Moderate-dose Vasopressin Therapy May Impair Gastric Mucosal Perfusion in Severe Sepsis

Klinzing, Stefan; Simon, Mark; Reinhart, Konrad; Meier‐Hellmann, Andreas; Sakr, Yasser

doi:10.1097/aln.0b013e318219d74f

Cited by 18 publications

(13 citation statements)

References 34 publications

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“…So far, few studies indicate that vasopressin decreases mesenteric and splanchnic blood flow. Results from studies in humans reported that vasopressin was responsible for this decreased flow even in the presence of additional catecholamines such as norepinephrine [13,[29][30][31]. Additionally, another interesting study demonstrated that addition of vasopressin resulted in decreased EN tolerability [26].…”

Section: Discussionmentioning

confidence: 99%

Vasopressors and Nutrition Therapy: Safe Dose for the Outset of Enteral Nutrition?

Covello

Gava-Brandolis

Ribeiro

et al. 2020

Critical Care Research and Practice

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Background and Aims. Patients with hemodynamic instability need to receive intensive treatment as fluid replacement and vasoactive drugs. In the meantime, it is supposed to initiate nutritional therapy within 24 to 48 hours after admission to the intensive care unit (ICU), as an essential part of patient’s intensive care and better outcomes. However, there are many controversies tangential to the prescription of enteral nutrition (EN) concomitant to the use of vasopressor and its doses. In this way, the present study aimed to identify what the literature presents of evidence to guide the clinical practice concerning the safe dose of vasopressors for the initiation of nutritional therapy in critically ill patients. Methods. This review was carried out in PubMed, ProQuest, Web of Science, and Medline databases. The descriptors were used to perform the search strategy: Critical Care, Intensive Care Units, Vasoconstrictor Agents, and Enteral Nutrition. Inclusion criteria were patients of both genders, over 18 years of age, using vasoactive drugs, with the possibility of receiving EN therapy, and articles written in English, Portuguese, and Spanish. In addition, exclusion criteria were case reports, non-papers, and repeated papers. Results. 10 articles met our inclusion criteria. Conclusion. It was observed that there are many controversies about the supply of EN in critically ill patients using vasopressor, especially about the safe dose, and it was not possible to identify a cutoff value for the beginning therapy. Despite the drug doses, clinical signs are still the most important parameters in the evaluation of EN tolerance.

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Section: Discussionmentioning

confidence: 99%

Vasopressors and Nutrition Therapy: Safe Dose for the Outset of Enteral Nutrition?

Covello

Gava-Brandolis

Ribeiro

et al. 2020

Critical Care Research and Practice

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“…Numerous investigators have shown that the administration of vasopressin to patients in septic shock leads to enteric and gastric hypoperfusion 14 – 17 . In a porcine surgical model of cardiopulmonary bypass, Bomberg and colleagues reported that vasopressin induced ischemia of the rectosigmoid region.…”

Section: Enteric Effects Of Pressorsmentioning

confidence: 99%

Feeding the Postoperative Patient on Vasopressor Support

Bruns

Kozar

2015

Nut in Clin Prac

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Initiating enteral nutrition in the postoperative patient can be challenging. Postoperative ileus and bowel edema, bowel anastomosis, and intra-abdominal pathology contribute to the reluctance and inability to achieve adequate nutrition in this patient population. The addition of vasopressors confounds the difficulties. Clinical data are sparse but suggest that most postoperative patients requiring vasopressor therapy can be safely initiated and advanced on enteral nutrition. Consideration of the vasopressor agent being utilized and its dose is imperative, as are individual patient characteristics. Temporal changes in the dosage should be closely monitored, as increasing doses may reflect worsening clinical status that can be due to intestinal ischemia. Well-designed prospective trials are clearly necessary to address this controversial topic.

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“…En ce qui concerne la microcirculation digestive, dans une autre étude, deux heures après avoir remplacé la noradrénaline par de l'arginine vasopressine (en moyenne 0,47 UI//min) avec un objectif de PAM stable à 70 mmHg, on constate un maintien du débit sanguin hépatosplanch-nique mesuré par la clairance du vert d'indocyanine malgré la baisse de l'index cardiaque, mais une augmentation de la différence artériogastrique du CO 2 (PCO 2gap ), plaidant en faveur d'une altération de la microcirculation avec hétéro-généité de perfusion aux dépens de la muqueuse gastrique [62]. Ces résultats étaient en accord avec ceux de Van Haren et al [63].…”

Section: Effets De La Vasopressine Sur La Microcirculation Chez L'animalunclassified

