Transcript Lorem Ipsum - NUS Yong Loo Lin School of Medicine

Alteration in Metabolism
in
Surgical Patients
Energy Metabolism

In order to mount a metabolic
response to injury the body uses
as a fuel glucose, fat and protein

How much fuel does the body
have?
Body Composition
Source
kg
kcal
Fat
Protein
14
125,000
skeletal muscle
other
6
6
24,000
24,000
Glycogen
muscle
liver
free glucose
0.15
0.075
0.02
600
300
80
Body Composition
Even though protein is used as a fuel
in stress, its depletion is detrimental
Body Composition
Glycogen - Fuel
Fat
- Fuel
Protein
- Structure (use as a fuel
should be minimised)
Protein & Amino Acid
Metabolism
Protein

15% body weight - ½ intracellular

Enzymes, transport, hormones, immune
Fx, muscle

It is not usually a food

when needed it is converted to glucose
Protein & Amino Acid
Metabolism
Total protein turnover
300g /day
Obligatory N loss in urine 12g /day
or 80g protein /day
Protein & Amino Acid
Metabolism
Nitrogen Balance
N balance = N intake - N out

Negative in starvation, injury,
severe infection
Response to
Starvation vs Injury
Parameter
BMR
Mediators
Major fuel
Ketone production
Hepatic ureagenesis
Neg N balance
Gluconeogenesis
Muscle proteolysis
Hepatic protein synthesis
Starvation
Trauma
Fat
+++
+
+
+
+
+
++
+++
Mixed
+/+++
+++
+++
+++
+++
Protein & Amino Acid
Metabolism
If protein is depleted via proteolysis –
ability to adapt in stress is compromised

protein depletion results in
decreased wound healing
 decreased immune response
 defective gut-mucosal barrier
 decreased mobility/ respiratory effort

Homeostatic Responses
to Stress

Designed to maintain homeostasis

Same response in controlled or
uncontrolled stress

Trigger mechanisms:




Volume loss
Tissue damage
Pain
Fear
Homeostatic Responses
to Stress
Volume Loss & Tissue Underperfusion

Pressure & Stretch receptors activated

HR / SV increased

ADH / Aldosterone secreted 
renal and hypothalamic mechanism
Need for adequate resuscitation
Homeostatic Responses
to Stress
Tissue Damage

Most important trigger

Neural pathways from wound




reach hypothalamus
efferents go to pancreas  glucagon insulin
efferents to adrenal   cortisol, catecolamines
Release of cytokines
Homeostatic Responses
to Stress
Pain & Fear

Increased levels of catecholamines

Fight or flight response
Homeostatic Response

Elective operation

min tissue damage

pain/fear managed

less hypotension

infection rare

stress response in controlled
Homeostatic Response

Trauma

major tissue damage

pain/fear excessive managed

hypotension common

infection common

Stress response uncontrolled
Homeostatic Responses
to Stress
Triggers
 Response
Volume loss
 Neurohormonal and
Tissue damage  Inflammatory arms
Pain & Fear

Mediators of
Stress Response

Neurohormonal arm


Catecolamines, glucocorticoids,
glucagon, ADH, aldosterone
Inflammatory arm

Cytokines, complement, eicisanoids,
PAF
Mediators of Stress Response
Neurohormonal Arm
- Counterregulatory Hormones
 catecholamines



glucagon


glycogenolytic, gluconeogenic
glucocorticoids?/ACTH


maintain circulation,
hepatic glycolysis, lipolysis,
gluconeogenesis,  BMR
mobilise muscle protein, gluconeogenesis
ADH. Aldosterone

Retain water and Na
Mediators of
Stress Response

Inflammatory Arm - Cytokines

TNF-alpha, IL-1, IL-2, IL-6,
IFN-gamma

Local effects - para or autocrine

Response to tissue injury
Mediators of
Stress Response
Cytokines

In elective surgery


confined to wound
Trauma/sepsis

spill over/ endocrine effect
Mediators of
Stress Response

Cytokines - local effect

Promote wound healing

Stimulate angiogenesis

White cell migration

Ingrowth of fibroblasts

Localise the wound
Mediators of
Stress Response

Cytokines - spill over

Mobilisation of AA, stimulation of
acute phase protein synthesis

Increase WBC counts/Hypoferremia

Fever, subjective discomfort, sleep
Mediators of
Stress Response
Cytokines - severe trauma /sepsis

Increased organ vascular permeability

Multiple organ dysfunction

Hypotension
Stress Response
The stress just described response
may be characterised as a adrenergic
corticoid phase
When the patient recovers the
adrenergic corticoid phase changes
to an anabolic phase
Stress Response
Adrenergic-Corticoid Phase

