Facebook Pet Education Archives - Page 3 of 8 - Animal Medical Center of Southern California

Platelet Rich Plasma Therapy

The usual protocol for the initial treatment of muscle and tendon injuries includes rest, ice, compression, and elevation of the injured area.

This combination prevents further injury, reduces pain, inflammation, and swelling and thereby encourages healing. Not exactly an easy task when dealing with dogs and cats. Physical therapy is usually applied when the acute stage of injury has subsided. It usually involves massage, stretching, and exercises, many times augmented with ultrasound and acupuncture therapy.  Non-steroidal and steroidal anti-inflammatory drugs are also commonly used. Surgery is reserved for the more severe and intractable injuries. However, a novel approach, very different from the usual methods and involving blood platelets, shows much promise and is causing much excitement in the orthopedic and sports injury world.

When tissue is injured, the inflammatory response is triggered. This is necessary even though the heat and swelling are unpleasant. Inflammation stops the spread of infection and clears away damaged tissue. However, healing of the tissues cannot take place until the inflammation process is switched off. The fact that platelets play a role in the control of both of these processes forms the rationale behind PRP treatment. Most everyone thinks of blood platelets as being responsible for blood clotting after injury, which is true. What many people do not know is that blood platelets serve two other important functions. Blood platelets are responsible for bringing the white blood cells to the injured area to clean up the remains of dead and injured cells. Most importantly to this discussion, blood platelets release growth factors that are directly responsible for tissue regeneration. These substances are called cytokines and include platelet-derived growth factor, epithelial growth factor, transforming growth factor, insulin growth factor, and other important growth factors. By ultimately inhibiting inflammation, platelets form part of the mechanism that switches the process off and stimulates healing by producing the various tissue growth factors mentioned above which stimulate new blood vessel growth. It is for these reasons that PRP treatment has been promoted for tendon, ligament, muscle, and joint injuries, which have been historically normally slow to heal.

Platelet-rich plasma, or PRP, is derived from blood that is drawn from the patient and runs through a special centrifuge, which separates the blood’s less dense components from its heavier ones. This process distills a portion of the blood to a platelet concentration level that is much richer than regular blood. At the same time, it helps to remove both red and white blood cells from the platelet rich part of the plasma.

Plasma containing this concentrated level of platelets provides an abundance of the previously mentioned growth factors, which are the proteins in the body that stimulate cells in the tendon, ligament, muscle, or joint to start the healing process. When PRP is injected into damaged tendons or ligaments, cells in the tissue—along with new cells circulating in the blood—are stimulated to bring even more new cells to the injured site. Therefore, the growth factors derived from platelets initiate connective tissue healing, bone regeneration, and repair, promote the development of new blood vessels, and generally stimulate the wound healing process by accelerating epithelial and epidermal regeneration. Because the patient’s own blood is used to make the specialized plasma—this is known as an autologous process—there is no risk of the treatment being rejected, as it might be if the blood had been provided by a donor.

Although PRP technology is considered cutting-edge technology, it was initially developed 20 years ago for heart surgery to aid in wound healing and blood loss. Its benefits are now being applied towards the facilitating of healing of muscle, tendons, ligaments, articular and meniscal injuries. PRP has also been utilized for bone repair; it can be added to harvested autogenous bone or to a mixture of autogenous bone and freeze-dried bone/alloplastic material to improve the consistency for handling during surgery and minimizing particulate migration as well as to add increased platelets (i.e. increased growth factors) into the area to stimulate healing.

In our practice, the utilization of PRP has been directed towards Achilles tendon injuries, cruciate ligament injuries, complicated orthopedic fractures and delayed bone healing,  and degenerative joint disease of the shoulder, elbow, hip, knee, and ankle. The number of injections performed depends upon the severity and type of condition being treated. The use of certain anti-inflammatory drugs is not recommended during PRP therapy as they may diminish the success of the procedure by interfering with the initial inflammatory reaction induced by the platelets. The use of omega 3 and 6 essential fatty acid fish oil supplements and other natural anti-inflammatory agents do not seem to work the same way as the non-steroidal anti-inflammatory agents and are therefore not restricted in use throughout the platelet facilitated the natural healing process. Depending upon the condition being treated, the pet may require nothing more than a local anesthetic for the administration of PRP or may require a ‘twilight’ anesthetic.  A real advantage to PRP therapy is that it may not only facilitate the healing process, it may in certain cases provide an alternative to surgery.

While platelet-rich plasma therapy offers a promising solution to accelerate the healing of bone, muscle, tendon, ligament, and joint conditions naturally without subjecting the patient to invasive surgical procedures and significant risks, there is no one, standard protocol. Frequently, chronic injuries require more than one injection. In both acute and chronic injuries, injections may be combined with an exercise or physical therapy program, acupuncture and/or Class IV laser therapy to enhance the success of the treatment.

Pain Management

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.
    • <\ul>

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.

Pharmacological intervention:

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.

Non-Pharmacological intervention:

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).

The Medical and Legal Implications of Veterinary Cosmetic Surgical Procedures

While at first, it might seem odd that pets are the recipients of cosmetic surgical procedures, upon further consideration it makes perfect sense.

The problem is the accepted definition of cosmetic or plastic surgery. In the human field, the term cosmetic surgery is usually reserved for those procedures which are beautifying, nonessential, and non-medical.  In the veterinary field, an ethical veterinarian would not subject his patients to such procedures. There is always the attendant risk of anesthesia and surgical complication (as there is in the human field) with any procedure, let alone cosmetic ones. A veterinary surgeon weighs those risks every time he contemplates a surgical procedure, and it is a judgment call of whether to proceed with surgery or not depending upon the risks versus the gain to each individual patient. It is more than a matter of semantics to consider essential veterinary plastic surgical procedures more appropriately as reconstructive dermatologic surgery rather than cosmetic surgery.

The non-pet owning public finds it fascinating that dogs are even mentioned in the same breath as plastic surgery. Pet owners, however, are well aware of the myriad number of procedures that dogs have routinely and maybe not so routinely undergone to improve their health and welfare. Among those procedures which are “cosmetic” by nature but are truly reconstructive in nature are entropion and ectropion surgery (“eye lift or tuck”), nasal alar fold and deviated septum surgery (“nosejob”), cheiloplasty (“facelift”), facial fold reductions, orthodontic and maxillofacial surgery,  breast reduction, vaginal fold and tail fold pyoderma surgery,  skin grafting and myocutaneous flap surgeries, and the placement of prosthetic implants for limb salvage procedures.

