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Metabolic Changes and Nutritional Management of Surgical Patients

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Metabolic Changes and Nutritional Management of Surgical Patients James Taclin C. Banez, MD, FPSGS, FPCS Majority of surgical patients: well nourished / healthy ... – PowerPoint PPT presentation

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Title: Metabolic Changes and Nutritional Management of Surgical Patients


1
Metabolic Changes and Nutritional Management of
Surgical Patients
  • James Taclin C. Banez, MD, FPSGS, FPCS

2
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

3
Surgical Patients that Needs Nutritional Support
  • To shorten the postoperative recovery phase and
    minimize the number of complications
  • Chronically debilitated from their diseases or
    malnutrition.
  • Suffered severe trauma, sepsis or surgical
    complications

4
Metabolic Changes in Surgical Patients
  • Metabolic events brought about by STIMULI
  • Injury
  • Starvation
  • Metabolic response is directed to restore
  • Homeostasis
  • Repair

5
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)

6
  • Proteolysis increase due to increase CORTISOL
    ------gt inc. urinary nitrogen first 4 days of
    starvation (8-12g/day 6.25g of muscle/g of
    nitrogen).

7
  • 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 -gt PARADOXICAL FOOD INTOLERANCE

8
  • 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)

9
Metabolism of Injured Patient
  • PHASES
  • Catabolic phase (Ebb, Adrenergic-Corticoid)
  • 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

10
Metabolism of Injured Patient
  • PHASES
  • Early anabolic phase (flow, corticoid-withdrawal)
  • tissue perfusion has been restored, may last for
    days to months depending on
  • 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

11
Metabolism of Injured Patient
  • PHASES
  • Late anabolic phase
  • several months after injury
  • occurs once volume deficit have been restored
  • slower re-accumulation of CHON
  • re-accumulation of body fat

12
Metabolism of Injured Patient
  • Carbohydrate Metabolism in Injured Patient
  • Hyperglycemia proportional to the severity of
    injury
  • Importance
  • Homeostatic significance
  • Ready source of energy to the brain
  • Adequate delivery

13
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

14
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 its level is
    higher, but hyperglycemia persist because of
    continuous gluconeogenesis

15
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

16
Metabolism of Injured Patient
  • Lipid metabolism
  • primary source of energy
  • Best stimulus for hormone-sensitive lipase is
    CATECHOLAMINE
  • RANDLE EFFECT is not present

17
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.

18
Metabolism of Injured Patient
  • Protein Metabolism
  • Ketoadaptation is inhibited ----gt gluconeogenesis
    persist ---gt 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 (gt in young, healthy and
    male)
  • (-) nitrogen balance can be reduced by high
    caloric nitrogen supplement

19
  • Traumatized Man

20
  • Injury of any type is associated with
  • Immobilization
  • Starvation
  • 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
  • reduced or absent nutritional intake
  • significant reduction of energy charge and ATP
    content during shock, hypoxia, sepsis, ischemia
    and wound -? anaerobic metabolism

21
  • 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.

22
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23
Nutritional Support
  • Fundamental goal of nutritional support
  • To meet the energy requirement for metabolic
    processes
  • To maintain a normal core body temperature
  • For tissue repair

24
Nutritional Support
  • Indication of nutritional support
  • Pre-morbid state
  • Age of the patient
  • Duration of starvation
  • Degree of the insult
  • Likelihood of resuming normal intake within
    finite period

25
Nutritional Support
  • Determination of Lean Body Mass
  • Displacement
  • Exchange of labeled ions (radioactive K)
  • Neutron activation analysis
  • Total body counter
  • Nuclear magnetic resonance
  • Clinical history and physical examination
  • 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)

26
Route of Administration
  1. ENTERAL ROUTE
  2. PARENTERAL ROUTE (TPN)
  3. COMBINATION

27
ENTERAL
  • Advantages
  • more physiological (liver not bypassed)
  • lesser cardiac work
  • safer and more efficient
  • better tolerated by the patient
  • more economical

