clinical signs Flexion test Intra-articular analgesia Radiography Ultrasonography Arthroscopy Treatment: Primary goals of treatment are To minimize ongoing degenerative change Repair of damaged articular cartilage Pain management Medical therapy with PSGAGS and hyaluronic acid Intra-articular corticosteroids (methyl prednisolone acetate @60-80mg for smaller joints and 120mg for large joints DMSO as an anti-inflammatory and bacteriostatic and to inactivate superoxide radicals @ 10-30 ml of 10-40% concentration NSAIDS – Phenylbutazone @ 4.4mg/kg daily for 1-2 days then 2.2mg/kg twice daily 3-5 day

 

INTERVERTEBRAL DISC PROLAPSE AND ITS MANAGEMENT

·  Thoracolumbar intervertebral disk (IVD) extrusion, a common disease encountered in dogs, is often associated with severe neurologic dysfunction. Presenting clinical signs include spinal hyperesthesia, ataxia, paresis, and paralysis. In severe cases, loss of deep pain perception to the pelvic limbs may occur.

·  Obesity, muscular fitness, and spinal length (i.e., long spine compared with leg length [e.g., dachshunds]) are other factors that have been implicated in increasing the risk of intervertebral herniation.

• Narrowing of the intervertebral foramen, radio opaque material (calcified disk material) in the intervertebral foramen, and collapse of the articular facets are evidence a disk extrusion is present

 

• Acute IVD disease occurs in all breeds of dogs; however, chondrodystrophoid Breeds are at greater risk.
• The dachshund reportedly has a 10- to 12-fold greater risk than all other breeds combined.
• Approximately 75% of disk herniations occur in animals between 3 and 6 years of age.
• Eighty-five percent of all disk herniations occur in the thoracolumbar region, and the most frequent sites are from T11-12 to L2-3.
• Although most animals with acute IVD extrusion usually present with serious neurologic dysfunction, spinal pain may be the only presenting clinical sign in some patients.
• Dogs commonly present non ambulatory in the pelvic limbs.
• Voluntary bladder control is often lost and pain sensation is altered, depending on the degree of spinal cord injury.
• Less severely affected dogs may present with varying degrees of ataxia and paresis that, if left untreated, can progress to complete paraplegia.
•  A thorough orthopedic examination should be included in the diagnostic workup of such animals.

·   

·  In 1952, Hansen classified IVD disease into two types of disk herniation.

o Type I lesions refer to the extrusion of material from the central portion of the disk through the outer fibrous layers into the vertebral canal.

o  In small, typically chondrodystrophoid breeds of dogs (e.g.,dachshunds, Pekingese,).

o Clinical signs are usually acute.

 

o Type II lesions refer to the protrusion of the outer fibrous layers of the disk  to protrude into the vertebral canal.

o It may present as a chronic condition.

 

·  Intervertebral disks are located in every intervertebral space along the spinal column, except in the atlantoaxial joint (C1-2).

·  Each disk comprises three distinct anatomic regions: the annulus fibrosus, nucleus pulposus, and cartilaginous endplates.

·   The dorsal and ventral longitudinal ligaments bind the IVD dorsally and ventrally .

·  The annulus fibrosus encircles the nucleus pulposus .

·  The nucleus pulposus is an amorphous, gelatinous mass consisting of water, collagen fibers, proteoglycan molecules, and a variety of other cells (e.g., chondrocytes, fibrocytes).

·  The annulus fibrosis being two to three times wider on ventral than the dorsal aspect.

·  The cartilaginous endplates resemble hyaline cartilage.

·   From the second to the tenth thoracic vertebra, the inter capital ligament between opposite rib heads lies ventral to the dorsal longitudinal ligament.

·   Hemorrhage from the vertebral sinuses can accompany disk extrusion or can obstruct visualization during surgical decompression.

·  The spinal cord is located within the bony vertebral canal and is further protected by the meninges (dura mater, arachnoid membrane, pia mater).

·  The cerebrospinal fluid (CSF) is contained within the subarachnoid space.

·  Rapid neurologic dysfunction is noted, and death due to respiratory failure may follow in 3 to 10 days.

 

Diagnosis Signs, history, and physical examination is essential to make a tentative diagnosis. A complete neurologic examination should be performed in all cases of suspected acute thoracolumbar IVD extrusion to accurately localize the lesion.  Disk extrusion at L4-S3 may have decreased  patellar, gastrocnemius, and perineal reflexes, indicative of lower motor neuron (LMN) disease. A positive crossed extensor reflex is a sign of UMN disease. Hyperesthesia in the area of the affected disk space. The cutaneous trunci (panniculus) reflex can be useful in localizing a lesion. Deep pain sensation is evaluated by pinching a hemostat across the bone of a digit.

