A prospective study of the pathophysiology of carcinoid crisis

Mary E. Condron, Nora E. Jameson, Kristen E. Limbach, Ann E. Bingham, Valerie Sera, Ryan B. Anderson, Katie J. Schenning, Shaun Yockelson, Izumi Harukuni, Edward (Ed) Kahl, Elizabeth Dewey, Su Ellen Johnson Pommier, Rodney Pommier

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Abstract

Background: Sudden massive release of serotonin, histamine, kallikrein, and bradykinin is postulated to cause an intraoperative carcinoid crisis. The exact roles of each of these possible agents, however, remain unknown. Optimal treatment will require an improved understanding of the pathophysiology of the carcinoid crisis. Methods: Carcinoid patients with liver metastases undergoing elective abdominal operations were studied prospectively, using intraoperative, transesophageal echocardiography, pulmonary artery catheterization, and intraoperative blood collection. Serotonin, histamine, kallikrein, and bradykinin levels were analyzed by enzyme-linked immunosorbent assay. Results: Of 46 patients studied, 16 had intraoperative hypotensive crises. Preincision serotonin levels were greater in patients who had crises (1,064 vs 453 ng/mL, P =.0064). Preincision hormone profiles were otherwise diverse. Cardiac function on transesophageal echocardiography during the crisis was normal, but intracardiac hypovolemia was observed consistently. Pulmonary artery pressure decreased during crises (P =.025). Linear regression of preincision serotonin levels showed a positive relationship with mid-crisis cardiac index (r = 0.73, P =.017) and a negative relationship with systemic vascular resistance (r=-0.61, P =.015). There were no statistically significant increases of serotonin, histamine, kallikrein, or bradykinin levels during the crises. Conclusion: The pathophysiology of carcinoid crisis appears consistent with distributive shock. Hormonal secretion from carcinoid tumors varies widely, but increased preincision serotonin levels correlate with crises and with hemodynamic parameters during the crises. Statistically significant increases of serotonin, histamine, kallikrein, or bradykinin during the crises were not observed.

Original languageEnglish (US)
JournalSurgery (United States)
DOIs
StateAccepted/In press - Jan 1 2018

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Carcinoid Tumor
Serotonin
Prospective Studies
Kallikreins
Bradykinin
Histamine
Transesophageal Echocardiography
Swan-Ganz Catheterization
Hypovolemia
Histamine Release
Vascular Resistance
Pulmonary Artery
Linear Models
Shock
Hemodynamics
Enzyme-Linked Immunosorbent Assay
Hormones
Neoplasm Metastasis
Pressure
Liver

ASJC Scopus subject areas

  • Surgery

Cite this

Condron, M. E., Jameson, N. E., Limbach, K. E., Bingham, A. E., Sera, V., Anderson, R. B., ... Pommier, R. (Accepted/In press). A prospective study of the pathophysiology of carcinoid crisis. Surgery (United States). https://doi.org/10.1016/j.surg.2018.04.093

A prospective study of the pathophysiology of carcinoid crisis. / Condron, Mary E.; Jameson, Nora E.; Limbach, Kristen E.; Bingham, Ann E.; Sera, Valerie; Anderson, Ryan B.; Schenning, Katie J.; Yockelson, Shaun; Harukuni, Izumi; Kahl, Edward (Ed); Dewey, Elizabeth; Pommier, Su Ellen Johnson; Pommier, Rodney.

In: Surgery (United States), 01.01.2018.

Research output: Contribution to journalArticle

Condron, ME, Jameson, NE, Limbach, KE, Bingham, AE, Sera, V, Anderson, RB, Schenning, KJ, Yockelson, S, Harukuni, I, Kahl, EE, Dewey, E, Pommier, SEJ & Pommier, R 2018, 'A prospective study of the pathophysiology of carcinoid crisis', Surgery (United States). https://doi.org/10.1016/j.surg.2018.04.093
Condron, Mary E. ; Jameson, Nora E. ; Limbach, Kristen E. ; Bingham, Ann E. ; Sera, Valerie ; Anderson, Ryan B. ; Schenning, Katie J. ; Yockelson, Shaun ; Harukuni, Izumi ; Kahl, Edward (Ed) ; Dewey, Elizabeth ; Pommier, Su Ellen Johnson ; Pommier, Rodney. / A prospective study of the pathophysiology of carcinoid crisis. In: Surgery (United States). 2018.
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abstract = "Background: Sudden massive release of serotonin, histamine, kallikrein, and bradykinin is postulated to cause an intraoperative carcinoid crisis. The exact roles of each of these possible agents, however, remain unknown. Optimal treatment will require an improved understanding of the pathophysiology of the carcinoid crisis. Methods: Carcinoid patients with liver metastases undergoing elective abdominal operations were studied prospectively, using intraoperative, transesophageal echocardiography, pulmonary artery catheterization, and intraoperative blood collection. Serotonin, histamine, kallikrein, and bradykinin levels were analyzed by enzyme-linked immunosorbent assay. Results: Of 46 patients studied, 16 had intraoperative hypotensive crises. Preincision serotonin levels were greater in patients who had crises (1,064 vs 453 ng/mL, P =.0064). Preincision hormone profiles were otherwise diverse. Cardiac function on transesophageal echocardiography during the crisis was normal, but intracardiac hypovolemia was observed consistently. Pulmonary artery pressure decreased during crises (P =.025). Linear regression of preincision serotonin levels showed a positive relationship with mid-crisis cardiac index (r = 0.73, P =.017) and a negative relationship with systemic vascular resistance (r=-0.61, P =.015). There were no statistically significant increases of serotonin, histamine, kallikrein, or bradykinin levels during the crises. Conclusion: The pathophysiology of carcinoid crisis appears consistent with distributive shock. Hormonal secretion from carcinoid tumors varies widely, but increased preincision serotonin levels correlate with crises and with hemodynamic parameters during the crises. Statistically significant increases of serotonin, histamine, kallikrein, or bradykinin during the crises were not observed.",
author = "Condron, {Mary E.} and Jameson, {Nora E.} and Limbach, {Kristen E.} and Bingham, {Ann E.} and Valerie Sera and Anderson, {Ryan B.} and Schenning, {Katie J.} and Shaun Yockelson and Izumi Harukuni and Kahl, {Edward (Ed)} and Elizabeth Dewey and Pommier, {Su Ellen Johnson} and Rodney Pommier",
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T1 - A prospective study of the pathophysiology of carcinoid crisis

