Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents*
Authors
Abstract
Surgery is of paramount importance in the management of solid tumors as definitive resection can be totally curative. Nonetheless, metastatic recurrence after surgery remains a major cause of morbidity and mortality. Interest in the impact of the perioperative period on cancer recurrence is now growing rapidly, with recent research suggesting that some anesthetics or anesthetic techniques may influence the pathophysiology of postoperative metastatic spread. Our review examines the most widely postulated mechanisms for this, including the impact of anesthesia on neuroendocrine and immune function. We also consider evidence for a direct impact on tumor cell signaling pathways based on findings from organ protection research. These studies have demonstrated that certain volatile anaesthetics confer cytoprotective properties to exposed cells and lead to significant upregulation of Hypoxia Inducible Factor-1α (HIF-1α). This ubiquitous transcription factor exerts many effects in cancer: its activity has been linked with more aggressive phenotypes and poorer clinical prognosis. It is proposed that such an upregulation of HIFs in tumor cells by these anesthetics may contribute to a tumor's recurrence by stimulating cytoprotective or protumorigenic behavior in residual cells. Conversely, other anesthetic agents appear to downregulate HIFs or cause negligible effect and thus may prove more suitable for use in cancer surgery. As anesthetic drugs are given at a point of potentially high vulnerability in terms of dissemination and establishment of metastases, there is an urgent need to determine the most appropriate anesthetic strategy for surgical oncology so that the optimal techniques are used to maximize long-term survival.
http://onlinelibrary.wiley.com/doi/10.1 ... 26448/full
Abbreviations
Akt: serine/threonine protein kinase; CMI: cell-mediated immune system; Erk1/2: extracellular signal-related kinases; GA: general anesthesia; HIF: hypoxia inducible factor; MMP: matrix metalloproteinases; mTOR: mammalian target of rapamycin; NK cell: natural killer cell; PCA: patient-controlled (opiate) analgesia pump; PI3K: phosphatidyl-inositol-3-kinase (PI3K); RA: regional anesthesia; RCC4: renal cell carcinoma cells (RCC4); TIVA: total intravenous anesthesia; VGEF: vascular endothelial growth factor
Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
Last edited by D.ap on Tue Jul 11, 2017 3:57 pm, edited 2 times in total.
Debbie
Re: Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
The Perioperative Period: A Critical Window for Cancer Recurrence
The body's response to the profound insult of surgery is a complex interplay of neuroendocrine, inflammatory, immune and metabolic pathways.18 Activation of multiple biological cascades leads to postoperative immunosuppression, affecting both humoral and cell-mediated responses.19, 20 It has been hypothesized that before metastasis occurs, equilibrium exists between the cell-mediated immune (CMI) system and novel tumorigenesis. In line with the theory of immunoediting,21 the immunosuppression caused by surgical intervention disrupts this delicate balance.
Despite meticulous surgical technique including minimal handling of the neoplasm, surgical resection of tumors causes measurable release of cancerous cells into the circulation.3–5 In addition to this seeding effect, undetectable micrometastases may already exist even in localized disease.22 The fate of these “proto-metastases” that escape detection and destruction seems to be significantly influenced by biochemical changes and perturbations of cellular signaling that occur following excision of the primary tumor.23, 24 Recent evidence suggests that adrenergic activation in itself can directly potentiate cancer cell growth.25 Thus, potentially curative surgical resection may paradoxically create a window of susceptibility, where residual cancer cells (either disseminated during surgery, or pre-existing micrometastases) are able to overcome host defenses and become established26 as distant metastatic disease, as has been demonstrated in animal models.27
The mechanism underlying the proposed beneficial effect of regional techniques has yet to be clearly defined. A leading theory states that immunosuppression is reduced by a combination of lessening exposure to immunosuppressive agents and reduced transduction of surgical stress, and hence neuroendocrine activation, secondary to regional neuronal blockade.28, 29 This dampening of the stress response helps maintain immune function, producing a less favorable environment for potential metastases to establish themselves during the critical perioperative time period.
The body's response to the profound insult of surgery is a complex interplay of neuroendocrine, inflammatory, immune and metabolic pathways.18 Activation of multiple biological cascades leads to postoperative immunosuppression, affecting both humoral and cell-mediated responses.19, 20 It has been hypothesized that before metastasis occurs, equilibrium exists between the cell-mediated immune (CMI) system and novel tumorigenesis. In line with the theory of immunoediting,21 the immunosuppression caused by surgical intervention disrupts this delicate balance.