“…Vasopressine -Remplacement de la noradrénaline avec objectif de stabilité de la PAM à 70 mmHg ; pas de modification de la clairance du vert d'indocyanine, mais aggravation de la PCO 2gap en tonométrie gastrique [62] -Augmentation de la PCO 2gap en ajoutant de la vasopressine à 0,04 UI/h, la PAM augmentant en moyenne à 68 mmHg [63] -Comparaison vasopressine à la noradrénaline, amélioration de la clairance de la créatinine [64] -Comparasion à la noradrénaline : pas de modification de la PCO 2gap et amélioration de la clairance de la créatinine [65] -Choc distributif en post-CEC, ajout de 4 UI/h de vasopressine à noradrénaline vs noradrénaline seule : diminution de la PCO 2gap , mais augmentation des taux de bilirubine [68] -Ajout de vasopressine jusqu'à 4,8 UI/h à de la noradrénaline, augmentation de la PCO 2gap , diminution du flux [69] -Amélioration du débit de filtration glomérulaire chez des patients sans état de choc en post-CEC, mais dégradation de l'oxygénation rénale [70] Terlipressine -Augmentation de la PAM de 65 à 75, pas de modification par rapport à la vasopressine ou la noradrénaline sur l'indice de flux microcirculatoire sublingual [71] -Bolus de 0,5 mg, amélioration des paramètres de flux microcirculatoire sublingual à h6 et de la clairance de la créatinine [61] -Bolus de 1 mg, diminution de la PCO 2gap et augmentation du flux sanguin gastrique [62] Liens d'intérêts : Les auteurs déclarent ne pas avoir de lien d'intérêt.…”

Section: Sepsis Périopératoireunclassified

Effets des vasoconstricteurs sur la microcirculation

et al. 2015

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Les théories physiologiques et les modèles animaux nous prédisent souvent un effet néfaste de l'obtention d'une vasoconstriction importante sur la microcirculation. La diminution de la pression capillaire (avec au maximum une fermeture des capillaires en cas de pression extramurale trop forte), de l'hématocrite microcirculatoire, possiblement du débit, et de la densité capillaire possible en sont autant de raisons. En fait, les effets des vasoconstricteurs à disposition sont impossibles à prévoir : la noradrénaline par exemple provoque un effet alphapositif entraînant une augmentation des résistances artériolaires, mais aussi veineuses, avec un effet possible d'augmentation du débit cardiaque par effet précharge et/ou par bêtastimulation. Les effets sur la perfusion intestinale, rénale et microcirculatoire (le plus souvent sublinguale) sont souvent neutres, voire positifs pour la noradrénaline et la terlipressine au décours du choc septique, pour peu qu'une hypovolémie importante ait été traitée auparavant et que les objectifs de pression artérielle moyenne ne dépassent pas 75 mmHg. La phényléphrine semble être difficile d'utilisation et dangereuse pour la microcirculation. La vasopressine requiert probablement des études complémentaires concernant la microcirculation. Enfin, la titration et la décrémentation en cas de signe de dysoxie tissulaire (marbrures cutanées, augmentation du lactate) semblent être de bon sens. Mots clés Microcirculation · Vasoconstricteurs · Sepsis · Noradrénaline · Terlipressine · Adrénaline · Vasopressine · PhényléphrineAbstract Physiology and animal models often predict microvascular negative effects of excessive vasoconstriction. The following are among them: a drop in capillary pressure (even closure of capillaries), a drop in microvascular haematocrit, a possible drop in flow, a possible decrease in capillary density. In fact, the impact of usual vasoconstrictors is difficult to predict, e.g. norepinephrine is an alpha agonist, which simultaneously increases arteriolar but also venular resistances together with a possible increase in cardiac output by beta stimulation or thanks to preload effect. Concerning norepinephrine and probably terlipressin, the effects on splanchnic, renal and most often sublingual microcirculation are globally either positive or neutral if a deep hypovolemia is treated before perfusion of the drug and if mean arterial pressure goal is below 75 mmHg. Phenylephrine seems deleterious and difficult to use. Vasopressin requires more studies concerning microcirculation. Careful titration and even decrementation of the drugs in case of tissue dysoxia (mottling of the skin, the increase of lactate levels) seems to be common sense.

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Moderate-dose Vasopressin Therapy May Impair Gastric Mucosal Perfusion in Severe Sepsis

Cited by 18 publications

References 34 publications

Vasopressors and Nutrition Therapy: Safe Dose for the Outset of Enteral Nutrition?

Vasopressors and Nutrition Therapy: Safe Dose for the Outset of Enteral Nutrition?

Feeding the Postoperative Patient on Vasopressor Support

Effets des vasoconstricteurs sur la microcirculation

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