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Intervertebral Disc Disease

Thoracolumbar intervertebral disc disease is a well-recognized entity in veterinary medicine.

The clinical incidence of intervertebral disc disease has been reported to be higher in the chondrodystrophoid breeds of dogs although disc degeneration occurs in all breeds. The pathophysiologic distinction between intervertebral disc disease in the chondrodystrophoid and nonchondrodystrophoid breeds has been reported in detail.

The severity of the spinal cord lesion resulting from intervertebral disk extrusion may be influenced by (1) the magnitude of the force of impact of the extruded disk material on the spinal cord; (2) the extent of the mechanical distortion of the spinal cord; (3) the chemical, neuronal, and vascular alterations within the spinal cord; (4) the rate of onset of spinal cord compression; and (5) the duration of attenuation.


The intervertebral disk is located between two adjacent vertebrae and acts as a “shock absorber” to handle forces along the spine. There are two parts of the disk which each work differently. The center portion, called the nucleus pulposus (NP), has a high water concentration and is positioned to help absorb the forces along the spinal column. The majority of the force of a compressive load is absorbed by the nucleus pulposus. The outer portion, the annulus fibrosis (AF), is more like a ligament. When forces impact the intervertebral disk, the nucleus pulposus spreads and transmits forces outwards to the annulus fibrosus, which also spreads. The annulus fibrosus, while flexible, is more rigid and maintains disk structure. When the forces along the intervertebral disk cease, the elasticity of the annulus fibrosus allows return to the normal shape of the disk. From the second to the tenth thoracic vertebra, the intercapital ligament between opposite rib heads lies ventral to the dorsal longitudinal ligament and dorsal to the disks. This thick ligament is thought to be the reason disk extrusion is uncommon in the cranial thoracic area. The paired vertebral sinuses lie in a ventrolateral position along the floor of the vertebral canal. Hemorrhage from the vertebral sinuses can accompany disk extrusion or can obstruct visualization during surgical decompression.

The intervertebral disk is found between all but the first two cervical (neck) vertebrae. Individually, an intervertebral disk is the largest organ in the body that does not get direct blood supply bringing nutrients and oxygen to and removing waste products from the cells of the disk. These functions are maintained mostly by diffusion from the end of the vertebral bones. This is a relatively inefficient process in relationship to the high metabolic activity of the cells that make up the intervertebral disk.

Disk degeneration is primarily a result of a breakdown in the process of diffusion leading to an environment in which the cells cannot maintain normal health and function. There is no clinical treatment that can prevent the degenerative changes, but daily controlled exercise can promote disk health by promoting diffusion in the spine.

Degeneration of the intervertebral disk leads to a change in function and chemical properties of the disk, which can result in progressive injury and failure (or rupture) of the disk. When the intervetebral disk fails, it usually does so in an upward direction into the spinal canal and this can lead to compression of the spinal cord.


Because most of the nervous system is inaccessible for direct examination, diagnosis of neurological problems depends on obtaining a good history, consideration of the species, breed, age, and gender of the patient, and conducting a thorough neurological examination in order to establish a neuroanatomic diagnosis.

There are two major types of disc disease in dogs. HansenType I disk degeneration is an early degeneration of the disk that is most commonly observed in chondrodystrophic breeds of dogs including the Dachshund, Shih Tzu, and Beagle. In this type of disk disease, as the disk ages, areas of the nucleus pulposus show signs of cellular necrosis, disintegration of the matrix, and calcification. The biochemical alterations associated with the degeneration of the nucleus pulposus are primarily a loss of water and proteoglycan molecules as well as an increase in collagen content. The poor biomechanical properties of the degenerating nucleus result in disruption of the lamellae of the annulus, which progresses until the calcified nuclear material erupts dorsally through the outer layers of the annulus and impacts on the spinal cord.  In this type of disk disease, it is not uncommon for the NP to extrude out of the center of the disk to result in rapid concussion as well as compression to the spinal cord. The age range of presentation is usually between two and twelve years of age, but peak incidence of dogs presenting with this type of disk disease is between 4-8 years of age, with an average age of 5.5 years of age.