Anybody familiar with Chows and Sharpeis is familiar with their ocular problems. These breeds are consistently afflicted with congenital and hereditary tendencies, which result in the eyelids rolling in toward the eyeball and predisposing the cornea to persistent pain, discomfort, infection, and injury, which may progress to vision loss or blindness.  Saint Bernards, Newfoundlands,  Great Pyrenees, Mastiffs, and others suffer from the opposite congenital tendency, which is to have the eyelids droop outwardly predisposing these breeds to similar ocular injury. No one in their right mind would contest the necessity of reconstructive procedures to alleviate the constant ocular pain and attendant complications these congenital tendencies provoke.  The corrective procedures, however, are “cosmetic” in origin as the surgeon is basically performing an eyelift or tuck. It’s just that the procedure is being performed for a truly medical and not a cosmetic result.  No one performs an eyelift surgery to make a 10-years-old dog look likes she’s 6-years-old. All that the dog understands is that he is more comfortable and is able to see again without pain.

Nose job surgeries are similarly indicated for those breeds with inherent upper respiratory distress syndromes. Boston Terriers, Pugs, Boxers, Bulldogs, and other chondrodystrophic breeds (ie., “smushed in faces”) are compromised by narrowed nostrils. The inability to breathe through their nose and the resultant obligatory mouth-breathing leads to and exacerbates a variety of upper respiratory problems. Surgically opening these narrowed nostrils is a simple, easy, and minimally invasive surgery, which tremendously improves the quality of life for these animals. Once again, no one is performing nose surgery because the owner doesn’t like the shape of their pet’s nose. It’s nice to be able to breathe without having to consistently make a coordinated effort to do so.

Everybody who spends their time around dogs has been “slimed” at one time or another by flying saliva. Mastiffs are the poster child for droopy lips and excessive, uncontrolled salivation. In the old days, veterinarians actually removed the sub-mandibular salivary glands to decrease the amount of saliva formed and secreted in an attempt to prevent a consistently wet skin fold and resultant chronic bacterial and yeast infection in the skin below the lips. In many cases, these skin infections spread systemically causing urinary tract infection, heart valve infections, and dental disease. Rather than remove the salivary glands, a “facelift” or cheiloplasty effectively alleviates the problem. The lips are alternately pulled up and back and rolled in to prevent salivary leakage. The majority of the procedure is performed within the oral cavity to be more cosmetic, but no one can deny the medical benefits to be gained by that portion of the canine population with chronic lip fold infections. It’s also much less invasive a surgery than removing the salivary glands.

As you can see, many of the “cosmetic” surgical procedures performed on dogs are performed because of the complications associated with abnormal skin folds. It is for this reason that breast reductions and some vaginal, facial, and tail surgeries are carried out. While I am a Board certified Veterinary Surgeon, my practice is not limited to veterinary surgery. I operate a full service veterinary facility open 24 hours a day 7 days a week. As such, I see a tremendous amount of general practice cases. Many clients have recently adopted dogs from the shelters, pounds, and/or rescue groups which need to be spayed. A good proportion of these intact females have had multiple pregnancies. As a result of these pregnancies, there is a tendency for pendulous breast tissue and secondary intra-mammary skin fold infections. It makes sense to reduce the pendulous and cystic breast tissue under the same anesthetic that a spay procedure is performed to eliminate the chronic maintenance that would otherwise be required of the new owner to prevent consistent skin infections in the area. As a result of multiple pregnancies as well as for a variety of other congenital and/or hereditary reasons, many female dogs have chronic irritation of the vaginal area and secondary ascending urinary tract infections because of excessive vaginal skin folds. The removal of these folds prevents excessive vaginal licking and irritation and urine scalding, resulting in a much more comfortable pet. The same is true for tail and facial fold infections commonly observed in Bulldogs and other chondrodystrophoid breeds. Cosmetic removal of the kinked tail effectively eliminates an area of chronic irritation and infection. By the same token, cosmetic removal of excessive and deep facial skin folds removes a source of chronic irritation from persistent fungal and bacterial infection.

Many animals that have suffered through a significant trauma or cancer may require skin grafts or the movement of large flaps of skin and the attached underlying musculature, a procedure known as myocutaneous flap transfer. Once again, while cosmetic in nature, these procedures obviously are medically beneficial to the patient. Recently, advancements in prosthetic surgery are making it possible to consider osseointegrated prosthetic limb implants for limb salvage. In these procedures, a stainless steel or titanium implant is placed within the bone of a limb to act as a scaffold for placement of a prosthesis that mimics both cosmetically and functionally a normal limb. The potential benefit to dogs, which would otherwise have lost a limb to amputation, is enormous.

The question comes down to where does an ethical veterinarian cross the line with regard to the procedures that some clients would consider frivolous and other clients would consider a necessity? All of the procedures that have been previously mentioned are medically beneficial and help tremendously improve a patient’s quality of life when applied intelligently and with discretion. I have been asked to perform botox, collagen, and restylane injections as well as testicular implant surgery.  My answer, whenever I have been asked, is a resounding “No!!” In my opinion, these procedures serve no known medical benefit for the patient. The pet owners that ask for such procedures to be performed on their pets would be better off spending their money on psychotherapy in order to understand why anthropomorphization of their pets is flat out crazy.

Stifle Luxation in the Dog and Cat

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.

Principles of External Skeletal Fixation

Numerous methods of fracture fixation are available to the veterinary surgeon.

External skeletal fixation is an effective method of fracture repair, which has experienced a resurgence in popularity in the last few years. Several types of external skeletal fixation devices are commonly utilized, including the Kirshner-Ehmer apparatus and the Synthes and Hoffman external fixators. Many configurations and various modifications have been described for the application of external fixators. A review of apparatus design has resulted in a classification of external skeletal fixators into three types, each possessing separate attributes and indications for use. Type 1 for unilateral splints uses fixation pins, which are inserted through both bone cortices but penetrate only on the skin surface. Type 2 or bilateral splints use fixation pins, which are inserted through both cortices and both skin surfaces. Type 3 or biplanar splints are a combination of unilateral and bilateral splintage employed in a three-dimensional configuration.

