ABSTRACT OF THE WEEK

Journal of veterinary emergency and critical care
Volume 26 | Issue 4 (July 2016)

Retrospective evaluation of acute liver failure in dogs (1995-2012): 49 cases.

J Vet Emerg Crit Care (San Antonio). July 2016;26(4):559-67.

Carrie Lester¹, Johanna Cooper², Rachel M Peters³, Cynthia R L Webster⁴

¹ Departments of Clinical, Cummings School of Veterinary Medicine at Tufts University, Grafton, MA, 01536.; ² Departments of Clinical, Cummings School of Veterinary Medicine at Tufts University, Grafton, MA, 01536.; ³ Biomedical Science, Cummings School of Veterinary Medicine at Tufts University, Grafton, MA, 01536.; ⁴ Departments of Clinical, Cummings School of Veterinary Medicine at Tufts University, Grafton, MA, 01536.

© Veterinary Emergency and Critical Care Society 2016.

Abstract

OBJECTIVE:To characterize the clinical presentation and outcome of dogs with acute liver failure (ALF).

DESIGN:Retrospective case series from January 1995 to December 2012.

SETTING:University teaching hospital.

ANIMALS:Forty-nine dogs were diagnosed with ALF defined as the acute onset of clinical signs accompanied by serum hyperbilirubinemia and coagulopathy (prothrombin time >1.5 times the upper limit of the reference interval) with or without signs of hepatic encephalopathy.

METHODS:Medical records were retrospectively analyzed for clinical presentation, history, physical examination findings, clinicopathologic data, diagnostic imaging findings, hepatic histopathology, treatment, and outcome.

MAIN RESULTS:Presenting signs included anorexia (28/49, 57%), vomiting (25/49, 51%), neurologic abnormalities (17/49, 35%), and polydipsia/polyuria (10/49, 20%). Neurologic impairment compatible with hepatic encephalopathy occurred at some point during hospitalization in 28/49 (57%) of dogs. Common clinicopathologic abnormalities on presentation other than hyperbilirubinemia and increased serum liver enzyme activity included thrombocytopenia (25/49, 51%), hypoalbuminemia (23/49, 46%), leukocytosis (17/49, 34%), anemia (14/49, 29%), hypokalemia (13/49, 27%), and hypoglycemia (10/49, 20%). The causes of ALF included neoplasia (13/49, 27%), presumptive leptosporosis (4/49, 8%), and ischemia (1/49, 2%). The remaining cases were idiopathic although 15 of these dogs had exposure to possible hepatotoxins. Common lesions in the 35/49 (71%) dogs that had hepatic histopathology were necrosis (19/39, 48%), lipidosis (16/39, 41%), vacuolar change (7/49, 14%), and inflammation (4/49, 8%). Complications included ascites (20/49, 41%), bleeding tendencies (14/49, 29%), pancreatitis (12/49, 24%), and acute tubular necrosis (11/49, 22%). Seven (14%) dogs survived to discharge. Survivors had higher alanine aminotransferase activity, and were more likely to maintain normal albumin concentrations and not develop clinical bleeding or ascites during hospitalization.

CONCLUSIONS:Canine ALF is associated with multiple etiologies and a high mortality rate. Strategies to increase survival are urgently required.

Companion Notes

Retrospective report on acute liver failure in 49 dogs

Introduction on acute liver failure (ALF) in human medicine:

- ALF = acute onset of severe hepatic insufficiency manifesting as:

- increases in serum transaminase activity and bilirubin

- coagulopathy

- signs of encephalopathy

- underlying causes include the following:

(in 20% of cases the etiology is unknown)

- viral infection

- drug-induced

- toxins

- metabolic disorders

- neoplasia

- auto-immune hepatitis

- overall survival without liver transplantation: ~ 15%

Study design

- study population: dogs seen at a University teaching hospital

- 49 dogs with acute liver failure

- inclusion criteria (derived from human medicine):

- acute onset of clinical signs

- serum hyperbilirubinemia

- coagulopathy

- prolonged prothrombin time (PT)

- prolonged >1.5 times upper limit of reference range

- with or without signs of hepatic encephalopathy (HE)

- in children, HE is often omitted from the diagnosis of ALF

- due to difficulty recognizing HE in early stages

- procedure: records from 01/95-12/12 retrospectively reviewed

Results

- history & signalment

- breeds represented by 5 or more cases

- Labrador retriever, 7 cases

- golden retriever, 5

- median weight: 24.5 kg with a range of 1.36-66.8

- mean age: 5.6 ± 3.7 years of age with a range of 1 month to 13 years

- presenting signs

- anorexia, 28 of the 49 (57%)