Hansen Type II disk degeneration is associated with normal aging changes. This is most often seen in middle-aged to older large breed dogs including but not limited to the German Shephard.  The changes in Type II disk degeneration include alterations in the NP causing it to become similar in cellular properties and chemistry to that of the AF. In this type of disk disease, the primary physical change is tearing in the fibers of the AF and bulging or protrusion of the annulus fibrosus into the spinal canal. The degree of compression to the spinal cord can vary from minimally to severely compressed within the spinal canal. The onset usually involves more gradual progression of weakness, and often, the owner does not know exactly when it started. However, an acute and large disk extrusion is occasionally seen with this type of disk degeneration.

Whether the onset of disk extrusion is rapid or chronic, the compression to the spinal cord leads to neurological dysfunction. This can range from mild gait change and ataxia (incoordination of the limbs behind the spinal cord region affected) to weakness or even paralysis. It is not uncommon to see pain as the only presenting sign even when there is significant spinal cord compression. The extent of the clinical symptoms exhibited depends upon the length of time the disc has been herniated, the degree of compression of the spinal cord, the force of impact that the degenerated disc has on the spinal cord, and the rapidity of disc herniation and the resultant spinal shock and contusion to the spinal cord.

The most common sites for intervertebral disk extrusions in the dog occur between T11-12 and L2-3 (approximately 85% of all disc herniation), the cervical intervertebral disc C2-C3, and the L7-S1 intervertebral disc space in the lower back. Males are more commonly affected than females. Lumbosacral disc disease, a cauda equina disease at L7/S1, occurs most frequently in large breed dogs (e.g., Shepherd dogs) and is associated with Hansen type II disc disease, vertebral instability, and spinal stenosis, and the complex is called degenerative lumbosacral stenosis, a situation similar to sciatica in people.

Clinical Signs of Disc Disease

Clinical signs of intervertebral disc disease (IVDD) include spinal pain and varying degrees of neurologic deficits. Acute intervertebral disk extrusions are often characterized by the sudden onset of dysfunction of the spinal cord and pain. Chronic intervertebral disk extrusions are more common in large-breed dogs. With the latter form of disc compression, slow, progressive dysfunction without pain is common. The slow, progressive dysfunction associated with chronic intervertebral disk extrusions often times worsens in a rapid fashion as the compensatory limits of the spinal cord are exceeded. Spinal pain without paresis may cause the animal to be agitated, aggressive, or more vocal. Some animals will lie quietly refusing to walk whereas others will walk constantly or pace. Thoracolumbar IVDD may cause animals to walk with an arched back whereas dogs with cervical disk disease will be reluctant to elevate their heads or shake their ears. If there is compression on a nerve root, the animal may hold the affected limb up and have decreased weight bearing. Clinical signs of L7-S1 IVDD include pain upon rising, reluctance to jump up and down or negotiate the stairs, hesitancy to jump into or out of the car, and difficulty defecating. Some animals will have spinal pain as their only clinical sign. Clinical signs of spinal pain in our patient may improve, remain static, or progress depending on the disease progression. The clinical signs of spinal cord compression have been attributed to direct mechanical derangement of nerve tissue and hypoxic changes resulting from pressure on the vascular system in the spinal cord. Other causes for the neurologic signs include ischemia, edema, and reperfusion injury that may result in more severe spinal cord degeneration and hemorrhagic myelomalacia. Progression of neurologic clinical signs is correlated to increasing compression of the spinal cord. The larger, heavily myelinated fibers that mediate proprioception are affected first, followed (in descending order) by the intermediate sized fibers involved in voluntary motor function; the slightly smaller fibers that mediate superficial pain sensation; and, finally, the small unmyelinated fibers that mediate deep pain sensation. The spinal cord heals in the reverse direction with deep pain perception returning first, followed by superficial pain, voluntary motor control, and proprioception. Therefore, increasingly severe clinical signs occur in the following order: spinal pain, ataxia, paresis, paralysis, and loss of deep pain sensation. The ability to perceive superficial pain is typically lost at the same time that voluntary motor control is lost. Ataxia is the loss of coordination and is characterized by a broad-based stance and incoordination of the trunk or limbs in IVDD. Clinically, we may see crossing over of the limbs when walking or an over-reaching gait. Postural reactions may be diminished or absent with an ataxic animal. Paresis (weakness) and paralysis are measures of an animal’s voluntary motor ability. Gradation is arbitrary and may be characterized as mild, moderate, or severe. It is more helpful to describe if the animal can support weight or advance the limbs. The last modality lost is the perception of deep pain. An animal that has lost deep pain perception has a guarded prognosis and for the best possible outcome should be considered an emergency surgical candidate. Deep pain sensation is cerebral recognition of the painful stimuli and is different from the flexor reflex. An animal with no deep pain may retract their leg, but does not cry out, attempt to bite the examiner, or move away from the stimuli.


