Basic Civil Engineering first year Notes- Chapter 4 Building.pptx
overview on "Metabolic response to injury"
1. Dr Farhad Uddin Ahmed
Asst Professor (Surgery)
Shaheed Suhrawardy Medical College
METABOLIC RESPONSE TO
INJURY/TRAUMA
2. Introduction
• The ‘Milieu Interior’–
the internal environment with the harmony
between systems in human body
• Homeostasis
The coordinated physiological process to maintain
body’s steady states
Vital organs acts as a whole.
3. ‘There is a circumstance attending accidental injury
which does not belong to the disease, namely that the
injury done, has in all cases a tendency to produce both
the deposition and means of cure’
-John Hunter
4. Responses to injury are, in general, beneficial to
the host and allow healing/survival.
5. • Closed loop system of homeostatic control by
negative feedback
• ‘Open Loop’ system
whereby only with medical/surgical resolution of the
primary abnormality is a must to return to classical
homeostatic system
6. • ‘Stress-free’ perioperative care helps to preserve
homeostasis following elective surgery
• Resuscitation, surgical intervention and critical care
can return the severely injured patient to a situation
in which homeostasis becomes possible once again
7. • Aims to Review the mediators of stress
response specially to surgical insult & trauma
8. • Body’s response to injury is always graded
• the more severe the injury, the greater the
response
9. Following elective surgery of
(intermediate severity)
transient and modest rise in
temperature,
heart rate,
respiratory rate,
energy expenditure and
peripheral white cell count.
10. Major trauma/sepsis
changes are accentuated
– systemic inflammatory response syndrome (SIRS),
– hypermetabolism,
– marked catabolism,
– shock
– multiple organ dysfunction (MODS).
22. Ebb phase
• Regulator players are
catecholamines,
cortisol &
aldosterone
• Response magnitude depends on
– Degree of blood loss
– Stimulation of somatic nerves at site of injury
23. FLOW PHASE
Catabolic phase 3-
10 days
Anabolic phase for
weeks
Mobilize energy stores for recovery &
repair, thus replacing damaged tissue.
Characterized by
– tissue edema (from vasodilatation
and increased capillary leakage)
– basal metabolic rate
(hypermetabolism)
– cardiac output,
– body temperature,
– oxygen consumption and
– gluconeogenesis.
24. counter-regulatory hormones
proinflammatory cytokines
Metabolic stress
responses
VISCIOUS CYCLE
significant fat and protein mobilisation
significant weight loss and
Increased urinary nitrogen excretion
significant insulin resistance
Prolonged
catabolism
26. Not all tissues are
catabolic at a time.
Reprioritization occurs to
utilize limited resources
27. Key factors
Hypermetabolism
Alterations in skeletal muscle protein
metabolism
Alterations in hepatic protein
metabolism: the acute phase protein
response
Insulin resistance
28. Hypermetabolism
• energy expenditures approximately 15–25% above
predicted healthy resting values.
• consuming high[ATP]-to maintain increased cardiac
output, protein turnover, nutritional support.
• intensive care (including bed rest, paralysis,
ventilation and external temperature regulation)
counteract the hypermetabolic driving forces
29. Alterations in skeletal muscle
protein metabolism
• Muscle protein turnover
rate 1–2% per day
• Synthesis & breakdown
equals in normal
circumstances
• Muscle protein
accretion by food &
exercise
30. During the catabolic phase
increased muscle protein degradation
SKELETAL MUSCLE
muscle wasting
Nitrogen loss
upto 10-20% in
severe sepsis
RESPIRATORY MUSCLE
hypoventilation,
chest infection
GUT MUSCLE
Decreased
motility
33. (APPR)
represents a ‘double-edged
sword’ for surgical patients
provides proteins important
for recovery and repair, but only at
the expense of valuable lean tissue
and energy reserves.
liver export proteins (the
negative acute phase reactants) fall
acutely following injury, e.g. albumin.
34. Insulin resistance
Following surgery or
trauma
Increased glucose
production ,
Decreased glucose uptake
in peripheral tissues.
postoperative
hyperglycaemia
35. The degree of insulin resistance
is proportional to the magnitude
of the injurious process
Insulin resistance may persist for
approximately 2 weeks.
The mainstay of management of
insulin resistance is intravenous
insulin infusion.
38. • The main labile energy reserve in the body is fat,
and the main labile protein reserve is skeletal
muscle.
• Protein turnover in the whole body is 150–200 g
per day.
• Excreted in urine as ammonia and urea
(i.e. approximately 14 g N/day).
39. Changes in body weight that occur in serious
sepsis, after uncomplicated surgery and in total
starvation • Critically ill patients
undergo massive changes
in body composition
• Body weight Increase by
ECF volm expansion in
24hrs, then goes to
negative balance
• body protein continued
loss ≥15% by 10 days even
in optimal care
.
40. How to
maintain body
weight and
nitrogen
equilibrium
following
major elective
surgery?
By blocking the neuroendocrine stress
response
– Careful Intraoperative
management of fluid balance,
– Avoidance of excessive
administration of intravenous
saline.
– Epidural analgesia/other
related techniques
– Providing early oral/enteral
feeding.
44. Effect
– reduced gastric emptying
– delayed resumption of food
intake
– prolonged hospital stay.
• Careful limitation of intraoperative
administration of balanced
crystalloids
45. Hypothermia
• Hypothermia results in
increased adrenal steroids
and catecholamines
• postoperative cardiac arrhythmias
• increased catabolism.
46. Hypothermia
• To maintain normothermia,
Upper body forced-air heating cover
• reduces wound infections,
• cardiac complications and
• bleeding and transfusion
requirements.
47. Tissue
edema
Systemic inflammation
Exudation of fluid,
plasma proteins, leukocytes,macrophages and
electrolytes leave the vascular space
accumulate in the tissues.
diminish the alveolar diffusion of
oxygen
reduced renal function.
48. Systemic inflammation and
tissue
underperfusion
endothelial activation
excessive, compromised
microcirculation
subsequent cellular hypoxia
risk of organ failure.
• Maintaining normoglycaemia with insulin
infusion during critical illness has been
proposed to protect the endothelium
49. Starvation
• obligate need to generate glucose to sustain
cerebral energy metabolism (100 g of glucose per
day).
• Mobilizes energy for cerebral metabolism from
– liver glycogen
– neoglucogenesis from lean tissue
– Fat from adipose tissue
– Ketone bodies
50. • 2 L of i/v 4% dextrose/0.18% sodium chloride as
maintenance fluid– protein sparing effect
• Avoiding unnecessary fasting
• early oral/enteral/parenteral nutrition
• allow intake of clear fluids up to 2 hours before
surgery, specially carbohydrate drink—prevents
postoperative insulin resistance
51. Immobility
• Potent stimulus for inducing
muscle wasting.
• Avoidance of unnecessary bed rest
• Active early mobilisation are
essential measures
