Clinical outcome of congenital extrahepatic portosystemic shunt attenuation in dogs aged five years and older: 17 cases (1992-2005)

OBJECTIVE: To assess the outcome of extrahepatic portosystemic shunt (EHPSS) treatment in dogs aged 5 years and older. DESIGN: Retrospective case series. ANIMALS: 17 client-owned dogs. PROCEDURES: Medical records for dogs (> or = 5 years old) that underwent surgical attenuation of an EHPSS (1992 through 2005) were evaluated; data, including clinical signs, clinicopathologic findings, surgical procedure, and outcome, were recorded. Follow-up information was obtained via patient examination or telephone interview with veterinarians and owners. RESULTS: Dogs (5 to 9 years old [median age, 6.6 years]) had neurologic (n = 12), urinary tract (8), and gastrointestinal tract (6) EHPSS-associated clinical signs. Serum bile acids and ammonia concentrations were abnormal in all evaluated dogs. Treatment of EHPSSs included complete (n = 6 dogs) or partial (2) suture attenuation or ameroid constrictor placement (9). Two dogs died following surgery. Follow-up information (6 to 120 months) was available for 13 dogs. Deaths were attributable to heart failure (n = 1), bacterial hepatitis (2; with pyelonephritis in 1 dog), and unknown causes (3). At a median of 23 and 25 months, serum bile acids concentrations had almost normalized in 5 of 8 dogs and ammonia concentrations were within reference limits in 3 of 5 dogs, respectively; dogs with abnormal liver function test results had no associated clinical signs. Median long-term survival time was 72 months. CONCLUSIONS AND CLINICAL RELEVANCE: Attenuation of EHPSS in > or = 5-year-old dogs ameliorated signs of liver dysfunction in surviving dogs, although return of normal liver function occurred less frequently than expected.     

Use of zinc acetate to treat copper toxicosis in dogs.

Zinc acetate was used for the treatment and prophylaxis of hepatic copper toxicosis in 3 Bedlington Terriers and 3 West Highland White Terriers. Two dogs of each breed were treated for 2 years, and 1 of each breed for 1 year. A dosage of 200 mg of elemental zinc per day was required to achieve therapeutic objectives related to copper, which included a doubling of plasma zinc concentration to 200 micrograms/dl and a suppression of oral 64 copper absorption. The dosage was later reduced to 50 to 100 mg/day to avoid an excessive increase in plasma zinc concentration. The preliminary clinical results were good. Three dogs had mild to moderate active liver disease and high liver copper concentrations at the time of initiation of zinc administration. Biopsy of the liver 2 years later revealed a reduction in hepatitis and copper concentrations. One other dog without active hepatitis also had a reduction in hepatic copper concentrations over a 2-year period. All 6 dogs have done well clinically. On the basis of these findings, we believe zinc acetate to be an effective and nontoxic treatment for copper toxicosis in dogs.     

RADIATION PNEUMONITIS IN THREE DOGS

Radiation pneumonitis developed within the radiation treatment field in three dogs with soft tissue sarcomas located on or adjacent to the thoracic wall. Radiographic signs compatible with a diagnosis of radiation pneumonitis developed from one (n = 2 dogs) to two (n = 1 dog) months after completion of therapy. The initial radiographic sign was an alveolar infiltrate in all three dogs. At subsequent examinations at variable time periods after treatment, radiographic findings included: bronchiectasis (n = 3 dogs), alveolar infiltrate (n = 2 dogs), decreased lung volume (n = 2 dogs), and unstructured interstitial opacification (n = 1 dog). Necropsy examination of one dog at fourteen months after the completion of radiotherapy showed evidence of pulmonary fibrosis within the irradiated lung. Necropsy examination of the second dog did not show any evidence of radiation induced changes. It is possible that histopathologic examination did not include irradiated lung. No clinical signs that could be attributed to the radiation pneumonitis were observed in any dog. It appears that approximately 25% of the lung can be safely irradiated to high doses, if indicated, in order to deliver an adequate dose of radiation to a primary tumor site.     