Diagnosis of intervertebral disc disease is based on the clinical presentation, history, and ultimately, the imaging findings. Survey radiography, myelography (contrast-assisted radiographs where a radiological contrast agent – dye – is injected into the spinal fluid to permit visualization of the otherwise radiographically invisible spinal cord on x-rays), contrast-assisted computed axial tomography (CAT Scans), and magnetic resonance imaging (MRI) are utilized to diagnose intervertebral disk disease and accurately localize the compressive spinal cord lesion. Radiographic findings suggestive of IVDD include collapse or wedging of the intervertebral disk, deformities of the intervertebral foramina, and the presence of radiopaque material in or around the spinal canal.  While routine spinal radiographs may give us the suspicion of disk disease, the spinal cord and canal are not adequately visualized and significant spinal cord compression and injury are not identified in the majority of cases. The most accurate methods of diagnosis of spinal cord compression caused by IVDD require imaging of the spinal cord with myelography, computed tomography (CT), or magnetic resonance imaging (MRI). All of these methods require general anesthesia.

Intervertebral Disc Disease


Neurological grading in canine IVDD is valuable to follow the progression of neurological deficits in time (improvement or worsening), to choose the mode of therapy, for prognosis, and for assessment of outcome after medical or surgical treatment.


  • Grade 5: normal.
  • Grade 4: cervical or thoracolumbar pain, hyperaesthesia.
  •  Grade 3: paresis (muscle weakness) with decreased proprioception, ambulatory (able to walk).
  •  Grade 2: severe paresis with absent proprioception, not ambulatory (not able to walk).
  • Grade 1: paralysis (not able to stand or walk), decreased or no bladder control, conscious deep pain perception present.
  • Grade 0: paralysis, urinary and fecal incontinence, no deep conscious pain perception.

There is a diversity of opinion regarding treatment options for dogs with IVDD, but general guidelines can be used for selecting therapy. Decisions regarding when and if surgical versus medical treatment for the spinal compressive disease is indicated depend primarily upon the severity of the neurological signs and the chronicity of the problem. In addition, treatment is modified in relation to the presumptive diagnosis, owner finances, and concomitant medical problems.

Patients with pain only (Grade 4) or pain with minimal neurologic deficits (Grade 3) can often be managed conservatively. It should be mentioned, however, that improper management of the dog with spinal pain with or without minimal neurologic deficits may result in the progression of clinical signs and a worse overall prognosis.

Ideally, any significant spinal cord compression (Grade 2-0) should be relieved surgically. While medications and time may improve the animal’s comfort and neurological function, compression on the spinal cord of these magnitudes most likely will remain and result in continued spinal cord injury and prevent complete return to normal function.  Removal of the extruded nuclear material and hemorrhage crushing the spinal cord is necessary to allow for revascularization, removal of toxic by-products within the spinal cord, and resolution of swelling or edema. Decompression is based upon the location of the extruded nuclear material and hemorrhage based upon myelographic, CT, or MRI findings. For the majority of dogs, if done early, surgery will result in a good to excellent outcome. The outcome for decompression of spinal cords that have been compressed for months to years becomes more difficult to predict. Some factors that will affect the outcome are irreversible spinal cord injury (from acute concussion or chronic compression), the animal’s overall health, and whether there are multiple levels of disk extrusion with spinal cord compression.

