Objective—To evaluate pituitary-adrenal function in critically ill dogs with sepsis, severe trauma, and gastric dilatation-volvulus (GDV).
Animals—31 ill dogs admitted to an intensive care unit (ICU) at Washington State University or the University of Pennsylvania; all dogs had acute critical illness for < 48 hours prior to admission.
Procedures—Baseline and ACTH-stimulated serum cortisol concentrations and baseline plasma ACTH concentrations were assayed for each dog within 24 hours after admission to the ICU. The change in cortisol concentrations (Δ-cortisol) was calculated for each dog. Morbidity and mortality data were recorded for each patient.
Results—Overall, 17 of 31 (55%) acutely critically ill dogs had at least 1 biochemical abnormality suggestive of adrenal gland or pituitary gland insufficiency. Only 1 (3%) dog had an exaggerated response to ACTH stimulation. Dogs with Δ-cortisol ≤ 83 nmol/L were 5.7 times as likely to be receiving vasopressors as were dogs with Δ-cortisol > 83 nmol/L. No differences were detected among dogs with sepsis, severe trauma, or GDV with respect to mean baseline and ACTH-stimulated serum cortisol concentrations, Δ-cortisol, and baseline plasma ACTH concentrations.
Conclusions and Clinical Relevance—Biochemical abnormalities of the hypothalamic-pituitary-adrenal axis indicative of adrenal gland or pituitary gland insufficiency were common in critically ill dogs, whereas exaggerated responses to ACTH administration were uncommon. Acutely ill dogs with Δ-cortisol ≤ 83 nmol/L may be more likely to require vasopressors as part of the treatment plan.
Objective—To determine the lowest ACTH dose that would induce a maximum increase in serum cortisol concentration in healthy adult horses and identify the time to peak cortisol concentration.
Animals—8 healthy adult horses.
Procedures—Saline (0.9% NaCl) solution or 1 of 4 doses (0.02, 0.1, 0.25, and 0.5 μg/kg [0.009, 0.045, 0.114, and 0.227 μg/lb]) of cosyntropin (synthetic ACTH) were administered IV (5 treatments/horse). Serum cortisol concentrations were measured before and 30, 60, 90, 120, 180, and 240 minutes after injection of cosyntropin or saline solution; CBCs were performed before and 30, 60, 120, and 240 minutes after injection.
Results—For all 4 doses, serum cortisol concentration was significantly increased, compared with the baseline value, by 30 minutes after administration of cosyntropin; no significant differences were detected among maximum serum cortisol concentrations obtained in response to administration of doses of 0.1, 0.25, and 0.5 μg/kg. Serum cortisol concentration peaked 30 minutes after administration of cosyntropin at a dose of 0.02 or 0.1 μg/kg, with peak concentrations 1.5 and 1.9 times, respectively, the baseline concentration. Serum cortisol concentration peaked 90 minutes after administration of cosyntropin at a dose of 0.25 or 0.5 μg/kg, with peak concentrations 2.0 and 2.3 times, respectively, the baseline concentration. Cosyntropin administration significantly affected WBC, neutrophil, and eosinophil counts and the neutrophil-to-lymphocyte ratio.
Conclusions and Clinical Relevance—Results suggested that in healthy horses, administration of cosyntropin at a dose of 0.1 μg/kg resulted in maximum adrenal stimulation, with peak cortisol concentration 30 minutes after cosyntropin administration.
Objective—To determine whether seasonal variations exist in endogenous plasma ACTH, plasma α-melanocyte—stimulating hormone (α-MSH), serum cortisol, and serum insulin concentrations and in the results of a dexamethasone suppression test for older, clinically normal geldings in Alabama.
Procedures—Sample collection was repeated monthly for 12 months. Dexamethasone (0.04 mg/kg [0.02 mg/lb], IM) was administered and cortisol concentrations were determined at 15 and 19 hours. Radioimmunoassays were used to measure ACTH, α-MSH, cortisol, and insulin concentrations at each testing time. Hormone concentrations were compared between months via repeated-measures ANOVA and correlated with age within each month.