Neurological Manifestations of Hypothyroidism: A Retrospective Study of 29 Dogs

Neuromuscular signs in association with hypothyroidism are described in 29 dogs. Eleven dogs had lower motor neuron signs, 9 had peripheral vestibular deficits, 4 had megaesophagus, and 5 had laryngeal paralysis. Primarily older (mean = 9.5 years), large-breed dogs were affected, and there was no sex or breed predisposition. Duration of clinical signs before presentation ranged from 2 to 8 weeks (mean = 5 weeks). The diagnosis was based on (1) results of neurological examination (29 dogs); (2) electromyographic abnormalities (18 dogs), including fibrillation potentials (n = 18), positive sharp waves (n = 15), and complex repetitive discharges (n = 4); (3) high serum cholesterol concentration (10 dogs; mean = 335 mg/dL); (4) low response to thyroid-stimulating hormone (29 dogs; mean T₄ prestimulation concentration = 0.8 μg/dL; mean T₄ poststimulation = 1.2 μg/dL); and (5) good response to thyroxine supplementation (26 dogs). Dogs with vestibular deficits had abnormal brainstem auditory-evoked responses (BAER), including increased latencies of P₁-P₆ and decreased amplitude of P_4,5-N₅. Seven other dogs had similar BAER abnormalities without manifesting clinical signs of vestibular involvement. Three dogs with vestibular signs had fibrillation potentials and positive sharp waves without exhibiting lower motor neuron signs. All dogs were supplemented with levothyroxine (0.02 mg/kg P0 bid). The follow-up period ranged between 6 and 30 months (mean, 14 months). Serum T₄ concentrations were measured at least 3 times for each dog every 2 months (mean T₄ concentration = 2.6 μg/dL). All but 1 dog with lower motor neuron signs and 1 dog with vestibular signs recovered after 2 months (mean, 57 days). Signs of megaesophagus became progressively less severe over 4 months. Dogs with laryngeal paralysis improved partially after 5 months. We suggest that either vestibular or lower motor neuron signs, megaesophagus, or laryngeal paralysis may be the only clinical signs of an underlying, more generalized polyneuropathy associated with hypothyroidism. Electro-diagnostic abnormalities may be detected before clinical disease develops.     

Association between liver copper concentration and subclinical hepatitis in Doberman Pinschers

The prevalence of subclinical hepatitis was investigated in a group of 106 randomly selected 3-year-old Doberman Pinschers. Histopathologic examination of liver samples from 65 dogs (52 dogs with high bile acids, alkaline phosphatase activity, or alanine aminotransferase activity or with copper granules in hepatocytes in a liver aspirate and 13 normal dogs) revealed subclinical hepatitis in 22 dogs (19 females and 3 males). Liver copper concentrations measured by instrumental neutron activation analysis was significantly higher (mean +/- SD; 419 +/- 414 microg/g dry matter) in dogs with hepatitis than those without liver disease (197 +/- 113 microg/g; P = .0008). At 2.6 +/- 0.6 years hepatitis persisted in 5 of 16 dogs available for examination. One dog with a high copper concentration but normal liver subsequently developed subclinical hepatitis after 3 years. During the follow-up period, the average copper concentration of the 6 dogs with persistent subclinical hepatitis was 939 +/- 299 microg/g and had continued to rise significantly (P = .02). The hepatitis in these dogs was associated with apoptotic hepatocytes and copper-laden Kupffer cells in centrolobular regions. The results of this study suggest that there is a relationship among copper storage, hepatocellular damage, and hepatitis in Doberman Pinschers.     

Clinical signs, clinicopathological findings, etiology, and outcome associated with hemoptysis in dogs: 36 cases (1990-1999)

Hemoptysis, the expectoration of blood or bloody mucus from the respiratory tract at or below the larynx, was retrospectively evaluated in 36 dogs. Cough, tachypnea, and dyspnea were common historical and physical examination signs. Anemia was documented in 11 dogs, but was severe in only one dog. Other clinicopathological findings reflected the underlying diseases. All thoracic radiographs obtained were abnormal; alveolar and interstitial patterns were most common. Diseases predisposing to hemoptysis included bacterial bronchopneumonia (n=7), neoplasia (n=5), trauma (n=5), immune-mediated thrombocytopenia (n=4), heartworm disease (n=4), rodenticide poisoning (n=3), lung-lobe torsion (n=1), left-sided congestive heart failure (n=1), pulmonary hypertension (n=1), and foreign-body pneumonia (n=1). Four additional dogs had more than one underlying disease process. Nine dogs were either euthanized or died in the hospital during the initial visit. While at least half of the 27 dogs discharged went on to completely recover, five dogs discharged were known to have either died or been euthanized as a result of their disease in <6 months.     

