Metabolism In Surgical patients

Proteinogenic Amino Acids

Essential Amino Acids

• Histidine (HIS) - H
• Isoleucine (ILE) - I
• Leucine (LEU) - L
• Lysine (LYS) - K
• Methionine (MET) - M
• Phenylalanine (PHE) - F
• Threonine (THR) - T
• Tryptophan (TRP) - W
• Valine (VAL) - V

Conditionally Essential Amino Acids

• Arginine (ARG) - R
• Cysteine (CYS) - C
• Glutamine (GLN) - Q
• Tyrosine (TYR) - Y

Nonessential Amino Acids

• Alanine (ALA) - A
• Asparagine (ASN) - N
• Aspartate (ASP) - D
• Glutamate (GLU) - E
• Glycine (GLY) - G
• Proline (PRO) - P
• Serine (SER) - S
• Selenocysteine (SEC) - U

Brown Adipose Tissue (BAT)

• Thermogenic Tissue:
  • Mesenchymal lineage.
  • Dark appearance due to abundant mitochondrial content and limited lipid droplets.
• Function:
  • Energy Sink:
    • Highly uncoupled mitochondria.
    • Potential treatment for obesity and diabetes.
• Distribution in Adults:
  • Small depots located above the clavicle, near the vertebrae, in the mediastinum, and around the kidneys.
• Mechanism of Thermogenesis:
  • Proton Gradient Dissipation:
    • Loss of proton gradient causes ATP synthase to run in reverse (acts as a proton pump).
    • Leads to exothermic hydrolysis of ATP.
  • Electron Transport Chain:
    • Increased oxygen consumption, producing H₂O.
• BAT Origin:
  • Cells are myogenic factor 5 positive.
  • Related to muscle cells rather than white adipose tissue cells.
• "Beiging" or "Browning" of White Adipose Tissue:
  • White adipose cells acquire BAT characteristics under stress.
  • Driven by Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha (PGC-1α), the "master regulator" of mitochondrial biogenesis.
  • Observed in patients after severe burns.

Lipid Metabolism: Cholesterol

• Cholesterol Overview:
  • Critical element of cell membranes, alongside phospholipids.
  • Steroid alcohol structure: 3 cyclohexanes and 1 cyclopentane.
• Biosynthesis:
  • Starting substrate: Acetyl-CoA.
  • Rate-limiting enzyme: β-Hydroxy β-methylglutaryl-CoA reductase (HMG-CoA reductase).
  • Targeted by statins (cholesterol-lowering drugs).
  • No dietary requirement since cholesterol is fully synthesized by the body.
• Role in Steroid Hormones:
  • Backbone of all steroid hormones.
  • Rate-limiting step: Conversion of cholesterol to pregnenolone by cholesterol side chain cleavage enzyme.
  • Sex steroids synthesis occurs in the endoplasmic reticulum.
  • Final reactions of aldosterone, corticosterone, and cortisol synthesis take place in the mitochondria.
• Sites of Synthesis:
  • Female sex steroids: Derived exclusively from gonadal tissues.
  • Intermediate androgens: Synthesized in adrenal glands and processed further in the gonads.
  • All mineralocorticoids and glucocorticoids: Derived from the adrenal glands.
• Triglycerides
  • Structure:
    • Composed of a glycerol molecule bound to three fatty acid tails.
  • Function:
    • Primary form of body fat: Storage and transport of lipids.
    • Stored in lipid droplets within adipose tissue.
  • Energy Release:
    • Hormonal signals (e.g., epinephrine or glucagon) activate hormone-sensitive lipase.
    • Lipase hydrolyzes the ester bond to release free fatty acids into circulation.
  • Clinical Relevance:
    • Transient elevations in blood-free fatty acids occur in the perioperative period due to stress hormones.
    • The clinical significance of these elevations is unclear.

