Many smaller breed dogs present with varying symptoms of neurologic compromise after having herniated a disc. They may appear to walk somewhat wobbly or off-balance or be totally paralyzed and dragging their rear end on the ground. Varying degrees of pain and discomfort are present or they may be so severely paralyzed that they appear non-painful because the spinal cord is “numbed out” from being squished. These three dogs illustrate the differing degrees of a presentation I commonly see at our hospital. The first dog was painful and reluctant to move and would stumble on its front limbs because of a herniating disc in the neck area. It responded well to a combination of special intravenous steroids as well as some other medications and can be seen walking normally within one day of aggressive medical management. While some veterinarians debate the usefulness of this regime to treat herniating disc injuries, the reality is that used intelligently it works very well with no adverse side effects as seen in this case. In spite of the debate, if you or I were to present similarly, we would unequivocably receive the same medical treatment administered to this dog. The second and third dogs presented acutely and totally paralyzed. A myelogram revealed extensive spinal cord compression (as seen on the x-ray) and so a combination of medical and surgical intervention was warranted. As seen in the video, the brown dog was back up and walking normally within 10 days of surgery. “Booger”, the black dog took a little longer but as can be seen in the video, is back up and walking well by 8 weeks after surgery; he should continue to make progress over the next few months and even the first full year after surgery. Prompt and aggressive medical and surgical intervention is warranted to achieve the best results in cases of paralysis, and success rates of approximately 90% (even in cases like Booger) can be expected.
Fractures involving the distal femoral physis are relatively common in immature dogs and cats with the greatest incidence occurring between the ages of 5 and 8 months.
Physel fractures have been classified by Salter and Harris into 5 categories: Type 1 traverse the physeal plate through the zone of hypertrophying cartilage; Type 2 involves the physis and continues through the mtaphysis; Type 3 involves the physis and continues through the epiphysis to involve the articular surface; Type 4 involves the articular surface, crosses the physis and continues into the metaphysis; and Type 5 a compression injury to the zone of resting cartilage of the physis.
Distal femoral physeal fractures are commonly Types 1 and 2; most physeal fractures in the dog are Type 2 while those in the cat are Type 1. This is due in part to the fact that the distal femoral metaphysis has four projections that correspond to four similar deep depressions in the epiphysis in the dog while in the cat, the projections are flatter and do not interdigitate as deeply with the corresponding epiphyseal depressions. Physeal fractures usually occur through the zone of hypertrophying cartilage, because this zone is characterized by large, vacuolated cells with minimal intercellular matrix. Therefore, this zone is the weakest.
A variety of treatment methods have been described for repair of distal femoral physeal fractures including closed reduction and external fixation, normograde or retrograde placement of a single intramedullary pin with or without an anti-rotational Kirshner wire, multiple intramedullary pins, paired Rush pins, Steinman pins, or Kirshner wires employed in Rush pin technique, cross pins, bone plates, and lag screws. The ultimate goal of treatment should be accurate reduction and rigid stabilization of these fractures with as little iatrogenic damage to the germinal cells of the physis and their blood supply as possible.
While closed reduction and external fixation may be successful in selected cases, every attempt should be made to satisfactorily stabilize the fracture internally so that early return to function is achieved and restricted joint movement is avoided. When closed reduction and external fixation is used, a good result is the most that one can expect.
Surgical exposure for open reduction and internal fixation is achieved via a lateral parapatella approach with reflection of the patella medially. Interference with growth is a consideration in the selection of the method of repair; however, recent studies have suggested that premature closure of the physis occurs more commonly as a result of the initial trauma than the method of treatment employed. Distal femoral physeal closure normally occurs between six and eight months of age; as the majority of physeal fractures occur in dogs and cats greater than five months of age, over 90 percent of their skeletal growth has already been achieved by the time of injury. Therefore, in animals over five months of age, while some degree of femoral shortening may occur, the overwhelming majority of animals clinically accommodate shortening by a change in stifle or hock angulation. In dogs and cats under five months of age with substantial growth potential, the method of fixation chosen should provide adequate stabilization but should not mechanically bridge the physis. Early implant removal may minimize premature physeal closure. Any implant, which traverses the growth plate, will result in some degree of permanent damage to the growth plate. The least damage occurs when round, smooth, non-threaded implants are placed perpendicularly to the long axis of the growth plate.