An external skeletal fixator (ESF) can be used as the primary method of fracture fixation or can be used to enhance the stability provided by another primary fixation modality. External fixators may be used in a variety of clinical situations including simple fractures, open or compound fractures, delayed and non-unions, highly comminuted fractures, fractures in which there is extensive soft tissue damage, and infected fractures. They are also frequently recommended in cases requiring transarticular stabilization and for stabilization of corrective osteotomies. When used properly, application of an ESF results in a number of advantages over other techniques of fracture repair, including minimal disruption of soft tissues attachments to bone and minimal disturbance of the blood supply to the bone. When used in difficult fracture situations involving open or compound wounds, osteomylitis and/or extensive soft tissue injury, the contaminated fracture sites are not disturbed by the presence of the fixation device and dissemination of the contamination is minimized.

As with any surgical technique, the use of an ESF is not without some disadvantages or potential complications. Disadvantages of an ESF include delayed healing under certain condition, ideal reduction is not always possible, the fixation may fail in cases of osteoporosis, and the ESF may catch on an object thereby ruining the fixation. Complications associated with the use of an ESF include pin tract drainage and infection, pin loosening, pin breakage, iatrogenic fractures, damage to vessels and nerves, and disturbed muscle function due to pin placement. The disadvantages and complications must be taken into consideration when deciding whether to use external fixation. The majority of the disadvantages and complications associated with an ESF can be alleviated if the important principles of application are followed carefully.

Historically, the major limitation for the use of external skeletal fixation has been its ability to adequately stabilize fracture fragments until healing has occurred. It is absolutely essential to maintain the holding power of the pins the bone and the stiffness of the fixation pins if rigid immobilization is to be maintained. Maximum stress of the fixation pins occurs at the pin-bone interface. Stress transfer from bone to metal and, over time, stress concentration at these sites can eventually lead to pin loosening, drainage, infection, or breakage. Information gathered from numerous studies and clinical experience indicates that stiffness, bone holding power, and clinical performance of an ESF is dependent upon numerous factors including configuration, diameter and number of connecting bars, pin diameter, number of pins, type of pin, angle and location of pins in cortical bone, length of pins from the connecting bars to the bone, method of pin insertion, and inherent stability at the fracture site. Each of these factors must be critically assessed by the surgeon to decrease the likelihood of pin loosening and loss of fixator stiffness and associated morbidity.

The method of fixation pin insertion used should avoid generating mechanical damage and bone necrosis. High speed power insertion of pins results in thermal necrosis of bone, while insertion by a hang drill results in excessive mechanical damage. Both techniques are associated with a decreased force required for axial extraction of the fixation pins. Current recommendations include predrilling with a smaller drill bit and either low speed power or hand chuck insertion of fixation pins to decrease the incidence of mechanical or thermal necrosis and subsequent premature pin loosening.

The type of pin used influences greatly the stability of the pin-bone interface, as well as fixators stiffness. While nonthreaded pins exhibit decreased bone holding power, they are stiffer, stronger, and more resistant to bending and breaking than threaded pins. A recent study indicated that single cortex partially threaded pins compare favorable to pins with threads engaging both cortices with regard to holding power. In addition, these pins provided more resistance to bending at the pin-bone interface than fully threaded pins. Essentially, the single cortex partially threaded pin combines the increased holding power of threaded pins with the stiffness of the nonthreaded pins. The use of partially threaded pins, either exclusively or in combination with nonthreaded pins, should be considered in clinical cases where prolonged external skeletal fixation is required. Other studies have indicated that morbidity decreased significantly with the exclusive use of threaded pins or a combination of threaded and smooth pins as compared to the exclusive use of the smooth pins. Prolonged stability of the pin-bone interface was considered to be the reason.

Numerous recommendations have been made with regard to the angle and location of fixation pin placement in cortical bone. Information gathered from many studies indicates that an angle of approximately 70 degrees to the long axis of the bone and inward (central) angling of the pins improves fixation stiffness. It may also reduce pin loosening, because nonparallel pins will tend to restrict the motion of their neighbor. The appropriate number of pins per fragment has not been objectively determined; however, a minimum of 2 and perhaps 3 or 4 pins per fragment should be used as increasing the number of fixation pins per fragment reduces the incidence of premature loosening. Each pin should be inserted through a separate stab incision in intact skin and avoid penetration of large muscles masses. This practice will help alleviate problems with incision or wound management, decrease the incidence of pin tract infection and make incision closure easier.

Bone-connecting bar distance should be minimized while avoiding interference with the skin. Doubling the bone-clamp distance reduces the fixator stiffness by 25%. Increasing the diameter of the fixation pins or the diameter and number of the connecting bars will increase fixator stiffness. The configuration of the fixators will also affect fixator stiffness, with Type 3, or biplanar splints, being the strongest configuration.

In conclusion, since fractures vary widely in type, stability, the condition of the soft tissues, and activity and size of the patient, it is obvious that no one configuration is best suited for all fractures. Providing that the proper principles of application are followed, external skeletal fixation can provide the stable fixation necessary for fracture healing and good to excellent post-operative limb function. The information presented should hopefully enable the surgeon in choosing the best ESF design for the fracture type under consideration.

Principles of Tendon Repair

A tendon is a dense band of fibrous connective tissue which acts as an intermediary component in the attachment of the muscle to bone.

When operating within a range of normal physiological forces, tendons exhibit high compliance, great tensile strength and low extensibility. When supraphysiologic forces are placed on tendons, their mechanical characteristics change, and apparently irreversible structural changes take place. Whether or not such changes eventually result in a clinical lesion is dependent upon a number of poorly defined factors. The healing of injured tendons presents the veterinary surgeon with a number of different management decisions as opposite objectives seem to be required in the same wound. Successful restoration of injured tendons requires a rapid gain in tensile strength without adherence to other tissues. For a single scare to provide strength in one area yet not restrict motion in another, a complex series of events must occur. This series of events is dependent upon the anatomy and vascular supply of the tendons and the adjacent tissues.

A tendon may receive its blood supply from four sources: the muscle or bone to which the tendon is attached (intrinsic vessels), a mesotendon within a synovial sheath, and the paratendon if no sheath exists (extrinsic vessels). Both intrinsic and extrinsic components can be involved in tendon healing. As tendon injuries are often accompanied by injuries to the surrounding soft tissues and/or bone, their healing does not take place in an isolated environment. The gain in tensile strength and adhesions that develop are part of a single healing process, resulting in the tendon and the surrounding tissues healing according to the “one wound-one scar” principle. There is no question that if the wounded tendon could be managed independently of the adjacent soft tissue wound, the problem of tendon repair would be simplified.