Amino Acid Metabolism

• Amino Acids Overview:
  • Small organic molecules with a carboxyl group, amino group, and various side chains.
  • 21 amino acids in human proteins, out of over 500 found in nature.
  • Functions beyond protein synthesis: precursors to neurotransmitters, nucleic acids, and fuel substrates (glucose and ketones).
• Proteinogenic Amino Acids:
  • Human proteins: Long chains of amino acids linked by covalent peptide bonds.
  • 21 amino acids appear in human proteins, but only 20 are directly coded by the genetic code.
  • Selenocysteine: Encoded by a stop codon under specific conditions.
• Sources of Amino Acids:
  • 12 amino acids synthesized by the body.
  • 9 essential amino acids must be consumed in the diet.
  • Branched-Chain Amino Acids (BCAAs): Isoleucine, leucine, valine.
    • Leucine: Important for signaling nutritional status in skeletal muscle.
    • BCAAs stimulate muscle protein synthesis.
• Amino Acids as Fuel:
  • Glucogenic amino acids (13): Can be oxidized into glucose.
    • Examples: Alanine, Arginine, Glycine, Histidine, Valine, Glutamine.
  • Ketogenic and Glucogenic amino acids (5): Can be converted to either ketones or glucose.
    • Examples: Isoleucine, Phenylalanine, Threonine.
  • Ketogenic amino acids (2): Only converted into ketones.
    • Examples: Leucine, Lysine.
  • Glucose-Alanine Cycle: Alanine converted to pyruvate and then glucose in the liver.
    • Similar to the Cori cycle.
  • BCAAs catabolism in skeletal muscle leads to the production of toxic ammonium ions.
    • Alanine is synthesized to offload ammonium, transported to the liver, and converted back to glucose.
• Amino Acids as Precursors to Neurotransmitters:
  • Tryptophan → Serotonin.
  • Tyrosine (product of Phenylalanine) → Catecholamines (Dopamine, Epinephrine, Norepinephrine).
  • Phenylalanine → Tyrosine and Phenylethylamine.
• Toxic By-Products of Amino Acid Metabolism:
  • Ammonia: Converted into water-soluble urea for excretion.
  • Liver: Principal organ for converting nitrogenous waste into urea.
  • Transport of Nitrogenous Waste:
    • Packaged into Glutamine and Alanine for blood transport to the liver.
  • Hepatic Encephalopathy: Risk in liver failure due to accumulation of urea and other toxins.
    • Caution needed in managing protein nutrition for liver failure patients.

Anabolic and Catabolic Hormones

Insulin

• Anabolic Peptide Hormone:
  • Facilitates cellular uptake of structural and fuel substrates.
  • Drives the uptake of glucose and promotes glycogen synthesis while suppressing glycogenolysis.
• Synthesis & Secretion:
  • Synthesized by the pancreas; secreted in response to elevated blood glucose.
  • Degraded by the liver and kidneys; half-life of 5-15 minutes.
• Mechanism:
  • Tyrosine kinase receptor signaling through phosphatidylinositol-3,4,5-triphosphate activates protein kinase B.
  • Stimulates GLUT-4 trafficking to cell membranes in skeletal muscle and adipose tissue.
  • Increases Na-K ATPase activity, reducing blood potassium levels.

Glucagon

• Catabolic Peptide Hormone:
  • Defends against hypoglycemia by stimulating gluconeogenesis and glycogenolysis in the liver.
  • Suppresses fatty acid synthesis and promotes fatty acid release via hormone-sensitive lipase.
• Synthesis & Secretion:
  • Synthesized by the pancreas; secreted in response to low blood glucose.
  • Secreted from alpha cells in response to falling blood glucose or epinephrine.
• Mechanism:
  • Binds to G-protein–coupled receptors signaling through cyclic adenosine monophosphate (cAMP).

Thyroid Hormones (T3 and T4)

• Energy Homeostasis:
  • Synthesized from tyrosine and iodine in the thyroid gland.
  • Essential minerals: Iodine and selenium.
• Function:
  • Regulated by the hypothalamic-pituitary axis.
  • Binds to thyroid hormone receptor (a nuclear receptor) to upregulate genes associated with glucose and lipid metabolism.
  • Increases heart rate and cardiac output.

Glucocorticoids (e.g., Cortisol)

• Catabolic Steroid Hormones:
  • Synthesized from cholesterol in the mitochondria of the zona fasciculata in the adrenal cortex.
  • Promotes gluconeogenesis, amino acid degradation, and lipolysis.
  • Cortisol is the most significant glucocorticoid.
• Response to Stress:
  • Controlled by adrenocorticotropic hormone (ACTH) from the pituitary gland.
  • Causes stress hyperglycemia due to high concentrations of glucocorticoids and catecholamines.
• Mechanism:
  • Binds to glucocorticoid receptor; translocates to the nucleus to regulate gene expression.
  • A subclass of receptors on the cell membrane mediates rapid, nongenomic responses.

