Objective—To determine morbidity and fatalities in cats with hepatic lipidosis that received propofol to facilitate placement of a feeding tube.
Study Design—Retrospective case series.
Animals—44 cats with presumed primary hepatic lipidosis anesthetized for placement of a feeding tube.
Procedures—Medical records from January 1995 through December 2004 were reviewed to identify cats that matched the inclusion criteria (histologic confirmation of hepatic lipidosis, anesthetized for placement of feeding tube, complete intensive care unit [ICU] records, and recorded outcome). Data extracted included age, body weight, sex, anesthetic drugs, drug dosages, type of feeding tube, duration of anesthesia, number of hours in ICU, administration of blood products, and survival until discharge from ICU.
Results—44 cats (21 females and 23 males) were included in the analysis. Age range was 3 to 15 years (median, 8 years), and body weight ranged from 1.8 to 9.0 kg (4.0 to 19.8 lb), with a median of 4.8 kg (10.6 lb). Twenty-seven cats were administered propofol. There was no significant association between the use of propofol or the dosage of propofol and any risk factor, need for blood products, number of hours in the ICU, or survival. There was no significant difference between cats that received propofol and cats that did not receive propofol with regard to interval until discharge from the ICU.
Conclusions and Clinical Relevance—The use of propofol did not increase morbidity or fatalities in cats with primary hepatic lipidosis. Thus, propofol can be used in these cats for placement of a feeding tube.
Objective—To determine total glutathione (GSH) and
glutathione disulfide (GSSG) concentrations in liver
tissues from dogs and cats with spontaneous liver
Sample Population—Liver biopsy specimens from
63 dogs and 20 cats with liver disease and 12 healthy
dogs and 15 healthy cats.
Procedure—GSH was measured by use of an enzymatic
method; GSSG was measured after 2-vinylpyridine
extraction of reduced GSH. Concentrations were
expressed by use of wet liver weight and concentration
of tissue protein and DNA.
Results—Disorders included necroinflammatory liver
diseases (24 dogs, 10 cats), extrahepatic bile duct
obstruction (8 dogs, 3 cats), vacuolar hepatopathy (16
dogs), hepatic lipidosis (4 cats), portosystemic vascular
anomalies (15 dogs), and hepatic lymphosarcoma
(3 cats). Significantly higher liver GSH and protein
concentrations and a lower tissue DNA concentration
and ratio of reduced GSH-to-GSSG were found in
healthy cats, compared with healthy dogs. Of 63 dogs
and 20 cats with liver disease, 22 and 14 had low liver
concentrations of GSH (µmol) per gram of tissue; 10
and 10 had low liver concentrations of GSH (nmol) per
milligram of tissue protein; and 26 and 18 had low
liver concentrations of GSH (nmol) per microgram of
tissue DNA, respectively. Low liver tissue concentrations
of GSH were found in cats with necroinflammatory
liver disease and hepatic lipidosis. Low liver concentrations
of GSH per microgram of tissue DNA
were found in dogs with necroinflammatory liver disease
and cats with necroinflammatory liver disease,
extrahepatic bile duct occlusion, and hepatic lipidosis.
Conclusions and Clinical Relevance—Low GSH values
are common in necroinflammatory liver disorders,
extrahepatic bile duct occlusion, and feline
hepatic lipidosis. Cats may have higher risk than dogs
for low liver GSH concentrations. (Am J Vet Res
Objective—To develop an assay to measure canine von Willebrand factor (vWF):collagen-binding activity (CBA) to screen for type 2 von Willebrand disease (vWD) in dogs.
Sample Population—293 plasma samples submitted for analysis of canine vWF antigen (vWF:Ag) and 12 control plasma samples from dogs with inherited type 2 or 3 vWD.
Procedure—Bovine collagens were evaluated for suitability as binding substrate for vWF. Assay sensitivity to depletion, proteolytic degradation, or a genetic deficiency of high-molecular-weight vWF were determined. Amounts of vWF:Ag and vWF:CBA were measured. The ratio of vWF:Ag to vWF:CBA was used to discriminate between type 1 and type 2 vWD.