- vomiting, 25 (51%)

- neurologic signs compatible with HE during hospitalization, 17 (35%)

- altered mentation (dull)

- circling

- head pressing

- seizures

- polydipsia/polyuria, 10 (20%)

- clinicopathologic abnormalities on presentation

- thrombocytopenia, 26 of 49 dogs (53%)

- median: 146 x 10⁹/L with range 9-653 x 10⁹/L

- leukocytosis 17 of 49 (34%)

- leukopenia in 1 dog

- anemia with PCV < 39%, 14 of 49 (28%)

- hemoconcentration, 5 of 49 (10%)

- hyperbilirubinemia, all 49

- median: 4.1 mg/dL with a range of 0.40-37.8

- increased serum alkaline phosphatase activity, 45 of 47

- median: 609 U/L with a range of 47-5166

- increased aspartate aminotransferase activity, 45 of 49

- median: 368 U/L with a range of 34-13,356

- increased alanine transaminase, 45 of 49

- median: 1048 U/L with a range of 44-48,531

- increased gamma glutamyl transpeptidase, 35 of 45

- median: 16 U/L with a range of 1-88 U/L

- hypoalbuminemia, 23 of 49 dogs (45%)

- hypoglycemia in 10 of 49 (20%)

- hypokalemia in 13 of 45 (26%)

- hyperkalemia in 9 of 49 (18%)

- hypernatremia in 10 of 49 (20%)

- hyponatremia in 9 of 49 (18%)

- hyperphosphatemia in 7 of 49 (14%)

- elevated blood ammonia, 7 of 11 (63%)

- elevated creatinine, 7 of 49 (15%)

- hyperlactatemia, 21 of 29 (56%)

- coagulation profile

- prolonged PT and activated partial thromboplastin time, all dogs

- both elevated, 12 dogs

- hypofibrinogenemia, 8 of 11 dogs

- causes included the following:

- neoplasia, 13 of 49 (27%)

- presumptive leptospirosis, 4 of 49 (8%)

- positive acute titers

- ischemia, 1 (2%)

- remaining 31 (63%) cases were idiopathic

- 15 had exposure to possible hepatotoxins

- several dogs got drugs involved in hepatotoxic reactions in dogs

- NSAIDs, 7 cases

- phenobarbital, 3

- trimethoprim sulfa, 1

- cephalexin, 1

- doxycycline, 1

- glucosamine manufactured for equine use, 1

- mushrooms, 1

- liver histopathology

- necrosis, 19 of 39 (48%)

- lipidosis, 16 (41%)

- vacuolar change, 7 (14%)

- inflammation, 4 (8%)

- complications included the following:

- ascites, 20 of 49 (41%)

- bleeding tendencies, 14 (29%)

- evidence of hemorrhage, 25

(based on signs of bleeding ante-mortem or at necropsy)

- melena, 14

- petechiation, 7

- bloody diarrhea, 3

- ecchymosis, 4

- gastrointestinal ulceration, 4

- hemoabdomen, 2

- hematuria, 2

- cerebral hemorrhage, 2

- adrenal hemorrhage, 1

- excessive bleeding from a catheter site, 1

- pancreatitis, 12 (24%)

- acute tubular necrosis, 11 (22%)

- outcome

- survival to discharge, 7 dogs (14%)

- parameters in these survivors

- higher alanine aminotransferase activity

- more likely to maintain normal albumin levels

- did not develop clinical bleeding or ascites during hospitalization

- median hospitalization time for all dogs: 3 days with a range of 1-12

- full necropsy performed in 23 cases

- concurrent renal lesions, 18 of the 23

- acute tubular necrosis, 11

- chronic membranous glomerulonephritis, 4

- interstitial nephritis, 3

- concurrent pancreatic and gastrointestinal lesions, 9

- gross evidence of thrombosis at necropsy, 4

- pulmonary thromboembolism, 2

- abdominal ultrasonography, performed on 38 dogs

- hepatomegaly, 17

- normal liver, 8

- inhomogeneous liver, 9; hypoechoic, 7; hyperechoic, 4

“In people with ALF, intracranial pressure is often monitored and measures to decrease intracranial pressure such as elevation of the head, control of systemic hypertension and minimization of agitation and pain are standard of care for patients with ALF….”

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