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

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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

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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

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Metabolic Changes in Surgical Patients

• Metabolic events brought about by STIMULI
• Injury
• Starvation
• Metabolic response is directed to restore
• Homeostasis
• Repair

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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)

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• 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).

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• 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

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• 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)

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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

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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

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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

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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

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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

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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

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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

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Metabolism of Injured Patient

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

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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.

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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

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• Traumatized Man

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• 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

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• 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.

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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

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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

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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)

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Route of Administration

1. ENTERAL ROUTE
2. PARENTERAL ROUTE (TPN)
3. COMBINATION

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ENTERAL

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

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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

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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

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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)

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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

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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

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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

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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

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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)

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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

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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

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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

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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

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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

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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).

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Parenteral Nutrition

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

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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.

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