Transcript Metabolic Changes and Nutritional Management of Surgical Patients James Taclin C. Banez, MD, FPSGS, FPCS.

Metabolic Changes and
Nutritional Management
of Surgical Patients
James Taclin C. Banez, MD, FPSGS, FPCS
Majority of surgical patients:
► well
nourished / healthy
► uncomplicated major surgical procedure
► has sufficient fuel reserve
► can withstand brief period of catabolic insult
and starvation of 7 days
 Postoperatively:
►can
resume normal oral intake
►supplemental diet is not needed
Surgical Patients that Needs
Nutritional Support
►
To shorten the postoperative recovery
phase and minimize the number of
complications:
1. Chronically debilitated from their diseases or
malnutrition.
2. Suffered severe trauma, sepsis or surgical
complications
Metabolic Changes in Surgical Patients

Metabolic events brought about by
STIMULI:
1. Injury
2. Starvation
 Metabolic response is directed to restore:
1. Homeostasis
2. Repair
Metabolic Response to
Starvation
►
►
HYPOGLYCEMIA – is primary stimulus
Hormonal Changes: increase cortisol, catecholamines,
glucagon, growth hormones
Primary gluconeogenic precursors by the liver & kidney:
a. lactate b. glycerol c. amino acid (alanine & glutamine)
►
► Proteolysis
increase due to increase CORTISOL -----> inc. urinary nitrogen first 4 days of starvation
(8-12g/day = 6.25g of muscle/g of nitrogen).
►
Protein catabolism for gluconeogenesis primarily comes
from SKELETAL muscle, but in pure starvation other
organs are involved
►
In liver. CHON loss is selective; spare enzymes for
gluconeogenesis and lipolysis.
In pancreas and GIT, enzymes for digestion and protein for
regeneration of epithelium is involved -> PARADOXICAL
►
FOOD INTOLERANCE
►
Rapid proteolysis of body CHON cannot proceed at 75
g/day for long, or else patient will die immediately
RANDLE EFFECT.
 decrease urinary excretion of nitrogen 2 – 4 gm/day due
to keto-adaptation of the brain
 decrease protein degeneration and major source of
energy is FAT (90%)
Metabolism of Injured Patient
PHASES:
1. Catabolic phase (Ebb, AdrenergicCorticoid):
 immediately following surgery or trauma
 characterized w/ hyperglycemia, increase
secretion of urinary nitrogen beyond the level
of starvation
 caused by increase glucagon,
glucocorticoid, catecholamines and
decrease insulin
 tries to restore circulatory volume and tissue
perfusion
Metabolism of Injured Patient
PHASES:
2. Early anabolic phase (flow, corticoidwithdrawal):
 tissue perfusion has been restored, may last for days
to months depending on:
a.
b.
c.
severity of injury
previous health
medical intervention
 sharp decline in nitrogen excretion
 nitrogen balance is positive (4g/day) indicating
synthesis of CHON and there is a rapid and
progressive gain in weight and muscular strength
Metabolism of Injured Patient
PHASES:
3. Late anabolic phase:




several months after injury
occurs once volume deficit have been restored
slower re-accumulation of CHON
re-accumulation of body fat
Metabolism of Injured Patient
Carbohydrate Metabolism in Injured
Patient:
Hyperglycemia = proportional to the severity
of injury

Importance:
1. Homeostatic significance
2. Ready source of energy to the brain
3. Adequate delivery
Metabolism of Injured Patient
Carbohydrate Metabolism:
Hyperglycemia:
 Caused by:
►Increased catecholamine (primarily), cortisol,
glucagon, GH, vasopressin, angiotensin II,
somatostatin and decrease insulin.
►Gluconeogenesis in liver and kidney and
impaired peripheral uptake of glucose
Metabolism of Injured Patient
Carbohydrate Metabolism:
Hyperglycemia:
 Insulin resistance:
►During
the Ebb phase there is reduction in beta cell
sensitivity to glucose due to Catecholamine,
somatostatin and reduced pancreatic blood
flow
►Resistance to exogenous administration on
insulin in both EBB and early FLOW phases
►In middle and late Flow phase, beta cell sensitivity
return to normal and it’s level is higher, but
hyperglycemia persist because of continuous
gluconeogenesis
Metabolism of Injured Patient
Carbohydrate Metabolism:
► Glucose
metabolism in wounded tissue:
 Increase glucose uptake and lactate
production because of anaerobic glycolysis due
to local tissue hypoxia
 (+) insulin insensitivity
Metabolism of Injured Patient
Lipid metabolism:
 primary source of energy
 Best stimulus for hormone-sensitive lipase is
CATECHOLAMINE
 RANDLE EFFECT is not present
Metabolism of Injured Patient
Protein Metabolism:
 Nitrogen urine excretion 30-50g/day due to
proteolysis; 20% utilized for energy
(calories) the rest for gluconeogenesis by
liver and kidney (cortisol, glucagon,
catecholamine).
 Primary source of protein is the skeletal
muscle and the visceral organs are spared.
Metabolism of Injured Patient
Protein Metabolism:
 Ketoadaptation is inhibited ---->
gluconeogenesis persist ---> proteolysis persist
(INTERLEUKIN I).
 The degree and duration (-) nitrogen balance is
related to severity of injury. The net CHON
catabolism depends on the age, sex and
physical condition of the patient (> in
young, healthy and male)
 (-) nitrogen balance can be reduced by high
caloric nitrogen supplement
Traumatized Man
Injury of any type is associated with:
1. Immobilization
2. Starvation
3. Repair
 the first two are associated with reduction in
energy requirement. While the third is
associated w/ increase energy requirement

