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Canine Hip Dysplasia-Part 1

Pathophysiology and Diagnosis

Canine hip dysplasia (CHD) is an inherited developmental disorder of the coxofemoral joint commonly affecting many of the larger breeds of dogs. Patients with clinical signs referable to CHD are regularly presented for evaluation and treatment, and selection of the most appropriate medical or surgical therapy requires a comprehensive orthopedic evaluation of each individual. The purpose of this series of articles is to describe the pathophysiology of the disease and the techniques employed for its successful diagnosis as well as the indications for the multitude of surgical procedures utilized to treat the condition.

Pathophysiology and Diagnosis

The cause and pathogenesis of canine hip dysplasia are still poorly understood; however, numerous studies over the last 15 years have indicated that CHD is a developmental disorder and that multiple factors can influence or modify the expression of the disease. No specific genetic pattern of inheritance has been demonstrated; however, the pattern of inheritance is multi-factorial. The spread of hip dysplasia is centered around the genetic transmission and heritability of a particular body size, type, confirmation, and growth pattern. The occurrence of hip dysplasia has been reduced by breeding dogs that have radiographically disease-free joints and by selecting dogs for breeding based on family performance and progeny selection. Unfortunately, many factors affect the choice of dogs used in breeding programs and breeding dogs for desirable traits (i.e., large size, temperament) may result in the inadvertent selection of dogs predisposed to CHD. Therefore, while CHD is a heritable disease, controlled breeding programs have only reduced the prevalence of hip dysplasia, but the disease has not been eliminated.

Dogs with the highest incident of hip dysplasia are large, rapidly growing and maturing breeds with a heavy body confirmation. It has been speculated that slow growth and late maturation favors the completion of ossification and development of the joint before the hips are subjected to possible injury from excessive extrinsic forces, especially excessive body weight. Rapid growth and early weight gain may result in disparities of tissue development triggering a series of events leading to subluxation, hip dysplasia, and degenerative joint disease. While the role of nutrition has been thoroughly investigated, diet has not affected the occurrence or course of CHD other than the mechanical effect of increased or decreased weight upon the hip.

Several hormones have been implicated as playing a role in causing CHD, including estrogen and relaxin. Based on the results of several studies, there is no evidence that hormonal influence (within the biologic range) is associated with the development of spontaneously developing hip dysplasia in the dog.

A causal relationship between pelvic muscle mass and/or muscle myopathies and hip dysplasia has also been advanced. The disparity between primary muscle mass and/or failure of the muscles to develop and reach maturity at the same rate as the pelvis may lead to alterations in the function of pelvic muscles and the development of CHD. There are substantial evidence that the consequence of hip joint laxity. Joint laxity is thought to precede hip joint remodeling and degenerative joint disease. The possibility that joint laxity may be associated with or influenced by pelvic muscle mass and/or maturation as well as by the anatomic structures important in maintaining hip stability (i.e., ligament of the head of the femur, joint capsule, joint confirmation) has been extensively explored. The available evidence, however, does not single out any one factor or variable, which would lead to increased joint laxity. In conclusion, the confirmation and stability of the hip is governed by a number of factors which influence the congruency of the articular surfaces between the femoral head and acetabulum, the integrity of the joint capsule and ligamentum teres, combined with the overall mass and strength of the associated pelvic musculature. The failure of one or more of the orthopedic or soft tissue supporting structures leads to joint laxity with stretching and confirmational change of the aforementioned structures, progressive subluxation, hip dysplasia, and resultant degenerative joint disease.

The clinical signs of hip dysplasia are many and varied, ranging from minimal to pronounced pain, lameness, and disability. Symptoms may be seen as early as four weeks of age, but are generally not detected until 4-6 months of age. Physical examination must include gait analysis, palpation, and precise radiography of the hip.

Observation of the gait may disclose a weight bearing lameness, which is more severe after exercise, a stilted or swaying rear limb gait, an audible “click” when walking, or walking with an arched back. There may also be pain and/or crepitation present upon manipulation of the hip and evidence of poorly developed musculature of the hind quarters.

Palpation of the hip has been utilized to determine the presence or absence of joint laxity and early CHD, especially in immature dogs. The ability to accurately quantitate hip joint laxity should provide key diagnostic and prognostic information for affected dogs. There are, however, a number of concerns, which must be addressed relating to the accuracy of palpation as a method of diagnosis. Palpation is at best a subjective evaluation and is influenced by practitioner experience, positioning of the dogs, amount of forced applied, and whether or not the dog is anesthetized. As of yet, an objective method of determining the amount of joint laxity of subluxation in dogs manifesting symptoms of CHD prior to the development of detectable radiographic changes. The two most common procedures employed are the Bardens’ method and the test for the Ortolani sign, both of which are described extremely well in the article authored by Chalman and Butler. The Bardens’ test detects movement of the femoral head in and out of the acetabulum as the femur is lifted horizontally. Elicitation of an Ortolani sign may be performed with the patient in either dorsal or lateral recumbancy. During testing, the application of pressure along the femoral shaft will subluxate the femoral head dorsally. As the limb is abducted, the femoral head will reseat within the acetablulum. The resulting sound and vibrations or “clicks” produced by this reseating is a positive Ortolani sign. The degree of grading residence of “click” gives an appreciation of the severity of the existing pathology. Dogs with extensive pathology, however, may have a negative Ortolani sign because distortion of the acetabular rim combined with a thickened joint capsule and osteophyte production may lead to an extremely limited range of motion. In these cases, however, radiographic evidence of joint distortion exists and diagnosis should be straightforward.

Although observation of the gait and palpation of the hip can indicate the possibility of CHD, radiographic examination is used to establish the diagnosis in the majority of cases. Historically, radiographic evaluation consists of a symmetric ventrodorsal radiograph of the pelvis and femors with the hind limbs extended and parallel to each other. Lateral pelvic views contribute minimally in the assessment of possible CHD. A major deficiency in this standard radiographic view is the failure to adequately delineate the weight bearing portion of the acetabulum. In addition, this hip extended position may mask the true potential hip joint laxity because in this position, the joint capsule tightens and may act to drive the femoral head into the acetabulum. The dorsal acetabular rim radiographic view has been recommended to evaluate the dorsal rim of the acetabulum for damage and secondary changes to show acetabular filling and congruency of the hip and to correlate palpation of joint laxity and crepitation with radiographic appearance.

The primary radiographic signs of CHD are a shallow acetabulum and a small flattened femoral head. The dorsal acetabular rim recedes and becomes less concave, and increased joint space and subluxation or luxation of the femoral head is observed. As dysplasia progresses, joint instability, synovitis, and cartilage degeneration increase as evidenced by radiographic indication of osteoarthritic changes including femoral neck and acetabular osteophyte development, sclerosis of subchondral bone, subcondral cysts of the femoral head, and ossification of the joint capsule.

While one study reports excellent success in obtaining pelvic radiographs of dogs for hip dysplasia without sedation or anesthesia, chemical restraint is usually employed to achieve proper positioning. Once again, while anesthesia allows for proper positioning, the effects of anesthesia on the relaxation of tissues in the hip joint region and how this may affect the radiographic diagnosis of CHD needs to be taken into consideration.

In conclusion, CHD is a developmental disorder, the expression of which is influenced by a multitude of factors. Gait analysis, palpation, and radiography are indicated to establish a correct diagnosis, but the incipient disease may be difficult to identify because interpretation of the aforementioned diagnostic procedures can be subjective and requires a great deal of skill and expertise for accuracy.

In the next article, we will discuss the treatment of the young growing dog with hip dysplasia. The third article will address the treatment of the mature dog with secondary osteoarthritic changes and degenerative joint disease.

Canine Hip Dysplasia


Canine Hip Dysplasia-Part 2

Surgical Treatment for the Immature Patient

A number of different surgical techniques have been employed to treat canine hip dysplasia. The procedure, which is ultimately selected, should be based upon careful observation and evaluation of the individual patient. Criteria, which must be addressed, include the age of the patient; the severity of subluxation (i.e., the angle of Wiberg); the angle of inclination and anteversion; the depth of the acetabulum; and the presence or absence of femoral head deformity and associated changes indicative of osteoarthritis.

Canine Hip Dysplasia

The surgical procedures most commonly recommended for treatment include triple pelvic osteotomy; intertrochanteric de-rotational femoral osteotomy; excision arthroplasty with or without a bicep sling; and total hip replacement.

The advantages, as well as the indication for each of these procedures, will be discussed in this and in a future article.

The primary goal of surgical intervention for the treatment of canine hip dysplasia in the majority of immature patients is re-direction of the acetabulum. The restoration of hip stability promotes a more normal development of the hip and results in a decrease or halt of the osteoarthritic changes typically associated with a degerenative joint disease.

Because the ultimate goal in a young dog is to help reshape the acetabulum so as to create more depth to accommodate the femoral head and save the hip joint, the technique of choice is the triple pelvic osteotomy (TPO). This procedure presupposes that the femoral component of the hip is normal. Triple pelvic osteotomy is not designed to correct the subluxation problems associated with coxa valga, i.e., increased angle of inclination or increased anteversion of the proximal femur. Such problems need to be addressed by performing a varus osteotomy and demonstrated, however, that if the acetabular component is repositioned such that normal congruency of the joint is maintained, the femoral changes will revert toward normal with time.

Fortunately, in my experience, a femoral osteotomy is usually not necessary, although several studies have indicated that functional results tend to be less satisfactory in dogs having the largest angles of anteversion. Varus and/or intertrochanteric osteotomy is most appropriate in the young dog with subluxation and femoral dysplasia without acetabular dysplasia. As acetabular dysplasia is frequently present, these techniques are seldom employed as a sole means of surgical correction. As previously mentioned, the overwhelming majority of patients exhibit acetabular dysplasia, and the resulting new position obtained by a TPO produces adequate acetabular depth to provide hip stability. However, femoral osteotomy needs to be considered as an ancillary procedure in some cases.

The ideal candidates for a TPO are immature dogs with pain and/or lameness associated with hip subluxation. Since the purpose of the TPO is to prevent the development of degenerative joint disease, only those joints with minimal or no preexisting degenerative joint disease should be considered as candidates for the procedure. When radiographic changes of osteoarthritis are present, excision arthroplasty or total hip replacement may be indicated as the likelihood of success with a TPO is minimized.

