The aim of the study was to retrospectively evaluate clinical signs, CBC, coagulation profile and serum biochemical profile in dogs with leptospirosis, which developed fatal pulmonary hemorrhage. These findings were compared to those of dogs affected by leptospirosis, which did not develop PH.16 dogs with acute leptospirosis (PCR and/or paired MAT) and referred for hemodialysis were divided into two groups (CG n=11; PH n=5), according to the development of pulmonary hemorrhage during hospitalization. At hospital admission values of CBC, PLT, serum creatinine, urea, total bilirubin, total protein, albumin, total calcium, phosphate, ALT, AST, ALKP, cholesterol, PT, aPTT, fibrinogen and ACT were recorded. Clinical signs of dyspnea, coughing, jaundice, melena, hematemesis, hematuria, hemoptysis and spontaneous mucous membrane bleeding were recorded. Data were tested for normality by Kolmogorov- Smirnov test. Mann-Whitney test was used to compare the laboratory parameters between CG and PH. The prevalence of different clinical signs in CG and PH was compared by Fischer’s test. Results were considered statistically significant for p<0.05. At hospital admission, no significant difference in CBC (p=0.16), PLT (p=0.17), serum creatinine (p=0.82), urea (p=0.15), total protein (p=0.69), albumin (p=0.64), total calcium (p=0.43), phosphate (p=0.70), cholesterol (p=0.60), PT (p=0.19), aPTT (p=0.95), fibrinogen (p=0.62) and ACT (p=0.16) was found between CG and PH. PH group showed significantly higher values of ALKP (p=0.07), AST (p=0.06), ALT (p=0.04) and bilirubin (p=0.04) compared with CG. According to clinical signs, in CG jaundice and melena were present in 7/11 dogs, and hemoptysis and coughing in 1/11. None of the patients of CG showed hematuria, or spontaneous mucous membrane bleeding. In PH group all patients were icteric and 4/5 dogs showed melena. Spontaneous mucous membrane bleeding was present in 2/5 dogs and hematuria in 1/5. None of the patients of PH showed hematemesis or hemoptysis. Dyspnea and hematemesis were absent in both CG and PH. No significant difference in the number of patients showing jaundice (p=0.24) or melena (p=1.0) was found between CG and PH. In the dogs of the present study, pulmonary hemorrhage developed as a sudden and dramatic event within hours from hospitalization. In our cohort, clinical signs, coagulation profile and degree of azotemia did not seem to be predictive of the risk for pulmonary hemorrhage. Instead, severely elevated bilirubin and jaundice were constantly found in all patients of HP, and may represent predisposing factors of pulmonary hemorrhage. [1] Barthelemy A. et al. Hemorrhagic, hemostatic and thromboelastometric disorders in 35 dogs with a clinical diagnosis of leptospirosis:a prospective study, JVIM, 31:69-80, 2017. [2] Marchiori E. et al. Clinical and imaging manifestations of hemorrhagic pulmonary leptospirosis: a state of the art review, Lung, 189:1-9, 2011. [3] Kohn B. et al. Pulmonary abnormalities in dogs with leptospirosis, JVIM, 24:1277-82, 2010.
RETROSPECTIVE EVALUATION OF LABORATORY AND CLINICAL FEATURES IN DOGS WITH FATAL PULMONARY HEMORRHAGE DUE TO LEPTOSPIROSIS
Lippi I;Mannarini C;Perondi F;Ceccherini G;Marchetti V;Guidi G.
2017-01-01
Abstract
The aim of the study was to retrospectively evaluate clinical signs, CBC, coagulation profile and serum biochemical profile in dogs with leptospirosis, which developed fatal pulmonary hemorrhage. These findings were compared to those of dogs affected by leptospirosis, which did not develop PH.16 dogs with acute leptospirosis (PCR and/or paired MAT) and referred for hemodialysis were divided into two groups (CG n=11; PH n=5), according to the development of pulmonary hemorrhage during hospitalization. At hospital admission values of CBC, PLT, serum creatinine, urea, total bilirubin, total protein, albumin, total calcium, phosphate, ALT, AST, ALKP, cholesterol, PT, aPTT, fibrinogen and ACT were recorded. Clinical signs of dyspnea, coughing, jaundice, melena, hematemesis, hematuria, hemoptysis and spontaneous mucous membrane bleeding were recorded. Data were tested for normality by Kolmogorov- Smirnov test. Mann-Whitney test was used to compare the laboratory parameters between CG and PH. The prevalence of different clinical signs in CG and PH was compared by Fischer’s test. Results were considered statistically significant for p<0.05. At hospital admission, no significant difference in CBC (p=0.16), PLT (p=0.17), serum creatinine (p=0.82), urea (p=0.15), total protein (p=0.69), albumin (p=0.64), total calcium (p=0.43), phosphate (p=0.70), cholesterol (p=0.60), PT (p=0.19), aPTT (p=0.95), fibrinogen (p=0.62) and ACT (p=0.16) was found between CG and PH. PH group showed significantly higher values of ALKP (p=0.07), AST (p=0.06), ALT (p=0.04) and bilirubin (p=0.04) compared with CG. According to clinical signs, in CG jaundice and melena were present in 7/11 dogs, and hemoptysis and coughing in 1/11. None of the patients of CG showed hematuria, or spontaneous mucous membrane bleeding. In PH group all patients were icteric and 4/5 dogs showed melena. Spontaneous mucous membrane bleeding was present in 2/5 dogs and hematuria in 1/5. None of the patients of PH showed hematemesis or hemoptysis. Dyspnea and hematemesis were absent in both CG and PH. No significant difference in the number of patients showing jaundice (p=0.24) or melena (p=1.0) was found between CG and PH. In the dogs of the present study, pulmonary hemorrhage developed as a sudden and dramatic event within hours from hospitalization. In our cohort, clinical signs, coagulation profile and degree of azotemia did not seem to be predictive of the risk for pulmonary hemorrhage. Instead, severely elevated bilirubin and jaundice were constantly found in all patients of HP, and may represent predisposing factors of pulmonary hemorrhage. [1] Barthelemy A. et al. Hemorrhagic, hemostatic and thromboelastometric disorders in 35 dogs with a clinical diagnosis of leptospirosis:a prospective study, JVIM, 31:69-80, 2017. [2] Marchiori E. et al. Clinical and imaging manifestations of hemorrhagic pulmonary leptospirosis: a state of the art review, Lung, 189:1-9, 2011. [3] Kohn B. et al. Pulmonary abnormalities in dogs with leptospirosis, JVIM, 24:1277-82, 2010.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.