Blood Arginine Vasopressin, Adrenocorticotropin Hormone, and Cortisol Concentrations at Admission in Septic and Critically Ill Foals and their Association with Survival

Hurcombe, Samuel D.A.; Toribio, Ramiro E.; Slovis, Nathan M.; Kohn, Catherine W.; Refsal, Kent R.; Saville, William J.; Mudge, Margaret C.

doi:10.1111/j.1939-1676.2008.0090.x

Cited by 91 publications

(161 citation statements)

References 59 publications

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“…In addition, if exhausted endogenous glucocorticoid synthetic capacity or adrenocortical resistance to ACTH is responsible for the lower cortisol concentrations seen in this group of foals, one would expect basal ACTH concentrations and ACTH : cortisol ratios to be higher rather than lower in hospitalized foals as compared with healthy foals. 21,22,29,30 Low ACTH concentrations in this group of foals thus suggest hypothalamic or pituitary suppression of the HPA axis, perhaps related to the effects of inflammatory cytokines stimulated by the foal's concurrent illness. [43][44][45] In contrast to previous reports, 29,30 significant differences in basal ACTH : cortisol ratios between surviving and nonsurviving hospitalized or septic foals were not identified in the present study population.…”

Section: Discussionmentioning

confidence: 99%

“…22,[24][25][26][27][28] In addition, recent studies have identified markedly increased ACTH : cortisol ratios (increased plasma ACTH concentration with correspondingly low serum cortisol concentration) in nonsurviving septic foals as compared with both healthy foals and surviving septic foals. 29,30 Low cortisol concentration in conjunction with increased ACTH concentration suggests that failure of cortisol synthesis is primarily at the level of the adrenal gland, whereas the central portions of the HPA axis appear intact.…”

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confidence: 99%

“…[31][32][33] Transient adrenal insufficiency has been described in 1 neonatal foal with concurrent septicemia and hypovolemic shock, 34 and recent evidence suggests that some degree of HPA axis dysfunction may occur in septic neonatal foals. 29,30,35 To the authors' knowledge, HPA axis function has not been evaluated in hospitalized or septic foals using a paired low-and high-dose ACTH stimulation testing protocol.…”

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confidence: 99%

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Hypothalamic‐Pituitary‐Adrenal Axis Dysfunction in Hospitalized Neonatal Foals

Hart

Slovis

Barton

2009

Veterinary Internal Medicne

124

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Background: Transient hypothalamic-pituitary-adrenal (HPA) axis dysfunction occurs frequently in critically ill humans and impacts survival. The prevalence and impact of HPA axis dysfunction in critically ill neonatal foals are not well characterized.Hypotheses: (1) HPA axis dysfunction occurs in hospitalized neonatal foals, and is characterized by inappropriately low basal serum cortisol concentration or inadequate cortisol response to exogenous adrenocorticotropic hormone (ACTH); (2) hospitalized foals with HPA axis dysfunction have more severe disease and are less likely to survive than hospitalized foals with normal HPA axis function.Animals: Seventy-two hospitalized foals and 23 healthy age-matched foals. Methods: Basal ACTH and cortisol concentrations were measured and a paired low-dose (10 mg)/high-dose (100 mg) cosyntropin stimulation test was performed at admission in hospitalized foals. HPA axis dysfunction was defined as (1) an inappropriately low basal cortisol concentration or (2) an inadequate increase in cortisol concentration (delta cortisol) after administration of cosyntropin, with cut-off values for appropriate basal and delta cortisol concentrations determined from results obtained in healthy age-matched foals.Results: Forty-six percent of hospitalized foals had an inappropriately low basal cortisol concentration and 52% had an inadequate delta cortisol concentration after administration of the 100 mg dose of cosyntropin. An inadequate delta cortisol response to the high (100 mg) dose of cosyntropin was significantly correlated with shock and multiple organ dysfunction syndrome in hospitalized foals, and with decreased survival in a subgroup of septic foals.Conclusions and Clinical Importance: HPA axis dysfunction occurs frequently in hospitalized neonatal foals, and negatively impacts disease severity and survival.

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Section: Discussionmentioning

confidence: 99%

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Hypothalamic‐Pituitary‐Adrenal Axis Dysfunction in Hospitalized Neonatal Foals

Hart

Slovis

Barton

2009

Veterinary Internal Medicne

124

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“…Possible mechanisms for these disturbances include reduced perfusion because of hypovolemia and hypotension,3, 4, 5, 6 activation of hormonal mechanisms including the renin angiotensin aldosterone system and vasopressin,7, 8, 9 tubular damage,10, 11 and perturbation of the hypothalamic–pituitary–adrenal axis 12. Plasma protein alterations might be caused by increased capillary leakage,12, 13 altered intravascular and tissue albumin distribution, imbalances between albumin synthesis and degradation14, 15 and failure of transfer of passive immunity (FTPI) 2…”

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confidence: 99%

Physicochemical Approach to Determine the Mechanism for Acid–Base Disorders in 793 Hospitalized Foals