Ureterocolonic anastomosis in clinically normal dogs

Ureterocolonic anastomosis was evaluated in 13 clinically normal dogs. Urinary continence was maintained after surgery, and the procedure was completed without technique errors in all but 2 dogs. Three dogs died within 5 weeks (2 of undetermined causes and 1 of aspiration pneumonia and neurologic disease), and 1 dog was euthanatized 4 months after surgery because of neurologic signs. Two healthy dogs were euthanatized 3 months after surgery for light microscopic evaluation of their kidneys. Five dogs were euthanatized 6 months after surgery for light microscopic evaluation of their kidneys. Gastrointestinal and neurologic disturbances developed in 4 dogs at various postoperative intervals. Plasma ammonia concentration measured in 2 dogs with neurologic signs was increased. Plasma ammonia concentration measured in 5 dogs without neurologic signs was within normal limits. All 5 dogs, in which metabolic acidosis was diagnosed, had high normal or above normal serum chloride concentration. Serum urea nitrogen values were increased after surgery because of colonic absorption of urea. Serum creatinine concentration was increased in 1 dog 6 months after surgery. Individual kidney glomerular filtration rate was reduced in 38% (3/8) of the kidneys from 4 other dogs at 6 months after surgery. Of 5 dogs euthanatized at 3 to 4 months after surgery, 4 had bilateral pyelitis, and 1 had unilateral pyelonephritis. Six months after surgery, pyelonephritis was diagnosed in 40% (4/10) of the kidneys from 5 dogs. The ureterocolonic anastomosis procedure is a salvage procedure that should allow complete cystectomy. However, variable degrees of metabolic acidosis, hyperammonemia, and neurologic disease may result.     

Copper toxicosis in Bedlington Terriers in the United Kingdom

This paper summarizes the clinical and laboratory data on two adult Bedlington Terriers with liver disease associated with copper toxicosis. The younger dog, at 3 years, had elevated serum levels of alanine aminotransferase and alkaline phosphatase with active parenchymal cell degeneration and hepatitis. The second dog developed chronic hepatic failure at 5 years with advanced cirrhosis. Both dogs had stainable copper granules in the liver and chemical analysis of their livers revealed elevated copper contents (1,027 and 10,728 μg/g dry weight; normal less than 300 μg/g). These are the first published cases of this inherited abnormality of copper metabolism in this breed in this country.     

Visceral mast cell tumors in dogs: 10 cases (1982-1997)

OBJECTIVE: To characterize the clinical features of visceral mast cell tumors (MCT) without associated cutaneous involvement in dogs. DESIGN: Retrospective study. ANIMALS: 10 dogs with histologically confirmed MCT without associated cutaneous lesions. PROCEDURE: Information on signalment, clinical signs, laboratory examinations, and time from first admission to death was obtained from the medical record of each dog. RESULTS: Purebred male dogs of miniature breeds appeared to have a higher prevalence of visceral MCT. Clinical signs included anorexia, lethargy, vomiting, and diarrhea. Anemia (n = 7), hypoproteinemia (5), and mastocythemia (5) were detected. Treatments, including glucocorticoids, were not successful. Primary sites of tumors were the gastrointestinal tract (n = 6) and the spleen or liver (1); the primary site was not confirmed in the remaining 3 dogs. In 7 dogs, tumors were categorized as grade II or III, on the basis of histologic findings. The prognoses were poor, and all dogs died within 2 months after first admission. CONCLUSIONS AND CLINICAL RELEVANCE: Visceral MCT is uncommon in dogs, and the prognosis is extremely poor. Biological behavior and drug susceptibility of visceral MCT may be different from cutaneous MCT. The lack of specific clinical signs may result in delay of a definitive diagnosis. The rapid progression of clinical signs and difficulty in diagnosis contributes to a short survival time.     