The dog’s age is also an important consideration, as rapid breakdown of the dorsal acetabular rim occurs from 4 to 8 months of age in dysplastic puppies. For these reasons, the surgery should be performed prior to nine to ten months of age to achieve best results. However, if the other criteria mentioned previously have been met, good clinical results can still be achieved in older dogs.

Another prerequisite of surgery is the ability to reduce the hip while the patient is under general anesthesia. If the hip cannot be reduced and stabilized by the femoral abduction and internal rotation, there is a diminished chance of success that a TPO would produce good hip stability. Dogs with complete luxation of the hip (grade IV hip dysplasia) however, have been successfully treated with this procedure.

As with any other surgical procedure, numerous techniques and variations of TPO have been developed and used over the last several years to enhance success and minimize complications. The earlier techniques advocated a stair-step osteotomy of the ilium and internal stabilization consisting of screw and wire fixation with or without trochanteric osteotomy. More recently, techniques have employed straight osteotomy of the ilium and rigid internal fixation utilizing bone plates with or without ischial wiring. My own personal preference is to use an oscillating saw to perform the pubic, ischial, and ilial osteotomies through three separate skin incisions. The freely movable acetabular segment is then rotated and tilted into its new position, and rigid stability is achieved and maintained by application of a special pre-contoured bone plate.

Canine Hip Dysplasia

Routine post-operative care consists of confinement and restriction of exercise throughout the immediate post-operative period. Strict rest and confinement should eliminate the potential complication of loss of fixation. Other complications include constipation, urethral impingement, and sciatic nerve injury. Constipation is usually easily alleviated with the administration of stool softener. The proper surgical technique should prevent complication related to urethral and/or sciatic injury. The overwhelming majority of animals will begin bearing weight on the operated limb within 24 to 48 hours, although significant additional time is required for complete healing.

All in all, a triple pelvic osteotomy is an extremely successful treatment of choice for hip dysplasia in the immature dog. This high degree of success, however, depends upon the careful selection of surgical candidates and familiarity with the surgical techniques available.

Canine Hip Dysplasia


Canine Hip Dysplasia-Part 3

Surgical Treatment for the Mature Patient

Although it is highly preferable to diagnose and treat canine hip dysplasia (CHD) in the immature patient, numerous dogs are presented with initial clinical signs of pain and lameness associated with hip subluxation once they have achieved maturity. While triple pelvic osteotomies are routinely performed on mature dogs with no or minimal pre-existing degenerative joint disease with a great degree of success, when moderate to severe radiographic changes of osteoarthritis are present, excision arthroplasty with or without a biceps sling or total hip replacement (THR) is indicated as the likelihood of success with a triple pelvic osteotomy is minimized. The purpose of this article is to discuss the advantages and disadvantages as well as the indication for each of these procedures.

Any discussion about the operative procedures utilized for degenerative disease of the canine coxofemoral joint must be preceded by mention of the fact that the procedure ultimately performed depends upon the surgeon’s experience and training. While this seems intuitively obvious, surgeons are extremely adamant in their views (also intuitively obvious) about which procedure is beset for management of degenerative hip dysplasia in the canine. While some surgeons consider a femoral head and neck excision, a salvage procedure one step short of an amputation, others feel that the inherent risks involved in a THR do not warrant its utilization as a form of treatment. In light of this fact, the discussion of the operative procedures available will proceed from the least aggressive to the most aggressive options rather than from worst to best or visa versa.

Femoral head and neck ostectomy (FHO) is a relatively simple procedure that has been used frequently to eliminate the pain experienced by dysplastic patients. Because the procedure does not reconstruct an intact coxofemoral joint, normal function of the joint is not restored. While the formation of a false joint often alleviates pain and produces increased weight bearing ability on the affected limb, post-operative sequellae including shortening of the affected limb, muscle atrophy, decreased range of motion of the pseudoarthrosis and continued pain, and/or lameness is not uncommon after simple excision of the femoral head and neck. Although these residual clinical signs may result from the biomechanical alterations associated with the formation of a false joint, they may also be attributable to persistent abnormal contact of the proximal femur with the pelvis. For these reasons, various modifications of the standard technique for excision arthroplasty have been developed to prevent bone on bone contact between the cut surface of the femoral neck and the acetabulum.

My own clinical observation has been that in dogs receiving excision, arthroplasty of the femoral head and neck alone increased morbidity, and generally overall, poorer results are achieved than if an ancillary, interpositional procedure is concurrently performed. It is therefore my own personal preference to discourage utilization of a simple FHO for treatment of degenerative joint disease of the canine hip and to rely instead on an ancillary interpositional procedure in combination with an FHO or total hip replacement. While a variety of tissues including the joint capsule and the deep gluteal and biceps femoris muscles have been mobilized to prevent bone on bone contact between the pelvis and the cut surface of the femoral neck, utilization of the biceps femoris allows for a wider and thicker flap of muscle to be mobilized easily for translocation.

The advantages and disadvantages of performance of a biceps sling compared to a simple FHO have been debated for a number of years. Surgeons that discourage its utilization argue that the increased operative time and potential morbidity (i.e., increased swelling or edema of the operated limb, wound infection, sciatic nerve entrapment), outweigh any potential benefits including excellent coverage of the ostectomy site, to decreased bone on bone contact, and the promotion of early post-surgical use of the limb.

Over the course of the last nine years, I have had considerable exposure to and experience with the biceps sling, and my clinical impression is that these patients, while perhaps not being restored to a totally normal state, fare far better than if a simple FHO had been performed. In fact, the overwhelming majority return to at least good, if not excellent, function over a relatively short period of time, free from pain, discomfort, and crepitation at the ostectomy site. Excision arthroplasty of the femoral head and neck utilizing a biceps femoris muscle sling is certainly an effective alternative to total hip replacement.

Total hip replacement is a rewarding method of treatment for canine hip dysplasia as the best approach to restoring normal hip function is to reestablish as closely as possible normal joint configuration. While standard operative procedures have been in use for more than 15 years, recent advances in surgical technique and modifications of the implants themselves have led to greater acceptance of the procedure as complication rates have decreased and long term success has been documented. The hesitancy to recommend THR as the primary means of treatment of canine hip dysplasia outside of limited availability and cost has been the potential for complications including prosthesis dislocation, deep infection, loosening of the implants, femoral fracture, and sciatic neuropraxia. Once again, by paying strict attention to detail, the potential for complications following THR is minimized and excellent long-term success rates can be achieved, clearly demonstrating the THR is an effective method of treating canine hip dysplasia.

In conclusion, it should be mentioned that patient selection for any of the aforementioned procedures is of the utmost importance. A dog that has hip dysplasia but has clinically sound ambulatory function is not a candidate for surgery. Many dogs function with minimal pain or impairment on medical management alone, despite tremendous bony changes. Others, with what appear to be minimal lesions, are severely hindered. It follows then that a reasonable effort at medical management must have been tried and failed. The point of medical failure must be clearly recognized, however, because continuing medical therapy after these treatments have become ineffective decreases the chances for surgical success. In addition, an accurate neurologic examination is mandatory, as many myelopathies co-exist in dysplastic dogs. If there is the presence of neurologic degeneration, the dog should not be considered a surgical candidate.

In response to the poor results consistently obtained with excision arthroplasty in large dogs, my recommendation is to avoid this procedure as a treatment for hip dysplasia and to rely instead on a biceps sling surgery or a total hip replacement. The determination of which of these two procedures to use depends upon the client’s expectations for return to function and the degree to which they are willing to accept the potential limitations and/or complications associated with each procedure.

canine hip-dysplasia


Total Ear Canal Ablation with Curettage of the Bulla for End State Otitis Externa

Although medical therapy is often effective in treating otitis externa, chronic otitis externa may progress to end-stage otitis necessitating surgical intervention.

Unsuccessful medical therapy for otitis externa may be due to the presence of horizontal or vertical ear canal neoplasia or polyps, generalized dermatological disease, simultaneous otitis media, and/or interna or irreversible hyperplastic ear canal disease. Total ear canal ablation combining bulla osteotomy and curettage is the surgical technique of choice in patients that have chronic, non-responsive ear disease that is unsuitable for or non-responsive to lateral ear canal resection.

While total ear canal ablation with bulla osteotomy (“TECA/BO”) may be the technique of choice, it is also a technique that should not be taken lightly, as post-operative complications can and do indeed occur. These complications are attributable to the technical difficulty of the surgical procedure and the potential for post-operative infection because of bacterial contamination of the surgical site, the most common post-operative complications encountered include facial nerve paralysis, head tilt, nystagmus, ataxia, hearing loss, hypoglossal nerve dysfunction, Horner’s syndrome, cellulites, abcessation, fistulation and/or dehiscence, and/or recurrent infection. In the majority of cases, the manifestation of these complications is temporary, however, because of the potential for long-term disability, excellent client communication is essential prior to surgical intervention. In addition, in those cases exhibiting aural manifestations of generalized dermatological disease, the client should be informed that persistent topical and/or systemic therapy may be indicated to control head shaking, pruritus, and odor even after aggressive surgical intervention.

In light of the association of otitis media with chronic end stage otitis externa, bulla osteotomy and curettage is indicated in conjunction with TECA to provide drainage of the tympanic bulla and reduce the post-operative complication rates experienced when TECA is performed alone. The surgical procedures advocated to achieve tympanic drainage are either ventral or lateral bulla osteotomy with curettage. In my experience, lateral bulla osteotomy is preferable to ventral bulla osteotomy because the patient does not have to be re-positioned after the TECA procedure. In addition, less soft tissue dissection is required of both procedures are performed through a single incision. Although it is difficult to perform a valid comparison of the two techniques because of the variability of the clinical features present in each case, the overall rates of recurrence or persistence of drainage appear to be lower when the lateral approach is utilized.