28
ENTERAL
  • Route
  • Naso-enteric tube feeding (blended food
    Casseinates and whole protein formulas)
  • Naso-esophageal or NGT / NJT.
  • Gastrostomy tube (blended food)
  • Stamm (sero-lined) temporary
  • Glassman (mucous-lined) permanent
  • Percutaneous endoscopic gastrostomy
  • Jejunostomy tube (elemental diet)
  • Roue-en-y - permanent
  • Witzel - permanent
  • Endoscopic

29
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31
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
  • 30 degree angle
  • Conscious
  • 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

32
Complication of Enteral Feeding
  • Malposition of the catheter (pharynx/trachea)
  • Inadvertently moved
  • Reinsert ideally w/ fluoroscopic guidance
  • Aspiration due to
  • Overloading
  • Supine position / unconscious
  • Change in gastric motility
  • Solute overloading --gt diarrhea, dehydration,
    electrolyte imbalance (hypokalemia,
    hypomagnesemia), hyperglycemia (hyperosmolar,
    nonketotic coma)
  • Avoided by gradual increase in the osmolality of
    the fluid
  • Perforation (rare)

33
Parenteral Nutrition
  • Components
  • CHON
  • Mixture of single amino acid of synthetic origin,
    largely produced from intelligent bacteria
    cultures
  • CHO
  • Provides calories hypertonic dextrose
  • Fat emulsion
  • 10 or 20 emulsion of soy or safflower oil
    emulsions, usually emulsified and stabilized with
    egg phosphatides and lecithin

34
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

35
Parenteral Nutrition
  • As Primary Therapy
  • 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

36
Parenteral Nutrition
  • As Supportive Therapy
  • 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

37
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Parenteral Nutrition
  • Contraindication of TPN
  • Lack of specific goal for severe metabolic
    management (inevitable dying).
  • Cardiovascular instability / severe metabolic
    derangement.
  • Feasible GIT feeding
  • Patient with good nutritional status
  • Infants with less than 3cm of small bowel
  • Irreversible decerebrate (dehumanized)

40
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

41
Parenteral Nutrition
  • Complication of TPN
  • Technical complication
  • Early - related to catheter insertion
  • Pneumothorax
  • Arterial laceration
  • Hemothorax
  • Mediastinal hematoma
  • Nerve injury to the brachial plexus
  • Hydrothorax
  • Air embolism
  • Catheter embolism

42
Parenteral Nutrition
  • Complication of TPN
  • Technical complication
  • Late
  • Erosion of the catheter to the bronchus or right
    atrium
  • Thrombosis
  • Upper arm swelling and pain at the base of the
    neck
  • Streptokinase / heparin ---gt coumadin
  • Septic thrombosis
  • Antibiotic therapy
  • Fogarty catheter embolectomy
  • Excision of the subclavian vein and superior
    venacava

43
Parenteral Nutrition
  • Complication of TPN
  • Metabolic complication
  • Inadequate administration of certain nutrient
  • Trace metal deficiency
  • Zinc deficiency
  • perioral pustular rash
  • darkening of the skin creases
  • neuritis
  • Copper deficiency
  • microcytic anemia

44
Parenteral Nutrition
  • Complication of TPN
  • Metabolic complication
  • Inadequate administration of certain nutrient
  • Essential Fatty Acid deficiency
  • Dry flaky skin w/ small reddish papules and
    alopecia
  • Disorder of Glucose metabolism
  • Hypoglycemia unexpected slowing of the glucose
    infusion / excessive insulin administration

45
Parenteral Nutrition
  • Complication of TPN
  • Metabolic complication
  • Disorder of Glucose metabolism
  • 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 ---gt dehydration, fever, obtundation and
    coma ---gt death.
  • Tx insulin 200 units/day and administration of
    large dextrose free hypoosmolar solution (0.45
    NSS w/ K).

46
Parenteral Nutrition
  • Complication of TPN
  • Metabolic complication
  • Liver function derangement
  • Adnormalities in SGOT / SGPT / Alk. PO4
  • Fatty infiltrate of liver ----gt fat emulsion

47
Parenteral Nutrition
  • Complication of TPN
  • Septic complication
  • Catheter infection
  • most lethal complication of TPN
  • Bacterial / fungal (candida)
  • Site of entry of the organism ---gt 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. ---gt removed
    catheter and culture the tip of the tube.

48
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49
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