Single intramedullary pin fixation, Rush pinning and modified Rush pin technique, and cross pinning are the most commonly employed techniques used to treat Salter Type 1 and 2 fractures. A single intramedullary pin should provide excellent alignment and stability if the opposing surfaces of the fracture interlock following anatomic reduction. However, in large dogs, single pin fixation may be inadequate to allow early use of the limb. In addition, femoral intramedullary pins existing the trochanteric fossa have been associated with sciatic nerve injury. Normograde pinning of distal femoral physeal fractures is less likely to induce sciatic nerve injury then retrograde pinning. Implant migration may also result in damage to the intra-articular surface of the stifle joint.
Although cross pin fixation works well, it is associated with more complications than other techniques including caudal malalignment and/or displacement of the distal fragment and quadriceps tie-down. In very immature animals, cross pin fixation may interfere with physeal growth because of the excessive pin angulation necessary for adequate stabilization.
Rush pins provide excellent fixation for distal femoral physeal fractures. Their disadvantage is the need for special instrumentation and the cost of the implants. Rush pins provide three point fixation, thereby increasing stabilization and making their application especially indicated in large dogs. If Rush pins are used in very immature animals, great care must be taken when driving the pins to prevent excessive compression of the germinal cell layer, which may result in growth arrest.
Steinman pins or Kirshner wires may be used in exactly the same way as Rush pins. Once the fracture is reduced, the pins are inserted laterally just cranial to the tendon of origin of the long digital extensor muscle, and medially on the distal medial bondyle symmetric to the later pin placement. The pins are alternately advanced in the medullary cavity. I prefer that the pins do not exit the trochanteric fossa so as to minimize the potential complication of sciatic nerve injury. Pre-bending the pins accentuates a three point fixation and results in rigid internal fixation and rotational stability. This technique can be used in very immature animals when fear of Rush pin compression of the germinal layer may be a factor. Such pins may be placed with relative minor trauma to the physis, and most animals continue to lengthen their femurs despite the pins through the growth plate. With proper alignment and internal fixation, an excellent result should be expected.
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.
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.
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
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 (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 oxime (Interceptor® & Sentinel® by Novartis) has benefits, which are similar to ivermectin.
Selamectin (Revolution® by Pfizer) is applied topically to prevent heartworm disease.
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).
Animals and people have similar neural pathways for the development, conduction, and modulation of pain.
This biological similarity makes the expression of both acute and chronic pain comparable. Like humans, dogs and cats develop myopathies and neuropathies that lead to muscle and neurological pain and discomfort. Other painful conditions, which may be similarly expressed include ear infections, dental conditions, sinus pain, skin lesions, and the pain of acute and chronic, repetitive trauma. Untreated pain decreases the quality of life in all patients and prolongs recovery from surgery, injury, or illness. Today, with a better understanding of how pain develops and is perpetuated, pain management has become an essential part of high quality and compassionate patient care in the veterinary field. Providing adequate pain management helps pets recover faster, improving the human-animal bond and the pet’s overall well-being.
Different kinds of pain
When a negative, painful insult is encountered, the body’s endocrine system produces substances such as cortisol, catecholamine, and other inflammatory mediators that alter normal physiologic parameters. As a result of the release of these substances into the general circulation, substantial changes occur at the tissue level including decreased oxygen delivery to tissues, increased cellular metabolic demands, impaired immune function, increased risk of infections, delayed wound healing, prolonged convalescence, and cardiovascular stress.
In the past, the pain was most commonly classified either as acute or chronic. Recently, a newer approach has been to consider pain as adaptive or maladaptive.
Adaptive pain is a normal response to tissue damage. It includes all types of pain involving the release of inflammatory mediators that will cause heat, redness, swelling, pain, and loss of function of the injured area. Inflammation is a major component of pain and can be present both in postoperative/trauma patients and in chronic pain states such as osteoarthritis.
If the adaptive pain is not properly managed, it will eventually result in physical changes in the spinal cord and brain, which will lead to maladaptive pain. In maladaptive pain, the central nervous system becomes more sensitive and the thalamus, which serves as a relay station for nerve impulses from the periphery to the cortex, becomes a spontaneous pain generator. The adjustment from thinking of pain as either acute or chronic to adaptive or maladaptive makes it easier to understand why pain can be so difficult to control in certain patients.
How do I know my pet is in pain?
There are numerous signs that an animal can exhibit while experiencing pain:
- They can fail to exhibit normal behavior, as evidenced by being more lethargic, with perhaps a decreased appetite or decreased grooming tendencies, especially in cats.
- They may express an abnormal behavior, such as an increase in vocalization, aggression, altered posture and/or facial expression, hiding (cats especially), restlessness, and inappropriate elimination.
