Dysplasia of the tricuspid valve in the dog and cat.

Dysplasia of the tricuspid valve in 14 dogs and 13 cats was studied. The clinical, electrocardiographic, radiographic, hemodynamic, angiocardiographic, and pathologic findings were reviewed in each species. Alterations of the tricuspid valve complex included long, thick septal leaflets adhered to the septum; absent or short, stout fused chordae tendineae; hypertrophic fused papillary muscles; insertion of papillary muscles directly into the lateral leaflets; incomplete development of the valvular tissue; and enlargement of the right atrium and ventricle. Additional intracardiac anomalies included malformation of the mitral valve complex (5 dogs and 3 cats), ventricular septal defect (3 dogs and 3 cats), pulmonary stenosis (1 dog and 1 cat), aortic stenosis (1 dog and 1 cat), and persistent left cranial vena cava (1 dog).     

Treatment and Long-Term Follow-up of 205 Dogs With Hypoadrenocorticism

Results of long-term treatment were evaluated in 200 dogs with primary hypoadrenocorticism and 5 dogs with spontaneous secondary hypoadrenocorticism. Fludrocortisone acetate initially was used for mineralocorticoid replacement in 190 of the dogs with primary hypoadrenocorticism. The daily dose of fludrocortisone required in these dogs increased significantly during the treatment period (median, 2.6 years) from an initial median dose of 13.1 μg/kg to a final dose of 22.6 μg/kg. In 27 of the 200 dogs, mineralocorticoid therapy was changed from fludrocortisone to desoxycorticosterone pivalate (DOCP) because of adverse effects, poor response, or financial considerations. The dose of DOCP required in the 33 dogs (27 dogs plus 6 dogs initially given DOCP) increased significantly during the treatment period (median, 3.5 years) from an initial median dose of 1.56 mg/kg to a final dose of 1.69 mg/kg; the interval between DOCP injections ranged from 14 to 35 days (median, 30 days). The dose of prednisone administered to the dogs with primary hypoadrenocorticism decreased significantly from an initial median dose of 0.3 mg/kg to a final dose of 0.2 mg/kg; the drug was discontinued in 22 dogs due to adverse effects. The 5 dogs with secondary hypoadrenocorticism received only glucocorticoid replacement therapy (prednisone) at initial and final daily dosages of 0.41 mg/kg and 0.25 mg/kg, respectively, during a median treatment period of 4.4 years. More than 80% of the dogs were considered to have a good to excellent response to therapy. The median survival time of all 205 dogs was 4.7 years. There were no differences in response to treatment or survival between dogs treated with fludrocortisone and those receiving DOCP, or between dogs with primary hypoadrenocorticism and those with secondary hypoadrenocorticism.     

Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease

Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.     

THE RADIOGRAPHIC APPEARANCE OF PRIMARY LIVER NEOPLASIA IN DOGS

The signalment, anamnesis, and histopathologic, gross pathologic, and radiographic findings in 22 dogs with nonvascular, nonhematopoletic primary liver tumors were reviewed. The tumor types represented were hepatoma (8), bile duct cystadenoma (1), hepatocellular carcinoma (5), and cholangiocellular carcinoma (8). The dogs averaged 11.1 years of age. Females were predisposed to cholangiocellular carcinoma. The most common presenting clinical signs were general malaise, anorexia, PU/PD, vomiting, and seizures. Tumors ranged in size from diffuse 0.5-1 cm nodules to an 18-cm solitary mass and were located in any of the liver lobes. Four of the five diffuse tumors were cholangiocellular carcinomas. The most common radiographic appearance for any type of liver tumor was a right cranial abdominal mass causing caudal and left gastric displacement. In 54.5% of the dogs, radiographic evidence of intraperitoneal disease was identified. Nodular interstitial pulmonary masses were seen in 3 of the 22 dogs.     