As mentioned previously, a high rate of complications may be observed if excellent attention to detail is not achieved throughout the surgical procedure. Facial nerve dysfunction may result from stretching or transecting the nerve because of its close association with the horizontal ear canal as it exits the stylomastoid foramen. Meticulous dissection of tissues as close to the perichondrium as possible should be performed to help prevent iatrogenic trauma. This perichondrial dissection sounds easier than it is, because the distortion of normal ear anatomy caused by fibrosis, ossification, and perioral abcessation make dissection difficult and may prevent visualization of the nerve. Iatrogenic damage to the structures of the middle and inner ear can occur during bulla curettage resulting in Horner’s syndrome, nystagmus, head tilt, and/or ataxia post-operatively. While affected tissue must be removed to reduce the risk of continued infection, gentle curettage avoiding the dorsomedial compartment of the bulla may help reduce the incidence of neurologic complication.

In an effort to achieve complete yet gentle curettage, I use sterile cotton swabs instead of a curette to remove the inflammatory tissue and associated debris from the bulla. Complete removal of the offending tissue is easily accomplished using the gentle curettage because of the degree of inflammation and infection of the epithelium of the middle ear is such that the tissue usually strips away from the bulla cleanly. Gentle yet copious lavage will usually remove any tags of tissue missed initially. Bacterial contamination of the surgical site is a given and thorough debridement and lavage must be performed to decrease the risk of post-operative sequelae. Cellulitis, drainage, fistulation, and reinfection is usually due to incomplete removal of the infected tissue, inadequate drainage, or primary closure of the surgical site. In order to avoid these complications, I place a penrose drain within the bulla and allow it to exit the ventral aspect of the incision to achieve optimal ventral drainage In addition, the incisional edges of tissue are not primarily closed, but are incompletely opposed with loose tacking sutures to allow the defect to fill in with granulation tissue.

The head is then bandaged and rebandaged as necessary (usually every 2 to 3 days) to prevent the accumulation of blood, pus, or serum within the wound. Drainage is maintained until the drain is non-productive, which is usually by the seventh day post-operatively. At this stage bandages may be changed every 5-7 days until contraction and reepithelialization is complete, which usually takes an addition 7-14 days.

Utilization of complete curettage, thorough debridement, lavage, drainage, and delayed closure affords an excellent opportunity for successful management of chronic otitis externa with a single surgical intervention. If reinfection and fistulation eventually develop, surgical exploration for remnants of infected cartilage or epithelium is required, as antibiotic therapy alone is usually fruitless and only ends up delaying the inevitable. If exploration is performed, a ventral bulla osteotomy is strongly recommended as fibrosis and loss of normal tissue plains makes identification of the facial nerve even more difficult.

In conclusion, TECA/BO and curettage is an effective means of treating end stage otitis externa. Long-term results are usually good to excellent and adherence to the principles outlined above will help minimize the occurrence of the unfortunate complications that can accompany surgical management for this disease.


Canine Mast Cell Tumors

Mast cell tumors (MCT) in dogs are very common, accounting for approximately 20% of all skin tumors in dogs.

For most dogs, the underlying cause promoting the development of the tumor is not known. Mast cells are specialized cells derived from stem cells in the bone marrow and play an important role in helping an animal respond to inflammation and allergies. They are found distributed throughout the body, predominantly near blood vessels, nerves, and beneath the skin. Mast cells become activated when antigens bind to receptors on their surface and subsequently release several biologically active chemicals stored in their granules when stimulated including histamine, heparin, serotonin, prostaglandins, proteolytic enzymes, and other pro-inflammatory molecules. Although these chemicals are vital to normal bodily function, they can be very damaging to the body when released in chronic excess. These chemicals can cause systemic problems that include gastric ulcers, internal bleeding, and a range of allergic manifestations.

Mast cell tumors can arise from any skin site on the body and can have a variety of appearances. MCT most commonly are seen as solitary lumps or masses in or underneath the skin; occasional dogs can have multiple masses. MCT can look like just about anything ranging from benign-appearing lumps, to more angry or ulcerated lumps, masses with a stalk, or focal thickenings in the skin. MCT may change quickly in size because of reactions around the mass and release of their vasoactive compounds. In most cases, evidence of an MCT is easily generated by examination of a fine-needle aspirate of the suspect mass, and aspiration is advised before removal of a mass to determine if it is an MCT, a finding that would demand a more aggressive surgical removal than for other more benign skin masses. Often, obtaining blood for a complete blood count and biochemical profile, buffy coat analysis, and a urinalysis will be advised as these can help assess overall health and provide information that potentially influences treatment recommendations. The CBC may reflect low or high white blood cell count, low platelet count, and/or elevated mast cell counts. The buffy coat is diagnostic (although subject to false-positives) and reflects mast cells circulating in the bloodstream where they are ordinarily not found in large numbers. A positive buffy coat suggests bone marrow involvement. Other tests may include lymph node aspirate, bone marrow aspirate, x-rays, and ultrasound evaluation.

As mentioned previously, canine mast cell tumors are among the most common skin tumors, which occur in dogs. Boxers, Rhodesian ridgebacks, Pugs, Boston terriers, Pit-bull terriers, and Weimaraners are at high risk (4 to 8 times more than the population) for developing MCT. Shar-Peis, particularly young dogs, are predisposed to developing MCT, and these tumors are often poorly differentiated and act more aggressively biologically than in other breeds.

One characteristic of mast cell tumors is the tendency for them to change in size, even on a daily basis. A tumor that gets bigger and smaller, seemingly on a whim, maybe an MCT. Another idiosyncrasy is the potential of the tumor to produce “Dariers sign” if poked and prodded. Handling these tumors – even a routine veterinary palpation or needle aspirate – can cause a heavy release of histamine that results in swelling, redness, itchiness, and/or hives. Symptoms are variable, depending on the location of the tumor and the degree to which it has developed and/or spread. Signs of systemic involvement may include: loss of appetite, vomiting, bloody vomit, diarrhea, abdominal pain, dark or black feces, itchiness, lethargy, anorexia, irregular heart rhythm and blood pressure, coughing, labored breathing, various bleeding disorders, delayed wound healing, enlarged lymph nodes.

Most mast cell tumors are considered locally invasive and can be difficult to remove completely because of the extent of local spread. The behavior of mast cell tumors is a reflection of their grade. When evaluating the tissue sample obtained from surgical removal of the mast cell tumor, the diagnosis of mast cell tumor will be confirmed, the mast cell tumor will be staged, and the width of the tissue margins, which are free of tumor will be measured. Staging and the width of the tissue margins which are free of tumor cells together with the location of the mass, the health of the dog, and the grade of the mast cell tumor will determine whether further treatment with radiation therapy or chemotherapy will be recommended.

Mast cell tumors have 3 grades. Tumor grade is associated with the degree of differentiation of the mast cells. Grade I tumors are well differentiated and are the least aggressive and least likely to metastasize (spread to other organs). Complete surgical excision of Grade 1 MCT is usually curative. Grade 2 tumors are moderately differentiated and the prognosis and treatment options are perhaps the most complicated and difficult to predict. Grade 3 tumors are poorly differentiated, very aggressive with a high likelihood of metastasis. They carry the poorest prognosis but are fortunately the least common grade encountered. Mast cell tumors show a predilection to spread to regional lymph nodes, liver, spleen, and bone marrow.

Grading of mast cell tumors, however, is very subjective. In one study, mast cell tumors were graded by a group of pathologists, and frequently, there was disagreement regarding the grade even amongst board-certified pathologists. In many cases, perhaps a better method of determining how malignant or benign a mast cell tumor will behave is to have a proliferative study performed. This includes PCNA (proliferating cell nuclear antigen), AgNOR (agyrophilc nuclear organizing regions), and Ki67. Tyrosine kinase receptors (a receptor for mast cell growth factor) are also important and tests related to this include cKIT mutations and KIT staining patterns.

Because mast cell tumors prefer to metastasize the above-mentioned sites, staging a dog with a mast cell tumor entails collecting cells from the regional lymph nodes for microscopic examination, imaging the thorax and abdomen (radiographs, abdominal ultrasound, ) for evidence of enlargement of the mesenteric lymph nodes, liver or spleen, and an assessment of potential bone marrow involvement, either via a bone marrow aspirate for microscopic examination, or examination of the white blood cells for circulating mast cells.

Surgical removal is the mainstay of treatment of canine mast cell tumors. Presurgical treatment with histamine blockers and/or steroids is recommended to prevent complications of mast cell degranulation during manipulation of the tumor mass for the duration of its removal. Because of their locally invasive behavior, wide margins of what appears to be normal tissue around the tumor needs to be removed to increase the likelihood that the tumor has been completely removed. Approximately 2-3 cm margins and one fascial plane of depth are attempted as surgical margins.  Recent research has shown that 1-2 cm clean margins of a grade 1 or 2 mast cell tumor can be curative.  For mast cell tumors that were not or because of location could not be completely removed with wide surgical margins, radiation therapy is often the best treatment for residual disease. Radiation therapy after surgical removal appears to be beneficial and may reduce the incidence of reoccurrence and increase survival rates. Radiation is most useful when the tumors have not spread to multiple areas of the body. Radiation therapy, however, is expensive and there may not be a facility able to offer this option within a convenient distance in many locations. Chemotherapy is sometimes used to treat mast cell tumors, but chemotherapy is usually reserved for dogs with grade 3 tumors. Mast cell tumors are notoriously unpredictable tumors with regards to response to chemotherapy, and chemotherapy for metastatic mast cell neoplasia does not offer consistent results. If the mast cell tumors have spread to multiple areas, combinations of anti-cancer drugs are commonly used along with surgery and radiation. These include vinblastine, lomustine, vincristine, doxorubicin, mitoxantrone, cyclophosphamide, and L-asparginase. These are all heavy-duty chemotherapy drugs with potential side-effects that include severe immunosuppression, vomiting, diarrhea, and/or liver damage. Palladia is a tyrosine kinase receptor blocker; the proliferative panel may be helpful to determine if the patient will respond to this type of medication. The tumor should be positive for cKIT mutations for this drug to be potentially effective. Unfortunately, mast cell tumors do not respond well to these drugs and several recent studies seem to demonstrate very limited efficacy in conjunction with surgery. It is important to remember that, while radiotherapy and chemotherapy are potentially useful adjuvant forms of therapy, aggressive surgery remains the mainstay of treatment for canine MCT and is sufficient to successfully treat the majority of MCT encountered in practice.