Proper medical therapy for the IVDD patient includes cage rest, non steroidal anti-inflammatory therapy ( deramax, metacam, rimadyl), corticosteroid therapy (dexamethasone sodium phosphate, solu medrol, prednisolone), muscle relaxants (robaxin), pain management (fentanyl patches, oxymorphone, buprenex, gabapentin, tramadol), and gastrointestinal protectants (fametodine, zantac, pepcid, tagamet). Non-steroidal and steroidal anti-inflammatory therapy should not be combined in the same treatment plan because of the increased risk of gastrointestinal ulceration. While some may consider corticosteroid therapy controversial in treating intervertebral disk disease, my personal opinion, based on over 20 years of experience as a board certified surgeon, is to give steroids. Used intelligently and judiciously, my experience is that steroids have absolutely had a positive effect on a substantial number of our spinal patients.

While physical therapy and massage therapy probably will not prevent IVDD disease, they are very useful in helping patients recover from spinal cord injury. In fact, these methods may be as important as any other factor in ensuring maximal recovery. In cases where surgery is not performed, physical therapy and massage therapy must be limited to the least aggressive methods. Massage therapy improves muscle and joint flexibility, increases blood supply (improving nutrient delivery and waste removal), and help prevent or breakdown scar tissue formation. It also helps relax muscle spasms and aids in patient comfort levels. Massage therapy for animals should be performed by massage therapist trained in animal behavior and anatomy, under the supervision of your veterinarian. Many of the basic principles can be learned by the owner under proper instruction. While acupuncture cannot prevent IVDD disease and should be used with the same caution as relieving pain by conventional measures, acupuncture provides many beneficial effects in treating IVDD disease or following surgical correction during the healing process. Acupuncture is widely accepted as a method to provide analgesia without the side-effects of drugs. More recently, Class IV laser therapy may be employed in the multi-modal approach for those patients managed medically as well as surgically.

The medically managed patient must be observed frequently for deterioration of neurologic signs. Client education is an important component of the medical management regime. The client should be informed of the severity of the disease and of the fact that the signs may suddenly become progressively worse in which case surgical therapy is indicated. Recurrent episodes are frequent and are commonly more severe than the previous one. Recurrence of clinical signs after non-surgical treatment occurs in 40% of patients. Overall recovery in dogs with grade 3-4 deficits is 80% to 90%. Paraplegic dogs with grade 2-0 deficits non-surgical treatment is rarely the treatment of choice because of the low response rate, high rate of recurrence, neurological worsening during treatment, and development of complications. In dogs with grade 0 neurological deficits, the duration of absence of conscious deep pain sensation is an important prognostic parameter. Dogs with grade 0 neurological deficits should be regarded as emergencies and require surgery within 12-24 hours. When grade 0 neurological deficits persist beyond 24-48 hours the result of any treatment (surgical or nonsurgical) becomes minimal. Medical management has been shown to be as ineffective as surgical therapy in the majority of patients with sensorimotor paralysis for more than 24-48 hours. However, some clients do not consider euthanasia as an immediate alternative in these cases and may request some form of therapy.

The surgical approach taken to appropriately decompress the spinal cord is determined by the location of the herniated disc material within the spinal canal and the exact intervertebral disc space affected. In the cervical or neck region, a ventral or anterior approach is favored. The dorsal or posterior approach procedures are sometimes necessary; however, excessive muscle hemorrhage, increased surgery time, the difficulty of removing disk material from the ventral spinal canal, and prolonged postoperative care make this approach undesirable as a routine procedure. The ventral approach is less traumatic and requires less surgery time. The ventral-slot technique allows direct access to the extruded disk material and direct visualization of the affected spinal cord. The major disadvantage of the ventral-slot technique is the potential for hemorrhage associated with laceration of the venous sinuses.

Dorsolateral hemilaminectomy is the most common surgical treatment for thoracolumbar disc disease.

Hemilaminectomy best preserves the mechanical and structural integrity of the spine while allowing for excellent access and decompression. Dorsal laminectomy is not recommended in the thoracolumbar area because it causes considerable biomechanical instability and may lead to neurological worsening. In the lower lumbar area (L7-S1), however, dorsal decompressive laminectomy is the procedure of choice.