COMPUTED TOMOGRAPHIC CHARACTERISTICS OF COLLATERAL VENOUS PATHWAYS IN DOGS WITH CAUDAL VENA CAVA OBSTRUCTION

Collateral venous pathways develop in dogs with obstruction or increased blood flow resistance at any level of the caudal vena cava in order to maintain venous drainage to the right atrium. The purpose of this retrospective study was to describe the sites, causes of obstruction, and configurations of venous collateral pathways for a group of dogs with caudal vena cava obstruction. Computed tomography databases from two veterinary hospitals were searched for dogs with a diagnosis of caudal vena cava obstruction and multidetector row computed tomographic angiographic (CTA) scans that included the entire caudal vena cava. Images for each included dog were retrieved and collateral venous pathways were characterized using image postprocessing and a classification system previously reported for humans. A total of nine dogs met inclusion criteria and four major collateral venous pathways were identified: deep (n = 2), portal (n = 2), intermediate (n = 7), and superficial (n = 5). More than one collateral venous pathway was present in 5 dogs. An alternative pathway consisting of renal subcapsular collateral veins, arising mainly from the caudal pole of both kidneys, was found in three dogs. In conclusion, findings indicated that collateral venous pathway patterns similar to those described in humans are also present in dogs with caudal vena cava obstruction. These collateral pathways need to be distinguished from other vascular anomalies in dogs. Postprocessing of multidetector‐row CTA images allowed delineation of the course of these complicated venous pathways and may be a helpful adjunct for treatment planning in future cases.     

MULTIDETECTOR ROW COMPUTED TOMOGRAPHY AND ULTRASOUND CHARACTERISTICS OF CAUDAL VENA CAVA DUPLICATION IN DOGS

Caudal vena cava duplication has been rarely reported in small animals. The purpose of this retrospective study was to describe characteristics of duplicated caudal vena cava in a large group of dogs. Computed tomography (CT) and ultrasound databases from two hospitals were searched for canine reports having the diagnosis “double caudal vena cava.” One observer reviewed CT images for 71 dogs and two observers reviewed ultrasound images for 21 dogs. In all CT cases, the duplication comprised two vessels that were bilaterally symmetrical and approximately the same calibre (similar to Type I complete duplication in humans). In all ultrasound cases, the duplicated caudal vena cava appeared as a distinct vessel running on the left side of the abdominal segment of the descending aorta and extending from the left common iliac vein to the left renal vein. The prevalence of caudal vena cava duplication was 0.46% for canine ultrasound studies and 2.08% for canine CT studies performed at these hospitals. Median body weight for affected dogs was significantly lower than that of unaffected dogs (P < 0.0001). Breeds with increased risk for duplicated caudal vena cava were Yorkshire Terrier (odds ratio [OR] = 6.41), Poodle (OR = 7.46), West Highland White Terrier (OR = 6.33), and Maltese (OR = 3.87). Presence of a duplicated caudal vena cava was significantly associated with presence of extrahepatic portosystemic shunt(s) (P < 0.004). While uncommon in dogs, caudal vena cava duplication should be differentiated from other vascular anomalies when planning surgeries and for avoiding misdiagnoses.     

Cytological Analysis of Bronchoalveolar Lavage Fluid in the Diagnosis of Spontaneous Respiratory Tract Disease in Dogs: A Retrospective Study

Results of cytological analysis of bronchoalveolar lavage (BAD fluid were compared with clinical diagnoses in dogs that presented with signs of respiratory disease to referral hospitals. Of 68 dogs in which a clinical diagnosis was possible, BAL cytological findings were considered definitive for the diagnosis in 17 cases (25%), supportive of the diagnosis in 34 cases (50%), and not helpful in 17 cases (25%). Findings were most often considered supportive of or definitive for the clinical diagnosis in dogs with alveolar or bronchial radiographic patterns, or the presence of pulmonary masses. BAL results among lung lobes differed in 23 of 63 dogs (37%) with diffuse radiographic patterns. Tracheal wash cytology differed from BAL fluid cytology in 45 of 66 dogs (68%). Bronchoalveolar lavage was a clinically useful procedure for the diagnostic evaluation of dogs with signs of respiratory disease.     

RADIOGRAPHIC APPEARANCE OF PRESUMED NONCARDIOGENIC PULMONARY EDEMA AND CORRELATION WITH THE UNDERLYING CAUSE IN DOGS AND CATS