Results—A significant time effect was found between months for α-MSH and insulin concentrations. Endogenous cortisol and ACTH concentrations remained within existing reference ranges. Significant correlations were detected between age and ACTH concentration for several fall and winter months and between age and insulin concentration for September.
Conclusions and Clinical Relevance—Older horses have higher ACTH concentrations in several fall and winter months and higher insulin concentrations in September than do younger horses. Seasonally specific reference ranges are required for α-MSH and insulin concentrations, with significantly higher concentrations detected in the fall. Practitioners should be advised to submit samples only to local laboratories that can provide such reference ranges for their local geographic region.
Objective—To evaluate pituitary-adrenal function in a
population of critically ill dogs by measuring serial
plasma concentrations of basal cortisol, ACTH-stimulated
cortisol, and endogenous ACTH.
Animals—20 critically ill dogs admitted to an intensive
care unit (ICU).
Procedure—Basal plasma cortisol, ACTH-stimulated
cortisol, and endogenous ACTH concentrations were
measured for each dog within 24 hours of admission
and daily until death, euthanasia, or discharge from
the ICU. Established reference ranges for healthy
dogs were used for comparison. Survival prediction
index (SPI) scores were calculated for each dog within
24 hours of admission.
Results—No significant difference was found
between initial concentrations of basal cortisol,
ACTH-stimulated cortisol, and endogenous ACTH in
13 dogs that survived and those in 7 dogs that died.
High initial basal endogenous ACTH concentrations
were correlated with subsequent high values. Low
basal ACTH-stimulated cortisol concentrations were
predictive of higher subsequent values. All basal and
ACTH-stimulated cortisol concentrations were within
or above the reference range in the 52 plasma samples
collected from the 20 dogs during hospitalization.
The SPI scores correlated with outcome (ie, alive or
dead), but none of the plasma hormone concentrations
correlated with SPI score or outcome.
Conclusions and Clinical Relevance—Results indicate
that none of the critically ill dogs in our study
population developed adrenal insufficiency during
hospitalization in the ICU. (J Am Vet Med Assoc
Objective—To assess serum 17-α-hydroxyprogesterone
(17OHP) and corticosterone concentrations in
dogs with nonadrenal neoplasia and dogs being
screened for hyperadrenocorticism.
Animals—16 clinically normal dogs, 35 dogs with
nonadrenal neoplasia, and 127 dogs with suspected
Procedure—ACTH stimulation tests were performed
in all dogs. Baseline serum cortisol and corticosterone
concentrations were measured in the healthy dogs;
baseline serum cortisol concentration and ACTH-stimulated
cortisol, corticosterone, and 17OHP concentrations
were measured in all dogs. Endogenous plasma
ACTH concentration was also measured before
administration of ACTH in dogs with neoplasia.
Results—In 35 dogs with neoplasia, 31.4% had high
serum 17OHP concentration and 22.9% had high
serum corticosterone concentration. Of the 127 dogs
with suspected hyperadrenocorticism, 59 (46.5%) had
high ACTH-stimulated cortisol concentrations; of those,
42 of 59 (71.2%) and 32 of 53 (60.4%) had high serum
17OHP and corticosterone concentrations, respectively.
Of dogs with serum cortisol concentration within reference
range after ACTH administration, 9 of 68 (13.2%)
and 7 of 67 (10.4%) had high serum 17OHP and corticosterone
concentrations, respectively. In the dogs
with neoplasia and dogs suspected of having hyperadrenocorticism,
post-ACTH serum hormone concentrations
were significantly correlated.
Conclusions and Clinical Relevance—Serum concentrations
of 17OHP or corticosterone after administration
of ACTH may be high in dogs with nonadrenal neoplasia
and no evidence of hyperadrenocorticism. Changes in
serum 17OHP or corticosterone concentrations after
administration of ACTH are proportionate with changes
in cortisol concentration. (J Am Vet Med Assoc 2005;227:1762–1767)