Despite meticulous surgical technique including minimal handling of the neoplasm, surgical resection of tumors causes measurable release of cancerous cells into the circulation.3–5 In addition to this seeding effect, undetectable micrometastases may already exist even in localized disease.22 The fate of these “proto-metastases” that escape detection and destruction seems to be significantly influenced by biochemical changes and perturbations of cellular signaling that occur following excision of the primary tumor.23, 24 Recent evidence suggests that adrenergic activation in itself can directly potentiate cancer cell growth.25 Thus, potentially curative surgical resection may paradoxically create a window of susceptibility, where residual cancer cells (either disseminated during surgery, or pre-existing micrometastases) are able to overcome host defenses and become established26 as distant metastatic disease, as has been demonstrated in animal models.27
The mechanism underlying the proposed beneficial effect of regional techniques has yet to be clearly defined. A leading theory states that immunosuppression is reduced by a combination of lessening exposure to immunosuppressive agents and reduced transduction of surgical stress, and hence neuroendocrine activation, secondary to regional neuronal blockade.28, 29 This dampening of the stress response helps maintain immune function, producing a less favorable environment for potential metastases to establish themselves during the critical perioperative time period.
Debbie
Re: Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
Anesthetics and Immunosuppression
Although surgical stress and pain can activate neuroendocrine cascades that inhibit NK-cells around the perioperative period, anesthetics and analgesics (which alleviate pain and the stress response) can also independently suppress immune function. This becomes less counterintuitive when considering that anesthetic agents depress almost all components of the immune system:43 cell-mediated and humoral, in human and animal subjects and both in vivo and in vitro.44 The magnitude of these effects varies depending on the specific agent used.43–45 Interferon α/β stimulates NK-cell function, an effect which is attenuated in the presence of halogenated anesthetics.46 Melamed et al. investigated the effects of propofol, thiopental, ketamine and halothane: all agents reduced the number of circulating NK-cells and all except propofol depressed NK-cell cytotoxicity.45 Ketamine has notable adrenergic activity and is profoundly immunosuppressive. Accordingly, its use leads to increased incidence of metastases in animal models. In keeping with the role of catecholamines in the stress response, preadministration of a β-adrenergic antagonist attenuated the immunosuppressive and prometastatic effects of ketamine anesthesia.45
Opioids are widely used in anesthesia to provide both intra- and postoperative pain-relief. Although undoubtedly efficacious analgesics, there is growing evidence of their potential for exerting negative consequences in those undergoing cancer surgery. Administration of morphine to mice in clinically relevant doses leads to increased angiogenesis and growth of breast tumors.47 In addition to effects on tumor cell biology, opioids interact with the immune system: indirectly via modulation of the hypothalamic-pituitary-adrenal axis and autonomic nervous system, and directly via opioid receptors on immune cells. Both acute and chronic exposure to opioids dampen the actions of the humoral and CMI systems; with a multitude of suppressive effects seen: NK-cell activity, phagocytic activity and production of antibodies and cytokines are all reduced.48 In particular, morphine has been demonstrated to reduce NK-cell activity in a dose-dependant fashion in rats49 and also reduces NK-activity following intravenous administration in humans, the effects persisting 24 hr after the cessation of the infusion.50 However, the opiate-immune system interaction is complex: perioperative morphine given to rats undergoing laparotomy attenuated the tumor-retentive effect of surgery, most markedly when given preoperatively.51 Morphine promoted cell death and apoptosis in an adenocarcinoma cell line.52 Additionally, endogenous and exogenous opioids have differing immunomodulatory properties, partly explained by the degree of their affinity to the different opioid receptor subtypes.
Although inhalational anesthetics and opioids appear to negatively affect immune parameters, growing evidence suggests use of RA lessens the immunosuppressive burden of surgery.18, 53 Blockade of afferent nerve impulses that signal tissue damage has occurred leads to reduced activation of intra- and postoperative neuroendocrine stress responses. Accordingly, plasma cortisol18, 53 and catecholamine levels54–56 are reduced; the latter may be especially important as immune cells have functional adrenoreceptors, and lymphoid organs are richly innervated by autonomic nerves.57 The use of intraoperative epidural lowered catecholamine and cortisol levels, and accordingly, showed blood lymphocyte numbers were higher than those who had received opiates.56 Similar preservation of NK-cell activity and reduced plasma stress hormone levels following epidural use have been shown in patients undergoing hysterectomy.53 Through these effects, RA reduces intra- and postoperative opioid requirement. Although opiates are often used in neuraxial anesthesia, the dose required is several orders of magnitude lower than that used when delivered intravenously. By reducing opiate-induced immunosuppression,58 RA use may also abrogate opiate-induced NK-cell suppression.