Noncardiogenic pulmonary edema is an important cause of respiratory disease in dogs and cats but few reports describe its radiographic appearance. The purpose of this retrospective case series study was to describe radiographic findings in a large cohort of dogs and cats with presumed noncardiogenic pulmonary edema and to test associations among radiographic findings versus cause of edema. Medical records were retrieved for dogs and cats with presumed noncardiogenic edema based on history, radiographic findings, and outcome. Radiographs were reviewed to assess lung pattern and distribution of the edema. Correlation with the cause of noncardiogenic pulmonary edema was evaluated with a Fisher's exact test. A total of 49 dogs and 11 cats were included. Causes for the noncardiogenic edema were airway obstruction (n = 23), direct pulmonary injury (n = 13), severe neurologic stimulation (n = 12), systemic disease (n = 6), near‐drowning (n = 3), anaphylaxis (n = 2) and blood transfusion (n = 1). Mixed, symmetric, peripheral, multifocal, bilateral, and dorsal lung patterns were observed in 44 (73.3%), 46 (76.7%), 55 (91.7%), 46 (76.7%), 46 (76.7%), and 34 (57.6%) of 60 animals, respectively. When the distribution was unilateral, pulmonary infiltration involved mainly the right lung lobes (12 of 14, 85.7%). Increased pulmonary opacity was more often asymmetric, unilateral, and dorsal for postobstructive pulmonary edema compared to other types of noncardiogenic pulmonary edema, but no other significant correlations could be identified. In conclusion, noncardiogenic pulmonary edema may present with a quite variable radiographic appearance in dogs and cats.     

Aortic to caudal vena cava ratio measurements using abdominal ultrasound are increased in dogs with confirmed systemic hypertension

Chronically sustained systemic hypertension in dogs can damage the kidneys, eye, brain, heart, and vessels. In human medicine, systemic hypertension has been implicated as the most common risk factor for aorta dilation, which can progress to an aneurysm. Abdominal ultrasound has been commonly used to monitor the size of the abdominal aorta in people with systemic hypertension. In this retrospective cross‐sectional abdominal ultrasound study, evaluation of the size of the abdominal aorta relative to the caudal vena cava was performed in 18 control dogs and 128 dogs with confirmed systemic hypertension. Preexisting conditions contributing to systemic hypertension in these dogs were renal disease, hyperadrenocorticism, diabetes mellitus, adrenal tumors, and previous administration of phenylpropanolamine or palladia. The abdominal aorta and caudal vena cava were assessed from longitudinal images cranial to the trifurcation with measurements made from outer border to outer border of the walls, being careful not to compress the caudal vena cava that would alter its size. Our hypothesis was the ratio of the diameter of the abdominal aorta to caudal vena cava would be higher in dogs with systemic hypertension compared to dogs with normal blood pressure. The mean abdominal aorta‐caudal vena cava ratio was 1.028 in control dogs with a normal blood pressure and 1.515 in dogs with systemic hypertension. In dogs with confirmed systemic hypertension, the abdominal aorta was dilated compared to the caudal vena cava in the caudal abdomen. An increase in the abdominal aorta‐caudal vena cava ratio in a dog should raise suspicion for the presence of systemic hypertension and prompt evaluation of blood pressure.     

Assessment of survey radiography and comparison with x-ray computed tomography for detection of hyperfunctioning adrenocortical tumors in dogs

Results of abdominal survey radiography and x-ray computed tomography (CT) were compared in 13 dogs with hyperadrenocorticism histologically attributed to adrenocortical tumors. X-ray computed tomography enabled accurate localization of the tumor in all 13 dogs. Apart from 2 poorly demarcated irregular-shaped and mineralized carcinomas, there were no differences between adenoma (n = 3) and carcinoma (n = 10) on CT images. In 1 dog, invasion of the caudal vena cava by the tumor was suggested on CT images and was confirmed during surgery. Suspicion of adhesions between tumors of the right adrenal gland and the caudal vena cava on the basis of CT images was confirmed during surgery in only 2 of 6 dogs. Survey radiography allowed accurate localization of the tumor in 7 dogs (4 on the right side and 3 on the left). In 6 of these dogs, the tumor was visible as a well-demarcated soft tissue mass and, in the other dog, as a poorly demarcated mineralized mass. The smallest tumor visualized on survey radiographs had a diameter of 20 mm on CT images. Six tumors with diameter less than or equal to 20 mm were not visualized on survey radiographs. In 1 of these dogs, a mineralized nodule was found in the left adrenal region, without evidence of a mass. In a considerable number of cases, survey radiography can provide presurgical localization of adrenocortical tumors in dogs with hyperadrenocorticism; CT is redundant in these instances. In the absence of positive radiographic findings, CT is valuable for localization of adrenocortical tumors.     