Sex Hormones

• Steroid Hormones:
  • Determine secondary sexual characteristics via altering gene transcription.
• Androgens:
  • Promote protein accretion, glucose uptake, and oxidation in skeletal muscle.
  • Synthetic analogues (e.g., oxandrolone) have varying degrees of androgenic and anabolic activities.
• Estrogens:
  • Decrease lipogenesis and promote overall glucose homeostasis.

Nutritional Assessment Scores

Key Nutritional Assessment Tools:

• Nutrition Risk Screening (NRS 2002)
• Nutrition Assessment in Critically Ill (NUTRIC) Score:
  • Includes severity of disease and nutritional factors.
• Other Assessment Tools:
  • Malnutrition Universal Screening Tool (MUST)
  • Mini Nutritional Assessment (MNA)
  • Perioperative Nutrition Screen (PONS):
    • Assesses need for dietician/nutrition consultation before surgery.

Serum Markers

• Historical Use:
  • Previously relied upon as measures of nutritional status.
  • Markers: Albumin, prealbumin, retinol-binding protein, transferrin.
• Current Understanding:
  • Limitations:
    • Normal serum markers may persist until severe malnutrition (e.g., BMI <12 or 6 weeks of starvation).
    • Inflammatory stress reallocates amino acids to inflammatory proteins, lowering serum concentrations even in adequately nourished patients.
    • Albumin synthesis remains unchanged after surgery, but albumin capillary leak correlates with inflammation, leading to reduced intravascular levels.
  • Clinical Studies:
    • Administration of albumin for low serum concentrations does not improve outcomes.
    • Relationship between albumin and outcomes is likely non-causal.
• Preoperative Use:
  • Good or excellent correlation between preoperative albumin/prealbumin levels and patient outcomes.
  • Consider serum markers as preoperative prognostic factors, not indicators of nutritional status.
• Assessment Strategy:
  • Combine screening to identify at-risk patients.
  • Recognize phenotypic and etiologic factors to reliably establish a patient’s nutritional state.

Imaging in Nutritional Assessment

• Purpose:
  • Used as an adjunct to history and physical exam.
  • Monitors trends in lean body mass, bone mineral/density, and adiposity.

Dual Emission X-ray Absorptiometry (DXA)

• Gold Standard:
  • Highly accurate for measuring bone and soft tissues.
  • Uses low-dose ionizing radiation at two different energies.
• Capabilities:
  • Differentiates soft tissues and bone.
  • Calculates body fat, lean body mass, and bone mineral density/content.
• Limitations:
  • Precision and reproducibility decrease if the standard protocol is not maintained.
  • Variables like clothing, nasogastric tubes, or prosthetics can alter results.

Ultrasound

• Rapid and Reliable:
  • Bedside method to assess muscle mass.
  • No radiation involved; individual muscles can be measured.
• Quantitative and Qualitative Measurements:
  • Combines muscle dimension measurement with muscular density.
  • Correlates well with DXA but requires standardized protocols due to operator dependency.
• Technique:
  • B-mode ultrasound can determine the cross-sectional dimensions of the rectus femoris at the midpoint of the femur.

Computed Tomography (CT)

• Lean Body Mass Calculation:
  • Uses computer algorithms (e.g., at the L3 vertebra using the psoas muscles).
  • Measures Hounsfield density units as a proxy for muscle quality.
• Limitations:
  • High cost and ionizing radiation exposure.
  • Should only be used for lean mass measurements on CT scans ordered for other reasons.

Weight and Body Measurements

Weight Monitoring

• Importance in Hospitalized Patients:
  • Essential for fluid resuscitation and nutrition monitoring.
  • Daily weights in ICU help monitor long-term trends and short-term fluctuations.
  • Weight increases early in ICU stay (likely due to fluid overload) are linked to higher mortality risk.
• Assessing Fluid Overload:
  • Use current weight minus historical dry weight (if available), intake/output recordings, and physical exam findings.
  • No verified method for calculating or estimating dry weight exists; it is clinically determined.