Clinical, clinicopathologic, and parasitologic observations of trypanosomiasis in dogs infected with North American Trypanosoma cruzi isolates

Nineteen purebred Beagles of various ages (4, 5, 13, and 47 weeks) were inoculated with North American Trypanosoma cruzi isolates obtained from an opossum (Tc-O), an armadillo (Tc-A), or a dog (Tc-D). Dogs were grouped on the basis of clinical outcome of infection. During the acute stage of disease, dogs of group 1 (n = 7 inoculated with Tc-O or Tc-A) died or were euthanatized because of the severity of disease. Dogs of group 2 (n = 5 inoculated with Tc-O or Tc-A) developed acute disease, but survived to develop chronic disease. Dogs of group 3 (n = 7 Tc-D-inoculated dogs) developed neither acute nor chronic disease. Dogs of group 4 (n = 4--2 dogs 13 weeks old and 2 dogs 47 weeks old) served as noninoculated controls. Clinical signs associated with severe acute myocarditis developed in dogs of groups 1 and 2 between postinoculation day (PID) 15 and 28. Generalized lymphadenopathy and lymphocytosis were observed in all dogs of groups 1, 2, and 3 between PID 14 and 17. Serum alanine transaminase and aspartate transaminase activities and urea nitrogen concentration were high, and glucose concentration was low prior to death of dogs in group 1. Serum activities of isoenzymes of creatine kinase were significantly (P less than 0.05) high in only 1 dog (group 1), whereas serum lactate dehydrogenase isoenzyme activities were not significantly high in any dog.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gallbladder disease in Shetland Sheepdogs: 38 cases (1995-2005)

OBJECTIVE: To determine risk, clinical features, and treatment responses for gallbladder disorders in Shetland Sheepdogs. DESIGN: Retrospective case-control study. ANIMALS: 38 Shetland Sheepdogs with gallbladder disease. PROCEDURES: Medical records were reviewed for signalment, history, physical findings, laboratory results, imaging features, coexistent illnesses, histologic findings, treatments, and survival rates. RESULTS: Mature dogs with gastrointestinal signs were predisposed (odds ratio, 7.2) to gallbladder disorders. Gallbladder mucocele was confirmed in 25 dogs. Concurrent problems included pancreatitis, hyperlipidemia, corticosteroid excess, hypothyroidism, protein-losing nephropathy, diabetes mellitus, cholelithiasis, and gallbladder dysmotility. Mortality rate was 68% with and 32% without bile peritonitis. Nonsurvivors had high WBC and neutrophil count and low potassium concentration. Although preprandial hypercholesterolemia, hypertriglyceridemia, and high serum liver enzyme activities were common, gallbladder disease was serendipitously discovered in 11 of 38 dogs. Histologic examination (n=20 dogs) revealed gallbladder cystic mucosal hyperplasia in 20 dogs, cholecystitis in 16, periportal hepatitis in 9, and vacuolar hepatopathy in 7. Surgery included cholecystectomy (n=17) and cholecystoenterostomy (4). In 1 hyperlipidemic dog without clinical signs, gallbladder mucocele resolved 6 months after beginning use of a fat-restricted diet and ursodeoxycholic acid. CONCLUSIONS AND CLINICAL RELEVANCE: Shetland Sheepdogs are predisposed to gallbladder disorders, with mucoceles and concurrent dyslipidemia or dysmotility in many affected dogs. Most dogs were without clinical signs during mucocele development. Low survival rate after cholecystectomy in clinically affected dogs suggested that preemptive surgical interventions may be a more appropriate treatment strategy.     

Results of thoracic duct ligation in dogs with chylothorax

Thoracic duct lymphangiography and ligation were done on 15 dogs with idiopathic chylothorax. Lymphangiography revealed thoracic lymphangiectasia in all dogs; none had a thoracic duct rupture. Lymphangiography immediately after ligation demonstrated missed branches of the thoracic duct in 4 of the 15 dogs. Eleven of the 15 dogs are alive and doing well. Eight of the 11 had no radiographic or clinical signs of pleural effusion (mean follow-up, 31.5 months; range, 4 to 75 months). The other 3 living dogs had persistent effusion; 2 were successfully managed with a pleuroperitoneal shunt (follow-up, 15 months) or pleurodesis (follow-up, 5 months), respectively, and 1 was not treated because the effusion was mild and the dog did not have clinical signs of disease (follow-up, 14 months). Four of the 15 dogs died or were euthanatized because of persistent effusion (mean follow-up, 11.5 months; range, 3 to 24 months). Considering the lack of treatment alternatives for dogs with idiopathic chylothorax, these results support thoracic duct ligation as a treatment method for dogs.     