The healing process of tendons can be further divided into healing of sheathed versus non-sheathed tendons. In a non-sheathed tendon, healing depends less on intrinsic blood supply because of the contributions of the wound bed from the paratendon and peritendonous tissues. In sheathed tendons under ideal conditions (i.e., if the primary intrinsic blood supply is not damaged), the potential for primary intrinsic repair exists. Maximization of the intrinsic healing and minimization of extrinsic healing will lead to fewer problems with peritendonous adhesions. Unfortunately, the majority of tendon injuries involves the tendon and tendon sheath and primary intrinsic repair is overshadowed by an extrinsic response by the peritendonous tissues. This response results in adhesion formation in addition to tendon healing and may preclude restoration of normal gliding function.

In an effort to erect an artificial barrier between the healing tendon and the rest of the wound, numerous materials have been placed around the anastomatic site. In all cases, retardation of the healing process has occurred. This is because in the overwhelming majority of tendon injuries, although numerous intrinsic vessels are present, these vessels are not capable of nourishing the tendon without collateral connections to extrinsic vessels. In addition, tendon healing is dependent upon migration of cells from outside the tendon into the defect between tendon ends. Therefore, successful isolation of a tendon anastomosis from the extrinsic tissues invariably results in failed healing. The best approach to minimizing adhesion formation and subsequent restricted gliding function is to use proper surgical technique and postoperative care.

Obviously, the importance of adhesions in tendon surgery depends upon the necessity for restoration of normal gliding function. The return of sufficient tensile strength may be more important than restoration of normal gliding function in a number of instances. For example, in treating injuries involving large weight-bearing tendons, provision of tensile strength adequate to prevent distraction during weight-bearing, rather than prevention of adhesions, should be the primary concern of the surgeon. This is because the formation of adhesions which would restrict the motion of these structure is rare, and a successful clinical outcome depends primarily on the maintenance of close opposition of the sutured tendon ends throughout healing.

The goals of tendon repair are apposition of the severed tendon ends with minimal disruption of blood flow, minimal suture bulk, and maximum strength of the overall repair. As is true with any surgical technique, suture materials and tendon suture patterns have been developed and recommended in an attempt to optimize results. These patterns have evolved in an attempt to maximize both tensile strength and normal gliding function.

Monofilament suture material is recommended for tendon repair because of its ability to glide within tissue and may be less likely to initiate tearing or separating of the tendon. While synthetic, monofilament, non-absorbable suture material has been the preferred suture material in the past, polydioxanone (PDS*) is absorbed slowly and loses its strength slowly. Therefore, enough strength would remain until the tendon begins to acquire intrinsic tensile strength. In addition, PDS* is less likely than non-absorbable suture materials to create a suture sinus in a contaminated environment.

As mentioned previously, several suture patterns have been designed for the surgical repair of severed tendons, including the Bunnell, Bunnell-Mayer, locking loop or modified Kessler, and three lopp pulley techniques. In the immediate postoperative healing period the sutures are relied upon to maintain tendon apposition and resist gap formation. They provide mechanical support and serve as a scaffold for initial cellular migration. The suture pattern should not restrict blood flow within the tendon or enhance scar formation by irritating the surrounding tissues. In light of these criteria, the locking loop and three loop pulley techniques are favored, as they are less restrictive of the intrinsic blood supply and provide greater tensile strength than do Bunnell sutures. The three loop pulley pattern has been shown to provide more tensile strength and resistance to gap formation than the locking loop pattern; however, it may compromise gliding function because of the quantity of suture material on the surface of the tendon. With this in mind, the locking loop pattern would seem best suited for use in situations where maximum gliding function is necessary, while the three loop pulley pattern may be used advantageously in high-load situations where provision of early tensile strength rather than restoration of normal gliding function is of primary concern.

Postoperative management of a surgical repair of a tendon rupture should consist of external support and immobilization for three weeks, followed by an additional three to four week period of restricted activity as the intrinsic tensile strength of the healing tendon increase. There should then be a gradual return to normal activity. Recent evidence indicates that limited passive motion aids in the longitudinal orientation of tendon fibrils in tendon repair while active motion will inhibit early repair of the tendon. When controlled passive motion is utilized, tendons heal more rapidly than in immobilized repairs. The difficulty encountered in veterinary surgery is how to conveniently implement limited passive motion without placing too much stress on the healing tendon too soon in a potentially uncooperative patient. Hopefully, additional advances will be made in the near future to help overcome these difficulties and to optimize the healing of tendon injuries in general.

Toxoplasmosis and Pregnancy

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.

Prevention and Treatment of Rattlesnake Bite in Dogs

Rattlesnakes live in a variety of habitats, ranging from wetlands, deserts, and forests, and from sea level to mountain elevations. Rattlesnakes are most active in warmer seasons, from Spring to Autumn. In southern latitudes (and here in Southern California) they are occasionally found year-round.

Dogs are at risk for rattlesnake bites; in fact, dogs are about 20 times more likely to be bitten by venomous snakes than people and are about 25 times more likely to die if bitten. Snake bites are life-threatening, extremely painful, expensive to treat, and can cause permanent damage even when the dogs survive. Dogs can encounter a rattlesnake anytime they are in rattlesnake habitat. You and your dog may live in rattlesnake habitat, or perhaps you travel through or frequently visit places where rattlesnakes are found. Maybe rattlesnakes are around when you take your dog hiking, camping or hunting. Like people, dogs may stumble over the location of a snake by accident. Curiosity or a protective instinct can place your dog at risk. When dogs encounter snakes during play or work in the snake’s natural habitat, most bites tend to occur on the face or extremities. The rattlesnake bite is generally “hemotoxic” which means that it exerts its toxin by disrupting the integrity of the blood vessels. The swelling is often dramatic with up to 1/3 of the total blood circulation being lost into the tissues in a matter of hours. The toxin further disrupts normal blood clotting mechanisms leading to uncontrolled bleeding. This kind of blood loss induces shock and finally death. Facial bites are often more lethal as the swelling may occlude the throat or impair ability to breathe. Less than a decade ago, a dog unfortunate enough to be bitten by a large Western Diamondback rattlesnake and injected with a full load of venom faced a grim fate, particularly if it was more than a couple of hours away from medical help. Since its availability in 2003, the Red Rock Biologics rattlesnake vaccine has helped provide the best protection against poisonous snakes and has become the standard of preventive veterinary care for dogs at high risk for rattlesnake bites.