AU - Condron, Mary E.

AU - Jameson, Nora E.

AU - Limbach, Kristen E.

AU - Bingham, Ann E.

AU - Sera, Valerie

AU - Anderson, Ryan B.

AU - Schenning, Katie J.

AU - Yockelson, Shaun

AU - Harukuni, Izumi

AU - Kahl, Edward (Ed)

AU - Dewey, Elizabeth

AU - Pommier, Su Ellen Johnson

AU - Pommier, Rodney

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Background: Sudden massive release of serotonin, histamine, kallikrein, and bradykinin is postulated to cause an intraoperative carcinoid crisis. The exact roles of each of these possible agents, however, remain unknown. Optimal treatment will require an improved understanding of the pathophysiology of the carcinoid crisis. Methods: Carcinoid patients with liver metastases undergoing elective abdominal operations were studied prospectively, using intraoperative, transesophageal echocardiography, pulmonary artery catheterization, and intraoperative blood collection. Serotonin, histamine, kallikrein, and bradykinin levels were analyzed by enzyme-linked immunosorbent assay. Results: Of 46 patients studied, 16 had intraoperative hypotensive crises. Preincision serotonin levels were greater in patients who had crises (1,064 vs 453 ng/mL, P =.0064). Preincision hormone profiles were otherwise diverse. Cardiac function on transesophageal echocardiography during the crisis was normal, but intracardiac hypovolemia was observed consistently. Pulmonary artery pressure decreased during crises (P =.025). Linear regression of preincision serotonin levels showed a positive relationship with mid-crisis cardiac index (r = 0.73, P =.017) and a negative relationship with systemic vascular resistance (r=-0.61, P =.015). There were no statistically significant increases of serotonin, histamine, kallikrein, or bradykinin levels during the crises. Conclusion: The pathophysiology of carcinoid crisis appears consistent with distributive shock. Hormonal secretion from carcinoid tumors varies widely, but increased preincision serotonin levels correlate with crises and with hemodynamic parameters during the crises. Statistically significant increases of serotonin, histamine, kallikrein, or bradykinin during the crises were not observed.

AB - Background: Sudden massive release of serotonin, histamine, kallikrein, and bradykinin is postulated to cause an intraoperative carcinoid crisis. The exact roles of each of these possible agents, however, remain unknown. Optimal treatment will require an improved understanding of the pathophysiology of the carcinoid crisis. Methods: Carcinoid patients with liver metastases undergoing elective abdominal operations were studied prospectively, using intraoperative, transesophageal echocardiography, pulmonary artery catheterization, and intraoperative blood collection. Serotonin, histamine, kallikrein, and bradykinin levels were analyzed by enzyme-linked immunosorbent assay. Results: Of 46 patients studied, 16 had intraoperative hypotensive crises. Preincision serotonin levels were greater in patients who had crises (1,064 vs 453 ng/mL, P =.0064). Preincision hormone profiles were otherwise diverse. Cardiac function on transesophageal echocardiography during the crisis was normal, but intracardiac hypovolemia was observed consistently. Pulmonary artery pressure decreased during crises (P =.025). Linear regression of preincision serotonin levels showed a positive relationship with mid-crisis cardiac index (r = 0.73, P =.017) and a negative relationship with systemic vascular resistance (r=-0.61, P =.015). There were no statistically significant increases of serotonin, histamine, kallikrein, or bradykinin levels during the crises. Conclusion: The pathophysiology of carcinoid crisis appears consistent with distributive shock. Hormonal secretion from carcinoid tumors varies widely, but increased preincision serotonin levels correlate with crises and with hemodynamic parameters during the crises. Statistically significant increases of serotonin, histamine, kallikrein, or bradykinin during the crises were not observed.

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