In addition to surgery, radiation therapy, and/or chemotherapy management of the tumors, many dogs will benefit from the administration of medications that tend to help fight the secondary local and systemic effects of the tumor. These usually include steroidal drugs like prednisone, and anti-histamines like Benadryl, Pepcid, or Zantac. These medications prevent the undue side-effects of histamine release commonly encountered in dogs with MCT.

Several prognostic factors (in addition to grade or stage) have been identified. Boxers have a higher percentage of low-grade tumors compared to most other breeds (It is important to recognize, though, that a high-grade mast cell tumor will behave just as aggressively in a boxer as in any other breed.) Smaller tumors and tumors that remain relatively static in size for prolonged periods (months or years) carry a better prognosis. Tumors that remain confined to the skin without metastasis to regional lymph nodes or distant sites carry a better prognosis. The presence of multiple cutaneous tumors does not affect long-term prognosis. Systemic illness (anorexia, vomiting, melena, gastrointestinal ulceration) is usually a reflection of a larger tumor burden and therefore carries a worse prognosis. Tumors located on the muzzle have a higher rate of spread to regional lymph nodes and therefore carry a more guarded prognosis. Historically, it has been suggested that tumors located in the inguinal area, perineum, and scrotum carry a more guarded prognosis, but this is based solely on anecdotal evidence, and two recent studies have refuted this claim.

The prognosis for completely removed grade I and grade II tumors is excellent. Even with complete surgical removal, however, because of the tendency of MCT to exhibit multicentric origination, new lesions may appear elsewhere, which are not the result of actual metastatic spread. For this reason, multiple surgeries over time may be necessary to control the disease process. The prognosis for incompletely removed grade I and II tumors treated with radiation therapy after surgery is also excellent with approximately 90-95% of dogs having no recurrence of tumor within 3 years of receiving radiation therapy. The prognosis for dogs with grade III tumors is considered guarded as local recurrence and/or spread is likely in most dogs. If your dog is diagnosed with a grade III MCT, most likely chemotherapy will be recommended as at least part of the protocol and a guarded prognosis is warranted.


Multiple Myeloma

Multiple myelomas or plasma cell myeloma is a neoplasm of well-differentiated B cell lymphocytes typically originating from the bone marrow.

Neoplastic cells can metastasize widely, having a predilection for bone and resulting in osteolysis. The malignant transformation of a single B cell can secrete a homogenous immunoglobulin product known as paraprotein, which will mimic the structure of normal immunoglobulins. Overabundant production of paraprotein, consisting of any of the immunoglobulin classes, will appear as a sharp, well-defined peak or monoclonal gammopathy on serum electrophoresis.

The most frequently encountered multiple myelomas secrete IgG or IgA paraproteins; however, IgM myelomas (macroglobulinemia) have also been diagnosed in companion animals. Light chain disease is caused by plasma cell overproduction of the light chain segment of the immunoglobulin complex, consisting of either the lambda or kappa light chain. These proteins are referred to as Bence-Jones proteins and are the most commonly observed immunoglobulin fragments in the monoclonal gammopathies. There are rare instances where a malignant plasma cell neoplasm will be nonsecretory. These tumors occur in approximately 1% of all cases of multiple myeloma and are referred to as nonsecretory multiple myeloma. In this type of neoplasm, malignant plasma cells produce either fragments or intact monoclonal immunoglobulins but do not secrete them from the cell. In rare cases of nonsecretory multiple myeloma, recognizable immunoglobulins are not produced.

Multiple myelomas have been described most commonly in dogs, humans, and cats. They account for

< 1% of all malignant canine tumors, ~ 8% of all malignant hematopoietic tumors in dogs, and 3.6% of all primary and secondary bone tumors diagnosed by biopsy. There is no current evidence suggesting any age, sex, or breed predilection; however, older dogs are most commonly affected with a mean age of 8 to 9 years. Multiple myeloma is even less common in cats with a median age of 12 to 14 years and possible male predisposition. The cause of multiple myeloma in companion animals is largely unknown although genetics, viral infections, chronic immune stimulation, and exposure to carcinogens have been identified as possible contributing factors.

The clinical manifestations of multiple myeloma are highly variable and may affect multiple organ systems. The pathologic conditions associated with multiple myeloma are related to the effects of the circulating paraprotein as well as organ or bone marrow dysfunction due to neoplastic infiltration. The presentation of a patient with multiple myeloma will depend on the type of neoplastic cell, type of immunoglobulin produced, location of the tumor, and severity of growth and infiltration. Affected dogs can exhibit signs of lethargy, weakness, lameness, bone pain, hemorrhage (e.g, petechiae on mucous membranes, gingival bleeding, and epistaxis), polyuria / polydypsia, and/or neurologic deficits. Other presenting signs of disease may include hypertension, ophthalmic abnormalities (e.g., venous dialation with sacculation, retinal hemorrhages, and retinal detachment), neurologic dysfunction (including seizures), organomegaly, and suggestion of multiple organ failure.

Hyperviscosity syndrome.
Hyperviscosity syndrome is an increase in the viscosity of the blood secondary to the high concentrations of circulating paraprotein, clinically manifesting in neurologic signs, retinopathy, and cardiomyopathy. IgA and IgM are most often associated with hyperviscosity syndrome because of their structure and size (IgA dimers and IgM pentamers). Cardiomegaly and cardiac disease may result secondary to increased cardiac workload and myocardial hypoxia caused by hyperviscosity. In a study of cats with multiple myeloma, two-thirds of the cats had cardiomegaly on thoracic radiographs and nearly half had a heart murmur.

Osteolysis.
Bone lesions associated with multiple myeloma include discrete radiolucent lytic areas (punched-out appearance) or diffuse osteopenia and commonly affect the axial skeleton and long bones. These lesions may be associated with severe bone pain, spinal cord compression, pathologic fracture, and hypercalcemia. However, only 50% of dogs have radiographic evidence of bone disease. And although cats are reported to have skeletal lesions (8% to 67%), the true incidence of lytic lesions in cats is unknown.

Bone lesion detection improves with focused imaging on specific regions or bones vs. routine survey abdominal and thoracic radiographs. In people, conventional radiography remains the gold standard imaging technique. Computed tomography and magnetic resonance imaging may also be useful; however, nuclear scintigraphy is generally not recommended since myeloma patients have inadequate skeletal uptake of technetium-99 secondary to osteoblast dysfunction.

Hemorrhagic diathesis.
Patients with multiple myeloma can manifest unique hemostatic disorders that predispose them to hemorrhage. Mechanisms include paraprotein-induced thrombocytopath, in which protein coating of platelets leads to platelet dysfunction and paraprotein interference with clotting factors. Other potential causes of bleeding include abnormalities in the formation and polymerization of fibrin, tissue fragility associated with amyloidosis, hypervolemia secondary to hyperviscosity syndrome, and thrombocytopenia. About one-third of dogs and cats with multiple myeloma have clinical signs of bleeding, most commonly epistaxis, intraocular hemorrhage, and gingival bleeding. These patients may have prolonged prothrombin and partial thromboplastin times and about 50% of cats and 30% of dogs are thrombocytopenic.

Cytopenias.
Patients with multiple myeloma can develop anemia from a variety of causes including chronic disease, hemorrhage due to coagulopathy, myelophthisis, and red blood cell destruction. Normocytic, normochromic, and nonregenerative anemia is one of the most common findings on a complete blood count (CBC); two-thirds of dogs and cats are affected. Pancytopenia may be seen in patients with marked bone marrow infiltration with neoplastic cells.

Hypercalcemia.
Hypercalcemia in cases of multiple myeloma can result from osteoclastic bone resorption, hypercalcemia of malignancy, or hyperglobulinemia. Bone stores of calcium can be released by osteoclasts secondary to cytokine secretion by myeloma cells (e.g. lymphotoxin, tumor necrosis factor alpha, interleukins 1, 3, and 6). Myeloma cells can also secrete parathyroid hormone-related peptide, resulting in paraneoplastic hypercalcemia of malignancy. Hyperglobulinemia results in calcium binding by the paraprotein increasing the total calcium concentration while the ionized calcium concentration remains normal. Ionized calcium measurement is, therefore, needed to confirm true hypercalcemia in patients with multiple myeloma.

Renal disease.
Renal disease occurs in about one-third of dogs and cats with multiple myeloma. Renal insufficiency is most commonly associated with excessive light chain production or hypercalcemia. First, excessive light chain production overwhelms the catabolic capacity of the renal tubular cells and the free light chains complex with proteins to form tubular casts leading to renal tubular obstruction. Endocytosis of light chains by tubular cells also induces cytokine release and inflammation resulting in further renal damage. Second, hypercalcemia can lead to prerenal azotemia secondary to antidiuretic hormone inhibition and eventual renal mineralization. Other potential causes of renal disease include amyloidosis, pyelonephritis, and decreased renal perfusion secondary to hyperviscosity syndrome.

Bacterial infection.
Increased susceptibility to bacterial infection is common in patients with multiple myeloma and infections can be life-threatening if not addressed. Immunodeficiency can be secondary to myelophthisis (which results in leukopenia), decreased production of functional immunoglobulin, and compromised B cell function.

Clinical signs and symptoms may be present for up to 1 year before a definitive diagnosis of multiple myeloma is made. Patients can also present with recurrent infections, non-regenerative anemia, pathologic bone fractures, and/or seizures. Complications secondary to multiple myeloma may include renal failure, infections secondary to immunosuppression, clotting disorders, chronic anemia, cardiac insufficiency, and neurologic dysfunctions such as senility.

A diagnosis of multiple myeloma may be made if there is radiographic evidence of osteolysis, there is a population of greater than 20% plasma cells in bone marrow aspirates or biopsies, a monoclonal gammopathy on serum electrophoresis exists, and/or Bence-Jones protinuria is present. Recent studies suggest that in cats’ visceral organ infiltration be included in the diagnostic criteria. Further studies suggest a primary extramedullary origin for neoplastic transformation in cats with multiple myeloma vs. primary intramedullary neoplastic transformation as accepted in the dog myeloma model.