The canine rattlesnake vaccine comprises venom components from Crotalus atrox (western diamondback). This vaccine is meant for use in healthy dogs to help decrease the severity of rattlesnake bites. The vaccine is produced from inactivated Crotalus atrox venom with an adjuvant and preservatives added. Dogs develop neutralizing antibody titers to C. atrox venom; the vaccine is specifically for the toxin of the Western Diamondback rattlesnake and provides the best protection against the venom of that particular rattlesnake, however the vaccine has been shown to provide cross protection against the venom of other types of rattlesnakes and copperheads since the venom of pit vipers share some of the same toxic components. In fact, most of the 15 species of rattlesnakes in the United States have fairly similar venom.  This is how one antivenin is able to cross-protect against so many rattlesnake species.  The protection afforded by the vaccine depends on the similarity of snake venoms to the Western Diamondback.

The vaccine however does not provide protection against the Mojave rattlesnake, Eastern Diamondback rattlesnake, cottonmouths or coral snakes.

The vaccine works by stimulating the dog’s immune system to produce antibodies against rattlesnake toxin. Initially, a dog should receive two subcutaneous doses about 30 days apart.  It is best to give vaccination boosters about 30 days before beginning of exposure to rattlesnakes. Protection peaks about 30 to 45 days after boosters and lasts about six months.  As the antibodies are short-lived and the vaccine typically only provides protection for six months, a booster shot is necessary either once a year one month before “snake season” or twice a year in areas where rattlesnakes are year-round risks. The protection level that a dog receives from the vaccine depends upon how well that individual dog produces these specific antibodies and may vary. Protective antibodies made by your dog in response to the vaccine start neutralizing venom immediately. On average, antibody levels in recently vaccinated dogs are comparable to treatment with three vials of antivenin. Almost no vaccine is effective 100% of the time.  There are undoubtedly some dogs whose immune systems just won’t produce as many antibodies necessary for maximum protection but the partial protection they receive may still be enough to save their lives or help them recover more quickly. Therefore, this vaccine should not be used solely as a means of protection against rattlesnake bites. It is meant to provide some protection and to reduce the severity of the snakebite.  Adverse events are reported in far less than one percent of all vaccinated dogs.  Most of these side effects are mild and need no veterinary care.  The most common side effect is the development of an injection site cellulitis; these vaccine site reactions can be treated with hot, moist compresses, antibiotics, and pain relief medication if necessary.  Systemic reactions (typically flu-like symptoms) are reported in fewer than one in 3,000 vaccinates and usually self-resolve in two to three days.

Even good antibody protection can be overcome in special snakebite circumstances. A vaccinated dog’s resistance to rattlesnake venom can be overcome with enough venom or special circumstances.  But what are those circumstances?  Special snakebite circumstances include smaller dogs, larger snakes, multiple snake bites to the same dog, and bites near vital organs.  Smaller dogs are always going to have a harder time fighting off the same amount of venom as larger dogs.  Larger snakes can produce and deliver larger doses of venom in a single bite.  Multiple snake bites to the same dog can naturally deliver larger quantities of venom.  Bites near vital organs allow the venom to start destroying those organs before the antibodies in the dog’s blood plasma have time to find and neutralize the harmful proteins in the rattlesnake venom.  Other special circumstances may include some dogs whose immune systems just don’t produce enough antibodies, intravenous bites, and some snake species that the vaccine has little or no protection against.

The reported benefits of vaccination include a delay in onset of symptoms, fewer symptoms, less severe symptoms, a decrease in mortality rate, faster recovery times, and little or no tissue necrosis.  In addition, most veterinarians also report less painful dogs, less lethargy, less swelling, that the swelling progression typically reversed within the first 1 to 2 hours, and that dogs had full recoveries in about 24 to 48 hours. As mentioned previously, according to Red Rock Biologics, the manufacturers of the rattlesnake vaccine, the antibody levels in recently vaccinated dogs are comparable to treatment with three vials of antivenin. So, although canines still need emergency veterinary treatment, they should experience less pain and a reduced risk of permanent injury from the rattlesnake bite. Snakebites are always an emergency. Even if your dog is vaccinated against rattlesnake venom, always get the pet to a veterinarian as soon as possible following any snakebite. Even non-venomous snake bites can lead to serious infections and antibiotic treatment may be needed. A veterinarian can determine what additional treatment is needed.

Since the most common mechanism of death from rattlesnake bite is circulatory collapse, intravenous fluid support, antibiotic therapy, cardiac and blood pressure monitoring, antihistamine administration and pain management are very important.  Fluids may be started at a relatively slow rate if the patient is stable but should signs of impending trouble occur, circulatory volume replacement and treatment for shock is indicated. Blood transfusion may be necessary if life-threatening blood loss has occurred. A minimum of twenty four hours of post-bite observation and hospitalization is prudent. In addition, treatment of snakebite should include antivenin administration. There are numerous misconceptions about antivenin. The first is simply the name of the product. It is not “anti-venom.” It is not a single injection that provides the antidote to snake bite venom. Antivenin is a biological product consisting of antibodies made in response to exposure to four common Crotaline venoms. The antibody serum is reconstituted into an intravenous drip that is run into the patient over at least 30 minutes or so. Antivenin is expensive (at least $600-$800 per vial) and a large dog with a severe bite is likely to require several vials. Antivenin is very helpful in the inactivation of snake venom but there is a narrow window in which it must be used. After about 4 hours post-bite, antivenin is less effective in countering the effects of snake venom.

In summary, rattlesnake envenomation is a serious life-threatening injury and immediate veterinary care is warranted for the best success rates in surviving the ordeal. The benefits of prophylactic vaccination include more time to get to a veterinary hospital, the reduction in the amount of pain and swelling experienced, faster recovery times and a decrease in the mortality rate. It is not meant as a sole means of protection. Emergency treatment consisting of an intravenous fluid support, antibiotic administration, antihistamines, pain management and antivenin will result in the best chance of successfully surviving a rattlesnake bite.


It’s never an easy decision to make, but perhaps the kindest thing you can do for a pet that is extremely ill or so severely injured that it will never be able to resume a life of good quality is to have your veterinarian induce its death quietly and humanely through euthanasia.

A decision concerning euthanasia may be one of the most difficult decisions you will ever make for your pet. Although it is a personal decision, it doesn’t need to be a solitary one. Your veterinarian, your family, and close friends can help you make the right decision and can support you as you grieve the loss of your pet.

What should I do?

Eventually, many owners are faced with making life-or-death decisions for their pets. Such a decision may become necessary for the welfare of the pet and your family. Consider not only what is best for your pet, but also what is best for you and your family. For example, if your pet has an injury or disease that requires more care than you and your family can give to make sure it has a good quality of life, euthanasia may be the right decision. Quality of life is important for pets and people alike.