Results—An assay for canine vWF activity was developed by use of mixed collagen (types I and III). When vWF:Ag was used to subtype vWD, 48% of the dogs were classified as clinically normal, 9% as indeterminate, and 43% as type 1 vWD. Inclusion of vWF activity resulted in reclassification of 5% of those identified as type 1 to type 2 vWD. However, vWF:CBA of the reclassified dogs was not persistently abnormal, a finding compatible with acquired type 2 vWD. Some Doberman Pinschers had lower antigen-to-activity ratios than other breeds with type 1 vWD, suggesting that Doberman Pinschers have more functional circulating vWF.
Conclusions and Clinical Relevance—Analysis of canine vWF activity should be included among the vWF-specific assays used to confirm type 2 vWD. The prevalence of inherited forms of type 2 vWD in screened dogs is lower than acquired forms that can result secondary to underlying disease.
Objective—To evaluate the effect of carprofen on
hemostatic variables in clinically normal dogs.
Animals—12 clinically normal Labrador Retrievers.
Procedure—10 dogs (6 females, 4 males) received
carprofen (2.2 mg/kg of body weight, PO, q 12 h) for
5 days. Two dogs (untreated control group; 1 female,
1 male) did not receive carprofen. Hemostatic variables
(platelet count, activated partial thromboplastin
time, prothrombin time, fibrinogen, platelet aggregation,
and bleeding time) were assessed for all dogs
prior to treatment, on day 5 of treatment, and 2 and 7
days after discontinuation of the drug (days 7 and 12).
Serum biochemical variables and Hct were assessed
prior to treatment and on days 5 and 12.
Results—In dogs receiving carprofen, platelet aggregation
was significantly decreased, and onset of
aggregation was significantly delayed on days 5, 7,
and 12, compared with pretreatment values.
Activated partial thromboplastin time was significantly
increased on days 5, 7, and 12 over pretreatment
values in treated dogs, but values remained within
reference ranges. Significant differences were not
detected in buccal mucosal bleeding time, other
serum biochemical and hemostatic variables, or Hct,
compared with pretreatment values and the internal
Conclusion and Clinical Relevance—Administration
of carprofen for 5 days causes minor but not
clinically important alterations in hemostatic and
serum biochemical variables in clinically normal
Labrador Retrievers. Carprofen is commonly used to
treat osteoarthritis and chronic pain in dogs, but prior
to this study, its effect on platelet aggregation and
hemostatic variables was unknown. (Am J Vet Res
Objective—To determine the effect of citrate concentration
(3.2 vs 3.8%) on coagulation tests in
Animals—30 clinically healthy dogs and 12 dogs with
hereditary hemostatic disorders.
Procedure—Blood was collected from all dogs directly
into collection tubes containing 3.2 or 3.8%
buffered citrate. Prothrombin time (PT), activated partial
thromboplastin time (aPTT), and fibrinogen concentration
were measured by use of 3 clot-detection
assay systems (2 mechanical and 1 photo-optic).
Factor VIII and factor IX coagulant activities (FVIII:C
and FIX:C, respectively) were determined by use of a
manual tilt-tube method and a mechanical clot-detection
Results—Significant differences were not detected in
median PT, fibrinogen concentration, FVIII:C, or FIX:C
between 3.2 and 3.8% citrate for any assay system.
A significant prolongation in aPTT for 3.2% citrate,
compared with 3.8% citrate, was found in 1 mechanical
Conclusions and Clinical Relevance—Citrate concentration
does not significantly affect results of most
coagulation assays, regardless of assay system. The
aPTT was mildly influenced by the citrate concentration,
although this was animal-, instrument-, and
reagent-dependent. The choice of 3.2 or 3.8% citrate
as an anticoagulant for coagulation tests has minimal
influence on assay results in healthy dogs or dogs
with hereditary hemostatic disorders. (J Am Vet Med
Objective—To define the relationship between clinical
expression of a type-1 von Willebrand disease
phenotype and genotype at 2 von Willebrand factor
marker loci in Doberman Pinschers.