Multifocal radiolucent lesions within the bone may be seen in ~ 40% of dogs suffering from multiple myeloma. In contrast, osteolytic lesions rarely are seen in cats. The bones most commonly involved in canine multiple myeloma include the spine, pelvis, ribs, skull, and proximal extremities. Malignant plasma cell tumors present in the bone marrow are often osteolytic. The presence of these tumors directly induces bone resorption by production of osteoclastic-activating factor from neoplastic cells. Osteolysis is also induced secondary to paraprotein binding of ionized calcium, which initiates secretion of parathormone (PTH) from the parathyroid gland. PTH acts directly on the bone to increase serum calcium concentration.

Survey radiographs may reveal focal, multifocal, or diffuse osteoporosis-type lesions approximately 3-4 weeks after bone changes have occurred. Clinically, the patient may present with pathologic fractures, rear limb lameness or paresis, or bone pain. Myelograms are an effective means of visualizing the changes to vertebral bodies, especially when the patient presents with rear limb lameness or paresis. Most commonly, the myelogram will show extradural compression of spinal cord in the area of the lesion. Plasma cell tumors producing IgM often infiltrate the spleen, liver, and lymph tissue rather than bone. Whole body survey radiographs may detect enlargement of these organs and tissues.

Dogs and cats with multiple myeloma may experience moderate to severe pain, and eliminating it should be a priority. Pain may be relieved by treating the underlying cancer and providing various analgesic therapies and supportive care. Antibiotic therapy may be needed to treat concurrent infections, such as urinary tract infection or bacterial pyoderma, as these can progress to life-threatening infections if left untreated. Intravenous fluid therapy is often needed initially to correct dehydration, improve cardiovascular status, and manage hypercalcemia and azotemia. Treatment with isotonic saline solution is preferred over other crystalloid replacement fluids in the initial management of hypercalcemic patients. Bisphosphonates, such as pamidronate, may be useful in managing hypercalcemia as well as reducing bone pain and decreasing osteoclastic bone resorption. Evaluation of blood urea nitrogen and creatinine concentrations in conjunction with urine specific gravity should be performed before using this medication since it is potentially nephrotoxic. The recommended dose of pamidronate is 1 to 2 mg/kg given intravenously in dogs and, anecdotally, 1 mg/kg given intravenously in cats every 21 to 28 days. This medication should be diluted in saline solution and administered as a slow infusion over two hours to minimize renal toxicosis. Bisphosphonates are an essential component of therapy for multiple myeloma in people, and their use is associated with significantly reduced skeletal-related events and improved survival times. Plasmapheresis is the best immediate treatment for hyperviscosity syndrome. Although rarely performed in veterinary medicine, this procedure involves withdrawing anticoagulated blood, separating blood components, removing the plasma, and reinfusing the remaining components with crystalloid fluids. Packed red blood cells or platelet-rich plasma transfusions may be required if marked hemorrhage or thrombocytopenia is present, respectively. Neoplastic plasma cells are sensitive to irradiation, and radiation therapy is a highly effective palliative treatment for multiple myeloma since it can relieve discomfort and decrease the size of the mass or tumor burden. Indications for radiation therapy include painful bone lesions, spinal cord compression, pathologic fracture (after fracture stabilization), or a large soft tissue mass.

Although a cure is unlikely, multiple myeloma can be a rewarding disease to treat since chemotherapy can greatly extend the quality and duration of life. The chemotherapy drugs most often used are alkylating agents, usually melphalan, combined with prednisone. However, eventual relapse during therapy is anticipated. In dogs, the recommended treatment protocol is melphalan administered orally once daily at a dose of 0.1 mg/kg for 10 days and then 0.05 mg/kg once daily until the disease relapses or myelosuppression occurs. Prednisone is given concurrently at a dose of 0.5 mg/kg given orally once daily for 10 days and then 0.5 mg/kg every other day for 30 to 60 days, at which time prednisone is discontinued. Pulse-dose therapy with melphalan has also been described, in which melphalan, at a dose of 7 mg/m2, is given orally once daily for five consecutive days every 21 days. The most common side effects associated with melphalan therapy are myelosuppression and delayed thrombocytopenia. A CBC should be performed every two weeks for the first two months of treatment and then monthly.

Combined melphalan and prednisone therapy can also be used in cats; however, cats appear to be much more susceptible to myelosuppression. The recommended treatment protocol is 0.1 mg/kg (or 0.5 mg total dose) melphalan given orally once daily for 10 to 14 days and then every other day until clinical improvement or leukopenia develops. A maintenance dose of 0.5 mg given every seven days is then recommended. Prednisone or prednisolone is given concurrently at a dose of 0.5 mg/kg orally once daily. If leukopenia develops, melphalan therapy should be discontinued until white blood cell counts return to normal; then, maintenance therapy may be attempted at the same or a lower dose.

Other chemotherapy agents used to treat multiple myeloma include chlorambucil and cyclophosphamide either alone or in combination with melphalan. In sick myeoma patients, in which a faster response to treatment is needed, cyclophosphamide may be administered intravenously at a dosage of 200 mg/m2 once at the time that oral melphalan therapy is initiated. Lomustine (CCNU) has also been used in combination with prednisone to treat multiple myeloma in cats.

In dogs with relapsing multiple myeloma or resistance to alkylating agents, single agent doxorubicin or the VAD (vincristine, Adriamycin [doxorubicin], and dexamethasone) protocol can be considered. This protocol combines vincristine (0.7 mg/m2 intravenously on days 8 and 15), doxorubicin (30 mg/m2 intravenously every 21 days), and dexamethasone sodium phosphate (1 mg/kg intravenously on days 1, 8, and 15); however, the reported duration of response to this protocol is only a few months.

The overall response rate for dogs treated with melphalan and prednisone chemotherapy is 92%, with 43.2% of dogs achieving a complete response and 48.6% achieving a partial response. The median survival time of dogs treated with this drug combination is 540 days, which is significantly longer than the survival time of 220 days in dogs treated with prednisone alone. Negative prognostic factors in dogs include hypercalcemia, light chain proteinuria, and extensive lytic bone lesions.

Response to therapy and duration of response appear to be more variable in cats. Factors associated with a more aggressive form of the disease and poor prognosis include bone lesions with pathologic fracture, anemia, light chain proteinuria, azotemia, and poor response to treatment. When treated with melphalan and prednisone chemotherapy, four cats classified as having aggressive disease had a median survival time of five days, whereas the median survival time of five cats with less aggressive disease was 387 days. Other studies have shown overall less promising results with a shorter duration of response to treatment and a survival time of six months or less in treated cats. In cats with multiple myeloma and other related disorders, the degree of plasma cell differentiation is significantly correlated with survival. Cats with well-differentiated tumors (< 15% plasmablasts) have a median survival of 254 days, whereas cats with poorly differentiated tumors (≥ 50% plasmablasts) have a median survival of 14 days.

In summary, multiple myeloma is a rare neoplasm in both cats and dogs. Conditions associated with multiple myeloma include hyperviscosity syndrome, bone lesions, hypercalcemia, renal disease, cytopenias, hemorrhagic diathesis, and increased susceptibility to bacterial infection. Multiple myeloma does not appear to have the same biologic behavior in dogs and cats and is best viewed as a heterogeneous disease with a different prognosis, clinical course, and response to therapy both within and between species. Although a good clinical response may be achieved with chemotherapy, eventual relapse of disease is to be expected.


Management of Sacroiliac Fracture/Luxation in the Dog and Cat

Injury to the sacroiliac joint in the dog and cat commonly occurs in association with fractures of the pelvis and pelvic limb.

Substantial soft tissue injury and neurologic dysfunction may also be present. A patient with a sacroiliac fracture/luxation has in all probability sustained a significant external blow to the pelvis, and because of the probability of multiple fractures and soft tissue injuries, a thorough physical and neurologic examination must be performed.

The sacroiliac joint is a combined synovial and cartilaginous joint which functions as a supportive bridge between the appendicular and axial skeletons. Because the pelvis and sacrum form a rigid rectangular or boxlike unit, unilateral displacement of the sacroiliac joint cannot occur without associated pelvic fractures or a pelvic symphyseal separation. Unilateral separation of the sacroiliac joint occurring in conjunction with other severe orthopedic injuries is much more common than bilateral sacroiliac joint injury. Few unilateral sacroiliac injuries are associated with ischial and/or pelvic fractures alone.

Clinical signs exhibited by the patient obviously depend on the severity of the trauma as well as the extent of the associated injuries. Caudal abdominal herniation, urethral laceration, intestinal perforation, urinary bladder rupture, diaphragmatic hernias, and pulmonary contusions have all been associated with fractures of the pelvis. It is imperative that associated soft tissue injuries be diagnosed, as they affect treatment and prognosis. The patient may be ambulatory or nonambulatory, depending on the nature of the associated orthopedic and/or neurologic injuries.

In fracture/luxation of the sacroiliac joint in dogs and cats, treatment is either conservative or surgical. Current recommendations indicate conservative treatment in subluxations or in complete luxations when the patient is ambulatory and exhibits minimal discomfort. Before a course on conservative therapy is chosen, a neurologic examination should indicate that there are no functional deficits of the lumbosacral trunk and/or sciatic nerve. Complications of conservative management include increased cranial or medial displacement of the hemipelvis and obstruction of the pelvic outlet. Conservative treatment may also prolong the period of instability and lameness and prolong the period of patient discomfort and client concern. In addition, if marked displacement is present, asymmetry of the acetabulae may result in an abnormal gait posttrauma.

Open reduction and internal fixation is indicated for fracture/luxations when one or more of the following clinical or radiographic signs are present: 1) marked instability and displacement of the hemipelvis, 2) neurologic deficits attributable to the luxation or 3) obstruction of the pelvic outlet is observed. Surgical intervention is of particular value when associated orthopedic injuries are present, as surgical stabilization allows the patient to become ambulatory earlier and provides a better prognosis for the return to a normal gait.

