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Medical treatment of acute spinal cord injury in the dog has traditionally involved use of intravenous corticosteroids. Dexamethasone sodium phosphate use has been replaced by the use of methyl prednisolone sodium succinate (MPSS; Solu Medrol) as the current standard of care in treatment of acute spinal cord injury in the dog. Recently, the benefits versus risks of MPSS have come into question in both human and veterinary medicine. A new development which shows promise in treatment of acute spinal cord injury is polyethylene glycol (PEG).
Polyethylene glycol and related polymers found initial use in the development of monoclonal antibodies by virtue of their ability to fuse cell membranes. It is this feature, the fusion of "leaky" cell membranes, which has led to their use and benefit in spinal cord injury. In injured spinal cord cells, it the loss of membrane stability and unregulated entry of calcium (and potassium) into the cytosol that seems to be the initiating, primary event in the subsequent progressive dissolution of the axon.
Application of PEG directly to the spinal cord of acutely injured guinea pigs has been show to lead to rapid and complete recovery of spinal cord function (Borgens RB, Shi R. FASEB J, 2000:14; 27-35). In that study, PEG was initially applied to the spinal cord within 15 minutes of the compressive injury used to create complete sensory loss caudal to the lesion. Approximately 80% of the treated animals recovered whereas ~ 85% of the sham-treated group did not recover. In a second experiment, PEG was applied to the spinal cord approximately 8 hours after injury. In that group, 90% of treated animals recovered as measured by cutaneous trunci muscle skin response.
PEG and another related polymer have also been used intravenously with promising results (Laverty, et al. J NEUROTRAMA, 2004:21;1767-1777). Dogs with complete hindlimb paraplegia were admitted to a study where PEG was administered intravenously within 72 hours of loss of deep pain sensation. In this study, initial treatment involved i.v. PEG on admission and at 4 to 5 hours. All dogs underwent myelography and decompressive surgery. PEG treated dogs exhibited improved, early return of neurological function as compared to historical results in dogs with similar neurological deficits and lesions. By the end of this study (6 to 8 weeks), 68% of the PEG treated dogs were ambulatory. Results must be interpreted in light of the multiple modalities used; all dogs were also administered MPSS (Solu Medrol) at a dose of 30 mg/kg and underwent surgical decompression.
Experimentally at least, treatment of spinal cord injury with PEG appears to show significant promise. Results in the above referenced group of dogs are especially encouraging in that all of these dogs had loss of deep pain for a duration of up to 72 hours prior to intervention.
We are currently participating in a clinical trial with PEG. Please call if you would like additional information.
Perineal hernia occurs when there is a breakdown involving the muscles of the pelvic diaphragm. This allows the rectum to deviate into the perineal space lateral to the anus, and can lead to clinical signs of tenesmus, chronic constipation, and visible swelling ventrolateral to the anus. Occasionally, dysuria or anuria may be noted if the urinary bladder retroflexes into the hernia sac, distends and becomes entrapped.
Most cases of perineal hernia occur in middle aged to older male dogs from 6 to 14 years of age, with a peak incidence in the 7 to 9 year old age group. It is felt there are several factors which may predispose this group of dogs to developing hernias. Progressive atrophy of the muscles of the pelvic diaphragm, especially the levator ani, occurs in some dogs. Certain breeds are more prone than others to developing perineal hernias. Boston terriers, Pekingese, Boxers and Collies all seem to have an increased risk. The role of hormones, particularly testosterone, has been the subject of much study, as most perineal hernias occur in the intact male dog. Other factors thought to influence development of perineal hernia include prostatic disease, chronic constipation and tenesmus, and concurrent rectal disease.
Diagnosis is relatively straightforward in most cases. A visible bulge noted lateral to the anus which is usually fairly soft and fluctuant may be described by the owner as varying in size, some days appearing larger than others. Rectal palpation usually confirms the presence of a hernia - the area lateral to the rectum will palpate as very "thin". The index finger placed in the rectum can be felt readily adjacent to the thumb outside the rectum, as it is within the hernia sac and there is no muscle interposed between the two fingers. If the hernia is unilateral (about 2/3 of cases), the opposite side should also be palpated for comparison. For unknown reasons, unilateral hernias are often right-sided.
Radiographs are occasionally helpful. The lateral view should include the caudal abdomen and this should be examined to identify the location of the urinary bladder. If it cannot be determined that the bladder is within the abdomen, it may be within the hernia sac. Entrapment of the bladder can become life-threatening. A cystogram can confirm exact location of the bladder.
Since many patients are older, a complete work-up including serum chemistries should be done prior to surgical correction. Underlying abnormalities can be identified and either corrected, or compensated for in the anesthetic used.