Ideal Body Weight (IBW)

• Calculation:
  • Males: 50 kg + 2.3 kg for every 2.54 cm over 152.4 cm.
  • Females: 45 kg + 2.3 kg for every 2.54 cm over 152.4 cm.
  • For patients over 5 feet tall; may underestimate IBW for women.
  • Alternatively, use BMI method for IBW:
    • 19-21 BMI range (21-23 for women).
• Adjusted Body Weight:
  • Adjusted body weight = IBW + 0.4 × (Current body weight - IBW).
  • Commonly used in bariatric surgery for energy calculations.

Height

• Measurement Considerations:
  • Usually only one measurement needed during hospitalization, except in pediatric patients with long stays.
  • ICU and infant heights often measured supine, while outpatient heights are measured standing—this difference should be noted to avoid misdiagnosis.

Body Mass Index (BMI)

• Calculation:
  • BMI = Weight (kg) / Height (m)².
  • Limitations: Does not differentiate between fat, muscle, and bone mass, making it a potentially misleading sole indicator of health/nutritional status.

Lean Body Mass

• Clinical Relevance:
  • Important adjunct to BMI.
  • Loss of lean body mass is associated with worse outcomes, including higher mortality rates, increased ventilator reliance, and longer ICU stays.

Energy Expenditure

Challenges in Estimating Energy Expenditure

• Indirect Calorimetry:
  • Gold standard for estimating nutritional needs.
  • High variability: Errors can be up to 13% within the same day, and up to 23% within the same week.
  • No significant benefit to outcomes when used to supplement caloric goals.
  • Strict protocols required for standardization if used.

Resting Energy Expenditure (REE) Estimation

• Harris-Benedict Equation: Gender, Weight, height, Age
  • Men: REE = 665.5 + 13.75 × Weight (kg) + 5.003 × Height (cm) - 6.755 × Age (years)
  • Women: REE = 655.1 + 9.563 × Weight (kg) + 1.85 × Height (cm) - 4.676 × Age (years)
• Other Equations:
  • Korth and WHO equations: Higher accuracy in normal-weight patients.
  • Harris-Benedict: Better prediction in obese patients.

Adjusting REE for Clinical Scenarios

• Stress and Activity Factor Multipliers:
  • Ranges from 1.2 for light activity to 2 for severe thermal injury.
  • Example Multipliers:
    • Resting: 1.1
    • Out of bed: 1.3
    • Skeletal trauma: 1.35
    • Cancer cachexia: 1.3-1.5
    • Major sepsis: 1.6
    • Severe thermal injury: 2.1
    • Febrile: 1 + 0.09 per 0.5°C >38.5°C

Nutritional Needs Considerations

• Avoiding Underfeeding/Overfeeding:
  • Underfeeding (<70% REE) can increase mortality.
  • Overfeeding can increase mortality, ventilator days, and length of stay.
• Additional Protein Needs:
  • Burn patients: 1.5 to 2.5 g/kg/day of protein.
  • Critically ill surgical patients: Equivalent to 40% total body surface area burn.
    • Require 15 to 30 g of extra protein per liter of intraperitoneal fluid lost.

Nutritional Support of the Surgical Patient

Preoperative and Postoperative Nutritional Support

• Importance:
  • Critical for improving surgical outcomes.
  • Address the gap between prescribed and actual administration of feeding (12%-20% feeding time can be interrupted).
  • Nurse-directed feeding with 24-hour goals can help meet nutritional needs.

Optimizing Preoperative Nutrition

• Chronically Ill Patients:
  • Omega-3 fatty acids and arginine reduce hospital stay and infection rates.
  • Omega-3s: Anti-inflammatory by competing with omega-6 fatty acids.
  • Arginine: Improves T-cell function and collagen synthesis.
• Obese Patients:
  • High-protein, low-fat, low-carb diet to preserve lean body mass and mobilize unnecessary triglycerides.
  • Caloric intake should be scaled to ideal body weight (65%-70% of REE).
  • Protein intake: 2.0-2.5 g/kg/ideal body weight/day.
  • Close monitoring for hyperlipidemia, hyperglycemia, and other complications.