In light of the fact that the overwhelming majority of sacroiliac fracture/luxations are associated with additional orthopedic injuries, my personal preference is to opt for early surgical repair. Even in cases of unilateral fracture/luxations with minimal associated orthopedic injuries, in my experience surgical intervention returns these animals to a normal gait more quickly and with a shorter convalescent period than if conservative therapy was chosen.

Sacroiliac fracture/luxations may be surgically repaired by either a dorsolateral or ventrolateral approach. The approach chosen may be dictated by the presence of additional pelvic injuries requiring open reduction and internal fixation, or surgeon preference. Both approaches provide adequate exposure for visualization of the sacroiliac joint.

Stabilization of sacroiliac fracture/luxations is most commonly accomplished with lag screw fixation. The two most important variables in the technique of lag screw fixation affecting sacroiliac stability are screw location and depth of screw placement. Screws placed within the sacral body have the lowest rate of loosened fixation compared to other areas of the sacrum. Proper positioning within the sacral body is also essential to prevent injury to the nerve roots within the spinal canal, and the lumbosacral trunk or sciatic nerve ventral to the sacral body. With regard to depth of screw placement, a cumulative screw depth/sacral width of 60% or more significantly reduces the likelihood of loosening of the fixation. While some authors have suggested that 2 screws be used routinely for sacroiliac stabilization, in all feline and most canine sacrums there is room for only one properly placed screw within the sacral body. In the giant breeds of dogs, a second screw or an intramedullary pin may be placed, but the placement of this additional screw or pin within the sacral body is dependent upon the accuracy of placement of the first screw. In addition, a recent study did not demonstrate a difference in the number of loosened fixations when one or two screws were used.

When a sacroiliac fracture/luxation occurs, most if not all of the fibrocartilage remains attached to the lateral surface of the sacral wing. When placing lag screws for fixation, the location of the sacral body must be determined by palpation as well as by the anatomical landmarks of the sacral wing. Screw placement should always be just caudal to the sacral wing notch.

Postoperative care should include restriction of exercise for a period of 6-8 weeks. A mild laxative may be administered if bowel movements appear to be painful during the immediate postoperative healing period. A significant number of sacroiliac fracture/luxations repaired with lag screw fixation may loosen and result in loss of reduction and sacroiliac instability. The guidelines for the location of screw placement mentioned here should improve the results of fixation and allow for a better prognosis for return to a normal gait and conformation.

Sacroiliac Fracture/Luxation

Sacroiliac Fracture/Luxation


Portosystemic Shunts

Portosystemic shunting is a macroscopic diversion of portal blood from the liver into the systemic circulation, which most commonly occurs because of a congenital malformation of the portal circulation.

Blood flow to the liver may be decreased by up to 95% of normal in shunt patients, resulting in a bypass of the body’s normal homeostatic liver detoxification mechanisms. Additionally, this lack of normal blood flow results in a deficiency of oxygenated blood, insulin, and growth factors that the liver requires for normal growth and function.  The anomalous connections may occur between the portal vein and the caudal vena cava, azygous vein, renal vein, phrenic vein, internal thoracic vein, and the umbilical vein remnant.  As mentioned previously, in most cases, the shunt is congenital in nature; however, there are cases of acquired shunting secondary to an increase in portal hypertension.

The liver carries out a number of important functions, including but not limited to the synthesis of glucose, glycogen, cholesterol, lipoproteins, albumin, fibrinogen, bile acids, and detoxification of the blood to remove hazardous circulating chemicals, bacteria, and bilirubin. In addition, the liver functions as a reservoir to store important nutrients, minerals, vitamins, and hormones. All of these functions are significantly impaired in patients with portosystemic shunts. The degree of impairment is in direct correlation with the percentage of blood bypassing the liver.

Portosystemic shunts may be either intra or extra hepatic in nature. Congenital extrahepatic portosystemic shunts are most common, accounting for 61% to 94% of congenital shunts and are most prevalent in the smaller terrier breeds. They are frequently observed in the Maltese, Yorkshire Terrier, Shih Tzu, Dachshund, and Poodle. Congenital extrahepatic shunts are also frequently observed in cats. The Persian and Himalayan breeds are over represented; however, mixed breed cats may also be affected.  Acquired Intrahepatic shunts represent between 6% and 40% of congenital shunts and are more common in large and giant breeds of dogs such as Irish Wolfhounds and Golden Retrievers. Hepatic microvascular dysplasia is an unusual form of intrahepatic portosystemic shunting in which no gross vascular abnormality can be identified. This rare condition is associated with somewhat milder clinical signs and appears to be the consequence of a developmental abnormality; it has a higher prevalence in Cairn Terriers, suggesting a hereditary basis. Since that time, this anomaly has been seen in many other smaller dog breeds. Clinical signs and diagnostic evaluations are similar to those discussed below, but no surgically identifiable or radiographically identifiable shunt is seen. The shunting is at the level of the hepatic portal vein capillaries, and thus, not correctable surgically.

Portosystemic shunts are most commonly observed and diagnosed while the animal is young, often less than six months of age. The affected pets are smaller in stature, have poor quality hair coats, appear weak, and often exhibit neurologic abnormalities. Particularly bizarre behavioral signs or loss of intellectual function, unpredictable bouts of maniacal or aggressive behavior, staggering, pacing, circling, head pressing, blindness, deafness, tremors, seizures, and coma may be seen. Other signs include pica and polyphagia. In many cases, the clinical signs have an episodic nature; they are present for a few hours to a day or two and the animal returns to normal. The clinical signs are often meal related neuro-encephalopathic signs or somnolence, nausea or vomiting, diarrhea or constipation, polyuria and polydipsia, intermittent fever, ptyalism, and signs attributable to ammonium biurate urolithiasis (chronic urinary tract infections, prolonged or difficult urination). Any dogs or cats in which a uric acid calculus is identified should be evaluated as a possible PSS case (except for Dalmations and Bulldogs). Dogs with portosystemic shunts also have increased susceptibility to infections because of the decreased function of their hepatic mononuclear phagocytes which serve to clear toxic cells from the body. Minor bite wounds, tick bites, subcutaneous infections, lacerations, and even vaccinations may lead to illness requiring hospitalization. The severity of clinical signs in symptomatic patients is highly variable and is largely affected by the quality of food being consumed and the percentage of shunting present.

The diagnosis of PSS is often suspect on presentation of the afore mentioned clinical signs, history, and physical examination.  The diagnosis is confirmed by performing laboratory testing, which includes complete hematology, serum chemistry, urinanalysis, abdominal radiography, and pre and post prandial bile acid values. Hematologic evaluation may indicate microcytosis with or without a mild non regenerative anemia and a leukocytosis secondary to infection. Serum chemistry evaluation may indicate decreases in glucose, albumin, cholesterol, blood urea nitrogen, and total protein values because of decreased production and capacity for storage by the smaller than normal liver. An increase in certain liver enzyme values including the serum ALT, AST, and ALP, can be observed because of injury to the hepatic cells.  Increased serum bile acid concentrations taken either after an overnight fast or 2 hours after a meal are usually strongly suggestive of a shunt abnormality.

A definitive diagnosis of intrahepatic, extrahepatic, or microvascular PSS is made with varying combinations of contrast radiography, ultrasonography, scintigraphy, CT scan, or MRI angiography. This generally requires specialized imaging techniques, and it is appropriate that these pets be referred to appropriate specialists. Survey radiographs normally taken in general practice veterinary facilities is an important first step because it may indicate the presence of a small liver and urinary bladder stone formation consistent with a presumed shunt abnormality.

Contrast radiography is a procedure whereby a marker dye is injected into the jejunal vein or splenic parenchyma, which provides excellent imaging of portal blood flow.  The procedure requires general anesthesia and laparotomy to be performed and, as such, often performed in combination with surgical correction (so that the dog has to be anesthetized only once) and is often referred to as operative mesenteric portography. This procedure was the diagnostic technique of choice prior to the emergence of the non-invasive imaging techniques currently utilized in specialty practices such as the Animal Medical Center of Southern California.

Ultrasonography is a useful, noninvasive tool for acquiring information about the liver and circulatory system as well as the detection of portosystemic shunts. The exact location of intrahepatic shunts may be more amenable to diagnosis via ultrasound examination. Abnormalities observed upon ultrasound evaluation of pets with intrahepatic shunts include microhepatica, decreased numbers of hepatic and portal veins, detections of the anomalous vessel, and the presence of renal and bladder uroliths. Unfortunately, extrahepatic shunts are more difficult to diagnose using ultrasound because of the obscurity of the lesion from the surrounding visceral organs.

Nuclear scintigraphy is an advanced non-invasive technique which is currently the state of the art procedure used to evaluate portal venous shunting.  In this technique, after the animal receives a warm water enema, the colon is infused with technetium 99m pertechnetate.  The animal is scanned with a gamma camera and the images are registered.  In normal animals, the radiochemical is transported through the portal system to the liver.  In animals with PSS, a greater percentage of the radiochemical is carried to the heart.  The deviation in the time curve provides the diagnosis of the presence of a shunt; however, it does not definitively prove its anatomical location.  Normal dogs have a shunt fraction of less than or equal to 15 % whereas dogs with PSS have a shunt fraction of 60% or greater.  An inaccurately low result can be caused by poor absorption of the radiochemical by the colon, excessive fecal material in the colon, or poor administration technique.  A false positive result is occasionally observed with rectal administration of the radiochemical as uptake by the caudal rectal artery may be misinterpreted as an increased absorption indicative of an extrahepatic shunt.

MRI angiography and CT scan both provide excellent three dimensional images of the shunt.  Both modalities require a general anesthesia and can be cost prohibitive.  There are many other techniques available; transjugular retrograde portography, cranial mesenteric angiography, exploratory laparotomy, etc…The choice is often dependent on the patient’s stability, the urgency for surgical correction, availability, and physician preference.

Once a diagnosis is made, there are two standard management options: surgical ligation of the shunt and/or medical management of the effects of shunting. Surgery is the treatment of choice where feasible; however, the decision to pursue medical management should be made on a case-by-case basis depending on the type and location of the shunt, the age of the animal, and the severity of clinical signs. There may also be significant financial considerations on the part of the owner. Hepatic functional failure tends to progress in most animals that are diagnosed prior to one year of age. Even though medical therapy may keep them relatively asymptomatic, they eventually become refractory to medical management and succumb to their disease. Thus, surgical attenuation or ligation of the shunting vessel is the best therapeutic option in order to provide reversal of signs, and long duration quality survival. The objective of surgery is to redirect shunting blood back into the liver providing hepatic parenchyma with hepatotropic factors necessary for normal growth and metabolism.