Surgical fixation of the hernia in most cases is an elective rather than an emergency procedure. Urinary bladder entrapment within the hernia should be considered an emergency, and either immediate surgery done, or the bladder evacuated via catheter or cystocentesis pending herniorrhaphy. Two techniques for fixation are commonly used in my practice for repair of the hernia(s). My preference is to transpose a "normal" muscle into the hernia defect in order to restore structural integrity to the pelvic diaphragm. The internal obturator muscle is utilized after elevating it from the pelvic floor, transposing it into the defect and suturing it in place using monofilament absorbable sutures. Closure of the most dorsal aspect of the defect as well as the most ventral and medial part is sometimes difficult with this technique, and careful attention to suture placement as well as avoiding excessive tension on the repair is important. A suture method for apposing the muscles of the pelvic diaphragm can also be used, however; recurrence rates are higher than with the internal obturator muscle flap technique. Recurrence rates in general range from 5% to 45%.
Concurrent castration is recommended in males despite the ambiguous role of testosterone in development of hernias. Shrinking of the prostate gland post-castration is thought to be beneficial in preventing recurrence also.
Please contact our office if you need additional information about perineal hernias.
Portosystemic shunts are vascular abnormalities which allow portal blood draining the intestines, pancreas, stomach and spleen to bypass the liver and enter the systemic circulation directly. This blood containing the byproducts of digestion which are normally metabolized in the liver (bile acids, ammonia, mercaptans, etc.) produces the clinical symptoms commonly referred to as hepatic encephalopathy.
The abnormal flow of blood around the liver may be caused by a single vessel bypassing the hepatic portal system, or by multiple vessels. Single vessels are usually congenital shunts, while multiple vessels are usually acquired shunts secondary to liver disease. The congenital, single shunts are further divided into extra-hepatic shunts and intra-hepatic shunts.
Extra-hepatic shunts are usually seen in small breeds (Yorkie, Min. Schnauzer, Poodle and Dachshund). Intra-hepatic shunts occur primarily in large breed dogs (German Shepherd, Golden Retriever, Doberman, Labrador, Irish Setter, Samoyed, Irish Wolfhound). Cats may be either extra- or intra-hepatic.
Clinical signs of hepatic encephalopathy should prompt a suspicion of a portocaval shunt, especially when noted in dogs less than a year of age. Typical signs are depression and lethargy, frequent persistent vomiting or diarrhea, changes in behavior (aggression, hysteria), hypersalivation (nausea), seizures or visual disturbances. Typically, symptoms are noted to be worse after the dog has been fed and digested a meal.
Diagnosis of a shunt is primarily by direct surgical observation of the shunt. Suspicion of a shunt, and the need for surgery, should be based not only upon clinical signs, but also upon laboratory testing documenting diminished liver function. The most common test performed is measurement of serum bile acids. Bile acids are very efficiently removed from the portal circulation in the normal animal. In the presence of a shunt, serum bile acids are markedly elevated. Basic protocol for bile acid testing is to obtain a fasted blood sample, feed a high protein meal and then obtain a post-prandial sample at 2 hours. Most cases in which there is a shunt will have a ten-fold increase in post prandial serum bile acids over normal fasting values (N - 2.3 umol/L). Resting (fasting) values are also elevated in shunt dogs. Normals for your lab should be referred to in interpreting bile acids.
Some animals may be managed conservatively for a variable period of time with a shunt. Low protein diets, lactulose, and metronidazole are all used to inhibit the production and absorption of ammonia from the gut.
Surgical management is aimed at restoring normal hepatic blood flow. The goal of surgery is to identify and ligate the abnormal vessel which is draining the portal blood directly into the vena cava. These vessels can be found in a myriad of locations, but typically occur with regularity in defined locations. An abdominal exploratory surgery is done and the portal blood system evaluated for abnormal vessels draining into the vena cava. Many are noted draining blood from the left gastric and splenic vein region into the vena cava. A large vessel which enters the vena cava cranial to the renal veins is considered abnormal.
Methods of shunt ligation have evolved from ligation of the shunt while directly measuring portal pressure. Since it is important to avoid a sudden, acute rise in portal pressure, as can occur when the abnormal vessel is suddenly ligated, methods for gradual occlusion over time have been developed. Today, most surgeons place either an ameroid constrictor or a cellophane band around the shunt. Both slowly occlude the shunt over time (weeks).
Success is good with single, extra-hepatic shunts managed surgically if the dog survives the immediate postop period. Problems after surgery can be severe and close monitoring of the patient is required. In one study, there was a 14% mortality rate after application of an ameroid constrictor.
Please contact us if you have questions about a portosystemic shunt case.