Metabolic Response To Injury

Surgery Presentation
Franz fanon university

Class MD4
topic: metabolic response to injury
Student :sharma’arke Ahmed
contents
1. Introduction
2. Metabolic response to injury
3. Phases of metabolic response
4. key catabolic elements of flow phase
5. metabolism after injury
6. Factors can be avoided to reduce
Metabolic response to injury(surgery)
1
Introduction
1.Introduction
• Stress response caused by events such as surgical trauma includes
endocrine, metabolic and immunological changes.
• Stress hormones and cytokines play a role in these reactions.
• More reactions are induced by greater stress, ultimately leading to
greater catabolic effects.
• the initial hours after surgical or traumatic injury are metabolically
associated with a reduced total body energy expenditure and urinary
nitrogen wasting.
2
Metabolic response to injury
Metabolic response to injury
• The body responds to trauma with :-

-tachycardia,
-an increase in the use of oxygen,
- an increase in respiratory rate,
-body temperature and
-catabolism
• In 1930, Sir David Cuthbertson divided the metabolic response to
injury in humans into ‘ebb’ and ‘flow’ phases
33
phases of metabolic
response to injury
1.Ebb phase
• The ‘Ebb phase’ begins at the time of surgery (injury) and is characterised
by
- hypovolaemia,
-depression of metabolic rate,
-reduced cardiac output,
-hypothermia,
-lactic acidosis and
- an overall reduction in energy expenditure
• The main hormones in this phase are catecholamines, cortisol and
aldosterone.
2.Catabolic phase
• In the catabolic phase, there is an increased catecholamine drive and
• energy is mobilised from adipose tissue and carbohydrate stores in
the liver and muscle to aid recovery and repair.
• This phase is characterised by tissue oedema, increased metabolic
rate, increased cardiac output, increased oxygen consumption and
increased gluconeogenesis.
• Moreover, there is an increased production of hormones
(catecholamines, cortisol, insulin, glucagons) and inflammatory
cytokines (IL-1, IL-6, TNF-α) that utilises fat and protein stores.
• This leads to weight and nitrogen loss.
• The increased production of insulin results in insulin resistance. During
this phase, the patient is at risk of infections and cardiac dysfunction.
3.Anabolic phase
• The anabolic phase occurs in conjunction with repair.

• There is weight gain, protein and fat stores increase, and the metabolic
response returns to normal.
4
KEY CATABOLIC ELEMENTS OF
THE FLOW PHASE
4 KEY CATABOLIC ELEMENTS OF THE FLOW
PHASE OF THE METABOLIC STRESS RESPONSE
• There are several key elements of the flow phase that largely
determine the extent of catabolism and thus rule the metabolic and
nutritional care of the surgical patient.
• During the response to injury, not all tissues are catabolic.
• the significance of this coordinated response is to allow the body to
rearrange limited resources away from peripheral tissues (muscle,
adipose tissue, skin) and towards key viscera (liver, immune system)
and the wound.
1.Hypermetabolism
• The majority of trauma patients (except those with extensive burns)

demonstrate energy expenditures about 15–25% above predicted
values .
• The most cause appears to be a complex interaction between the
central control of metabolic rate and peripheral energy utilisation.
• several features of standard intensive care (including bed rest,
paralysis, ventilation and external temperature regulation) counteract
the hypermetabolic driving forces of the stress response.
• the skeletal muscle wasting experienced by patients with prolonged
catabolism actually limits the volume of metabolically active tissue .
2.Alterations in skeletal muscle
protein metabolism
• Muscle protein is continually synthesised and broken down with a loss