In addition to surgically decompressing the spinal cord to allow for spinal cord recovery, preventing further extrusions by the removal of the nucleus from the offending disk and other discs which can rupture is sometimes performed in breeds with a high incidence of repeat disc extrusions. This procedure is termed a fenestration. It is not a risk free procedure and in some cases can exacerbate the already existing clinical signs of spinal cord disease. It is also not a guarantee that the prophylactically fenestrated discs will not herniate at a later date as up to 20% of nucleus may be missed with this procedure. For these reasons, it is not commonly performed at our facility. Patients that are grades 2-0 are considered immediate surgical candidates. Grade 3-4 animals that have surgery performed within 48 hours have an excellent recovery rate to useful limb function (95%). Grade 0 animals (lose the perception of deep pain) that are operated on within 12-24 hours still have a fair to good prognosis for recovery (80-90%). If an animal has lost deep pain for more than 48 hours, a guarded prognosis should be given to the owner although one recent review indicated a 50% recovery rate.

The syndrome of myelomalacia is an important consideration in prognosticating the outcome of spinal trauma. Durotomy is performed when either an edematous spinal cord or discoloration suggestive of myelomalacia is present. Durotomy is ineffective as a method of treating compressive spinal cord trauma unless performed immediately (less than 2 hours) after the trauma has been suspected. Durotomy does, however, permit direct observation of the cord to see if myelomalacia is present. Myelomalacia occurs when severe, acute spinal cord trauma results in nearly complete destruction of nervous tissue. The cause and progression of myelomalacia is not completely understood, but the ischemia-reperfusion cascade results in lipid peroxidation and necrosis of myelin, and axons is suspected. Dogs with myelomalacia that have no deep pain perception and neurologic signs may progress cranial and caudal to the original injury. The typical clinical picture is an acute onset of paralysis with loss of deep pain followed by ascending and/or descending signs of neurologic dysfunction with ascending analgesia. Oftentimes, these patients are ill, febrile, and have extreme pain at the cranial edge of the lesion. Myelomalacia carries a hopeless prognosis.

Whether managed medically or surgically, paralyzed patients need to be maintained with excellent nursing care. Bladder management prevents urinary tract infections, overdistension, and urine scalding. The bladder needs to be expressed manually every 6-8 hours. If the bladder cannot be expressed, we recommend intermittent bladder catheterization using a sterile technique. Medication that assists with the ease of manual bladder expression include phenoxybenzamine and bethanacol,. These medications can be used together. Animals must also be maintained in a clean environment to prevent decubital ulceration (pressure sores). Frequent turning (every 4-6 hours) and proper bedding of sheepskin pads or foam “egg crate” bedding helps to lessen irritation. The skin needs to be closely monitored for the development of pressure sores as they are easier to prevent than reverse.

Postoperative recovery is often aided by the aforementioned medical therapy, controlled exercise and physiotherapy, acupuncture, and laser therapy afforded the medically managed patient. The best success rates combine medical therapy and surgical intervention. Functional improvement may be noted as early as 3-5 days following medical and surgical intervention. The continued gradual improvement over the following 4-6 weeks is expected. The prognosis for functional recovery is good for dogs with grade 2, 3, and 4 lesions irrespective of the treatment choice. Dogs with grade 1 lesions have better prognosis after surgical treatment than after nonsurgical treatment. In dogs with grade 0 lesions that are treated within 24-48 hours of onset, the animal has a chance of making a functional recovery.  Careful selection of surgical candidates should be based on the findings of a complete physical and neurologic examination, radiography, and specialized non-invasive diagnostic modalities (myelography, computed tomography, magnetic resonance imaging). In conclusion, the combination of medical and surgical therapy yields an optimal recovery.

MRI of Cervical Herniating Disc

MRI of Cervical Herniating Disc

MRI of Cervical Herniating Disc

MRI of Cervical Herniating Disc

MRI of Cervical Herniating Disc

MRI of Cervical Herniating Disc

Portosystemic Shunts

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Portosystemic Shunts

Portosystemic Shunts

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

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

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