Once the decision for euthanasia has been made, it is sometimes easier to discuss what you want done with the remains of your pet’s body before your pet is euthanized—by making arrangements prior to euthanasia; it can bring some degree of comfort to know what will be done with your pet’s body, and you will not have to focus on these decisions while you are grieving the recent loss of your beloved pet. Your veterinarian can provide information about burial, cremation, and other alternatives.

How will I know when?

If your pet can no longer experience the things it once enjoyed, cannot respond to you in its usual ways, or appears to be experiencing more pain than pleasure, you may need to consider euthanasia. Likewise, if your pet is terminally ill or critically injured, or if the financial or emotional cost of treatment is beyond your means, euthanasia may be a valid option. Sometimes asking yourself the question, “Does my pet have more bad days than good days?” can help you make the decision. Euthanasia might be necessary if a pet has become vicious, dangerous, or unmanageable. Some undesirable and abnormal behavior can be changed, so it is important to discuss these situations with your veterinarian. You and your family’s safety should always be taken into consideration.

Your veterinarian understands your bond with your pet and can examine and evaluate your pet’s condition, estimate its chances for recovery, and discuss any potential disabilities, special needs, and long-term problems. He or she can explain medical and surgical options as well as risks and possible outcomes. Because your veterinarian cannot make the euthanasia decision for you, it is important that you fully understand your pet’s condition. If there is any part of the diagnosis or the possible effects on your pet’s future that you don’t understand, ask questions that will help you understand. Although there are times when the decision needs to be made immediately, you usually will have some time to review the facts and discuss it with your family and friends before making the decision.

How do I tell my family?

Family members usually are already aware of a pet’s problems. However, you should review with them the information you have received from your veterinarian. Long-term medical care can be a burden that you and your family may be unable to bear emotionally or financially, and this should be discussed openly and honestly. Encourage family members to express their thoughts and feelings. Even if you have reached a decision, it is important that family members, especially children, have their thoughts and feelings considered.

Children have special relationships with their pets and should not be excluded from the decision-making process because they might seem too young to understand. Preventing children from participating in the process may only complicate and prolong their grief process. Children respect straightforward, truthful, and simple answers. If they are prepared adequately, children usually are able to accept a pet’s death.

Will it be painless?

Euthanasia is most often accomplished for pets by injection of a death-inducing drug. Your veterinarian may administer a tranquilizer first to relax your pet. Following injection of the euthanasia drug, your pet will immediately become deeply and irreversibly unconscious as the drug stops brain function. Death is quick and painless. Your pet may move its legs or head or breathe deeply several ties after the drug is given, but these are reflexes and don’t mean that your pet is in pain or is suffering.

How can I say goodbye?

The act of saying goodbye is an important step in managing the natural and healthy feelings of grief and sorrow following the loss of a beloved friend and companion.

Once the euthanasia decision has been made, you and other family members may want to say goodbye to your pet. A last evening with your pet at home or a visit to the pet at the hospital may be appropriate. Family members who want to be alone with the pet should be allowed to do so. Some pet owners choose to be present during their pet’s euthanasia, but others choose to say goodbye beforehand and not be present during euthanasia. This is a very personal decision and you should do what feels right for you. Do not let others pressure you into making a choice that makes you uncomfortable.

How can I face the loss?

After your pet has died, it is natural and normal to feel grief and sorrow. For some people, spending some time with their pet after euthanasia is helpful. The grieving process includes accepting the reality of your loss, accepting that the loss and accompanying feelings are painful, and adjusting to your new life that no longer includes your pet. By understanding the grieving process, you will be better prepared to manage your grief and to help others in the family who share this loss.

Sometimes well-meaning family and friends may not realize how important your pet was to you or the intensity of your grief. Comments that make may seem cruel and uncaring although they were not meant to be taken that way. Be honest with yourself and others about how you feel. If you feel despair, talk to someone who will listen to your feelings about the loss of your pet. Talk about your sorrow, but also about the fun times you and your pet spent together, the activities you enjoyed, and the memories that are meaningful to you.

The stages of grief

There are many stages of grief, but not everyone experiences them all or in the same order. The stages include denial, anger, guilt, depression, acceptance, and resolution. The grief can seem to come in waves, may be brought on more intensely by a sight or sound that sparks your memory, and may seem overwhelming at times.

Your first reaction may be denial—an unwillingness to accept the fact that your pet has died or that death is unavoidable. Denial may begin when you first learn the seriousness of your pet’s illness or injuries. Often, the more sudden the death, the more difficult the loss is to accept and the stronger the denial.

Anger and guilt often follow denial. Your anger may be directed toward people you normally love and respect, including your family, friends, or your veterinarian. People coping with death will often say things that they do not really mean, unintentionally hurting those whom they do not mean to hurt. You may feel guilty or blame others for not recognizing the illness earlier, for not doing something sooner, for not being able to afford other types of or further treatment, or for being careless and allowing your pet to be injured.

Depression is a common experience after the death of a special pet. The tears flow, there are knots in your stomach, and you feel drained of all your energy. Day-to-day tasks can seem impossible to perform and you may feel isolated and alone. Many depressed people will avoid the company of friends and family. It might be hard to get out of bed in the morning, especially if your morning routine involved caring for your pet’s needs. Sometimes you may even wonder if you can go on without your pet. The answer is yes, but there are times when special assistance may be helpful in dealing with your loss. If you are suffering from profound depression, seek professional assistance.

Eventually, you will come to terms with your feelings. You can begin to accept your pet’s death. Resolution has occurred when you can remember your pet and your time with them without feeling the intense grief and emotional pain you previously felt. Acceptance and resolution do not mean that you no longer feel a sense of loss, just that you have come to terms with the fact that your pet has died.

Even when you have reached resolution and acceptance, feelings of anger, denial, guilt, and depression may reappear. If this does happen, these feelings will usually be less intense, and with time, they will be replaced with fond memories.

Although everyone experiences the stages of grief, grieving is always a very personal process. Some people take longer than others to come to terms with denial, anger, guilt, and depression, and each loss is different. If you understand that these are normal reactions, you will be better prepared to cope with your feelings and to help others face theirs. Family and friends should be reassured that sorrow and grief are normal and natural responses to death.