Enhanced Recovery After Surgery (ERAS) Protocols

• Preoperative:
  • Carbohydrate loading via clear liquids up to 2 hours before surgery.
• Postoperative:
  • Minimize opioid use, balance pain control, and initiate a regular diet as soon as possible.
  • ERAS protocols can shorten hospital stay and improve outcomes.

Safe Initiation of Postoperative Nutrition

• Enteral Nutrition (EN):
  • Safely begin within 24 hours postoperatively unless contraindicated.
  • Early EN decreases mortality and may reduce nausea/vomiting.
  • Solid diet initiation is recommended over clear liquid diets unless contraindicated.
  • Continue EN or parenteral nutrition until 60% of caloric needs can be met by oral intake.
• Gastrointestinal Anastomoses:
  • EN is beneficial for anastomotic healing.
  • If oral intake isn't feasible, parenteral nutrition should be initiated after 5-7 days for low-risk patients or earlier for high-risk patients.
• Hemodynamic Instability/Vasopressor Use:
  • Hold EN during instability due to risk of intestinal necrosis.
  • Consider EN when weaning off vasopressors, with close monitoring for intestinal ischemia.

Post-Discharge Nutrition

• Ongoing Support:
  • Nutrition supplementation should continue post-discharge to reduce readmission rates.

Enteral Versus Parenteral Nutrition

ASPEN Guidelines (Box 5.1)

• Preference for Enteral Nutrition (EN):

  • Recommended over parenteral nutrition based on evidence.
  • Early EN is associated with reduced infectious complications (e.g., catheter-related bloodstream infections) and shorter hospital stays.

  

Parenteral Nutrition (TPN)

• Indications:
  • Beneficial for critically ill patients with baseline malnutrition.
  • Society for Critical Care Medicine guidelines: Early TPN recommended for patients with:
    • NRS 2002 score ≥5.
    • NUTRIC score ≥5.
    • Severe malnourishment and intolerance to EN.
• Tolerance to Starvation:
  • Patients with low-risk nutrition scores (NRS ≤3, NUTRIC ≤5) can tolerate starvation for up to 7 days if clinical improvement is expected.

Benefits of Enteral Nutrition

• Gut Health:
  • Improves intestinal blood flow.
  • Causes the release of bile salts and gastrin.
  • Assists in tight junction maintenance in the gut.
  • Prevents dysbiosis of the gut microbiome, reducing the risk of sepsis and multisystem organ failure.
• Debate on Net Effect:
  • Mixed literature on EN's impact on gut and immune response (benefits to intestinal villi and structural integrity vs. potential worsening of the inflammatory response).

Location of Enteral Feeding

• Gastric vs. Small Bowel Feeding:
  • Studies show no significant differences in pneumonia, length of stay, or mortality.
  • Some evidence of improved nutrient delivery with small bowel feeding compared to gastric feeding.
  • Gastric feeding is generally safe unless there's a high risk of aspiration.
  • Postpyloric feeding recommended if aspiration risk is high, to reduce aspiration and pneumonia.

Routes for Tube Feeding

1. Nasogastric Tube

• Suitability: Short-term, functional GI tract.
• Insertion Method: Blind at bedside; fluoroscopy guided.
• Advantages:
  • Easy to insert, replace.
  • Can monitor gastric pH and residual volume.
  • Capable of bolus feeding.
• Disadvantages:
  • Misplacement complications, sinusitis, esophagitis.
  • Risk of nasal necrosis, esophageal strictures.

2. Nasoduodenal/Nasojejunal Tube

• Suitability: Short-term, functional GI tract but poor gastric emptying, reflux, aspiration risk.
• Insertion Method: Blind at bedside; fluoroscopy or endoscopy guided.
• Advantages:
  • Reduced aspiration risk.
  • Some tubes enable decompression of the stomach while feeding into the jejunum.
• Disadvantages:
  • Easily clogged or displaced.
  • Requires continuous infusion; cannot check gastric residuals.

3. Gastrostomy Tube

• Suitability: Long-term, good gastric emptying.
• Insertion Method: Surgical, percutaneous, endoscopic, radiologic.
• Advantages:
  • Bolus feeding possible.
  • Large-bore tube less likely to block.
• Disadvantages:
  • Procedure risks include bleeding, infection, and aspiration.
  • Risk of dislodgment and peritoneal contamination.