 

GRADING

·  Based on Neurologic Signs

o Grade 1: Spinal hyperesthesia (pain) only

o Grade 2: Mild ataxia with enough motor function for weight-bearing

o Grade 3: Severe ataxia without weight-bearing ability

o Grade 4: No motor function, but deep pain sensation is present

o Grade 5: No deep pain sensation is present

·  An assessment of bladder function should also be obtained during the history and via abdominal palpation.

·  Differential Diagnosis:In anesthetized patients, plain radiography aids in ruling out diskospondylitis, Vertebral neoplasia and spinal fracture/luxation. Narrowing or wedging of the IVD space.

·  Narrowing of the intervertebral foramen, radio opaque material (calcified disk material) in the intervertebral foramen, and collapse of the articular facets are evidence a disk extrusion is present

·  Myelography is performed under general anesthesia and requires the injection of a radio opaque contrast agent into the subarachnoid space.

Prognosis

·  Dogs with grade 1 and 2 disease are candidates for appropriate medical management and that dogs exhibiting clinical signs consistent with grades 3,4, and 5 are candidates for decompressive spinal surgery.

·  Development of progressive hemorrhagic myelomalacia carries a grave prognosis.

·   Animals with loss of ambulation are not considered candidates for surgery

Medical management

·  Dogs with grades 1 and 2 clinical signs based on thorough neurologic examination may be considered candidates for medical management.

Confinement therapy

·  The key factor in confinement therapy is strict immobilization of animals in a cage or crate for at least 3 weeks.

·  Leash walking is permitted for urination and defecation.

·  Nonambulatory animals require intensive recumbency management.

·   In dogs that have lost the ability to urinate voluntarily, bladder expression should be performed three to four times daily.

·  Urinary catheterization (intermittent or indwelling) may be necessary.

·  Soft, dry, padded bedding material provided to prevent decubital ulcers.

·  Physical therapy, including gentle massage combined with exercise therapy

·   The use of carts and other walking aids should be used for permanent paralysis.

Pharmacologic therapy

• Drugs acting on the lower urinary tract
• Alpha antagonist –Phenoxybenzamine- Dog 0.25–0.5 mg/kg PO.
• Alphaantagonist- Prazosin Dog 1 mg /15 kg PO
• Alphaantagonist -Terazosin -Dog Per dog—1–2 mg up to 11 kg.
• Skeletal muscle -Diazepam -Dog Per dog—2–10 mg PO

·  Methyl prednisolone is believed to be beneficial because of its inhibition of oxygen free-radical lipid peroxidation in the spinal cord at 30 mg/kg.

HEMILAMINECTOMY AND PEDICULECTOMY Hemilaminectomy and pediculectomy are surgical methods for Spinal cord decompression and removal of extruded disk material. Extruded disk material can be removed through the bony window that is created, thereby decompressing the spinal cord. A standard dorsal approach to the selected side of the vertebral column is made centered on the affected IVD space. Visualizing the cranioventrally projected transverse process of the first lumbar vertebra (L-1) and the lateral transverse process and rib head of the thirteenth thoracic vertebra (T-13) makes identification of the correct disk space possible. Initially, the articular processes over the disk space are removed using a bone rongeur. The laminar bone is then removed to the level of the floor of the vertebral canal. This can be performed using rongeurs; Hemorrhage is controlled with bipolar cautery and bone wax. After the inner cortical layer of bone is gently removed with the drill, a small nerve-root retractor or dental scaler is used to open the periosteum and expose the spinal cord. Extruded disk material is often readily seen and is removed using small forceps or a nerve-root retractor .The dura is elevated with small forceps or a hooked hypodermic needle and then incised with a No. 11 or 12 scalpel blade along the length of the hemilaminectomy site. Oozing a “paste like” substance from the durotomy site indicates that myelomalacia is present and the prognosis for neurologic recovery is poor. Placement of a free fat graft over the hemilaminectomy site before closure of the surgical wound has been advocated to prevent perineural fibrosis and dural adhesion. The thoracolumbar fascia and subcutaneous tissues are closed thoroughly to eliminate dead space. Pediculectomy Pediculectomy is the removal of the lateral bony wall of the spinal canal between the vertebral body and the articular processes. This technique is reportedly less destabilizing to and minimizes manipulation of the spinal cord compared with hemilaminectomy but still provides spinal cord decompression and allows removal of extruded disk material.