- An increase in body tension and reaction to touch, or hyperpathia, is also consistent with an animal experiencing pain in a specific injured body area or region. A distinct change in physiologic parameters such as an elevated heart rate, respiratory rate, blood pressure, and/or pupilary dilation is also indicative of pain.
What can I do to help my pet?
Understanding the circumstances that can lead to the development of pain may help anticipate and properly manage the emergence of pain as a clinical condition. Attention must be paid to the development or presence of unusual bumps, scrapes, bruises, or sensitivities. Any change in an animal’s desire or ability to run, jump, play, or otherwise ambulate normally must be evaluated.
Simple basic lifestyle changes such as controlled exercise regimes and weight management can help reduce joint pain and stress.
Providing favorable environmental conditions to help prevent or alleviate pain and discomfort such as ensuring easy access to litter boxes, soft bedding, non slippery surfaces, limited access to stairs, and “warming up” your pet appropriately prior to exercise will help reduce the need for pharmacologic intervention in many cases.
How do we manage pain?
At our hospital, we utilize both pharmacological and a non-pharmacological treatments for pain management. Your doctor will recommend the best way to individually manage your pet’s painful condition.
Prior to an elective surgical procedure, appropriate opioids will be administered. Based upon the type of procedure performed, the addition of local anesthetics, epidurals, and steroidal or non-steroidal anti-inflammatory will provide pre and intra-operative comfort and a better postoperative recovery period. Throughout the anesthetic recovery period, hospitalization and the immediate post-operative recovery period at home, additional non- steroidal anti-inflammatory drugs (NSAIDs), opioids or opioid patches will be provided to your pet.
For maladaptive types of pain not associated with an elective procedure, numerous different options may be chosen by your veterinarian.
NSAID’s and Corticosteroids are the drugs of choice for many of the inflammatory conditions resulting in pain, acting by inhibiting substances released at multiple levels along the biochemical pain pathway.
Topical anesthetics are useful to manage well-delineated painful areas such as small burns or urine scalding.
When aberrant pain is refractory to traditional analgesics, specific drugs like Gabapentin, which acts on the central nervous system, may be required to restore normal central nervous system transmission and control pain and discomfort.
However, many patients with long term chronic, intermittent pain often benefit from the combination of pharmacological as well as non pharmacological therapy.
The newly developed high power Class IV lasers generate visible and invisible light beams that are absorbed as light energy by cells (photobiostimulation). This results in the activation of biological reactions, which have been shown to result in an increase in circulation to the damaged area thus creating an optimal healing environment.
Acupuncture has long been recognized by renowned medical associations for its analgesic properties. One of the ways acupuncture works is by slowly releasing an animal’s own opioid-like substances (endorphins) from the brain, spinal cord, and peripheral nerves to help alleviate pain at its source.
Rehabilitation therapy is crucial to help the patient return to normal function or to help improve overall body condition. Rehabilitative techniques include heat and cold therapy, passive range of motion exercises, stretching, balancing exercises, massage, joint mobility, and controlled walking exercises.
Nutrition or “food therapy” is a science that selects food or herbs customized to each individual based upon their inborn tendencies, age, species, personality, and disease process. A specifically formulated diet can help prevent or help in the management of many painful conditions including but not limited to certain skin diseases, osteoarthritis, cancer, and gastrointestinal problems.
Nutraceuticals (glucosamine, chondroitin, msm, creatine) may decrease joint inflammation and assist in cartilage repair. Additional products, which have demonstrated to be of help by decreasing inflammation and modifying the progression of osteoarthritis and therefore pain, include the omega-3 and omega-6 fatty acids and chondroprotective agents such as polysulfated glycosaminoglycans (Adequan).
Total derangement or dislocation of the stifle joint is a serious injury usually caused by severe direct or indirect trauma to the knee.
The type of dislocation observed depends upon the direction and location of the inciting trauma. Luxation of the stifle joint is not a very common injury because of the many soft tissue structures that interact to provide stability for the joint. These structures include the cranial and caudal cruciate ligaments along with the medial and lateral collateral ligaments. In addition, some support may also be derived from the quadriceps muscle and patella tendon cranially and the oblique poplitcal muscle, hamstring muscles, and the gastroenemius muscle, caudally. In many cases, fractures may accompany dislocations. Other structures are also likely to be injured including the menisci, joint capsule, popliteal artery, and peroneal nerve. Vascular integrity and neurologic function must be carefully evaluated as these complications usually are the limiting factor in the outcome of the injury.