rate in humans of 1–2% per day , a greater bulk of changes in protein
synthesis than breakdown .
• Normally, synthesis equals breakdown and muscle bulk remains
constant.
• Physiological stimuli that promote net muscle protein actual growth
include feeding (especially extracellular amino acid concentration)
and exercise.
• unclearly during exercise, skeletal muscle protein synthesis is
depressed, but it increases again during rest and feeding.
• During the catabolic phase of the stress response, muscle wasting
occurs as a result of an increase in muscle protein degradation
(via enzymatic pathways),
• coupled with a decrease in muscle protein synthesis.
• The major site of protein loss is peripheral skeletal muscle, although
nitrogen losses also occur in the respiratory muscles and gut
• predesposing patient to hypoventilation and chest infections and
reducing gut motility (Cardiac muscle mostly spared) .
• Under extreme conditions of catabolism (e.g. major sepsis), urinary
nitrogen losses can reach 14–20 g/day; this is equal to the loss of
500 g of skeletal muscle per day.
• muscle catabolism cannot be inhibited fully by providing artificial
nutritional support as long as the stress response continues.
• Hyperalimentation(form of nutritinon) represents a metabolic stress
in itself, and nutritional support attenuates rather than replace
energy and protein losses.
• The predominant mechanism involved in the wasting of skeletal
muscle is the ATP-dependent ubiquitin–proteasome pathway
• the lysosomal cathepsins and the calcium–calpain pathway play
facilitatory and accessory roles.
3 . Alterations in hepatic protein metabolism:
the acute phase protein response
• The liver and skeletal muscle together account for >50% of daily body
protein turnover(loss).
• liver has higher protein turnover rate (10–20% per day).
• Skeletal muscle has a large mass but a low turnover rate
• Albumin is the major export protein produced by the liver and is
renewed at the rate of about 10% per day.
• The transcapillary escape rate (TER) of albumin is about ten times the
rate of synthesis, and short-term changes in albumin concentration
• are most probably due to increased vascular permeability.
• The transcapillary escape rate (TER) of albumin is about ten times the
rate of synthesis,
• and short-term changes in albumin concentration are most probably
due to increased vascular permeability.
• Albumin TER may be increased three-fold following
majorinjury/sepsis.
• In response to inflammatory conditions, including surgery, trauma,
sepsis, cancer or autoimmune conditions, circulating blood
mononuclear cells secrete IL-1, IL-6 and TNFα.
• These cytokines, in particular IL-6, promote the hepatic synthesis of
positive acute phase proteins, e.g. fibrinogen and C-reactive protein
(CRP).
• The acute phase protein response (APPR) represents a ‘double-edged
sword’ for surgical patients as it provides proteins important for
recovery and repair, but only at the expense of valuable lean tissue
and energy reserves.
• in contrast to the positive acute phase reactants, the plasma
concentrations of other liver export proteins (the negative acute
phase reactants) fall acutely following injury, e.g. albumin.
• This fall reflects increased transcapillary escape
• thus increased hepatic synthesis of positive acutephase reactants is
not compensated for by reduced synthesis of negative reactants.
4 Insulin resistance
• Following surgery or trauma, postoperative hyperglycaemia develops
as a result of increased glucose production combined with decreased
glucose uptake in peripheral tissues.
• Decreased glucose uptake is a result of insulin resistance which is
transiently induced within the stressed patient.
• Mechanisms for this phenomenon include the action of
proinflammatory cytokines and the decreased responsiveness of
insulin-regulated glucose transporter proteins.
• The degree of insulin resistance is proportional to the magnitude of
the injurious process.
• in upper abdominal surgery, insulin resistance may persist for
approximately 2 weeks.
• Postoperative patients with insulin resistance behave in a similar
manner to individuals with type II diabetes mellitus.
• The mainstay (chief support) of management of insulin resistance is
intravenous insulin infusion.
• Insulin infusions may be used in either an intensive approach (i.e.
sliding scales are changed to normalise the blood glucose level) or
• a conservative approach (i.e. insulin is administered when the blood
glucose level exceeds a defined limit and discontinued when the
level falls).
• The risks of adverse events following significant hypoglycaemia as a
consequence of intensive insulin therapy have led most ICUs to adopt
a more conventional approach to glycaemic control.
• It should be noted that diabetic patients whose glycaemic control has
been poor prior to their critical illness pose a particular challenge.
5
Metabolism After
Injury
5 Metabolism After
Injury
• Injuries or infections induce

unique neuroendocrine and
• immunologic responses
that differentiate injury
metabolism from that of
unstressed fasting.
• the magnitude of metabolic • with the more severe insults
expenditure over time appears associated with increased
to be directly proportional to the “metabolic hibernation.”
severity of insult, • However, by week 2, the total
• with thermal injuries and severe energy expenditure increases
infections having the highest dramatically.
energy demands see figure 2-18
• the first few days following both
sepsis and trauma are not
hypermetabolic states,
• The increase in energy expenditure is mediated in part by sympathetic activation
and catecholamine release
• Lipid metabolism after injury becomes the primary source of energy during
stressed states .
Lipid Metabolism After Injury
• Lipids are not merely nonprotein, noncarbohydrate fuel sources

that minimize protein catabolism in the injured patient.
• Lipid metabolism potentially influences the structural integrity of cell
membranes as well as the immune response during systemic inflammation.
• Fat mobilization (lipolysis) occurs mainly in response to catecholamine
stimulus of the hormone-sensitive triglyceride lipase.Other hormonal
influences that potentiate lipolysis include
adrenocorticotropic hormone (ACTH),catecholamines, thyroid
hormone, cortisol, glucagon, growth hormone release, and reduction in
insulin levels.
• adipose tissue provides fuel for the host in the form of free fatty acids
and glycerol during critical illness and injury.
• Oxidation of 1 g of fat yields approximately 9 kcal of energy.
5
4
factors can be avoided
4 factors can be avoided to reduce
the metabolic response to surgery
• Continued haemorrhage (volume loss)

• Hypothermia
• Tissue oedema
• Poor tissue perfusion
• Starvation
• Immobility
Thanks
prepared by
sharm'arke ahmed
reffrences
1 baily and love 27 edition
2.schwartz 's principle of surgery
3 double click
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4379844/#:~:text=ME
TABOLIC%20RESPONSE%20TO%20TRAUMA,negative%20nitrogen%20b
alance%2C%20i.e.%20catabolism.

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Surgery Presentation

Franz fanon university

• The body responds to trauma with :-

• The anabolic phase occurs in conjunction with repair.

• The majority of trauma patients (except those with extensive burns)

• Muscle protein is continually synthesised and broken down with a loss

• Injuries or infections induce

Lipid Metabolism After Injury

• Lipids are not merely nonprotein, noncarbohydrate fuel sources

• Continued haemorrhage (volume loss)

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