The amount of energy produced in injured
pt. is not optimum, to supply necessary
energy for the repair due to:
1. reduced or absent nutritional intake
2. significant reduction of energy charge and ATP
content during shock, hypoxia, sepsis,
ischemia and wound - anaerobic
metabolism
REE (Resting energy expenditure)
by Harris and Benedict:
(MEN) 66.47 + 13.75 (W) + 5.0 (H) – 6.76 (A)
= Kcal/day
(Female) 65.51 + 9.56 (W) + 1.85 (H) – 4.68 (A)
= Kcal/day
Fever: increase resting energy expenditure of
approximately 7% for each degree of F of fever.
Nutritional Support
Fundamental goal of nutritional support:
1. To meet the energy requirement for
metabolic processes
2. To maintain a normal core body
temperature
3. For tissue repair
Nutritional Support
Indication of nutritional support:
1. Pre-morbid state
2. Age of the patient
3. Duration of starvation
4. Degree of the insult
5. Likelihood of resuming normal intake
within finite period
Nutritional Support
Determination of Lean Body Mass:
5.
Displacement
Exchange of labeled ions (radioactive K+)
Neutron activation analysis
Total body counter
Nuclear magnetic resonance
6.
Clinical history and physical examination
1.
2.
3.
4.
 History of weight loss, anorexia and disease process
that interfered with intake
 Anthropometric data (skin fold thickness , arm
circumference measurement, thenar eminence)
 Biochemical determination (TP, albumin, globulin, liver
profile, kidney function test)
Route of Administration:
1.
ENTERAL ROUTE
2.
PARENTERAL ROUTE (TPN)
3.
COMBINATION
ENTERAL
►
Advantages:
1.
2.
3.
4.
5.
more physiological (liver not bypassed)
lesser cardiac work
safer and more efficient
better tolerated by the patient
more economical
ENTERAL
Route:
1.
Naso-enteric tube feeding (blended food –
Casseinates and whole protein formulas)
 Naso-esophageal or NGT / NJT.
2.
Gastrostomy tube (blended food)
 Stamm (sero-lined) – temporary
 Glassman (mucous-lined) – permanent
 Percutaneous endoscopic gastrostomy
3.
Jejunostomy tube (elemental diet)
 Roue-en-y - permanent
 Witzel - permanent
 Endoscopic
ENTERAL
Hyperosmolar solution are better tolerated by the
stomach:




Gastric feeding – increase osmolality first then the
volume
Small bowel – volume first is increase then osmolality
Precautions to be observe to prevent
reflux/aspiration:
1. 30 degree angle
2. Conscious
3. Stop feeding at 11 pm


Use French 10 and after administration of food
clean the tube
Prolonged used render the cardia incompetent and
sometimes caused stricture
Complication of Enteral Feeding
1.
Malposition of the catheter
(pharynx/trachea):
 Inadvertently moved
 Reinsert ideally w/ fluoroscopic guidance
2.
Aspiration due to:
 Overloading
 Supine position / unconscious
 Change in gastric motility
3.
Solute overloading --> diarrhea, dehydration,
electrolyte imbalance (hypokalemia,
hypomagnesemia), hyperglycemia
(hyperosmolar, nonketotic coma)
 Avoided by gradual increase in the osmolality of the
fluid
4.
Perforation (rare)
Parenteral Nutrition
Components:
1. CHON:
 Mixture of single amino acid of synthetic
origin, largely produced from “intelligent
bacteria” cultures
2.
CHO:
 Provides calories; hypertonic dextrose
3.
Fat emulsion:
 10 or 20% emulsion of soy or safflower oil
emulsions, usually emulsified and stabilized
with egg phosphatides and lecithin
Parenteral Nutrition
Indications:
 Principal
indication is found in seriously ill
patients suffering from Malnutrition, Sepsis,
severe surgical or accidental trauma when
the use of the Gastrointestinal tract for
feeding is not possible.
 Can be supplemental in patients with
inadequate oral intake
Parenteral Nutrition
As Primary Therapy:

1.
2.
3.
4.
5.
6.
7.
TPN influence the disease process:
GIT fistula
Renal failure (ATN)
Short Bowel Syndrome
Acute Burn (severe trauma)
Hepatic failure
With normal bowel length but with
malabsorption syndrome due to SPRUE,
enzymatic or pancreatic insufficiency, Ulcerative
colitis, regional enteritis
Anorexia nervosa
Parenteral Nutrition
As Supportive Therapy:

1.
2.
3.
4.
5.
6.
7.
Nutritional support can be achieved but alteration in
the disease process have not been established.
New born GIT anomalies (TIF, gastrochisis,
omphalocele)
Alimentary tract obstruction (achalasia, stricture,
carcinoma, pyloric obstruction)
Acute radiation enteritis
Acute chemotherapy toxicity
Prolonged ileus
Prolonged respiratory support
Large wound losses
Parenteral Nutrition
Contraindication of TPN:
1. Lack of specific goal for severe metabolic
management (inevitable dying).
2. Cardiovascular instability / severe
metabolic derangement.
3. Feasible GIT feeding
4. Patient with good nutritional status
5. Infants with less than 3cm of small bowel
6. Irreversible decerebrate (dehumanized)
Parenteral Nutrition
Route of TPN:
 Central
hyperalimentation
 Subclavian vein
 Internal jugular vein
 Femoral vein
Gauge 16, 8-12 inches
radio-opaque catheter
end at SVC
 Checked position w/
x-ray

Parenteral Nutrition
Complication of TPN:
I.
Technical complication:
A.
Early: - related to catheter insertion
1.
2.
3.
4.
5.
6.
7.
8.
Pneumothorax
Arterial laceration
Hemothorax
Mediastinal hematoma
Nerve injury to the brachial plexus
Hydrothorax
Air embolism
Catheter embolism
Parenteral Nutrition
Complication of TPN:
I.
Technical complication:
A.
Late:
1.
2.
3.
Erosion of the catheter to the bronchus or right
atrium
Thrombosis:
 Upper arm swelling and pain at the base of the
neck
 Streptokinase / heparin ---> coumadin
Septic thrombosis:
 Antibiotic therapy
 Fogarty catheter embolectomy
 Excision of the subclavian vein and superior
venacava
Parenteral Nutrition
Complication of TPN:
II. Metabolic complication:
A.
Inadequate administration of certain
nutrient
1.
Trace metal deficiency:
a) Zinc deficiency:
 perioral pustular rash
 darkening of the skin creases
 neuritis
b) Copper deficiency:
 microcytic anemia
Parenteral Nutrition
Complication of TPN:
II. Metabolic complication:
A.
Inadequate administration of certain
nutrient:
2.
B.
Essential Fatty Acid deficiency:
 Dry flaky skin w/ small reddish papules and
alopecia
Disorder of Glucose metabolism:
1.
Hypoglycemia – unexpected slowing of the
glucose infusion / excessive insulin administration
Parenteral Nutrition
Complication of TPN:
II. Metabolic complication:
B.
Disorder of Glucose metabolism:
2.
Hyperglycemia – most dangerous metabolism
complication in TPN
 Due to rapid infusion (60 ml/hr the increase of
20ml/hr every 24-48 hrs)
 DM (Hyperosmolar nonketotic coma) due
to osmotic diuresis ---> dehydration, fever,
obtundation and coma ---> death.
 Tx: insulin 200 units/day and administration of
large dextrose free hypo=osmolar solution
(0.45% NSS w/ K+).
Parenteral Nutrition
Complication of TPN:
II. Metabolic complication:
C.
Liver function derangement:


Adnormalities in SGOT / SGPT / Alk. PO4
Fatty infiltrate of liver ----> fat emulsion
Parenteral Nutrition
Complication of TPN:
III. Septic complication:
A.
Catheter infection:





most lethal complication of TPN
Bacterial / fungal (candida)
Site of entry of the organism ---> site of catheter
Symptom: - sudden spike of fever
Management:
− Change TPN bottle, tubes and filter – culture /
investigate for presence of pneumonia, UTI,
wound infection, etc.
− If fever persist after 8 hrs. ---> removed
catheter and culture the tip of the tube.
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