If you or a family member have great difficulty in accepting your pet’s death and cannot resolve feelings of grief and sorrow, you may want to discuss these feelings with a person who is trained to understand the grieving process and can support and help you as you mourn your loss. Your veterinarian certainly understands the relationship you have lost and may be able to suggest support groups and hot lines, grief counselors, clergymen, social workers, physicians, or psychologists who can help.

Remembering your pet

The period from birth to old age is much shorter for most domestic animals than for people, and death is a normal part of the lifecycle. It cannot be avoided, but understanding and compassion can help you, your family, and your friends manage the grief associated with it.

For some people, a memorial service or ritual (such as releasing balloons or spreading cremated remains) can be therapeutic. You may choose to keep and display reminders of your beloved pet. Such as photos or mementos or anything that helps you recall and treasure the good times you spent with them. You may also wish to make a memorial contribution to a charity in honor of your pet and the deep bond you shared. Just as the grieving process varies from person to person, so does the method of remembering the pet that shared your life.

Should I get another pet?

The death of a beloved pet can upset you emotionally, especially when euthanasia is involved. Some people may feel they would never want another pet. For some, the thought having—and eventually losing—another pet may seem unbearable. These feelings may pass with time. For others, a new pet may help them recover from their loss more quickly. Just as grief is a personal experience, the decision of when, if ever, to bring a new pet into your life is a personal one.

If a family member is having difficulty accepting the pet’s death, getting a new pet before that person has resolved his or her grief may make them feel that you think the life of the deceased pet was unworthy of the grief that is still being felt. Family members should agree on the appropriate time to bring a new pet in to their lives. Although you can never replace the pet you lost, you can find another to share your life.

OCD of the Shoulder Joint: Pathogenesis and Surgical Treatment

Osteochondrosis (OC) is a pathologic process in growing cartilage.

Its main feature is a disturbance of endochondral ossification that leads to excessive retention of cartilage. The increase of epiphyseal volume, in growing animals, occurs through endochondral ossification within the epiphyseal cartilage. Multiplication of cartilage cells within a germinal layer leads to thickening of the growth cartilage towards the metaphysis. As the cartilage grows, the cells left in the newly formed matrix undergo a maturation, or degenerative process, while the ground substance becomes mineralized. Capillary buds then invade the mineralized cartilage from the metaphysis, following a front of chondroclasts that remove the cartilage. The latter is then replaced by bony tissue, synthesized by osteoblasts around the buds. Thus, normal growth of long bones results from a precise balance between cartilage growth and its gradual replacement by bone. Osteochondrosis can occur in any particular point within the cartilage and lead to a failure of the phenomena allowing capillary invasion and replacement of the cartilage by bone. Consequently, the cartilage tissue becomes abnormally thickened in that area. The process can be self-limiting. In this case, it remains clinically silent, although it may be detected as an incidental finding on survey radiographs. It may, on the other hand, evolve into a more significant lesion, associated with inflammation and clinical symptoms: this is referred to as “osteochondritis dissecans” (OCD). In shoulder OCD, the caudal aspect of the humeral head is usually affected. The epiphyseal cartilage is avascular, so that it only receives its nutrition via osmosis from the synovial fluid. In cases of OCD, the cartilage thickens markedly and the diffusion of nutrients into its deeper portion is poor, leading to degeneration and necrosis of the fragile cartilage cells. A fissure may develop at the necrotic site. Initially limited to the depth of the cartilage, it gradually extends towards the articular surface. This micro-fracture corresponds to the osteochondritis stage and is referred to as ‘dissecans’ (‘dissecting’) due to the formation of cartilage flaps separating from the subchondral bone. If a flap is completely detached, it may become free within the joint, forming one or more ‘joint mice,’ which may become localised in any joint recesses, though more particularly in the caudal recess or in the bicipital groove in the shoulder. A joint mouse can occasionally be gradually resorbed, or increase in size and become mineralised. Cartilage fissuring and the resulting cartilage breakdown products released into the synovial fluid contribute to inflammation and pain.  Invasion of the cracks by synovial fluid, thus coming into contact with subchondral bone also promotes inflammation. Clinical signs of lameness may occur at this point as lameness and pain become evident once synovial fluid establishes contact with subchondral bone. Osteochondrosis is a common and serious problem in many breeds of dogs. Large and giant breeds, especially Great Dane, Labrador Retriever, Golden Retriever, Newfoundland, Rottweiler, Bernese Mountain dog, English Setter, and Old English Sheepdog are most commonly affected. The age of onset of clinical signs is typically 4-8 months of age and bilateral shoulder involvement is seen in up to 67% of cases presented for evaluation. Males are more commonly affected than females.

The cause of OCD is considered to be multifactorial. Trauma, hereditary factors, rapid growth, nutritional factors and ischemia all seem to contribute to the pathogenesis of OCD. The initial clinical symptoms exhibited by dogs afflicted with OCD may be subtle and difficult to detect. Often times the dog may demonstrate nothing more than stiffness after rest which resolves relatively quickly, but typically the lameness worsens with exercise. The severity of clinical signs does not always correlate with the extent of the radiographic evidence of disease.

There may be episodes of spontaneous improvement for one or several weeks but the pain persists despite anti-inflammatory or analgesic therapy. Manipulation of the limb yields marked pain upon hyperextension of the scapulo-humeral joint and, to a lesser degree, upon forced flexion or deep palpation of the caudal joint recess. An accurate diagnosis is usually achieved with survey radiography, a mediolateral projection being most useful. The shoulder joint should be isolated as well as possible to improve visualization of the caudal aspect of the humeral head. The affected limb is radiographed with firm traction placed on it to pull the shoulder cranially and ventrally to avoid superimposition of the neck and thorax.  The opposite limb is pulled caudally to avoid any radiographic overlap while the affected thoracic limb is being evaluated. The typical radiographic appearance of OCD consists of an altered subchondral bone contour in the caudal aspect of the humeral head. It may be surrounded by a sclerotic bone area characterised by increased radiodensity and loss of trabecular pattern.

Conservative treatment (non surgical) is controversial for this condition. Regardless of the conservative approach used, a higher percentage of dogs go on to have permanent lameness and secondary joint changes associated with osteoarthritis when conservative treatment is used instead of a surgical approach. Conservative management of OCD usually consists of a combination of exercise restriction, body weight management, symptomatic pain management with analgesics and either steroidal or non-steroidal anti-inflammatory drugs, nutraceuticals and regimes of polysulfated glycosaminoglycans. The recent additions of Class IV laser therapy and platelet-rich plasma administration to the conservative treatment regime show promise in alleviating progressive arthritis usually observed with the conservative approach but definitive clinical studies have yet to be performed. None the less, the medical treatments described above are recommended in the postoperative recovery period to enhance and optimize the outcome of surgery.