Plasma L-carnitine concentration in healthy dogs and dogs with hepatopathy

BACKGROUND: L-Carnitine has an essential role in lipid metabolism. Disturbances of L-carnitine metabolism can influence the energy supply of the organism. L-Carnitine is synthesized exclusively in the liver. Hence, we hypothesized that liver disease can influence L-carnitine metabolism. OBJECTIVES: The goal of this study was to compare plasma L-carnitine concentrations in dogs with different liver diseases of differing severity with the plasma L-carnitine concentrations of healthy dogs. METHODS: Sixteen dogs with inflammatory liver disease and 12 dogs with liver neoplasia were included in the study. Liver disease was diagnosed by clinical chemistry, ultrasonography, and histology of liver biopsy specimens. L-Carnitine concentration was measured in plasma samples using mass spectrometry, and compared among groups using unpaired Student's t-tests. RESULTS: Compared with healthy controls (24.4 +/- 8.4 micromol/L), the plasma L-carnitine concentration in dogs with liver disease (44.2 +/- 23.7 micromol/L) was significantly higher (P<.0001). The difference in L-carnitine concentration between dogs with moderate (n=8; 33.6 +/- 13.7 micromol/L) and severe (n=8; 57.4 +/- 22.9 micromol/L) hepatitis was also significant (P=.02). No difference in plasma L-carnitine concentration was found between dogs with hepatitis and those with liver tumors. CONCLUSIONS: Liver disease in dogs was accompanied by elevated plasma L-carnitine concentration. The severity of hepatitis appears to influence L-carnitine concentration.     

Signs consistent with syringobulbia may be detected in dogs undergoing MRI

Syringobulbia is a pathologic condition characterized by one or more fluid‐filled cavities within the brainstem. This retrospective case series describes observations in eight dogs with syringobulbia diagnosed during MRI. All dogs were adult, small‐breed dogs with concurrent syringomyelia and neurologic deficits localized to sites rostral to the spinal cord, which cannot be explained by syringomyelia (eg, six dogs had vestibular signs). On MRI, the fluid‐filled cavities had signal intensity characteristics like cerebrospinal fluid, were in the medulla oblongata, and were solitary in each dog. Initially, the shape of the cavity was a slit in five dogs and bulbous in two dogs. Magnetic resonance imaging was repeated in five dogs (6‐55 months of age). One dog had progression of syringobulbia from slit‐like to bulbous, and four dogs had unchanged slit‐like syringobulbia. One dog developed slit‐like syringobulbia after cranioplasty. A variety of medical and surgical treatments were performed with improvement of some but not all clinical signs. One dog died following surgery due to cardiopulmonary failure and the other seven dogs were alive at least 1 year after the initial diagnosis, which was the least time of follow‐up. One surviving dog developed a unilateral hypoglossal nerve deficit 2 months after the initial diagnosis and megaesophagus 14 months later. In conclusion, detecting a fluid‐filled cavity in the medulla oblongata consistent with syringobulbia is possible in dogs undergoing MRI. The cavity is likely acquired, slit‐like or bulbous, progressive, or static, and might be associated with breed size and neurologic signs localized to the medulla oblongata.     

A method for intervertebral space distraction before stabilization combined with complete ventral slot for treatment of disc-associated wobbler syndrome in dogs

Objective— To evaluate the use of a modified K-wire spacer for maintaining intervertebral distraction after ventral decompression and during stabilization as a treatment for disc-associated wobbler syndrome in large breed dogs.
Study Design— A retrospective study.
Animals— Dogs (n=7) with disc-associated wobbler syndrome.
Methods— Medical records (2003–2006) of dogs treated by a modified surgical method were evaluated. Data retrieved were signalment, onset and duration of clinical signs, neurologic abnormalities, diagnostic methods, surgical procedure, immediate, and long-term (≥1 year) postoperative clinical and radiographic outcome.
Results— Mean duration of clinical signs was 4.8 months. Neurologic signs included ataxia (2), ambulatory tetraparesis (2), and non-ambulatory tetraparesis (3). Three dogs had disc protrusion in 2 sites, 2 dogs had the procedure in 1 location and stabilization of both affected sites. All dogs improved dramatically and remained for 1–3 years. One dog had recurrence of cervical discomfort 13 months later.
Conclusions— Despite the limited number of dogs, overall initial successful outcome with only 1 dog having mild recurrence 13 months later supports further use and evaluation of this technique.
Clinical Relevance— Distraction using a K-wire spacer after ventral decompression followed by stabilization should be considered in dogs with disc-associated wobbler syndrome to prevent collapse of the intervertebral space.     

