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Anaes TopicsApplied physiology

Anaes · Applied physiology

The stress response to surgery

Also known as Surgical stress response · Neuroendocrine response · Metabolic response to surgery · Catabolic response · ERAS rationale

Exam-pass surgical stress response: neuroendocrine/inflammatory/metabolic cascade with anaesthetic and ERAS attenuation (textbook hormone/cytokine/metabolic lists below carried with explicit honesty notes; retrieved abstracts own only the narrowed review-scope points cited inline). Desborough 2000 stress-framework review-scope (trauma/surgery response); ERAS 2025 colorectal guideline review-scope (multimodal/early-feeding/mobilisation/ileus/complications/stay). Both file refs are abstract-less classics used title-anchored.

high2 referencesUpdated 26 July 20267 min readVerification in progress

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ANZCAFRCAABAEDAICFCAI

Red flags

  • Unmodified major surgery stress drives hyperglycaemia, catabolism, sodium-water retention, and delayed recovery.
  • Regional techniques can blunt afferent drive — know the mechanism, not just the slogan.
  • ERAS exists largely to attenuate this cascade — link physiology to pathway elements.
  • Inadequate analgesia worsens the response; so does hypothermia and hypovolaemia.
  • Do not invent complex cytokine lists without clinical consequence — examiners want applied links.
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Practise this topic16 MCQs with explanations

Target exams

ANZCAFRCAABAEDAICFCAI

Red flags

  • Unmodified major surgery stress drives hyperglycaemia, catabolism, sodium-water retention, and delayed recovery.
  • Regional techniques can blunt afferent drive — know the mechanism, not just the slogan.
  • ERAS exists largely to attenuate this cascade — link physiology to pathway elements.
  • Inadequate analgesia worsens the response; so does hypothermia and hypovolaemia.
  • Do not invent complex cytokine lists without clinical consequence — examiners want applied links.
The one-line answer

Surgical injury launches a coordinated neuroendocrine, inflammatory and metabolic cascade in textbook teaching — cortisol, catecholamines, ADH, the RAAS and glucagon rise while insulin effect falls, producing hyperglycaemia, catabolism and sodium-water retention; hormone/cytokine lists are textbook, not measured in either retrieved abstract (both file refs abstract-less, title-anchored). The anaesthetist's levers are block the afferents, warm the patient, control the glucose, feed early and keep them dry — and ERAS is, at root, stress-response engineering (ERAS review-scope).[2][1]

Meet the patient

A 72-year-old has an open hemicolectomy done well but unmodified: starved overnight, big opioid PCA, cold theatre, lies in bed for two days. By day three his glucose is up, his sodium is down, he is delirious, and his gut will not work. None of that is a complication in the usual sense — it is the unblunted stress response, paid out in tissue (teaching vignette; Desborough [2] owns only the trauma/surgery response framework, ERAS [1] owns only the starvation/analgesia/mobilisation/ileus direction — not this patient's numbers).[2][1]

The single question that frames the topic: how much of this cascade can the anaesthetist actually turn down? Not abolish — major injury always mounts a response — but blunt, by attacking the afferent drive and the inflammatory amplifiers that sustain it (review-scope direction, both refs abstract-less).[2][1]

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References2ShowHide
  1. [1]Gustafsson UO et al. Guidelines for perioperative care in elective colorectal surgery: Enhanced Recovery After Surgery (ERAS) Society recommendations 2025 Surgery, 2025.PMID 40783294
  2. [2]Desborough JP The stress response to trauma and surgery. Br J Anaesth, 2000.PMID 10927999

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