Congenital Interruption of the Portal Vein and Caudal Vena Cava in Dogs: Six Case Reports and a Review of the Literature

Objective —To describe six dogs with congenital abnormalities involving the portal vein, caudal vena cava, or both.
Animals —Six client-owned dogs with congenital interruption of the portal vein or the caudal vena cava, or both.
Methods —Portal vein and caudal vena cava anatomy was evaluated by contrast radiography and visualization at surgery. Vascular casts or plastinated specimens were obtained in three animals.
Results —Portal blood shunted into the caudal vena cava in four dogs and the left hepatic vein in one. Two of these five dogs also had interruption of the caudal vena cava with continuation as azygous vein, as did an additional dog, in which the portal vein was normally formed. Portal vein interruption was present in 5 of 74 (6.8%) dogs with congenital portosystemic shunts evaluated at the Veterinary Teaching Hospital during the study period.
Conclusions —Serious malformations of the abdominal veins were present in more than 1 in 20 dogs with single congenital portosystemic shunts.
Clinical Relevance —Veterinarians involved in diagnosis and surgery for portosystemic shunts should be aware of these potential malformations, and portal vein continuity should be evaluated in all dogs before attempting shunt attenuation.     

Correlation between thoracic radiographs and postmortem findings in dogs with hemangiosarcoma: 77 cases (1984-1989).

Thoracic radiographic and postmortem findings were compared in dogs with histologically confirmed hemangiosarcoma (HSA). On the basis of results of radiography, a false-negative diagnosis was made for pulmonary HSA in 10 (21.7%) of 46 dogs, and in 26 (53.1%) of 49 dogs for cardiac HSA. The incidence of false-negative radiographic diagnosis for pulmonary HSA was lower in dogs when left and right lateral views were obtained. The radiographic sensitivity was 78%, and the negative-predictive value was 74% for pulmonary HSA. The radiographic sensitivity was 47%, and the negative-predictive value was 43% for cardiac HSA.     

Diagnosis by ultrasonography of congestion of the caudal vena cava secondary to thrombosis in 12 cows

This paper describes the clinical, ultrasonographic, radiographic and postmortem findings in 12 cows with thrombosis of the caudal vena cava. The principal clinical signs were chronic bronchopneumonia and fever in 11 cows; one cow had epistaxis and one cow bled from the mouth; eight cows had anaemia and leucocytosis, and the clotting time for the glutaraldehyde test was markedly decreased in all the cows; in nine of the cows the activity of gamma-glutamyltransferase was high, suggesting chronic hepatic congestion. The most important ultrasonographic finding was congestion of the caudal vena cava attributable to thrombosis of the vein. In all the cows the caudal vena cava was round to oval on cross-section, rather than the normal triangular shape. The hepatic, splenic and portal veins were dilated in five, three and one cow, respectively. The results of radiography and endoscopy supported a diagnosis of bronchopneumonia, but there were radiographic changes in the diaphragmatic lung lobes that supported a diagnosis of vena caval disease in only four cows. Postmortem there was a thrombosis of the caudal vena cava in all the cows, and the thrombi were located in the thoracic, subphrenic and abdominal part of the caudal vena cava at the level of the liver in four, one and seven cows, respectively. In three cows, the thrombus was situated where a hepatic abscess had broken into the caudal vena cava, and in one cow it was at the site of a diaphragmatic abscess. In another cow, there was a fistula between the major bronchus of the right diaphragmatic lung lobe and the caudal vena cava where the thrombus was situated. Three cows had liver abscesses that had not broken into the caudal vena cava. There was severe bronchopneumonia in 11 of the cows, some of which also had multiple pulmonary abscesses.     

Aldosterone-to-renin and cortisol-to-adrenocorticotropic hormone ratios in healthy dogs and dogs with primary hypoadrenocorticism

In dogs with primary hypoadrenocorticism, hypocortisolism and hypoaldosteronism usually are present, but these deficiencies also may occur in isolated forms. The diagnosis is commonly made by measuring plasma cortisol concentration before and after stimulation with ACTH, thereby ignoring aldosterone. In search of an alternative approach that would include assessment of glucocorticoid and mineralocorticoid production, 2 pairs of endocrine variables were measured: (1) plasma concentration of cortisol and ACTH, and (2) plasma aldosterone concentration and plasma renin activity. In addition, the cortisol-to-ACTH ratio (CAR) and the aldosterone-to-renin ratio (ARR) were calculated. Reference intervals were established in a population of 60 healthy dogs. In these dogs, CAR ranged from 1.1 to 26.1 and ARR ranged from 0.1 to 1.5. The variables were compared with those of 22 dogs with spontaneous primary hypoadrenocorticism. Plasma concentration of cortisol and ACTH in both groups of dogs overlapped, whereas CAR did not. Similarly, plasma aldosterone concentration and plasma renin activity overlapped, whereas ARR did not. These observations indicate that measurement of these endogenous variables (in one blood sample) allows the specific diagnoses of primary hypocortisolism and primary hypoaldosteronism.     

Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005)

OBJECTIVE: To compare dogs with glucocorticoid-deficient hypoadrenocorticism (GDH) with those with mineralocorticoid- and glucocorticoid-deficient hypoadrenocorticism (MGDH) and determine prevalence, historical and clinicopathologic markers, and outcome of dogs with GDH. DESIGN: Retrospective case series. ANIMALS: 46 dogs with hypoadrenocorticism. PROCEDURES: Records in the veterinary medical database at Purdue University were searched for dogs in which hypoadrenocorticism had been diagnosed at the Veterinary Teaching Hospital from 1985 to 2005. Data pertaining to signalment, history, a minimum clinicopathologic database, treatment, and outcome were collected. Dogs with hypoadrenocorticism were classified as having MGDH if hyponatremia, hyperkalemia, or both were detected and as having GDH if hyponatremia and hyperkalemia were absent. Dogs were excluded if they had ever been treated with mitotane or had been treated with > 1 dose of corticosteroids within a month prior to the ACTH-stimulation test. RESULTS: 35 dogs with MGDH and 11 dogs with GDH met the inclusion criteria. Dogs with GDH were older at the time of diagnosis and had a longer duration of clinical signs prior to diagnosis than those with MGDH. Dogs with GDH were more likely to be anemic, hypoalbuminemic, and hypocholesterolemic than dogs with MGDH. CONCLUSIONS AND CLINICAL RELEVANCE: GDH was more common than reported in a referral hospital population of dogs with primary hypoadrenocorticism. Definitive diagnosis of GDH remains a clinical challenge. Absence of a stress leukogram in dogs with signs of illness (especially relating to the gastrointestinal tract) warrants further investigation. Most dogs with primary cortisol deficiency do not develop mineralocorticoid deficiency.     

Diagnosis and treatment of naturally occurring hypoadrenocorticism in 42 dogs

Hypoadrenocorticism was diagnosed in 42 dogs over a two-and-a-half-year period. The disease occurred more commonly in young to middle-aged dogs, with a female:male ratio of 2:1. Most dogs had chronic intermittent signs (eg, poor appetite, lethargy and vomiting), but more than a third were in acute adrenal crisis at the time of diagnosis. Serum biochemical testing revealed azotaemia, hyperphosphataemia, hyper-kalaemia and hyponatraemia in almost all the dogs. In all dogs, results of adrenocorticotrophic hormone (ACTH) stimulation testing revealed a low to low-normal serum baseline Cortisol concentration that failed to increase after ACTH administration. In two dogs with persistently normal serum electrolytes concentration, one had a markedly high plasma ACTH concentration diagnostic for primary hypoadrenocorticism, whereas the other had a low concentration confirming secondary hypoadrenocorticism. Fludrocortisone acetate was initially used for mineralocorticoid replacement in 33 of the 37 treated dogs withprimary hypoadrenocorticism (final median dosage, 27-0 μg/kg/day), but supplementation was changed to desoxycorticos-terone pivalate (DOCP) in four dogs because of poor response or adverse effects. Seven dogs with primary hypoadrenocorticism were treated with DOCP (final median dosage, 2-02 mg/kg/month). Prednisone, initially administered to 36 dogs, was discontinued in 11 dogs because of side effects. Of the dogs treated with fludrocortisone, the response was considered good to excellent in 26 dogs (78.8 per cent), fair in three, and poor in four. All dogs treated with DOCP responded well.     

Evaluation of circulating amino terminal-pro-B-type natriuretic peptide concentration in dogs with respiratory distress attributable to congestive heart failure or primary pulmonary disease