4. Jejunostomy Tube

• Suitability: Long-term, functional GI tract but poor gastric emptying, reflux, gastric dysfunction.
• Insertion Method: Surgical, percutaneous, endoscopic, radiologic.
• Advantages:
  • Theoretical reduced aspiration risk.
• Disadvantages:
  • Higher risks: bleeding, infection, perforation.
  • Difficult to replace, requires continuous infusion.

Metabolism in Critical Illness

Ebb and Flow Phases

• Ebb Phase:
  • Occurs 12 hours post-trauma or surgical stress.
  • Characterized by low energy expenditure, decreased oxygen consumption, and reduced temperature.
• Flow Phase:
  • Followed by increased energy expenditure and hypermetabolism.
  • Can progress to chronic catabolic state if primary injury is severe.

Systemic Inflammatory Response Syndrome (SIRS)

• Triggered by toll-like receptor activation on immune cells.
• Shifts amino acids to the liver for acute phase protein production (e.g., C-reactive protein).
• Glutamine becomes the preferred energy source for immune cells.

Compensatory Anti-inflammatory Response Syndrome (CARS)

• Results from overcompensation of immune responses leading to immunosuppression.
• Can progress to persistent inflammation, immunosuppression, and catabolism syndrome (PICS).

Biology of Acute Catabolism

• Mineral and Antioxidant Alterations:
  • Anemia due to reduction in blood iron and zinc.
  • Serum zinc and iron decrease; plasma copper increases (due to ceruloplasmin rise).

• Protein Wasting and Nitrogen Balance:

  • Breakdown of lean body mass during critical illness.
  • Daily nitrogen balance can be calculated to assess protein turnover.

  

Anabolic Resistance:

• Increased muscle breakdown and resistance to building lean body mass.
• Requires 1.2 to 2.0 g/kg/day of protein to overcome anabolic resistance.
• Early mobilization and physical therapy can reduce anabolic resistance.

Refeeding Syndrome

• Potentially fatal condition post-starvation.
• Hallmark: Hypophosphatemia, often accompanied by thiamine deficiency, hypomagnesemia, and hypokalemia.
• Prevention:
  • Electrolyte correction before initiating nutritional support.
  • High-potency B vitamins and daily vitamin supplementation recommended.
  • Start feeding at 10 kcal/kg/day with slow increases over 4-7 days.

Inflammatory Diseases Without Hypermetabolism

Transplant Patients

• Increased REEs up to 1 year post-transplant due to surgical stress and inflammation.
• Side effects of immunosuppressants: Nausea, vomiting, dyspepsia, diarrhea.
• Nutritional Recommendations:
  • Caloric intake: 30-35 kcal/kg/day.
  • Protein intake: 1.3-1.5 g/kg/day.
• Opportunistic infections: Nutrition optimization helps reduce risk.

Inflammatory Bowel Disease (IBD) & Short Bowel Syndrome (SBS)

• IBD:
  • Prone to protein-calorie malnutrition and micronutrient deficiencies (e.g., selenium, vitamin D).
  • Dysbiosis with reduced bacterial diversity; strategies include prebiotics, probiotics, and dietary changes.
  • Diet:
    • High-protein, low-fat, low-carb;
    • avoid simple sugars, high meat, and alcohol.
• SBS:
  • Treatment: Aggressive enteral support to stimulate villi hypertrophy.
  • Home TPN: Improves survival, with supplementation of growth hormone and glutamine.
  • Nutritional optimization: Fiber supplementation and elemental feeds, although evidence is limited.

Enterocutaneous Fistula

• Preferred treatment: TPN to increase spontaneous closure rate without increasing mortality.
• EN may be attempted if fistula output is low (<200 mL/day) with close monitoring.

