SU1.1-2 | Homeostasis and Metabolic Response to Injury — Summary & Reflection

KEY TAKEAWAYS

Injury sets off a single integrated programme aimed at survival. After the initial ebb phase (hypometabolic, hypovolaemic, vasoconstricted, cool) comes the flow phase (hypermetabolic, first catabolic then anabolic) — the Cuthbertson model. It is driven by a neuroendocrine arm (cortisol, catecholamines and glucagon as counter-regulatory hormones causing hyperglycaemia and catabolism; ADH and aldosterone causing salt-and-water retention) and an inflammatory arm (IL-1, IL-6 and TNF-alpha causing fever and the hepatic acute-phase response). The result is hyperglycaemia, muscle breakdown with negative nitrogen balance, fat mobilisation and fluid retention. The magnitude is proportional to injury and, importantly, modifiable: prompt resuscitation, warmth, analgesia, minimally invasive surgery and early enteral feeding all blunt the harmful excess. Reading where a patient sits on this curve is the foundation of sound surgical fluid, nutrition and critical-care decisions.

REFLECT

Think back to a surgical or trauma patient you have seen who was cold, oliguric and tachycardic in the first day, or who lost noticeable muscle bulk over a week despite treatment. Map their course onto the ebb-and-flow model: which mediators explain each sign? Then ask which of the modifiable factors — warmth, resuscitation, analgesia, early feeding — were optimised and which could have been improved. How would understanding this programme change the way you prescribe fluids and nutrition for your next post-operative patient?