Every patient diagnosed with a PSS should be appropriately medically managed prior to surgical intervention in order to provide more strength and stability to the patient in anticipation of undergoing an invasive surgical procedure.  Initially, the correction of fluid and electrolyte abnormalities, glucose imbalance, and hepatic encephalopathy are of utmost importance. Other pre-operative goals include minimizing lower urinary tract disease and reducing the metabolic load on the liver. The chief components of medical management strategies are dietary modifications and the administration of oral antibiotics.

Dietary protein is restricted because it is a significant source of nitrogenous wastes and toxins that are in part responsible for symptoms of hepatic encephalopathy. Other additional toxins are derived from the bacterial flora found within the large intestine which is responsible for the production of ammonia and ammonia by products. The production of these toxins is reduced by limiting the total amount of protein ingested and ensuring that the dietary protein ingested is high quality and biologically available with little waste protein being generated during digestion. The utilization of these diets results in the reduction of the amount of waste protein that reaches the large intestine, thereby decreasing the substrate load the colonic bacteria have available to produce circulating toxins. Further reductions may be attained by feeding smaller meals more frequently to maximize the digestive capacity of the small intestine. These special high quality, lower total protein, high caloric diets are ideal because they provide a balanced protein-calorie intake, which is important for the control of hepatic encephalopathy. Including dietary fiber in the daily ration assists in acidifying the colonic environment and limiting toxin production and also acts as a mild laxative to increase the elimination of toxic factors in feces. Lactulose, a soluble fiber, is often prescribed as a supplement for this purpose. Antibiotics are used in most cases to reduce the bacterial population within the large intestine that are responsible for the production of circulating neurotoxins.

Surgical ligation of the shunt vessel is a sophisticated technique which requires an experienced surgeon and support staff in order to best ensure a successful surgical outcome. At the Animal Medical Center, our Board Certified Surgeon has successfully diagnosed and treated PSS patients for over 27 years. A thorough exploratory laparotomy is performed.  All the viscera in the abdomen are gently explored. The venous drainage system is explored and the shunt located.  Single extra hepatic shunts are usually identified as tortuous, abnormal vessels. The most common locations for an extrahepatic shunt include an abnormal vessel visualized rostral to the renal veins at the level of the caudal vena cava, along the greater or lesser curvature of the stomach, along the venous drainage of the spleen, and an abnormal vessel coursing dorsally to the azygous vein and disappearing beneath the diaphragm.  The shunt is ligated as close to it’s insertion site as possible so that the blood flow from potential tributaries of the shunt is redirected.  More specifically, portacaval shunts are occluded at their termination at the caudal vena cava and portoazygous shunts can be occluded at the abdominal side of the diaphragm.

A potentially fatal complication from shunt ablation is portal hypertension, which occurs when intrahepatic vessels are unable to cope with the additional volume of blood that is diverted to the liver after closure of the shunt vessel. Failure to recognize and alleviate hypertension and resulting pain can lead to the development of bloody diarrhea and endotoxic shock leading to death in 2 to 24 hours after surgery. Approximately 40-68% of dogs and cats that undergo shunt attenuation can only tolerate partial ligation. Before permanent ligation, the shunt is temporarily occluded using gentle digital pressure for 3-5 minutes and the portal and systemic blood pressures are carefully monitored for hypertension and the intestines and pancreas are inspected for signs of cyanosis indicative of the inability of the body to cope with the redistribution of blood flow through the liver. These complications were much more prevalent when shunt attenuation was accomplished by ligature placement around the shunting vessel. In order to decrease the incidence of complications observed with the older technique of immediate, complete occlusion of the shunting vessel by ligature placement, an ameroid ring constrictor was developed.  An ameroid ring is made of casein on its inner side and stainless steel on the outside.  The casein interior is composed of a hygroscopic substance that slowly swells as it slowly absorbs fluid from the abdominal cavity.  The ameroid ring is placed around the shunt vessel and locked in a closed position. The resultant inward swelling causes the vessel to gradually occlude over a 4-5 week period.

Portosystemic Shunts

Portosystemic Shunts

Dogs generally have dramatic clinical and biochemical improvement following shunt correction. They are usually clinically improved within 24 to 48 hours. Follow-up function studies significantly improve, but rarely return to normal postoperatively. Occasional animals will have persistently abnormal, but improved, ammonia tolerance tests or slightly elevated bile acid values but remain clinically asymptomatic and require no special therapy. A number of post-operative portal angiograms have been reported and all show improved portal circulation of the liver, but the perfusion pattern is aberrant. The overall prognosis for dogs with single extrahepatic shunts appears to be excellent if they survive the surgery and immediate post-operative period. For intrahepatic shunts, the outlook is more guarded, but numerous successful surgeries have been performed by surgeons knowledgeable in the intricacies of this procedure. If urinary calculi cannot be removed during the surgery to correct the shunt, they may be either removed at a later date or managed medically. Spontaneous dissolution of renal calculi (presumed to be ammonium urate) following shunt correction alone may be observed. Calculi present in the bladder may also be successfully dissolved using a combination of a reduced purine diet (Prescription diet-u/d) combined with allopurinol, 10 mg/kg every 8 hours, and sufficient sodium bicarbonate to alkalinize the urine. Calculi may disappear in 4 to 12 weeks on this therapy. Recurrences of calculi should not be a problem once the shunt is corrected, as metabolic abnormalities causing increased urinary ammonia and uric acid excretion should cease.

Immediate postoperative therapy should include fluid therapy, temperature and blood pressure monitoring, packed cell volume, total protein and glucose testing. All dogs undergoing surgical ligation should continue to receive medical therapy as discussed above for 2 to 4 weeks postoperatively.  Liver regeneration occurs rapidly and returns to normal to near normal hepatic function can be observed by 8 weeks post-operatively.

In conclusion, the portosystemic shunt is a common disease process encountered in dogs and cats. While the origin of the disease is obscure the disease is considered to be congenital; however, breed predisposition does exist, indicating a hereditary origin. Symptoms vary but all result in central nervous system disorders called hepatic encephalopathy. Puppies and kittens that fail to maintain the same growth rate as their siblings are suspect. Specific urinary crystals develop due to increased concentrations of ammonium. The degree or percentage of vessel shunting may explain why some animals are without symptoms until later in life. Small liver size coupled with bizarre neurological signs in young dogs and cats is highly suggestive of the disease. Medical or surgical treatment is available; however, without corrective surgery, an animal will eventually succumb to the progressive disease process. Prompt and effective surgical intervention utilizing an ameroid constrictor and medical management results in effective and long lasting alleviation of the clinical signs induced by this congenital anomaly.


Flexural Tendon Contracture (Flexural Deformity) In Kittens

This condition is commonly called tendon contracture even though the tendons don’t actually contract. Rather, it is generally a soft tissue problem that involves the flexure tendons, the muscles, ligaments and joint capsules of the distal extremities.

If caught early, preferably at birth or within a day or two, there is a reason to excellent chance that the condition can be rectified with a combination of massage, physiotherapy (stretching/flexing the limb), warm compresses (to ease muscles which have locked into position) and by splinting (or very rarely pinning) the leg into the proper position. One thing that is certain is that the longer the elapsed time between birth and treatment of a twisted contracted limb, the less likely it is that the kitten will fully recover due to atrophy of nerves and muscles. This is particularly important in rescue work where a litter may not be found until the kittens are several weeks old or older. By that stage, the twisted limbs may be beyond correction, or at the very least, require more extensive treatment and time to recover.

Clinically, the kittens present as healthy animals with an inability to walk normally because their feet are twisted and contracted. In some longer standing cases, the kittens are walking on the front of their ankles or wrists as their toes are pointed straight back. In this case, Oliver (“Twist”) presented as an older kitten with a long-standing history of deformity. After a few months of physical therapy and corrective splinting (with a very patient, understanding and attentive mom) Oliver’s bilateral rear limb deformities were corrected and he has returned to normal function, as can be seen in the before and after photos as well as the video where he can be seen running and jumping and playing with his bro. With appropriate and consistent care and time, many of these kittens will do very well with physical therapy and splinting and can live out a normal happy and healthy life as fully active cats.


Heartworm Disease

Canine heartworm infection is widely distributed throughout the United States. Heartworm infection has been found in dogs native to all 50 states. All dogs, regardless of their age, sex, or habitat, are susceptible to heartworm infection. Although there are differences in frequency of infection for various groups of dogs, all dogs in all regions should be considered at risk, placed on prevention programs and frequently examined by a veterinarian.

Heartworm disease is caused by Dirofilaria immitis, a parasitic worm that lives as an adult in the right side of the dog’s heart and large blood vessels leading to the lungs. Heartworms do most of the damage in the adult stage. Dogs are considered the definitive host for heartworms, however, heartworms may infect more than 30 species of animals (e.g., coyotes, foxes, wolves and other wild canids, domestic cats and wild felids, ferrets, sea lions, etc.) and humans as well. When a mosquito carrying infective heartworm larvae bites a dog and transmits the infection, the larvae grow, develop and migrate in the body over a period of several months to become sexually mature male and female worms. These reside in the heart, lungs and associated blood vessels. As mature adults, the worms mate and the females release their offspring (microfilariae) into the bloodstream. Offspring can be detected in the blood (pre-patent period) about six to seven months after the infective larvae from the mosquito enter the dog. The male heartworms (four to six inches in length) and the females (10-12 inches) become fully grown about one year after infection, and their lifespan in dogs appears to average up to five to seven years.