Acute and Chronic Pancreatitis

• Acute Pancreatitis:
  • Early feeding within 48 hours of admission is safe.
  • Diet: Low-fat, peptide-based, medium-chain fatty acid-enriched.
  • If EN not tolerated, parenteral options include amino acids and hypertonic glucose with essential fatty acids.
• Chronic Pancreatitis:
  • Diet: Low fat, low carbohydrate, high protein (0.8–1.0 g/kg/day).
  • Jejunal EN can improve nutritional status without worsening abdominal pain.
  • Supplementation: Calcium, vitamin B, and fat-soluble vitamins.
  • Pancreatic enzyme supplements: Limited evidence for routine use.

Inflammatory Diseases With Hypermetabolism

Burn Injury and the Metabolic Stress Response

• Metabolic Impact of Burn Injury:
  • Severe burn injuries induce a hypermetabolic state that can last for years, characterized by increased catecholamines, glucocorticoids, and glucagon levels.
  • Leads to gluconeogenesis, glycogenolysis, and protein catabolism.
  • Insulin resistance develops, making glucose management difficult.
  • Peripheral lipolysis increases, leading to the breakdown of fat stores.
• Persistent Effects:
  • Negative nitrogen balance and significant lean body mass loss are common even with aggressive nutritional support.
  • Long-term effects can include delayed rehabilitation due to ongoing protein catabolism.
• Nutritional Interventions:
  • Early Enteral Nutrition (EN):
    • Start as soon as possible to reduce REE and improve immune responses.
    • Focus on high-protein, high-carbohydrate, low-fat diets to offset hypermetabolism.
  • Pharmaceutical Interventions:
    • Propranolol (a non-selective β-adrenergic receptor blocker) reduces thermogenesis, tachycardia, and REE in burn patients.
    • Oxandrolone (an anabolic steroid) aids in preserving lean body mass.
  • Exercise and Rehabilitation:
    • Structured exercise programs are beneficial in mitigating muscle wasting.
  • Early Excision of Burn Eschar:
    • The most effective intervention to reduce total energy demand and improve outcomes.

Nutrition Support in Sepsis

• Preventative Measures:
  • Limit the use of invasive procedures like central lines to reduce infection risks.
  • Early mobilization and DVT prophylaxis help prevent complications.
• Nutritional Recommendations:
  • Trophic EN:
    • Low volume, slow rate feeding to maintain gut integrity and prevent bacterial translocation.
    • Recommended during the acute phase to avoid overfeeding and its complications.
  • Protein Requirements:
    • Acute phase: 1.0 g/kg/day.
    • Convalescent phase: Increase to >1.5 g/kg/day to support recovery.
  • Macronutrient Considerations:
    • Avoid high carbohydrate intake to prevent worsening respiratory function due to increased CO2 production (high RQ).
    • Balance with fats, but avoid excessive omega-6 fatty acids due to potential lung injury.
• Controversies in Immunonutrition:
  • Glutamine and arginine supplementation are not recommended in septic patients due to potential exacerbation of the inflammatory response.

Nutrition Support in AIDS and Cancer

• Mechanisms of Cachexia:
  • TNF-α ("cachexin"), IL-1, and IL-6 drive protein wasting and cachexia in both AIDS and cancer.
  • Chronic inflammation and immune system activation lead to immunosuppression and severe malnutrition.
• Nutritional Challenges:
  • Opportunistic infections: Affect the aerodigestive tract, leading to further difficulties in maintaining adequate nutrition.
  • Side Effects of Treatments:
    • Antiretroviral therapy (AIDS) and chemotherapy (cancer) often cause gastrointestinal issues, reducing appetite and nutrient absorption.
• Support Strategies:
  • Enteral or Parenteral Nutrition:
    • Essential when oral intake is inadequate due to digestive side effects or physical obstructions.
  • Supplementation:
    • Correct deficiencies in iron, zinc, and B vitamins to improve nutritional status.
    • Consider medications to reduce nausea and improve gut motility.
  • TPN:
    • Important for patients post-radiation with malabsorption issues until enteritis resolves.
  • Dietary Interventions:
    • Omega-3 fatty acids: Improve cancer cachexia in certain cancers.
    • Vitamin D, dietary fiber, and coffee: Shown to lower the risk of cancer recurrence and improve survival.