These combined benefits of RA on NK-cell function may, therefore, reduce metastatic potential postresection. Animal models validate this phenomenon: Wada et al. demonstrated the addition of spinal block to sevoflurane GA reduced liver metastasis following laparotomy by over a third.42 Similarly, Bar-Yosef et al. showed that adding spinal blockade to halothane GA reduced the tumor retentive effects of laparotomy by 70%,29 a finding that supports the results seen in retrospective human studies. In addition, T-helper (Th) cells (CD4+ CD25+) appear to be important in explaining the protective effects of RA on CMI. Precursor cells undergo functional differentiation into either Th1 or Th2 subtypes, secreting an array of cytokines that augment the cell-mediated or humoral immunity, respectively. Therefore, the Th1/2 ratio can determine the profile of subsequent immune responses. Although surgery conducted under GA reduced the normal Th1/2 ratio, the addition of spinal anesthesia to GA preserved this ratio42 and accordingly immune cell cytotoxicity. Similar results have been recorded from patients undergoing transurethral resection of the prostate: preservation of the Th1/2 ratio, without alteration of total T-helper cell numbers.59 Thus, use of RA may promote a shift toward CMI that helps maintain NK-cell numbers during the period where they are most required to neutralize “proto-metastases.”
Although surgical stress and pain can activate neuroendocrine cascades that inhibit NK-cells around the perioperative period, anesthetics and analgesics (which alleviate pain and the stress response) can also independently suppress immune function. This becomes less counterintuitive when considering that anesthetic agents depress almost all components of the immune system:43 cell-mediated and humoral, in human and animal subjects and both in vivo and in vitro.44 The magnitude of these effects varies depending on the specific agent used.43–45 Interferon α/β stimulates NK-cell function, an effect which is attenuated in the presence of halogenated anesthetics.46 Melamed et al. investigated the effects of propofol, thiopental, ketamine and halothane: all agents reduced the number of circulating NK-cells and all except propofol depressed NK-cell cytotoxicity.45 Ketamine has notable adrenergic activity and is profoundly immunosuppressive. Accordingly, its use leads to increased incidence of metastases in animal models. In keeping with the role of catecholamines in the stress response, preadministration of a β-adrenergic antagonist attenuated the immunosuppressive and prometastatic effects of ketamine anesthesia.45
Opioids are widely used in anesthesia to provide both intra- and postoperative pain-relief. Although undoubtedly efficacious analgesics, there is growing evidence of their potential for exerting negative consequences in those undergoing cancer surgery. Administration of morphine to mice in clinically relevant doses leads to increased angiogenesis and growth of breast tumors.47 In addition to effects on tumor cell biology, opioids interact with the immune system: indirectly via modulation of the hypothalamic-pituitary-adrenal axis and autonomic nervous system, and directly via opioid receptors on immune cells. Both acute and chronic exposure to opioids dampen the actions of the humoral and CMI systems; with a multitude of suppressive effects seen: NK-cell activity, phagocytic activity and production of antibodies and cytokines are all reduced.48 In particular, morphine has been demonstrated to reduce NK-cell activity in a dose-dependant fashion in rats49 and also reduces NK-activity following intravenous administration in humans, the effects persisting 24 hr after the cessation of the infusion.50 However, the opiate-immune system interaction is complex: perioperative morphine given to rats undergoing laparotomy attenuated the tumor-retentive effect of surgery, most markedly when given preoperatively.51 Morphine promoted cell death and apoptosis in an adenocarcinoma cell line.52 Additionally, endogenous and exogenous opioids have differing immunomodulatory properties, partly explained by the degree of their affinity to the different opioid receptor subtypes.