Gómez

Biermann

Sanchez

2015

Veterinary Internal Medicne

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BackgroundThe quantitative effect of strong electrolytes, unmeasured strong anions (UAs), pCO 2, and plasma protein concentrations in determining plasma pH can be demonstrated using the physicochemical approach. Plasma anion gap (AG) and strong ion gap (SIG) are used to assess UAs in different species.HypothesesStrong ions are a major factor influencing changes in plasma pH of hospitalized foals. AG and SIG accurately predict severe hyper‐l‐lactatemia ([l‐lac−] > 7 mmol/L).AnimalsSeven hundred and ninety three hospitalized foals < 7 days old.MethodsRetrospective study. The relationship between measured pH and physicochemical variables, and the relationship between plasma [l‐lac−] and AG and SIG, were determined using regression analyses. Optimal AG and SIG cut points to predict hyper‐l‐lactatemia were identified using an ROC curve analysis.ResultsCombined, the measured strong ion difference and SIG accounted for 54–69% of the changes in the measured arterial pH of hospitalized foals. AG and SIG were significantly associated with plasma [l‐lac−] (P < .0001). The receiver operator characteristics (ROC) AUC of AG and SIG for prediction of severe hyper‐l‐lactatemia were 0.89 (95%CI, 0.8–0.95; P < .0001) and 0.90 (95%CI, 0.81–0.96; P < .0001), respectively. Severe hyper‐l‐lactatemia was best predicted by AG > 27 mmol/L (sensitivity 80%, 95%CI, 56–94, specificity 85%, 95%CI, 73–93; P < .0001) and SIG <−15 mmol/L (sensitivity 90%, 95%CI, 68–98; specificity 80%; 95%CI, 68–90; P < .0001).Conclusion and clinical relevanceAltered concentrations of strong ions (Na+, K+, Cl−) and UAs were the primary cause of acidemia of hospitalized foals. AG and SIG were good predictors of hyper‐l‐lactatemia and could be used as surrogate tests.

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“…The use and the clinical benefits of vasopressin in adult horses during CPR have not been determined (Muir and Hubbel 2009). The benefit of vasopressin is discussed controversial (Valverde et al 2006, Hurcombe et al 2008, Dembek et al 2014. Some authors even do not mention vasopressin when listing vasopressors (Holcombe 2006).…”

Section: Introductionmentioning

confidence: 99%

Vasopressin is life threatening for horses under isoflurane anaesthesia

Wollanke¹,

Reimold²,

Gerhards³

2015

PHK

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Summary: The aim of the study was to examine the effects of vasopressin on the cardiovascular system of horses under isoflurane anaesthesia. For this purpose ten horses of various breeds were taken which had to be euthanized under general anaesthesia. Decision for euthanasia was made either during surgery or during radiographic examination due to diagnosis of a fatal condition. The horses consisted of 7 geldings, 2 mares, and 1 male foal, aged 14±8,5 (mean±SD) years and weighing 499,5±105,1 (mean±SD) kg. Before euthanasia was performed during general anaesthesia, vasopressin was administered. Five horses obtained an intravenous injection of 0,2IU vasopressin/kg and five horses were given an infusion of 0,08IU vasopressin/kg minute over a 10 minute period. Mean arterial blood pressure, heart rate, colour of mucous membranes, capillary refill time, ocular reflexes, ECG, and respiratory frequency and volume were determined. Furthermore, arterial blood gas analysis, capnography and pulse oximetry were performed. Additionally, cardiac ultrasound and heart auscultation were conducted in four horses. The results were that the blood pressure increased within 30-60 seconds of vasopressin administration and that all horses developed a high degree of ischemia of the mucous membranes during the 30-60 seconds after either vasopressin injection or vasopressin infusion. Eight horses died due to cardiac failure. Cardiac arrest occurred in four horses within 5 minutes of vasopressin injection as well as in four horses during the 10 minutes of vasopressin infusion. In four horses an ultrasound examination during vasopressin administration revealed acute cardio dilation causing cardiac arrest. It can be concluded that Vasopressin is fatal for horses under general anaesthesia. The use of vasopressin must be avoided in horses. Vasopressin must not be used as an alternative drug for adrenaline in horses.Keywords: Vasopressin / horse / isoflurane anaesthesia / cardiac dilation / cardiac arrest / lethal / anesthesiology Citation: Wollanke B., Reimold R., Gerhards H. (2015) Vasopressin is life threatening for horses under isoflurane anaesthesia. Pferdeheilkunde 31, 341-345

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Blood Arginine Vasopressin, Adrenocorticotropin Hormone, and Cortisol Concentrations at Admission in Septic and Critically Ill Foals and their Association with Survival

Cited by 91 publications

References 59 publications

Hypothalamic‐Pituitary‐Adrenal Axis Dysfunction in Hospitalized Neonatal Foals

Hypothalamic‐Pituitary‐Adrenal Axis Dysfunction in Hospitalized Neonatal Foals

Physicochemical Approach to Determine the Mechanism for Acid–Base Disorders in 793 Hospitalized Foals

Vasopressin is life threatening for horses under isoflurane anaesthesia

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