Nutrition Support in Hepatic Insufficiency

• Metabolic Stress in Liver Disease:
  • Hypermetabolism similar to sepsis or burn injury due to increased levels of TNF-α, IL-1, and IL-6.
  • Loss of liver function leads to glycogen depletion and reliance on proteins and lipids for energy.
• Nutritional Management:
  • Focus on maintaining lean body mass with sufficient caloric intake while managing fluid balance.
  • BCAA supplementation: May reduce protein wasting, although evidence is limited.
  • Protein Restriction:
    • Necessary (<40 g/day) to prevent hepatic encephalopathy due to ammonia accumulation.
  • Supplementation:
    • Address deficiencies in potassium, magnesium, and zinc.
  • Oral Intake Optimization:
    • Improve sensory perception of meals, increase meal frequency, and ensure adequate support from healthcare staff.
• Management of Ascites:
  • Sodium restriction and diuresis are key; paracentesis may be required in severe cases.

Nutrient Deficiencies in Bariatric Patients

Overview of Bariatric Surgery and Nutrient Deficiencies

• Appetite Control:
  • Ghrelin: Main orexigenic hormone released when fewer calories are consumed. Bariatric surgery may reduce ghrelin levels by removing parts of the stomach that secrete it, leading to reduced appetite.
• Types of Bariatric Surgery:
  • Restrictive Procedures:
    • Reduce gastric volume, triggering satiety with smaller portions.
    • Examples: Adjustable gastric banding, vertical banded gastroplasty, sleeve gastrectomy.
  • Malabsorptive Procedures:
    • Reroute normal absorption, often removing part of the gut to reduce nutrient absorption.
    • Examples: Jejunoileal bypass (JIB), biliary-pancreatic diversion (BPD), BPD with duodenal switch (BPD-DS), Roux-en-Y gastric bypass (RYGB).

Common Nutrient Deficiencies by Procedure

1. Adjustable Gastric Band (AGB)
   • Nutrient Deficiency:
     • Iron deficiency is most common.
   • Clinical Note:
     • Lowest rate of nutrient deficiencies among bariatric procedures.
     • High rates of reoperation and failure for weight loss.
2. Sleeve Gastrectomy (SG)
   • Nutrient Deficiency:
     • Vitamin B12 deficiency due to decreased intrinsic factor production from the resected stomach fundus.
   • Clinical Presentation:
     • Symptoms include pallor, fatigue, and megaloblastic anemia.
3. Roux-en-Y Gastric Bypass (RYGB)
   • After RYGB, patients have increased glucagon like peptide-1 (also known as “incretin”), which has been shown to contribute to decreases in appetite.
   • Nutrient Deficiencies:
     • Iron deficiency anemia is the most common.
     • Risk of deficiencies in protein-bound nutrients (iron, intrinsic factor, vitamin B12) and those absorbed in the proximal small bowel (iron, vitamin D, copper, calcium).
   • Clinical Benefits:
     • Provides significant, sustained weight loss and improvements in conditions like obstructive sleep apnea and metabolic syndrome.
4. Biliary-Pancreatic Diversion (BPD) and BPD with Duodenal Switch (BPD-DS)
   • Nutrient Deficiencies:
     • Most Common is Protein malnutrition: Hypoalbuminemia (3% to 11% incidence).
     • Iron deficiency anemia: Incidence ranges from 5% to as high as 12%-47%.
     • Deficiencies in calcium, zinc, and fat-soluble vitamins (due to 70% reduction in fat absorption).
   • Clinical Note:
     • High rates of nutritional deficiencies; only undertaken after careful patient selection.

General Recommendations for Nutritional Optimization in Bariatric Patients

• Preoperative Nutritional Counseling:
  • Begin months prior to surgery.
  • Preoperative weight loss trial to assess compliance with dietary restrictions and improve surgical outcomes.
  • Even a 10% weight loss significantly improves surgical visualization and reduces postoperative complications.
• Postoperative Nutritional Management:
  • Daily multivitamins for all bariatric patients.
  • Additional iron and vitamin B12 supplementation, especially after restrictive-malabsorptive procedures.
  • Close follow-up in outpatient clinics to monitor nutrient levels and adjust supplementation as needed.
• Screening and Supplementation:
  • Follow guidelines from the American Society for Metabolic and Bariatric Surgery for screening and supplementation based on the specific bariatric procedure.
  • Address potential preoperative deficiencies, such as iron, which is common in 44% of adults before bariatric surgery.