kathmandu medical college, department of surgery

1. Metabolic Response To Trauma
Dr. Uttam Laudari
1st year Resident
KMCTH

2. Objectives understanding MRI
• Elective surgical procedures seeks to reduce the need for
homeostatic response by minimizing the primary insult.(
minimal access surgery, stress free peri op care)
• Emergency surgery- need to augment artificially homeostatic
response ( Resuscitation)

3. • Mediators of stress response
• Physiological changes
• Biochemical changes
• Changes in body composition following
surgical injury

4. Homeostasis
• The coordinated physiological process which maintains most of
steady states of organism
• Respose to injury are in general beneficial to the host and allow
healing and survival
• Metabolic response to injury is directly propotional to the severity
of injury
• This concept is applied to physiological, metabolic, immunological
changes and sequelae

5. In elective surgeries (intermediate severity)
There is increase in
• Temperature (transient)
• Heart rate
• Respiratory rate
• Energy expenditure
• White blood cells

6. In major trauma and sepsis
Above mentioned changes are accentuated by
• SIRS
• Hyper metabolism
• Marked catabolism
• Shock
• MODS

7. Mediators of Metabolic response to
injury
• Neuro endocrine response to injury/ critical illness
• Proinflammatory cytokine response of the innate immune
system

8. HYPOTHALAMIC-PITUITARY CIRCUIT

9. ENDOCRINE STRESS RESPONSE
HORMONE TIME EFFECT
Catecholamines Stress dependent
immediate and continues
for 24-48 hrs
1. Hyperglycemia
2. Raises metabolic rate
3. Mobilize fatty acids
4. Haemodynamic stability
ADH Immediate to 1 week 1. Promotes reabsorption of water
2. Peripheral vasoconstrictor
Renin-
Angiotensin
1. Vasoconstrictor
2. Release of Aldosterone
• Conserves sodium and eliminates
potassium
Insulin First hours: Decrease
secretion
Later anabolic: Increase
release of insulin
1. Glycolysis
2. Glycogenesis
3. Lipogenesis
4. Proinflammatory activity
Growth Hormone Anabolic Phase 1. Protein synthesis
2. Ketogenesis

10. OTHER ENDOGENOUS SUBSTANCES
Glucagon 1. Catabolic role
2. Glycogenolysis, lipolysis and
ketogenesis
3. Levels increase within 24 hrs
Renin-Angiotensin 1. Promotes volume homeostasis
2. Potent vasoconstrictor, inotropic
3. Release of Aldosterone
• Conserves sodium and eliminates
potassium
Thyroid Hormones 1. Decrease thyroid hormone activities
*Decrease T4 levels following injury are
predictive of mortality
Endogenous Opioids 1. B- endorphins attenuate pain
receptors
2. Immuno and GI modulators

11. Role of proinflammatory mediators
• The innate immune system principally macrophages interact
with adaptive immune system (T cells and B cells)
• Release proinflammatory cytokines IL-1,1L-6, TNF alfa, IL-8
with in 24 hours hypothalamus pyrexia
• directly act on muscle causing proteolysis
• Acting on liver to produce Acute phase protein
• Development of peripheral insulin resistance

12. IMMUNOLOGICAL RESPONSE

13. • Increased proinflammatory cytokines endogenous cytokine
antagonist enter the circulation and act to control the
proinflammatory response
• Later further development of a Th2 type counter-
inflammatory response(IL-3,5,9,13 & TGFB) is accentuated
and prolonged in critical illnessCARS ( depressed
immunity nosocomial infection)

14. EBB AND FLOW MODEL
• Physilogical resoponse to injury includes:
Immobility, anorexia and catabolism.
• EBB and flow Model given by Sir David
Cuthbertson in 1930

15. Ebb phase
• Onset- at time of injury
• Last for 24-48 hours
• Attenuated partially by resuscitation
• Features of ebb phase:
1. Hypovolemia
2. Decresed BMR
3. Decresed cardiac output
4. Hypothermia
5. Lactic acidosis

16. Ebb phase
Phenomenon Effect
 blood glucose
 lactate
free fatty acids
 catecholamine
 glucagon
 cardiac output
Below normal core
temperature
 oxygen consumption

17. • Regulators of Ebb phase- catecholamines, cortisol, and
aldosterone (RAAS)
• These regulators directly promotional to the degree of blood
loss and stimulation of somatic afferent nerve at site of injury

18. OUTCOME OF PATIENT IN THE Ebb PHASE
• Succumb from lack of oxygen and nutrient supply to major
organs
• Survive if prompt resuscitation is given

19. Flow phase
• Resuscitation in ebb phase flow phase
1. Catabolic phase 3-10 day
2. Anabolic phase – weeks
Flow phase
• Hyper metabolic phase
• Mobilization of body energy of stores for recovery
and repair
• Replacement of lost or damaged tissue

20. • Characteritic of flow phase
– Increase tissue oedema
– Increse BMR
– Increase CO
– Increase temperature
– Increase WBC
– Increse Oxygen consumption
– Increase gluconeogenesis