Results of the Multicenter Spaniel Trial (MUST): Taurine-and Carnitine-Responsive Dilated Cardiomyopathy in American Cocker Spaniels With Decreased Plasma Taurine Concentration

Fourteen American Cocker Spaniels (ACS) with dilated cardiomyopathy (DCM) were studied to determine if individuals of this breed with DCM are systemically taurine-or carnitine-deficient and to determine if they are responsive to taurine and carnitine supplementation. American Cocker Spaniels with DCM were identified using echocardiography, and plasma was analyzed for taurine and carnitine concentrations. Each dog was randomly assigned to receive either taurine and carnitine supplementation or placebos. Echocardiograms and clinical examinations were repeated monthly for 4 months. During this period, the investigators and owners were blinded with respect to the treatment being administered. Each dog was weaned off its cardiovascular drugs (furosemide, digoxin, and an angiotensin converting enzyme inhibitor) if an echocardio-graphic response was identified. At the 4-month time period, each investigator was asked to decide whether he or she thought his or her patient was receiving placebo or taurine/ carnitine, based on presence or absence of clinical and echocar-diographic improvement. Unblinding then occurred, and dogs receiving placebos were switched to taurine and carnitine supplementation and followed monthly for 4 additional months. All dogs were reexamined 6 months after starting supplementation; survival time and cause of death were recorded for each dog. Data from 3 dogs were not included because of multiple protocol violations. Each dog had a plasma taurine concentration <50 nmol/mL (mean ±SD for the group 15 ± 17 nmol/ mL) at baseline; normal range, 50–180 nmol/mL. The plasma taurine concentration did not exceed 50 nmol/mL at any time in the dogs receiving placebos (n = 5), but increased to 357 ± 157 nmol/mL (range 140–621 nmol/mL) during taurine and carnitine supplementation (n = 11). Plasma carnitine concentration was within, only slightly below, or slightly above reported limits of normality at baseline (29 ± 15 μmol/L); did not change during placebo administration; and increased significantly during supplementation (349 ±119 μmol/L; n = 11). Echocardiographic variables did not change during placebo administration. During supplementation, left ventricular end-dia-stolic and end-systolic diameters, and mitral valve E point-to-septal separation decreased significantly in both groups. Shortening fraction increased significantly but not into the normal range. Echocardiographic variables remained improved at 6 months. All dogs were successfully weaned off furosemide, an angiotensin converting enzyme inhibitor, and digoxin once an echocardiographic response was identified. Nine of the dogs have died since the onset of the study in 1992. One dog died of recurrence of DCM and heart failure 31 months after starting supplementation; six dogs died of noncardiac causes. Two dogs developed degenerative mitral valve disease and died of complications of this disease. Dogs less than 10 years of age lived for 46 ± 11 months, whereas dogs older than 10 years of age lived for 14 ± 7 months. Two of the 11 dogs were alive at the time of publication, having survived for 3.5 and 4.5 years, respectively. We conclude that ACS with DCM are taurine-deficient and are responsive to taurine and carnitine supplementation. Whereas myocardial function did not return to normal in most dogs, it did improve enough to allow discontinuation of cardiovascular drug therapy and to maintain a normal quality of life for months to years.     

Dietary Management of Hepatic Copper Accumulation in Labrador Retrievers

Background: Copper-associated chronic hepatitis (CACH) recently has been recognized in the Labrador Retriever as an inherited disorder with a late onset of clinical signs. No studies have investigated dietary management for the long-term treatment of this disease or for its potential in delaying the onset of clinical signs in subclinical cases.
Objectives: To investigate the effects of a low-copper diet and zinc gluconate on hepatic copper concentrations in Labrador Retrievers with abnormal hepatic copper concentrations.
Animals: Twenty-four client-owned Labradors that were related to patients affected with CACH and that had been diagnosed with increased hepatic copper concentrations.
Methods: Hepatic copper concentrations were assessed before and after an average of 8 and 16 months of treatment. During this time, all dogs were fed exclusively a low-copper diet. In addition, dogs were assigned to 1 of 2 groups in a randomized double-blind manner to receive a supplement of zinc gluconate or placebo.
Results: Twenty-one dogs completed the study. Hepatic copper concentrations decreased in both groups at recheck 1 (n = 21; group 1, P < .001; group 2, P = .001) and at recheck 2 (n= 16; group 1, P = .03; group 2, P = .04). No difference in hepatic copper concentrations was found between the 2 groups before treatment ( P = .65), at recheck 1 or at recheck 2 ( P = .52–.79).
Conclusions and Clinical Relevance: Feeding low-copper diets to Labradors is effective in decreasing hepatic copper concentrations. Adjunctive treatment with zinc does not appear to increase the copper-lowering effects of dietary management.     