SPONDYLOSIS DEFORMANS

Introduction

·  Spondylosis is the term used to describe a non inflammatory and proliferative bony changes which occur on the ventral and the lateral aspects of the vertebral bodies.

·   It was proposed earlier that spondylosis was caused by stretching of the vertebral longitudinal ligament as a result of ventral disk protrusions.

·  More common in larger breeds and older animals. Affected  disk spaces will be narrowed.

·   Occurs more commonly at the lumbosacral junction.

·  Etiology

o Bony spurs create pressure on the exiting spinal nerve roots.

·  Spondylosis deformans may occur due to instability of the ivd’s in conditions like congenital vertebral deformitiesfollowing disk surgeries,trauma and also disk or vertebral body infection.

·  Pathogenesis

o Osteophytes occur on the ventral margins of the vertebral end plates which grow larger, bridge the gap between the neighbouring vertebrae-bridging spondylosis.

o  Advanced cases-disk tissue almost disappears,bone of adjacent vertebrae is ground and appears polished.

o Degeneration occurs mainly due to calcification of the nucleus. Pathogenesis of spondylosis is mostly associated with disk degeneration.

·  Clinical significance

·   It may result in nerve root compression due to impingement of the proliferated bone as they exit from i-v foramina.

·   Lumbosacral junction most common site of nerve root pain and as a part of ‘wobbler syndrome’ in combination with stenosis of intervertebral foramina.

·  Radiology

o Radiographic signs consist of osteophytes which are most easily visible on the ventral margins of the vertebral end plates. These may grow to large size and span the gap between neighbouring vertebrae-termed ‘bridging spondylosis.

o Care must be taken to distinguish between spondylosis which is a degenerative condition associated with bony proliferation and spondylitis which is an inflammatory condition in which bony destruction as well as proliferation occurs.

·  In general

o Spondylosis may occur at the site of instability.

o  Spondylosis occurs with considerable frequency at the lumbosacral junction.

o Spondylosis is usually regarded as an incidental finding and rarely is a cause of neurological symptoms in itself, although it may give rise to pain or stiffness.

o The affected vertebral bodies are sclerotic and disk spaces narrowed.

o Although symptoms of pain caused by spondylosis in dogs are generally mild, or even symptomic, certain individuals may be very severely incapacitated.

o  In cats, severe spondylosis can be found as a result of vitamin A intoxication, which frequently affects the cervical region of the vertebral column in this species and can cause a dramatic reduction in its mobility.

·  Treatment

o NSAID’s can be used as symptomatic treatment.

SPONDYLITIS

·  It is also called diskospondylitis. It refers to infection of the vertebral disks and the neighbouring vertebral end plates.  Spondylitis refers to osteomyelitis of the vertebrae alone.

·  Areas of spine most commonly affected are lumbosacral junction, cervicothoracic region, thoracic junction and mid thoracic disks.

·  Diskospondylitis most commonly affects young large breed dogs and the most commonly affected is T5\6 followed by L7 and the caudal cervical region.

·  Symptoms include subtle lameness, difficult jumping, anorexia, depression, weight loss.

·  The hallmark of patients with diskospondylitis is spinal hyperpathia(ie, neck or back pain on deep palpation) associated with systemic disease.

·  The typical sign is pain, which maybe severe.

·  The cause of the condition is usually systemic infection, with haematogenous spread of  bacteria, fungal and cryptococcal and in many cases is thought to originate from the urinary system.

·  In some cases foreign body migration from the digestive or respiratory tracts allows grass seed awns to find their way to the ventral aspect of L1\L2 region and lodge in the intervertebral disks and cause diskospondylitis.

·  Immunosuppressed patients may also be predisposed to diskospondylitis. Rarely, bacteria migrate dorsally and cause epidural abscess formation.

·  The most common bacterial isolates are staphylococci most of which are penicillin resistant.

·  Diagnosis of diskospondylitis can usually be made from plain radiographs. There is destruction of dense bone of the vertebral end plates with some bony proliferation at the margins of the lesion. Radiographically it is possible to confuse spondylosis with discospondylitis; however, in spondylosis there is only bony proliferation whereas in diskospondylitis there is concurrent bony destruction.

·  Signs as sclerotic changes and ventral osseous proliferation with varying degree of bridging spondylosis.

·  Mylelography is mandatory in patients requiring surgical intervention. Bone scintigraphy is also helpful in early diagnosis of diskospondylitis.

·  Diagnosis of the type of bacteria involved is usually not required for initial treatment.

·  Appropriate antibiotic treatment should be given for about 3 months or more

·   Exploratory surgery is likely to be required in such cases allowing cord decompression and retrieval of material for microbial culture.