Long-term outcome of dogs recovering from acute kidney injury: 132 cases.

BACKGROUND: Information regarding long-term outcome of dogs recovering from acute kidney injury (AKI) is limited. OBJECTIVES: Determine the long-term outcome of dogs recovering from AKI and identify predictors for serum creatinine concentration (sCr) normalization and long-term outcome. ANIMALS: One hundred thirty-two dogs with AKI that survived ≥30 days postdischarge. METHODS: Retrospective study. Search of medical records of dogs diagnosed with AKI that survived to discharge. Follow-up data were retrieved from medical records and by telephone interviews with the owners or primary care veterinarians or both. RESULTS: Estimated median survival time (MST) was 1322 days (95% confidence interval [CI], 1147-1626), and 76% of the dogs were alive at last contact. Normalization of sCr was documented in 55% of the dogs at discharge and in additional 20% during the follow-up period. The proportion of dogs with sCr normalization decreased with increase in AKI grade (P = .02). Long-term survival was not associated with sCr normalization (P = .63). Etiology was associated with the long-term outcome (P = .004). CONCLUSION AND CLINICAL IMPORTANCE: Long-term survival of dogs with AKI is longer than previously described. Normalization of sCr in 99 dogs (75%) occurred, either at discharge or within the follow-up period. Normalization of sCr was not associated with long-term survival. Estimated MST of dogs with sCr normalization was not different compared with dogs that developed azotemic chronic kidney disease (CKD), presumably because of slow CKD progression rate. Etiology is an important factor determining sCr normalization and long-term survival, emphasizing the importance of the reversibility of renal injury rather than its severity.

Acute kidney injury in dogs: Etiology, clinical and clinicopathologic findings, prognostic markers, and outcome.

BACKGROUND: Acute kidney injury (AKI) is a common, potentially fatal condition. OBJECTIVES: To characterize the etiologies, clinical and clinicopathologic findings, hospitalization period, and outcome of dogs with AKI and to identify markers of negative prognosis. ANIMALS: Two hundred forty-nine client-own dogs diagnosed with AKI and hospitalized at a veterinary teaching hospital. METHODS: Retrospective study. Search of medical records for dogs with AKI. RESULTS: Common clinical signs included lethargy (225/249, 90%), anorexia (206/249, 83%), and vomiting (168/249, 68%). Etiologies included ischemic/inflammatory (144/249, 58%), infectious (19/249, 8%), nephrotoxicosis (14/249, 6%), or other (13/249, 5%). Hospital-acquired AKI was diagnosed in 9% (23/249) of the dogs. Median presentation and peak serum creatinine (sCr) concentrations were 4 mg/dL (range, 1.1-37.9) and 4.6 mg/dL (range, 1.1-43.1), respectively. Dogs were classified to AKI grades as follows: Grade I, 6 (2%), Grade II, 38 (15%), Grade III, 89 (36%), Grade IV, 77 (31%), and Grade V, 39 (16%). One hundred and sixty-four (66%) dogs survived. There was a positive association between death and AKI grade (P = .009). The case fatality rate was higher among dogs with anuria compared with dogs without anuria (50% vs 28%, respectively; odds ratio [95% confidence interval]: 2.5 [1.39-4.6]; P = .002). Forty-seven (18.8%) dogs underwent hemodialysis, of which 60% survived. CONCLUSION AND CLINICAL IMPORTANCE: Two-thirds of dogs with AKI survived. Hospital-acquired AKI was common. The severity of AKI, as reflected by presence of anuria, AKI grade, and other body organs involvement, was associated with the outcome.

Lethal acute hemorrhage from an aortoesophageal fistula following endoscopy-assisted esophageal foreign body removal in a dog.

OBJECTIVE: To describe the clinical presentation of a dog with fatal hemorrhage from an aortoesophageal fistula (AEF) immediately following endoscopic removal of an osseous esophageal foreign body. CASE SUMMARY: A 12-year-old, male mixed-breed dog presented to a university hospital with a 6-day history of gagging, hematemesis, and anorexia. Physical examination upon arrival was unremarkable. Blood work revealed leukocytosis without anemia. Thoracic radiographs from the referring veterinarian demonstrated the presence of an osseous esophageal foreign body at the level of the heart base. Subsequently, esophagoscopy was performed under general anesthesia. A triangular-shaped, osseous esophageal foreign body was visualized at the level of the heart base and successfully removed. Following its removal, a deep, nonbleeding, presumably nonperforated, esophageal ulcer was revealed. While recovering from anesthesia, the dog's condition acutely deteriorated, with absence of spontaneous respiration, severe tachycardia, hypotension, white-pale mucous membranes, and hypothermia. Severe anemia was present, with hypovolemic shock likely secondary to acute, postprocedural bleeding. Medical management included rapid packed red blood cell transfusion, crystalloid fluid therapy, and tranexamic acid. Despite initial stabilization, several hours later, the dog suffered cardiac arrest and cardiopulmonary resuscitation (CPR) was unsuccessful. At postmortem examination, a 1-mm AEF was identified on the ventral aspect of the aorta that communicated with the overlying esophagus. NEW OR UNIQUE INFORMATION PROVIDED: Aortoesophageal fistulas should be considered in any patient with severe bleeding following esophagoscopy. A history of hematemesis in a dog with an esophageal foreign body should raise suspicion of an AEF and dictate case management accordingly.