21. Flow phase
Phenomenon Effect
 catecholamine
 glucagon
 cortisol
 insulin
 cardiac output
 core body
temperature
 aldosterone
 ADH
IL1, IL6, TNF
spillage from
wound
 consumption
of glucose, FFA,
amino acid
 O2 consumption
fluid retention
systemic inflammatory
response
N or  glucose
N or  FFA
normal lactate
 CO2 production
 heat production
multi-organ
failure

22. Catabolic phase
• Increase in Counter regulatory hormones and inflammatory
cytokines
• Result in significant fat and protein mobilization
• Resulting weight loss and increase urinary nitrogen excretion
• Insulin resistance infection and CVS complications
• Complications further aggravates neuroendocrine and
inflammatory response vicious catabolic cycle

23. Key catabolic phase of the flow phase
• Hyper metabolism
• Alteration in skeletal muscle protein
metabolism
• Alternation in hepatic protein metabolism
•
• Insulin resistance

24. causes of hypermetabolism
• majority of trauma cases, energy expenditure of 15- 25 %
• Central thermodysregulation cytokines
• Increase sympathetic activity
• Abnormal wound circulation lactate, metabolized by ATP
consuming hepatic Cori cycle
• Hyperaemia  increase cardiac output
• Increase protein turn over
• controlled by routine critical care
– Bed rest
– Paralysis
– Ventilator
– External temperature regulation

25. Alteration in skeletal muscle protein
metabolism
• peripheral skeletal muscles(major)
• Respiratory muscle ( hypoventilation and chest infection)
• Gut- decrease gut motility
• Extreme catabolism- urinary nitrogen loss is more than
20gm/day ~ 500gm of skeletal muscle loss/day
• Mechanism involved in skeletal muscle wasting- ATP
dependent ubiquitin-proteasome pathway
• features- asthenia, fatigue, decrease functional ability,
decrese quality of life , increase morbidity and morbidity
• Critical illness myopathy( impaired excitation contraction
coupling )

26. The acute phase protein response
• Proinflammatory cytokines promote synthesis of positive
acute phase proteins( fibrinogen, CRP) in liver
• While the negative acute phase reactants fall ( albumin)

27. Insulin resistance
• Following trauma there in increase in blood sugar and also decreased in
glucose uptake
• Decreased in glucose uptake results in insulin resistance
• Following routine abdominal surgery, insulin resistance may persist up to 2
weeks.
• Postperative patient with insulin resistance behave as T2DM and incresed
risk of sepsis , deteriorating renal function ,polyneuropathy and death
• Treatment- intravenous insulin( sliding scale or conservative approach)

28. Changes in body composition following injury
• Catabolism leads to decrease in fat mass and skeletal muscle
mass
• Body weight may paradoxically increase because of expansion
of ECF fluid space with in 24 hours
• There after total body protein diminishes by 15% in next 10
days
• Body weight will reach negative balance as the expansion of
ECF resolves.
• Blocking the neuroendocrine response stress response with
epidural analgesia and providing early enteral feeding body
weight and nitrogen balance can be maintained

29. METHODS TO MINIMISE METABOLIC
RESPONSE
1. Replace fluid and blood losses to maintain BP
2. Maintain Oxygenation and Ventilation
3. Cardiovascular support by inotropes
4. Give adequate nutrition
5. Provide analgesia
6. Antibiotics
7. Avoid Hypothermia

30. MACRONUTRIENTS DURING STRESS
Carbohydrate
• At least 100 g/day needed to prevent ketosis
• Carbohydrate intake during stress should be between 30%-
40% of total calories
• Glucose intake should not exceed 5 mg/kg/min
Fat
• Provide 20%-35% of total calories
• Maximum recommendation for intravenous lipid infusion: 1.0
-1.5 g/kg/day
• Monitor triglyceride level to ensure adequate lipid clearance

31. Protein
• Requirements range from 1.2-2.0 g/kg/day during
stress
• Comprise 20%-30% of total calories during stress

32. METABOLIC RESPONSE TO OVERFEEDING
• Hyperglycemia
• Hypertriglyceridemia
• Hypercapnia
• Fatty liver
• Hypophosphatemia, hypomagnesemia, hypokalemia

33. Take home message
• Understanding current trends in metabolic res

34. Avoidable factors that compound the
response to injury
• Volume loss
– Aldosterone and ADH release, RAAS activation natural
oliguria with increase water and sodium retention in ECF
– Aggravated by saline rich fluids peripheral edema and
even visceral edema decrease gastric emptying, delayed
resumption to food intake and prolong hospital stay.
So careful administration on intraoperative crystalloid and
colloid is must such that there is no weight gain following
elective surgery

35. Hypothermia
• Hypothermia increase in adrenal steroids and
catecholamines
• Increasing two to three fold postoperative cardiac arrhythmias
and increased catabolism
RCT has showed maintaining normothermia by upper body
forced air heating covers reduces wound infection, cardiac
complications and bleeding and transfusion requirements

36. • Systemic inflammation and tissue under perfusion
– Leads to compromised microcirculation and subsequent cellular
hypoxia organ failure