It is generally agreed that surgical intervention is the best treatment option in order to prevent continued degeneration of the joint. Given the course of the disease and the associated problems described earlier, it is probably not surprising that the treatment of choice for most cases of OCD is surgical removal of the cartilage flap as well over 90% of dogs diagnosed with OCD of the shoulder have a successful recovery with surgery.  The caudolateral approach between the acromial and the scapular part of the deltoid muscle, with cranial retraction of the teres minor and caudal retraction of the teres major, is sufficient to provide adequate visualization of the lesion. This approach via a longitudinal myotomy of the acromial head of the deltoid was developed because of the minimal surgical trauma caused by this approach. Prior to its development, other more traumatic approaches (osteotomy of the acromial process, tenotomy of the infraspinatus and teres minor, etc), were being utilized but they were associated with a much higher postoperative morbidity. I’m proud to say that the technique was developed while I was a surgical resident and is still considered the least invasive approach to the shoulder joint for the treatment of OCD in use today (Schulman, A.J.; Lusk, R.; Ettinger, S.J.; Lippincott, C.L.:  Longitudinal Myotomy of the Acrimonial Head of the Deltoid:  A Modified Approach for the Treatment of Osteochondritis Dessicans in the Dog.  JAAHA 1986; 22: 475-479.). Once the affected area of the caudal humeral head is visualized, the cartilage flap is cut free and all the abnormal cartilage around the lesion is trimmed with a curette to create vertical walls. Aggressive curettage of the floor of the lesion is of questionable value. Multiple drill holes are created in the bed of the lesion (forage) with a 1-2mm drill or a small kirschner wire to allow bleeding to occur in the subchondral bone. This enhances the migration of pleuropotential stem cells into the damaged area to stimulate the formation of fibrocartilage in the articular surface defect. The joint is then lavaged to help flush out any remaining debris, including free fragments of cartilage which should always be looked for in the caudal cul-de-sac of the joint. The prognosis for shoulder OCD is usually excellent. Dogs with this disease often return to normal function after surgery, unless the lesion has been long-standing and significant degenerative arthritis has already set in.

Minimally invasive arthroscopic approaches are also successfully utilized to manage OCD lesions of the shoulder in addition to the standard arthrotomy approach described above. Surgical arthroscopy allows enhanced visualization of intra-articular structures and is also associated with limited postoperative morbidity.  Arthroscopy entails less disruption of the periarticular soft tissue and decreased soft tissue disruption leads to less postoperative pain.  This is especially true when multiple joints are involved and are operated arthroscopically under the same anesthetic procedure. Whether the standard arthrotomy or arthroscopic approach is utilized, the response of OCD to surgical intervention is rapid and rewarding. A good to excellent prognosis is warranted in the overwhelming majority of cases when combined with appropriate postoperative medical therapy.

Jean-Pierre Genevois: Shoulder Osteochondrosis-Shoulder Synovial Chondromatosis-Shoulder Dysplasia. Main Proceedings, 27 WSAVA Congress.

Schulman, A.J.; Lusk, R.; Ettinger, S.J.; Lippincott, C.L.:  Longitudinal Myotomy of the Acrimonial Head of the Deltoid:  A Modified Approach for the Treatment of Osteochondritis Dessicans in the Dog.  JAAHA 1986; 22: 475-479.


ACL tear adenocarcinoma Antivenin arterial shunt artery arthritis back surgery Bacterial infection B cell lymphocytes bilateral bite bone lesion bone marrow broken leg cancer Canine hip dysplasia carcinoma cat cat litter CHD chemotherapy chronic ear infections chronic otitis externa chronic pain compressed spinal cord congestive heart failure Conservative management corticosteroids cosmetic surgical procedures coughing counseling coxofemoral joint Coxofermoral Luxations Cranial cruciate ligament (CrCL) injury Cranial cruciate ligament deficiency CrCL cremation Cruciate disease cruciate ligament CT Cytopenias degeneration of the joint degenerative joint disease derangement Dirofilaria immitis disc degeneration disc surgery disease dislocated hip dislocation distal Distal Femoral Physeal Fractures distal humeral fractures dog dysplasia ear ablation ear canal ablation with bulla osteotomy ear infection ear surgery echocardiogram elbow emergency euthanasia exploratory laparotomy exposure External Skeletal Fixation eye lift femoral fracture femoral head and neck ostectomy fetal heart FHO fixation pins Flexural Deformity Flexural Tendon Contracture fracture fracture fixation fracture repair front leg grade 1 grade 2 grade 3 grief heart heart surgery heartworm Hemilaminectomy Hemorrhagic diathesis herniated disc hip dysplasia hip implant Hip luxation hip surgery humeral fractures Hypercalcemia Hyperviscosity syndrome immiticide injury intervertebral disc disease IVDD Ivermectin kitten knee injury lameness laminectomy life-threatening ligament limping liver liver shunt liver surgery lobectomy loss of weight lung lobe malignant mast cell tumor MCT medial luxation Melarsomine dihydrochloride Milbemycin Monofilament suture mosquitoes Moxidectin MRI Multiple myelomas myelogram neoplasm neurologic non-sheathed tendon nose job NSAID Nuclear scintigraphy nutraceuticals osteoarthritic osteoarthritis Osteolysis otitis externa pain painless pain relief paralysis paralyzed parasite parasites patent ductus arteriosis Pathogenesis and Surgical Treatment: Osteochondrosis PDA pelvic limb pelvis permanent lameness plasma cell myeloma plastic surgery platelet rich plasma Portosystemic portosystemic shunt pregnancy protozoan parasite PRP PSS Pulmonary neoplasia puppy putting pet to sleep quality of life rare rattlesnake bite rattlesnake vaccine reduced tolerance of exercise Renal disease respiratory tract disease sacroiliac fracture sacroiliac joint sacroiliac luxation Selamectin Shoulder joint shoulder luxation shoulder surgery shunt shunting skin folds skin graft skin tumor soft tissue soil Spinal Injuries spine surgery stem cells stifle joint stifle joint luxation surgery Surgical arthroscopy surgical intervention TECA/BO tendon tendon contracture tendon injuries Tendon Repair tendon rupture tension Thoracolumbar intervertebral disc disease threaten unborn child Total hip replacement toxoplasmosis TPLO TPO trauma triple pelvic osteotomy tumor tumors