Animals—102 client-owned Doberman Pinschers.
Procedures—Dogs were recruited on the basis of
plasma von Willebrand factor concentration, clinical
history, and pedigree. Blood samples and response to
a history questionnaire were obtained for each dog.
Plasma von Willebrand factor concentration was measured
by use of an ELISA, and genotyping was performed
via polymerase chain reaction for 1 intragenic
and 1 extragenic von Willebrand factor marker.
Amplification product size was determined by use of
polyacrylamide gel electrophoresis (intragenic marker)
or automated sequence analysis (extragenic marker).
Western blots were prepared from a subset of
dogs with low plasma von Willebrand factor concentration
to evaluate multimer distribution.
Results—Strong associations were detected
between plasma von Willebrand factor concentration
and von Willebrand factor marker genotype. Twentyfive
dogs had substantial reduction in plasma von
Willebrand factor concentration and multiple hemorrhagic
events. All were homozygous for a 157-basepair
intragenic marker allele and homozygous or compound
heterozygous for 1 of 4 extragenic marker alleles.
These marker genotypes were exclusively
detected in dogs with low plasma von Willebrand factor
concentration, although some dogs with these
genotypes did not have abnormal bleeding.
Conclusions and Clinical Relevance—Type-1 von
Willebrand disease in Doberman Pinschers is associated
with the von Willebrand factor gene locus; however,
the expression pattern in this breed appears
more complex than that of a simple recessive trait.
(Am J Vet Res 2001;62:364–369)
Objective—To determine sensitivity and specificity of
assays of D-dimer concentrations in dogs with disseminated
intravascular coagulation (DIC) and healthy
dogs and to compare these results with those of
serum and plasma fibrin-fibrinogen degradation product
Animals—20 dogs with DIC and 30 healthy dogs.
Procedure—Semi-quantitative and quantitative
D-dimer concentrations were determined by use of
latex-agglutination and immunoturbidometry, respectively.
Fibrin-fibrinogen degradation products were
measured by use of latex-agglutination. A reference
range for the immunoturbidometric D-dimer concentration
assay was established; sensitivity and specificity
of the assay were determined at 2 cutoff concentrations
(0.30 µg/ml and 0.39 µg/ml).
Results—Reference range for the immunoturbidometric
D-dimer concentration assay was 0.08 to
0.39 µg/ml; median concentrations were significantly
higher in dogs with DIC than in healthy dogs. Latexagglutination
D-dimer and serum and plasma FDP
assays had similar sensitivity (85 to 100%) and specificity
(90 to 100%); the immunoturbidometric assay
had lower specificity (77%) at the 0.30 µg/ml cutoff
and lower sensitivity (65%) at the 0.39 µg/ml cutoff.
Sensitivity or specificity of the latex-agglutination
D-dimer assay was not significantly improved when
interpreted in series or parallel with FDP assays.
Conclusions and Clinical Relevance—Measurement
of D-dimer concentrations by latex-agglutination
appears to be a sensitive and specific ancillary test for
DIC in dogs. Specificity of D-dimer concentrations in
dogs with systemic disease other than DIC has not
been determined, therefore FDP and D-dimer assays
should be performed concurrently as supportive tests
for the diagnosis of DIC in dogs. (Am J Vet Res 2000;61:393–398)
Objective—To determine disorders associated with vacuolar hepatopathy (VH), morphologic hepatic and clinicopathologic abnormalities, and affiliation with steroidogenic hormone excess in dogs.
Design—Retrospective case series.
Animals—336 dogs with histologically confirmed moderate or severe VH.
Procedures—Information on signalment, results of diagnostic testing, definitive diagnoses, and exposure to glucocorticoids (ie, exogenous glucocorticoid administration or high endogenous concentrations of steroidogenic hormones) was obtained from medical records. Dogs were grouped by underlying disorder, glucocorticoid exposure, acinar zonal distribution of lesions, and histologic severity.