OBJECTIVE: To evaluate assessment of circulating amino terminal-pro-B-type natriuretic peptide (NT-proBNP) concentration as a means to discriminate between congestive heart failure and primary pulmonary disease in dogs. DESIGN: Prospective case series. ANIMALS: 46 dogs with signs of respiratory distress or coughing. PROCEDURES: All dogs underwent physical and thoracic radiographic examinations. Dogs with evidence of heart disease (eg, murmur, arrhythmia, or large cardiac silhouette detected by radiography) also underwent echocardiography. Dogs with no evidence of heart disease or failure were included if they underwent bronchoalveolar lavage (with cytologic examination and bacterial culture of the lavage fluid). Blood samples for NT-proBNP assay were obtained within 12 hours of the diagnosis of heart failure or prior to bronchoalveolar lavage in dogs with primary pulmonary disease. Circulating concentrations of NT-proBNP were compared between groups and correlated with radiographic and echocardiographic measures of cardiac size. RESULTS: Congestive heart failure and primary pulmonary disease were diagnosed in 25 and 21 dogs, respectively. Dogs with congestive heart failure had significantly higher median serum or plasma NT-proBNP concentration (2,554 pmol/L; interquartile [25% to 75%] range, 1,651.5 to 3,475.5 pmol/L) than dogs with primary pulmonary disease (357 pmol/L; interquartile range, 192.5 to 565.5 pmol/L). Radiographic vertebral heart score and echocardiographic left atrial-to-aortic diameter ratio were not correlated with NT-proBNP concentration. Left ventricular end-diastolic diameter (measured echocardiographically) and NT-proBNP concentration were weakly correlated. CONCLUSIONS AND CLINICAL RELEVANCE: Serum or plasma NT-proBNP concentration assessment may be useful for discrimination of congestive heart failure from primary pulmonary disease in dogs with respiratory distress or cough.     

Ultrasonographic measurement of caudal vena cava to aorta ratios for determination of volume depletion in normal beagle dogs

A noninvasive method for quantifying hydration status would be helpful for clinical management and for research applications in dogs. This prospective, experimental, pilot study aimed to assess the feasibility of ultrasonographic measurement of the caudal vena cava to aorta ratio as a method for quantifying volume depletion in dogs. In 12 normal beagle dogs, furosemide was administered intravenously at a dose of 1 mg/kg, every 2 h, for 8 h, to induce consecutive volume depletion. Every 30 min after administration, ultrasonographic images of the caudal vena cava and aorta, and physical and biological parameters related to dehydration were acquired. On transverse and longitudinal planes of caudal vena cava and aorta images, the height and area of the caudal vena cava and aorta were measured to calculate the caudal vena cava/aorta ratios. All images were acquired by approaching from the right intercostal space with the dogs in left lateral recumbency. A negative correlation was present between the percentage of weight loss in dogs and all four investigated caudal vena cava/aorta ratios (transverse plane width of the caudal vena cava [TW]/aorta; transverse plane height of caudal vena cava [TH]/aorta; longitudinal plane area of the caudal vena cava [TA]/aorta; and longitudinal plane maximal height of the caudal vena cava [L]/aorta). Significant differences (P < 0.001) were seen between dogs with and without clinical signs of dehydration for all caudal vena cava/aorta ratios. Findings indicated that ultrasonographic caudal vena cava/aorta ratios are feasible methods for quantifying volume depletion and for use as an adjunct to standard subjective methods for estimating hydration status in dogs.     

Radiographic findings in dogs with pulmonary blastomycosis: 125 cases (1989-2006)

OBJECTIVE: To identify radiographic patterns in dogs with pulmonary blastomycosis and radiographic factors associated with outcome. DESIGN: Retrospective case series. ANIMALS: 125 dogs with pulmonary blastomycosis. PROCEDURES: Medical records were reviewed, and for each lung lobe, the primary radiographic pattern and percentage of lobar involvement at the time of initial examination were recorded. RESULTS: 79 dogs survived, 38 died, and 8 were euthanized without treatment. The initial radiographic pattern was variable and not significantly associated with outcome. Mean half-time for radiographic resolution of pulmonary infiltrates was 41.4 days for all patterns except masses, for which mean half-time to resolution was 90.8 days. Transient radiographic worsening was seen in 20 of 87 (23%) dogs but was not associated with a poor prognosis. Pulmonary bullae were seen in 20 (16%) dogs, most often in association with an alveolar pattern. Accuracy of using percentage of right caudal lung lobe involvement ( 20%) to predict outcome was 74.4%; accuracy of using number of affected lobes (< 4 vs >or= 4) to predict outcome was 65.8%. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that a nonuniform distribution of pulmonary infiltrates was equally as likely as a diffuse nodular interstitial pattern in dogs with pulmonary blastomycosis. On the basis of half-time for resolution of pulmonary infiltrates, follow-up radiography should be performed no more often than every 4 to 6 weeks in clinically stable patients. Transient radiographic worsening that occurred during the initial weeks of treatment was not associated with a poorer prognosis.