Successful treatment of a stifle joint luxation must allow the animal to regain functional use of the limb. Good results achieved by a variety of methods support the notion that various techniques, which maintain reduction and stability, can be successful clinically. Initial maintenance of reduction and stability encourages well-organized periarticular collagen formation to provide long term joint stability. Closed reduction maintained with external coaptation, open reduction with extraarticular or intraarticular ligament reconstruction with transarticular external skeletal fixation and open reduction with transarticular pinning have been successful methods of treatment for stifle joint luxations. Although successful return to function has been reported following use of these techniques, some authors recommend stifle joint arthrodesis as the primary surgical treatment because of the severe general disruption sustained by the periarticular soft tissues at the time of injury. Based upon my experience, the results of surgical reduction and stabilization are generally good to excellent, and primary arthrodesis should only be attempted after attempts at reconstruction fail.
Because of the relatively infrequent occurrence of stifle joint luxation, only a few articles have appeared over the last several years comparing the results of various techniques of surgical intervention. It is generally agreed that it is difficult to accurately achieve and maintain reduction by closed methods alone. To provide a stable environment for healing of the soft tissues leading to well organized collagen formation and long term joint stability, surgical intervention is recommended.
A standard lateral parapatella approach and lateral arthrotomy is used to gain access to the stifle joint and allow inspection of the intraarticular and periarticular soft tissue damage. Because ligaments can appear to be grossly intact while having lost any load carrying ability, all ligaments should be inspected while undergoing stress palpation. Numerous different combinations of ligament damage have been reported with rupture of both cruciate ligaments and one of the collateral ligaments occurring most frequently. Interestingly, despite severe ligamentous and soft tissue damage, there is usually minimal, if any, gross articular damage observed at surgery. Remnants of the damaged cruciate ligament or ligaments should be removed and partial meniscectomy performed in animals with meniscal tears or avulsions. It is at this point that the various options available to this surgeon to achieve and maintain reduction and stability come into play.
In one technique, although the collateral ligaments are assessed for damage, they are not repaired; and reduction is achieved and maintained by placement of a transarticular pin while the stifle joint is held in a functional angle of approximately 135-140 degrees. While the technique is generally effective in cats and small dogs, transarticular pinning is not an especially rigid fixation. Distal pin migration and bending of the pin where it crosses the joint occur frequently, and failure of the technique may be due to reliance upon the transarticular pin to provide most of the stability of the fixation. It is quick, inexpensive, and easy to perform compared to other techniques, however, and may be the technique of choice in debilitate or muli-trauma patient in which anesthesia time should be limited. The authors of the technique conclude, however, by mentioning that better success would be achieved when the pin is used to maintain reduction while additional fixation in the form of a transarticular external skeletal fixators is used to provide sufficient rigidity to allow adequate healing of periarticular soft tissues. Such additional fixation would absolutely be necessary when repairing stifle luxations with this technique in medium and large sized dogs.
In another technique, the stifle luxation is maintained in reduction with multiple extraarticular sutures while transarticular external skeletal fixation is used to provide rigid fixation. In this technique, damaged collateral ligaments are repaired and extraarticular suture stabilization is performed for the damaged cruciate ligaments. Extraarticular stabilization is considered technically easier and may avoid further soft tissue disruption and instability of the joint when compared to intraarticular ligament reconstruction techniques. Transarticular external skeletal fixation augments joint stability while the tissues progress through the stages of inflammation and repair. Consistently, good to excellent functional results have been achieved in cats and all sizes of dogs with this surgical protocol.
My own personal preference is to use extraarticular stabilizing sutures and transarticular external skeletal fixation for medium and large sized dogs. In small dogs and cats, extraarticular stabilization and external coaptation consisting of a modified Bobby Jones bandage have consistently resulted in good to excellent results. While the majority of animals experience a loss of stifle joint range of motion in extreme flexion, the loss of flexion does not seem to interfere with clinical limb function. The development of mild to moderate degenerative joint changes has been observed radiographically. However, there does not appear to be a correlation between radiographic changes and functional limb use. The periarticular bone formation observed may be induced by the inciting trauma and not by post-operative instability or abnormal joint mechanics.
In conclusion, stifle joint luxation is an uncommon injury resulting from severe trauma. With proper surgical treatment, good to excellent clinical results and a return to normal or near-normal function can be expected in the majority of patients.
Toxoplasmosis is an infection caused by the protozoan parasite Toxoplasma gondii that can threaten the health of an unborn child if a woman becomes infected with Toxoplasma for the first time while she is pregnant.