Protease inhibitors, inflammatory markers, and their association with outcome in dogs with naturally occurring acute pancreatitis.

BACKGROUND: Acute pancreatitis (AP) presumably is associated with pancreatic protease activation, protease inhibitor (PI) depletion, and inflammatory mediator secretion. OBJECTIVES: Examine PIs and inflammatory mediator concentrations in dogs with AP and their association with death. ANIMALS: Thirty-one dogs diagnosed with AP based on clinical signs, ultrasonographic findings, and increased canine pancreatic lipase immunoreactivity (cPLI) and 51 healthy control dogs. METHODS: Antithrombin and α2 -antiplasmin activity (ATA and α2 AP, respectively) and concentrations of α1 -proteinase inhibitor (α1 PI), α2 -macroglobulin (α2 MG), C-reactive protein (CRP), interleukins (ILs)-2,6,8 and tumor necrosis factor-α (TNF-α) were prospectively measured. Severity of AP was assessed by clinical severity scoring systems. RESULTS: Mortality rate was 19%. Antithrombin activity was lower (P = .004) and maximal CRP, IL-6, and TNF-α concentrations higher (P < .04) in the AP group compared to the controls, whereas IL-2, IL-8, α1 PI, and α2 AP concentrations did not differ between groups. Serum α2 MG concentration was not reliably detected. Serum cPLI, CRP, and IL-6 concentrations were significantly and positively correlated. The ATA was lower (P = .04), and canine acute pancreatitis severity (CAPS) scores higher (P = .009) in nonsurvivors compared to survivors. Higher CAPS scores were associated (P < .05) with decreased ATA and increased cPLI, CRP, and IL-6 concentrations. CONCLUSIONS AND CLINICAL IMPORTANCE: Systemic inflammation in dogs with AP is manifested by increased inflammatory mediator concentrations, correlating with cPLI and CRP concentrations. Hypoantithrombinemia is associated with death. Serum concentrations of α2 AP and α1 PI are less useful prognostic markers. The CAPS score is a useful prognostic marker in dogs with AP.

Prognostic markers and assessment of a previously published clinical severity index in 109 hospitalised dogs with acute presentation of pancreatitis.

BACKGROUND: Acute pancreatitis (AP) is common in dogs. Nevertheless, validated clinical severity index (CSI) scoring systems to assess severity and guide treatment in current, large-scale studies are unavailable. METHODS: This is a retrospective study including 109 dogs. Pancreatitis was diagnosed based on clinical signs, abdominal sonographic evidence, positive pancreatic lipase assays and experts' assessment consensus. RESULTS: The survival rate was 75 per cent (82 dogs). Azotaemia and presence of local complications (ie, ascites) and secondary complications (ie, acute kidney injury and acute respiratory distress syndrome) were significantly associated with death. In agreement with the previously published CSI, respiratory anomalies were significantly associated with death. However, in disagreement with that study, high scores in the kidney and local abdominal complication categories and the sum of scores of all nine categories, but not high gastrointestinal category score, were also significantly associated with death. A final CSI score of at least 4 was associated with death. CONCLUSIONS: This study has validated a nine-category CSI, proven a useful assessment tool in dogs with AP. Several previously reported and novel prognostic markers were assessed.

A prospective randomized study of efficacy of 2 treatment protocols in preventing recurrence of clinical signs in 51 male cats with obstructive idiopathic cystitis.

BACKGROUND: Urethral obstruction (UO) is a common complication of feline idiopathic cystitis (FIC). Robust treatment recommendations to prevent its recurrence are scarce. OBJECTIVES: To evaluate meloxicam treatment for prevention of clinical recrudescence in male cats with obstructive FIC. ANIMALS: Fifty-one client-owned cats. METHODS: Prospective, randomized clinical trial. Every male cat with FIC-associated UO was deemed eligible for the study and was recruited during hospitalization. After discharge, cats were treated with phenoxybenzamine and alprazolam for 2 weeks, with (24 cats) or without (27 cats) low-dose meloxicam (0.025 mg/kg/day PO) and monitored for 6 months. RESULTS: Cumulative number (%) of cats with recurrent UO at 10 days, 1-, 2-, and 6-months after discharge was 1 (2%), 2 (4%), 4 (8%), and 8 (16%), respectively. Overall, 12 (24%) cats experienced signs of recurrent FIC within 6 months, with (8 cats) or without (4 cats) concurrent UO. No difference in the cumulative incidence of UO within 6 months was detected with addition of meloxicam (odds ratio [95% confidence interval], 0.63 [0.13-2.97]; P = .70). All cats were alive at 6 months. CONCLUSIONS AND CLINICAL IMPORTANCE: No clinical benefit was detected with the addition of low-dose meloxicam to phenoxybenzamine and alprazolam treatment for 2 weeks after discharge. Nevertheless, this study was underpowered to identify potential differences, and its findings must be corroborated in larger studies.