Although inhalational anesthetics and opioids appear to negatively affect immune parameters, growing evidence suggests use of RA lessens the immunosuppressive burden of surgery.18, 53 Blockade of afferent nerve impulses that signal tissue damage has occurred leads to reduced activation of intra- and postoperative neuroendocrine stress responses. Accordingly, plasma cortisol18, 53 and catecholamine levels54–56 are reduced; the latter may be especially important as immune cells have functional adrenoreceptors, and lymphoid organs are richly innervated by autonomic nerves.57 The use of intraoperative epidural lowered catecholamine and cortisol levels, and accordingly, showed blood lymphocyte numbers were higher than those who had received opiates.56 Similar preservation of NK-cell activity and reduced plasma stress hormone levels following epidural use have been shown in patients undergoing hysterectomy.53 Through these effects, RA reduces intra- and postoperative opioid requirement. Although opiates are often used in neuraxial anesthesia, the dose required is several orders of magnitude lower than that used when delivered intravenously. By reducing opiate-induced immunosuppression,58 RA use may also abrogate opiate-induced NK-cell suppression.
These combined benefits of RA on NK-cell function may, therefore, reduce metastatic potential postresection. Animal models validate this phenomenon: Wada et al. demonstrated the addition of spinal block to sevoflurane GA reduced liver metastasis following laparotomy by over a third.42 Similarly, Bar-Yosef et al. showed that adding spinal blockade to halothane GA reduced the tumor retentive effects of laparotomy by 70%,29 a finding that supports the results seen in retrospective human studies. In addition, T-helper (Th) cells (CD4+ CD25+) appear to be important in explaining the protective effects of RA on CMI. Precursor cells undergo functional differentiation into either Th1 or Th2 subtypes, secreting an array of cytokines that augment the cell-mediated or humoral immunity, respectively. Therefore, the Th1/2 ratio can determine the profile of subsequent immune responses. Although surgery conducted under GA reduced the normal Th1/2 ratio, the addition of spinal anesthesia to GA preserved this ratio42 and accordingly immune cell cytotoxicity. Similar results have been recorded from patients undergoing transurethral resection of the prostate: preservation of the Th1/2 ratio, without alteration of total T-helper cell numbers.59 Thus, use of RA may promote a shift toward CMI that helps maintain NK-cell numbers during the period where they are most required to neutralize “proto-metastases.”
Debbie
Re: Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
Discussion: Clinical Considerations and Future Directions
Retrospective human evidence6–8, 10–15, 108–110 suggests anesthetic technique acts as a prognostic factor, independent of known factors such as stage and grade of tumor. However, the extent to which anesthetic technique may affect long-term outcomes and the contribution of individual perioperative factors to the overall risk of cancer recurrence remain unclear. As multimodal anesthesia is the norm, it becomes difficult to isolate the respective contributions of a particular drug. Even within the basic science literature, there is limited information regarding the specific properties of individual anesthetic agents in relation to tumor cell biology and/or the immune system. Compounding this is the huge variety of methods of inducing and maintaining general and RA and the inevitable interaction between the different techniques. Similarly, there is a lack of standardization across many of the trials in this regard. Future studies are likely to require large numbers of patients with prolonged follow-up.
The only prospective randomized controlled trial in this field has several limitations, which limit its applicability. Investigators are planning multicenter, prospective, randomized trials to clarify the role of anesthetic technique111 (in particular use of RA) in recurrence in cancers of the breast (NIH clinical trial: NCT00418457) and colon (NIH Clinical Trials: NCT00684229 & NCT00684229). These are welcome but as it will be several years before meaningful conclusions can be drawn, other forms of investigation must continue in the meantime, particularly in the laboratory and in health informatics.
Given the difficulties entailed in adequately accounting for so many variables in perioperative management in clinical studies, basic research has a vital role in guiding future efforts by focusing attention on defined hypotheses with a sound biomolecular basis and a demonstrable effect in experimental models. We have postulated that the cytoprotective properties of certain anesthetics seen in organ protection studies would be detrimental in the context of cancer, and our laboratory is working to confirm whether or not this is the case. However, genetic aberrations of key pathways in the HIF system in cancer are frequent. and the tumor microenvironment plays host to a number of confounding stimuli, such as growth factors and inflammatory cytokines. This makes it quite likely that the extent to which different anesthetics affect HIF-mediated cellular changes will vary according to the tumor's pathology and tissue of origin. For that reason, the effects of individual anesthetics on tumors need to be defined in a diverse range of cell types at the molecular and cellular level and then followed up in in vivo models of cancer surgery and metastasis. The most significant effects have been observed in melanoma10 and cancers of the breast,6 prostate,13 colon8, 9 and rectum.7 Indeed, certain tumors are more prone to recurrence, and it may be wise to investigate these as a priority.