The infection is usually contracted by handling soil or cat litter that contains cat feces infected with the parasite. Cats generally pick up these organisms when they hunt and eat infected prey. Healthy cats rarely get sick themselves from the parasite, but when they are infected for the first time, they can shed it in their feces. It can also be contracted from eating undercooked meat from animals infected with the parasite or from uncooked foods that have come in contact with contaminated meat. Cats excrete the pathogen in their feces for a number of weeks after contracting the disease, generally by eating an infected rodent. Even then, cat feces are not generally contagious for the first 1-3 days after excretion, after which the cyst matures and becomes potentially pathogenic. Studies have shown that only about 2% of cats are shedding oocysts at any one time, and that oocyst shedding does not recur even after repeated exposure to the parasite.
With rare exception, women who have been infected at least 6 to 9 months before conception develop immunity to and do not pass it on to their baby. If you have been infected with Toxoplasma once, you usually will not become infected again.A positive antibody titer indicates previous exposure and immunity and largely ensures the unborn baby’s safety. A simple blood draw at the first pre-natal doctor visit can determine whether or not a woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to toxoplasmosis while pregnant, the baby is at particular risk. According to the Organization of Teratology Information Services (OTIS), when the mother gets infected between weeks 10-24 of pregnancy, the risk for severe problems in the newborn is about 5-6%. Effects on the baby include premature birth, low birth weight, fever, jaundice, abnormalities of the retina, mental retardation, abnormal head size, convulsions, and brain calcification. During the 3rd trimester, a fetus has an increased risk of becoming infected, but the risk of damage to the fetus is decreased since most of the important development has already occurred.
Now that you have an understanding of the risks involved if a pregnant woman is exposed to and subsequently contracts toxoplasmosis during the initial stages of her pregnancy, you can understand why I have a problem with the recommendations made by OB/GYNE doctors to their pregnant patients. Many of my clients schedule an office visit after learning of their pregnancy because they are scared to death that the family cat will cause the death or disfigurement of their unborn child and that they need to get rid of their cats while they were pregnant, or at the very least have their cat tested for toxoplasmosis. These recommendations drive me absolutely crazy! To recommend that a pregnant woman get rid of her cat(s) is taking the easy way out. It might take a bit of effort and time for a doctor to explain the real risks of toxoplasmosis and how to reduce them, but that is exactly what needs to be done to protect babies as well as prevent unnecessary suffering for mothers, families, and family pets.
These are the facts:
1. People become infected with toxoplasmosis when they inadvertently eat the parasite. The risk of contracting toxoplasmosis from ingesting cat feces is much lower than it is from handling and eating undercooked pork. So if doctors are going to counsel that pregnant women “get rid” of anything, it should actually be pork, not their pet cats.
2. If anybody is going to be tested for toxoplasmosis, it should be the pregnant woman, not the cat. A cat will come up positive if it has been exposed to the parasite at any point in its life, but it only poses a risk if it is shedding the parasite in its feces, which generally occurs for a very short period. Therefore, a positive feline test is meaningless in this situation. Testing a pregnant woman, on the other hand, can be helpful. If her test is positive already, perfect. She has been infected in the past and even if she is exposed again during her pregnancy her unborn child will not be affected. If she is negative, then she should take precautions.Pregnant women can protect themselves and their babies from toxoplasmosis by following these simple rules:
- Cook foods at safe temperatures and use a food thermometer to ensure that meat is cooked thoroughly.
- Peel or thoroughly wash fruits and vegetables before eating.
- Wash cutting boards, dishes, counters, utensils and hands with hot, soapy water after they have come in contact with raw foods.
- Wear gloves when gardening and during any contact with soil or sand because it might contain cat feces. Wash hands thoroughly after coming in contact with soil or sand.
- Avoid changing cat litter if possible. Better yet, get someone else in the household to change the litter box. If a pregnant woman does have to clean out the litter boxes, she should scoop them at least once daily. The parasite must spend 24 to 48 hours outside of the cat’s body before it is capable of causing an infection, so frequently cleaning the box will virtually eliminate the chances of disease transmission. If you must do it, wear gloves and wash your hands thoroughly afterward. Keep your cat inside and do not handle stray or adopted cats. Do not feed your cat raw or undercooked meats.
In my experience, I have never had a client contract toxoplasmosis, let alone pass it on to their unborn child. In fact, I have never known a female veterinarian that tested positive for exposure to toxoplasmosis. These women have subsequently become pregnant and all have given birth to happy, healthy children, all the while continuing to work in a veterinary practice throughout the majority of their pregnancies. The risk of toxoplasmosis causing birth defects in an unborn child because there is a cat in the household is, therefore, tremendously overblown. While there is always a potential risk, following simple precautions and employing common sense should eliminate the fear that your pet cat is a danger to your unborn child.