Surgical management of left-divisional intrahepatic portosystemic shunts: outcome after partial ligation of, or ameroid ring constrictor placement on, the left hepatic vein in twenty-eight dogs (1995-2005)

OBJECTIVES: To evaluate outcome in dogs with left divisional intrahepatic portosystemic shunts (PSS) treated by partial ligation (PL) or ameroid ring constrictor (ARC) placement on the left hepatic vein. DESIGN: Retrospective study. ANIMALS: Dogs (n=28) with left divisional intrahepatic PSS. METHODS: Retrieved data from medical records of dogs with left divisional intrahepatic PSS that had PL (n=17) or ARC (n=11) were signalment, history, clinical signs, preoperative blood work, portal pressure measurements, ARC size, complications and postoperative technetium scintigraphy. Outcome assessed by owner interview 6 months-10 years after surgery was classified as excellent, good or poor. Differences were tested by exact chi2 test. RESULTS: Major complications occurred in 3 dogs: coagulopathy (1 PL dog died), ascites (1 PL dog survived) and seizures (1 ARC dog died). Eight PL dogs had technetium portal scintigraphy; 1 dog was negative and 7 dogs positive for persistent shunting. Seven ARC dogs had scintigraphy; 4 dogs were negative and 3 positive for persistent shunting. In PL dogs, long-term clinical outcome was excellent (92%) or good (8%) whereas, in ARC dogs it was excellent (20%), good (50%) or poor (30%). This outcome difference between treatment groups was significant (P=.0012). CONCLUSION: Dogs treated by PL had significantly better long-term outcome compared with ARC treated dogs. CLINICAL RELEVANCE: Based on these data, ARC placement on the left hepatic vein in dogs with left-divisional intrahepatic PSS cannot be recommended.     

Improvement in liver pathology after 4 months of D-penicillamine in 5 doberman pinschers with subclinical hepatitis

Five female Doberman Pinschers with increased hepatic copper concentrations and persistent (3-4 years) subclinical hepatitis were treated with D-penicillamine for 4 months. Before and after treatment, the dogs underwent clinical, hematologic (red blood cell, white blood cell, and differential and thrombocyte counts), and clinical chemistry (creatinine, alkaline phosphatase, alanine aminotransferase, and total bile acid concentrations) examinations, and liver biopsies were examined histologically and their copper content measured quantitatively. No adverse effects were observed during treatment, and CBC and serum chemistry test results did not change. The mean liver copper concentration was 1,036 mg/kg dry matter before treatment and decreased to 407 mg/kg after treatment (P = .03). The copper concentrations had decreased (by between 134 and 1,135 mg/kg dry matter) in all of the dogs. The histopathologic appearance had improved or returned to normal in all 5 dogs. We conclude that D-penicillamine effectively reduced copper retention in these dogs and improved the histopathologic appearance of the lesions. However, because D-penicillamine has both copper-chelating and anti-inflammatory properties, it is not possible to draw conclusions on the etiology of this disease.     

Neurologic abnormalities as the predominant signs of neoplasia of the nasal cavity in dogs and cats: seven cases (1973-1986)

Neurologic abnormalities were the predominant historic and physical findings in 5 dogs and 2 cats with primary nasal cavity tumors that had invaded the cranial vault. Seizures, behavior changes, and obtundation were the most common signs. Other neurologic signs included paresis, ataxia, circling, visual deficit, and proprioceptive deficit. Although 1 dog and 2 cats had historic findings of mild respiratory disease, no physical abnormalities related to the respiratory tract were found in any of the 7 animals. Nasal cavity neoplasia was suggested by radiographic and computed tomographic studies and was confirmed histopathologically in each case. The nasal tumor types in the 5 dogs were epidermoid carcinoma (n = 1), adenocarcinoma (n = 2), solid carcinoma (n = 1), and anaplastic chondrosarcoma (n = 1). An esthesioneuroblastoma was found in each cat. Radiation therapy was effective for 3 months in palliating the clinical signs in the 2 dogs in which it was used. Neoplasia of the nasal cavity should be considered in the differential diagnosis for animals with neurologic signs suggestive of cerebral disorders.