The scientific literature cannot yet offer a definitive strategy for optimal anesthetic management in cancer patients. However, the huge pharmacopoeia available to anesthesiologists means that numerous alternatives are ready to replace drugs that prove detrimental. For example, it may become favorable to use propofol for total intravenous anesthesia in place of volatiles. RA may also feature more often, especially as it offers superior perioperative pain control compared to opiods.112 It should be noted that any putative benefit of one particular anesthetic technique over another in terms of cancer recurrence is likely to be small. Nonetheless, when scaled up to incorporate the huge numbers of patients undergoing cancer surgery worldwide, such a potential improvement merits thorough investigation.
In summary, the primary focus of curative cancer surgery is on complete resection and clearance. Paradoxically, the profound neuroendocrine and immune responses to physiological trauma that inevitably occur during surgery have been linked with prometastatic activity. Anesthetic agents can attenuate or potentiate these effects. Anesthetic drugs also appear to have direct actions on neoplastic cells, possibly by upstream effector-mediated activation of the HIF system. Optimal combinations of anesthetic agents and techniques may have a role in improved cancer survival.
Retrospective human evidence6–8, 10–15, 108–110 suggests anesthetic technique acts as a prognostic factor, independent of known factors such as stage and grade of tumor. However, the extent to which anesthetic technique may affect long-term outcomes and the contribution of individual perioperative factors to the overall risk of cancer recurrence remain unclear. As multimodal anesthesia is the norm, it becomes difficult to isolate the respective contributions of a particular drug. Even within the basic science literature, there is limited information regarding the specific properties of individual anesthetic agents in relation to tumor cell biology and/or the immune system. Compounding this is the huge variety of methods of inducing and maintaining general and RA and the inevitable interaction between the different techniques. Similarly, there is a lack of standardization across many of the trials in this regard. Future studies are likely to require large numbers of patients with prolonged follow-up.
The only prospective randomized controlled trial in this field has several limitations, which limit its applicability. Investigators are planning multicenter, prospective, randomized trials to clarify the role of anesthetic technique111 (in particular use of RA) in recurrence in cancers of the breast (NIH clinical trial: NCT00418457) and colon (NIH Clinical Trials: NCT00684229 & NCT00684229). These are welcome but as it will be several years before meaningful conclusions can be drawn, other forms of investigation must continue in the meantime, particularly in the laboratory and in health informatics.
Given the difficulties entailed in adequately accounting for so many variables in perioperative management in clinical studies, basic research has a vital role in guiding future efforts by focusing attention on defined hypotheses with a sound biomolecular basis and a demonstrable effect in experimental models. We have postulated that the cytoprotective properties of certain anesthetics seen in organ protection studies would be detrimental in the context of cancer, and our laboratory is working to confirm whether or not this is the case. However, genetic aberrations of key pathways in the HIF system in cancer are frequent. and the tumor microenvironment plays host to a number of confounding stimuli, such as growth factors and inflammatory cytokines. This makes it quite likely that the extent to which different anesthetics affect HIF-mediated cellular changes will vary according to the tumor's pathology and tissue of origin. For that reason, the effects of individual anesthetics on tumors need to be defined in a diverse range of cell types at the molecular and cellular level and then followed up in in vivo models of cancer surgery and metastasis. The most significant effects have been observed in melanoma10 and cancers of the breast,6 prostate,13 colon8, 9 and rectum.7 Indeed, certain tumors are more prone to recurrence, and it may be wise to investigate these as a priority.
The scientific literature cannot yet offer a definitive strategy for optimal anesthetic management in cancer patients. However, the huge pharmacopoeia available to anesthesiologists means that numerous alternatives are ready to replace drugs that prove detrimental. For example, it may become favorable to use propofol for total intravenous anesthesia in place of volatiles. RA may also feature more often, especially as it offers superior perioperative pain control compared to opiods.112 It should be noted that any putative benefit of one particular anesthetic technique over another in terms of cancer recurrence is likely to be small. Nonetheless, when scaled up to incorporate the huge numbers of patients undergoing cancer surgery worldwide, such a potential improvement merits thorough investigation.
In summary, the primary focus of curative cancer surgery is on complete resection and clearance. Paradoxically, the profound neuroendocrine and immune responses to physiological trauma that inevitably occur during surgery have been linked with prometastatic activity. Anesthetic agents can attenuate or potentiate these effects. Anesthetic drugs also appear to have direct actions on neoplastic cells, possibly by upstream effector-mediated activation of the HIF system. Optimal combinations of anesthetic agents and techniques may have a role in improved cancer survival.