 ACTH and cortisol


Catecolamines



Salt and water retention
 Insulin and  glucagon (via epinephrine)


circulatory adjustment
metabolic response if prolonged
Aldosterone and ADH


mobilises proteingluconeogenesis
gluconeogenesis
Cytokines confined to wound
Stress Response
Adrenergic - corticoid phase

Remains until insult corrected

Hypermetabolism-BMR increases
10-15% in elective operation
25% in long bone fracture
200% in 50% burn
Stress Response
Adrenergic - corticoid phase

Altered Glucose Metab

Normal/low insulin and insulin resistance

persisting hyperglycaemia

injured tissue uses glucose
Stress Response
ADRENERGIC - CORTICOID PHASE

Altered protein metabolism




Extensive muscle protein release
extensive urine N loss
reduced by feeding
Altered fat metabolism



Accelerated lipolysis via hormone sensitive
lipase
Ketosis blunted
Stress Response
ANABOLIC PHASE

 gluconeogenesis

 catecolamines

 aldosterone and ADH


 insulin and  glucagon


Salt and water loss
protein anabolism
cytokines reduction
Elective Operations

Adrenergic corticoid phase



period of catabolism
lasts 1-3 days
Anabolic phase




starts D3-D6
positive N balance
protein synthesis
recovery of lean mass
Nutritional Support
for Elective Operations
Because the adrenergic-corticoid phase is
short in elective, uncomplicated surgery
– Fluid therapy with 5% dextrose is
enough for up to 5-7 days
Nutritional Support
for Severe Stress

The adrenergic-corticoid phase is
prolonged in




severe injury
Malnourished patients
Infected patients
Nutritional therapy is needed
Stress Responses
The response is affected

Malnutrition

Age

Gender

Infection
Consequences
of Malnutrition

Metabolic response needs increased energy
expenditure

If intake < expenditure - protein/fat mass lost

Loss of 15% BW interacts with disease
process to





compromise immune response - sepsis, MOF
poor wound healing
edema due to  albumin
reduced mobility,  respiratory muscle strength &
vital capacity  pneumonia
altered GI function/breached mucosal barrier
Normal Post Op Drip

Energy provided as dextrose

1 L of D5W - 50g or 170 kcal

Typical post op patient gets 500 kcal/d


enough to stimulate pancreatic insulin
not enough to support a severe stress
reaction

Need for nutritional support to match
energy expenditure if stress is prolonged
Metabolic Response
to Trauma /
Severe Surgical Stress

Unfed trauma patients rapidly use their
protein and fat stores resulting in
increased susceptibility to effects of
haemorrhage, operations and infection
resulting in organ system failure, sepsis
and death

Malnourished patients are at greater risk
Determinants of Host
Responses to Surgical Stress
Age

Fat mass increase with age

Loss of muscle mass

Loss of strength with immobility

Decreased sensitivity to perturbations

Decreased effectiveness to maintain
homeostasis
Determinants of Host
Responses to Surgical Stress
Gender

Lean body mass less in
females

N loss more pronounced in
muscular males
Determinants of Host
Responses to Surgical Stress

Invasive Infection

May complicate any operation / injury

Results in increases metabolic rate fever, hyperventilation, etc

Nutritional depletion synergystic
Metabolic Response
to Trauma /
Severe Surgical Stress
Cuthbertson described in 1930 the
 Ebb or shock phase
 Flow phase
Cuthbertson
Ebb
Flow
not described
Modern
unresuscitated
adrenergic-corticoid
anabolic
Metabolic Response
to Trauma /
Severe Surgical Stress
Cuthbertson

Ebb or shock phase




12-24 hours
 BP,  CO,  Temp,  O2 consumption
due to haemorrhage, hypoperfusion,
lactic acidosis
Flow phase (adrenergic - corticoid)


hypermetabolism,  CO, Urine N loss,
altered glucose, tissue catabolism
similar to elective surgery but greater
Questions ?
A 64 year old 70 kg man comes for a gastrectomy.
Prior to operation he had been eating poorly for 4
weeks. On the 7th POD after Billroth II gastrectomy
he was drowsy and febrile. There was green fluid
coming from his drain.
Describe the metabolic responses this patient has.
What are the confounding factors that may
complicate his recovery?
Coming soon to a
Lecture Theatre near you
– Nutritional Support
In a severely injured patient the priorities
are: - resuscitation
- wound care

Nutritional support usually after 48 hrs

The next lecture will cover all aspects
of nutrition
Questions