Results—12 disease groups (neoplastic, acquired hepatobiliary, neurologic, immune-mediated, gastrointestinal tract, renal, infectious, cardiac disease, diabetes mellitus, portosystemic vascular anomaly, adrenal gland dysfunction, and miscellaneous disorders) were identified. There were 186 (55%) dogs with and 150 (45%) dogs without evidence of glucocorticoid exposure. Acinar zonal distribution of hepatic vacuolation and clinicopathologic values did not differ between dogs with and without evidence of glucocorticoid exposure. However, a 3-fold increased likelihood of severe VH was associated with steroidogenic hormone exposure. Of 226 dogs with high serum alkaline phosphatase activity, 102 (45%) had no evidence of glucocorticoid exposure.
Conclusions and Clinical Relevance—Results suggest that neoplasia and congenital or acquired hepatobiliary disease are common in dogs with VH and provide support for the suggestion that VH, high alkaline phosphatase activity, and illness-invoked physiologic stress may be associated. Histologic confirmation of VH should initiate a diagnostic search for a primary disease if glucocorticoid treatment and hyperadrenocorticism are ruled out.
Objective—To determine the diagnostic value of protein C (PC) for detecting hepatobiliary disease and portosystemic shunting (PSS) in dogs.
Animals—238 clinically ill dogs with (n = 207) and without (31) hepatobiliary disease, including 105 with and 102 without PSS.
Procedures—Enrollment required routine hematologic, serum biochemical, and urine tests; measurement of PC activity; and a definitive diagnosis. Total serum bile acids (TSBA) concentration and coagulation status, including antithrombin activity, were determined in most dogs. Dogs were grouped into hepatobiliary and PSS categories. Specificity and sensitivity were calculated by use of a PC cutoff value of 70% activity.
Results—Specificity for PC activity and TSBA concentrations was similar (76% and 78%, respectively). Best overall sensitivity was detected with TSBA, but PC activity had high sensitivity for detecting PSS and hepatic failure. Protein C activity in microvascular dysplasia (MVD; PC ≥ 70% in 95% of dogs) helped differentiate MVD from portosystemic vascular anomalies (PSVA; PC < 70% in 88% of dogs). A receiver operating characteristic curve (PSVA vs MVD) validated a useful cutoff value of < 70% activity for PC.
Conclusions and Clinical Relevance—Combining PC with routine tests improved recognition of PSS, hepatic failure, and severe hepatobiliary disease and signified a grave prognosis when coupled with hyperbilirubinemia and low antithrombin activity in hepatic failure. Protein C activity can help prioritize tests used to distinguish PSVA from MVD and sensitively reflects improved hepatic-portal perfusion after PSVA ligation.
Objective—To determine whether dogs that received eyedrops containing phenylephrine and scopolamine would have a higher mean arterial blood pressure (MAP) when anesthetized than would dogs that did not receive the eyedrops.
Animals—37 nondiabetic and 29 diabetic dogs anesthetized for phacoemulsification and 15 nondiabetic dogs anesthetized for corneal ulcer repair (control dogs).
Procedures—Medical records were reviewed to identify study dogs. Dogs undergoing phacoemulsification received 2 types of eyedrops (10% phenylephrine hydrochloride and 0.3% scopolamine hydrobromide) 4 times during a 2-hour period prior to the procedure. Control dogs did not receive these eyedrops. Heart rate and MAP were measured before surgery in all dogs 10 and 5 minutes before, at the time of (t0), and 5 (t5) and 10 (t10) minutes after atracurium administration.
Results—MAP was greater in the 2 groups that received the eyedrops than in the control group at t0 and t5; at t10, it was greater only for the nondiabetic dogs that received eyedrops. Nine nondiabetic dogs and 1 diabetic dog anesthetized for phacoemulsification had at least 1 MAP value > 131 mm Hg; 73% of MAP values > 131 mm Hg were detected within 10 minutes after atracurium administration. At no time did a control dog have an MAP value > 131 mm Hg.
Conclusions and Clinical Relevance—Anesthetized dogs pretreated with eyedrops containing phenylephrine and scopolamine had higher MAP values than dogs that did not receive the eyedrops, suggesting the drops caused hypertension. Atracurium may interact with the eyedrops and contribute to the hypertension.