Debbie
Re: Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
Relationship between Volatile Anesthetics and Tumor Progression: Unveiling the Mystery
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Summary
A series of factors can be involved in the perioperative period to cause an increase in cancer-related mortality. Unfortunately, volatile anesthesia might aggravate the deleterious effects. In this article, we review the association of diverse volatile anesthetic agents with immune system and cancer cell biology, and examine the effects on angeogenesis and postoperative metastasis or recurrence. Isoflurane, haloflurane and enflurane enhance immunosuppression and upregulate hypoxia-inducible-factor 1 and matrix metalloproteinases, leading to the cancer malignant progression, whereas roles of desflurane and sevoflurane are still unclear. As the effects of volatile anesthetics on tumor immunity have been known, it will be beneficial for using selective drugs into anesthesia and operation in cancer patients.
https://link.springer.com/article/10.10 ... 018-1970-6
From
“Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents*
Pay to view-
Summary
A series of factors can be involved in the perioperative period to cause an increase in cancer-related mortality. Unfortunately, volatile anesthesia might aggravate the deleterious effects. In this article, we review the association of diverse volatile anesthetic agents with immune system and cancer cell biology, and examine the effects on angeogenesis and postoperative metastasis or recurrence. Isoflurane, haloflurane and enflurane enhance immunosuppression and upregulate hypoxia-inducible-factor 1 and matrix metalloproteinases, leading to the cancer malignant progression, whereas roles of desflurane and sevoflurane are still unclear. As the effects of volatile anesthetics on tumor immunity have been known, it will be beneficial for using selective drugs into anesthesia and operation in cancer patients.
https://link.springer.com/article/10.10 ... 018-1970-6
From
“Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents*
Abbreviations
Akt: serine/threonine protein kinase; CMI: cell-mediated immune system; Erk1/2: extracellular signal-related kinases; GA: general anesthesia; HIF: hypoxia inducible factor; MMP: matrix metalloproteinases; mTOR: mammalian target of rapamycin; NK cell: natural killer cell; PCA: patient-controlled (opiate) analgesia pump; PI3K: phosphatidyl-inositol-3-kinase (PI3K); RA: regional anesthesia; RCC4: renal cell carcinoma cells (RCC4); TIVA: total intravenous anesthesia; VGEF: vascular endothelial growth factor
Debbie
Re: Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
Good to know, but do we have a say in what drug is used when the surgery conducted? Not likely. I hope that medical community updates their understanding though and considers this.
Olga
Re: Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents* Authors
Hello Olga,
Absolutely the medical community has to be more educated when it comes to anesthesia choices and their immune suppressive tendencies.
When Josh had his liver cryoablation performed we discussed this type of choices that were going to be used with his procedure.
Of course he had a choice to whether to be put completely under or using conscious sedation.
With surgical tumor removals , I’m not sure if there are a lot of choices .
Here’s an article on some less immune suppressive anesthesias
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774104/
Absolutely the medical community has to be more educated when it comes to anesthesia choices and their immune suppressive tendencies.
When Josh had his liver cryoablation performed we discussed this type of choices that were going to be used with his procedure.
Of course he had a choice to whether to be put completely under or using conscious sedation.
With surgical tumor removals , I’m not sure if there are a lot of choices .
Here’s an article on some less immune suppressive anesthesias
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774104/
Debbie
Effects of surgery and anesthetic choice on immunosuppression and cancer recurrence
Effects of surgery and anesthetic choice on immunosuppression and cancer recurrenceD.ap wrote: ↑Sun Aug 28, 2022 11:16 am Hello Olga,
Absolutely the medical community has to be more educated when it comes to anesthesia choices and their immune suppressive tendencies.
When Josh had his liver cryoablation performed we discussed this type of choices that were going to be used with his procedure.
Of course he had a choice to whether to be put completely under or using conscious sedation.
With surgical tumor removals , I’m not sure if there are a lot of choices .
Here’s an article on some less immune suppressive anesthesias
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774104/
Abstract
Background
The relationship between surgery and anesthetic-induced immunosuppression and cancer recurrence remains unresolved. Surgery and anesthesia stimulate the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS) to cause immunosuppression through several tumor-derived soluble factors. The potential impact of surgery and anesthesia on cancer recurrence was reviewed to provide guidance for cancer surgical treatment.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774104/
Debbie