The onset and severity of disease in the dog is mainly a reflection of the number of adult heartworms present, the age of the infection and the level of activity of the dog. Dogs with higher numbers of worms are generally found to have more severe heart and lung disease changes. Until the number of mature heartworms exceeds 50 in a 25-kg dog, nearly all of the heartworms reside in the lower caudal pulmonary arteries. Higher numbers of heartworms result in their presence in the right chambers of the heart. In such infections, the most common early pathological changes caused by heartworms are due to inflammatory processes that occur in and around the arteries of the lower portion of the lungs in response to the presence of heartworms. Later, the heart may enlarge and become weakened due to an increased workload and congestive heart failure may occur. A very active dog (e.g., working dog) is more likely to develop severe disease with a relatively small number of heartworms than an inactive one (e.g., a lap dog or couch potato). Occasionally, a dog with a large number of heartworms may not only have worms in the heart, but also in the caudal vena cava between the liver and the heart. If the heartworms are not removed surgically, this syndrome causes sudden collapse and death within two to three days.

Canine heartworm infection is widely distributed throughout the United States. Heartworm infection has been found in dogs native to all 50 states. All dogs, regardless of their age, sex, or habitat, are susceptible to heartworm infection. The highest infection rates (up to 45%) in dogs (not maintained on heartworm preventive) are observed within 150 miles of the Atlantic and Gulf coasts from the Gulf of Mexico to New Jersey and along the Mississippi River and its major tributaries. Other areas of the United States may have lower incidence rates (5% or less) of canine heartworm disease, while some regions have environmental, mosquito population and dog population factors that allow a higher local incidence of heartworm infection. Regions, where heartworm disease is common, have diagnosed infections in dogs as young as one year of age, with most areas diagnosing infections primarily between the ages of three and eight years. Although there are differences in frequency of infection for various groups of dogs, all dogs in all regions should be considered at risk, placed on prevention programs and frequently examined by a veterinarian.
Heartworm disease may cause a combination of medical problems in the same dog including dysfunction of the lungs, heart, liver and kidneys. Signs of heartworm disease may occur within 6 months of infection or may not appear at all depending upon the number of adult worms that are present. In most cases, signs will begin within 1-2 years after infection. Typical signs include coughing, labored breathing, weakness, and tiring with exercise. Since the signs vary, the disease may be well advanced before the dog begins to show any problems, or signs may be mistaken for another problem. In advanced stages, the heart and lungs can be severely damaged. Eventually, heart failure can occur and the dog can die from damage cause by heartworms unless appropriate treatment is instituted. The disease may have an acute onset but usually begins with barely detectable signs resulting from a chronic infection and a combination of physiologic changes. Dogs with a low number of adult worms in the body that are not exercised strenuously may never have apparent signs of heartworm disease. However, in most dogs, the heart and lungs are the major organs affected by heartworms with varying degrees of clinical signs.

Clinical Signs Associated with Canine Heartworm Disease:
Early Infection- No abnormal clinical signs observed
Mild Disease -Cough
Moderate Disease -Cough, exercise intolerance, abnormal lung sounds
Severe Disease- Cough, exercise intolerance, dyspnea (difficulty breathing), abnormal lung sounds, hepatomegaly (enlargement of the liver), syncope   (temporary loss of consciousness due to poor blood flow to the brain), ascites (fluid accumulation in the abdominal cavity), abnormal heart sounds, death

DISEASE TRANSMISSION

Heartworms are transmitted from dog to dog by mosquitoes. There are three stages in the development of heartworms in the dog.

1. The adult female, living in the right side of the heart and/or major vessels to the lungs, produces immature worms called “microfilariae” that circulate in the blood stream. The microscopic microfilariae can live for up to 3 years.

2. When a mosquito bites an infected dog, it takes in blood containing microfilariae. The microfilariae mature in the mosquito over a period of two weeks to become infective larvae.

3. The mosquito, carrying infective larvae, deposits them in other dogs during blood meals. Larvae develop over 3-6 months and migrate to the right heart. Within 6 months, the larvae develop into adult heartworms that are responsible for the disease process in the heart and lungs. The adult heartworms can live up to 7 years. The adults produce microfilariae, hence completing the life cycle.

To identify heartworm infection, a blood sample is taken from the dog. This test detects specific antigens primarily found in adult female heartworms and are used with much success to detect canine heartworm infection. Currently, tests are available as in-clinic tests as well as at many veterinary reference laboratories. Most commercial tests will accurately detect infections with one or more mature female heartworms that are at least seven or eight months old, but the tests generally do not detect infections of less than five months duration. The identification of the offspring (microfilaria) of heartworms from a blood sample indicates infection with adult heartworms. Identifying offspring can also be accomplished through either one of two concentration tests: the modified Knott’s test (a technique requiring spinning the blood sample in a mechanical device called a centrifuge) or a filter test. Practitioners will often do a quick examination of a blood smear to look for the presence of the offspring (microfilaria), but this procedure is not sensitive enough to rule out heartworms and only verifies the presence of an infection. Another parasitic infection of dogs that is capable of producing circulating microfilariae, detectable upon examination of the blood, is called Acanthocheilonema (Dipetalonema) reconditum. A reconditum is a non-disease-causing parasite that matures in the tissues beneath the skin of dogs. Its offspring can be differentiated from those produced by heartworms through microscopic examination evaluating size, shape and their movement.

Radiographic abnormalities develop early in the course of the disease. Radiographs of the heart and lungs are the best tool available to evaluate the severity of the disease. Typical changes observed are enlargement of the following structures: right-side of the heart, main pulmonary artery, and pulmonary arteries in the lobes of the lung. Blunting and thickening of pulmonary arteries, along with tortuosity is often noted. Evidence of inflammation in the lung tissue that surrounds the pulmonary arteries is often found.

The elimination of heartworms from your dog requires medication to kill the adult heartworms and microfilariae. Most dogs infected with heartworm can be successfully treated. The goal of treatment is to kill all adult worms with an adulticide and all microfilariae with a microfilaricide. It is important to try to accomplish this goal with a minimum of harmful effects from drugs and a tolerable degree of complications created by the dying heartworms. Heartworm infected dogs showing no signs or mild signs have a high success rate with treatment. Patients with evidence of more severe heartworm disease can be successfully treated, but the possibility of complications and mortality is greater. The presence of severe heartworm disease within a patient in addition to the presence of other life-threatening diseases may prevent treatment for heartworm infection.

There is currently one drug approved by the FDA for use in dogs for the elimination of adult heartworms. This drug is an organic arsenical compound. Dogs receiving this drug therapy will typically have had a thorough pretreatment evaluation of its condition and will then be hospitalized during the administration of the drug. Melarsomine dihydrochloride (Immiticide®, Merial) has demonstrated a higher level of effectiveness and safety than any other adult heartworm treatment previously available. It is administered by deep intramuscular injection into the lumbar muscles. One injection is administered intramuscularly and then the dog returns for an additional injection 30 days later. Following treatment with an arsenical compound, the dog must be rested for 4-6 weeks, during which time the dead adult heartworms will slowly be reabsorbed. The primary post-adulticide complication is the development of severe pulmonary thromboembolism. Pulmonary thromboembolism results from the obstruction of blood flow through pulmonary arteries due to the presence of dead heartworms and lesions in the arteries and capillaries of the lungs. If heartworm adulticide treatment is effective, some degree of pulmonary thromboembolism will occur. When dead worms are numerous and arterial injury is severe, widespread obstruction of arteries can occur. Clinical signs most commonly observed include fever, cough, hemoptysis (blood in the sputum) and potentially sudden death. It is extremely important to not allow exercise in any dog being treated for heartworms. Often dogs with severe infections will also require the administration of anti-inflammatory doses of corticosteroids.

The microfilariae must also be eliminated so the dog will not be a source of infection for other dogs. Elimination of the microfilariae is monitored by using blood tests that can easily identify microfilariae in the blood. The most effective drugs for this purpose are the macrocyclic lactone (ML) anthelmintics, i.e.,milbemycin oxime, selamectin, moxidectin and ivermectin. These drugs are the active ingredients in commonly used heartworm preventives. Although their usage as microfilaricides has not been approved by the FDA, they are widely used by veterinarians as there are no approved microfilaricidal drugs currently available. It is recommended that microfilariae positive dogs being treated with these macrocyclic lactones be hospitalized for at least eight hours following treatment for observation of possible adverse reactions, including those resulting from rapid death of the microfilariae. Circulating microfilariae usually can be eliminated within a few weeks by the administration of the ML-type drugs mentioned above. Today however, the most widely used microfilaricidal treatment is to simply administer ML preventives as usual, and the microfilariae will be cleared slowly over a period of about six to nine months. In some cases, not all microfilariae can be eliminated and the veterinarian may recommend retreatment of your dog for adult heartworms and microfilariae.

While treatment of canine heartworm disease is usually successful, prevention of the disease is much safer and more economical. There are a variety of options for preventing heartworm infection, including daily and monthly tablets and chewables and/or monthly topicals. These products are extremely effective and when administered properly on a timely schedule, heartworm infection can be prevented. The American Heartworm Society is now recommending year-round prevention, even in seasonal areas. One reason for this is compliance – to make sure the medicine has been given properly by the pet owner. In addition, most monthly heartworm preventives have activity against intestinal parasites. Many of these same intestinal parasites that infect dogs can also infect people, with estimated infections occurring in three to six million people every year. So this added benefit of monthly deworming makes great sense.

The products listed below are intended to be given on a monthly basis and are highly effective in preventing heartworm disease if given as directed.

Ivermectin
Ivermectin (Heartgard® & Heartgard® Plus by Merial, Iverhart® Plus & Iverhart MAX™ by Virbac and Tri-Heart® Plus by Schering-Plough) was the first in this family of drugs to be approved for preventing heartworm infection. An infection with larvae as long as two months prior to the initiation of ivermectin treatment will be blocked from development.

Milbemycin
Milbemycin oxime (Interceptor® & Sentinel® by Novartis) has benefits, which are similar to ivermectin.

Selamectin
Selamectin (Revolution® by Pfizer) is applied topically to prevent heartworm disease.

Moxidectin
Moxidectin (Advantage Multi™ by Bayer) is available in a topical formulation, in combination with a flea control product, imidacloprid. Moxidectin is also available as a six-month injectable product for dogs (ProHeart®6 (moxidectin) Sustained Release Injectable for Dogs, by Fort Dodge Animal Health).


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