Ahmed Badrek- Alamoudi FRCS

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

IntroductionIntroduction

The Wider Physiological Response, MetabolicThe immune responseEndocrine response

Injury:Surgical & TraumaticThermal/ Electrical (Burns)Infectious ( septicemia)

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Introduction

The Aim:Identify and quantify the injurious agent.Maintain Critical Organ functionRestore HomeostasisMobilize Energy reservesProvide substrate for tissue repairRepair of dysfunctional tissueEradicate sepsis

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Response to InjuryResponse to Injury

Ebb Phase Flow Phase

Injury

Catabolism

Anabolism

Death

Minutes Hours Days…………………Weeks

Energy

Temperature

O2 Consumption

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Factors influencing the Extent and Duration of the Metabolic Response

Pain and Fear Surgical Factors:

Type of surgeryRegionDurationPreoperative support

Extent of the trauma and degree of resuscitationPost traumatic complications:

HemorrhageHypoxia Sepsis and FeverStarvationIleusRe-operation

Pre-existing nutritional statusAge and sex

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Pain, Fear, Anxiety Mediators from IT Nociceptors Baroreceptor

Hypothalamic Pituitary Axes

Autonomic Axes

ACTH Cortisol Aldesterone

TSH GH Prolactin Endo-Opiods ADH

AD/NA Aldesterone Insulin Glucagon

Target Organ

Cell Surface Receptors

Intracellular Receptors

Hormone Time Effect Catecholamines Stress dependant

Immediate and continues for: 24-48 hours

1. Hyperglycaemia: Gycogenlysis Gulconeogenesis Suppression of Insulin

secretions Stimulation of

Glucagon Inhibits Glucose

Uptake 2. Raises the Metabolic Rate 3. Mobilizes Free Fatty acids 4. Hemodynamic Factors 5. It lowers Immunity

ADH

Immediate to 1 week

1. Promotes reabsorption of water 2. Peripheral vasocontrictor

Renin-Angiotensin

1. Vasoconstrictors 2. Release of Aldesterone

Cortisol

Stress dependant To 4 weeks

1.Glycogenlysis 2. Cluconegenesis 3. Increases insulin resistance 4. Protein break-down and release of lactate 5. Immunosuppression

Aldesterone

1. Conserves sodium 2. Eliminates Potassium

Insulin

First hours: Decrease insulin release Later Anabolic: Increase insulin release

1. Facilitate entry of glucose. 2. Stimulates Glycogenesis 3. Lipogenesis 4. Glycolysis 5. Proinflammitory activity

Growth Hormones

Anabolic Phase 1. Protein Synthesis 2. Ketogenesis

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Other Endogenous Substances

Glucagon Catabolic roleGlycogenlysis, Lipolysis and ketogenesisLevels increase with in 24 hours

Renin-Angiotensin

Promotes volume homeostasisPotent vasoconstriction, inotropic Effects glucose metabolism

TRH / TSH Decrease thyroid hormone activities (euthyroid sick syndrome)Reduce levels of T4 in severely injured are predictive of mortality

Endogenous Opioids

B-endorphins attenuate pain receptorsImmune & GI modulators

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Water Balance

Under the influence of ADH

Results in WATER RETENTION.

Inappropriate ADH SecretionLow Plasma Osmolarity

High Urine Osmolarity

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Sodium Balance

• Early Retention

• Plasma levels: normal/ raised

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Potassium Balance• Initial Decrease• Intracellular K is released by injured tissue

K Loss, Duration/ days Amount/day

Mild Trauma 1 20 mmol

Gastrectomy 2-3 50 mmol

Major Trauma 7-8 70- 100 mmol

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Protein Balance• Protein loss depends on

– the severity of the injury– The body tissue affected– Gender, age and state of health of the

patient– The nutritional status of the patient

• Degree of Protein break-Down may be limited by glucose infusion.

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Nitrogen Balance

N2 loss/ day in g days Hernia repair 5 1 Gastrectomy 15 5 Major laparotomy 20 10 Sepsis & Burns 30 weeks

1g N2 = 6.25g Protein = 30g wet muscle

Daily intake= 120g prot = 20g N2

Daily Loss= 2-3 g N2

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

A Schematic Diagram Showing Nitrogen and Sodium Balance

+ve

-ve Trauma 4 8 20

Days N2 Balance

Na Balance

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Glucose Balance• Immediate increase in glucose level

• This continues in to the early catabolic Phase

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Change in Metabolic Rate

Injury % Change in Metabolic Rate Gastrectomy < 15 Multiple fractures >20 Moderate sepsis >20 Severe Sepsis >40 Major Burns >90

Other Changes Vitamines

Retention of Vit.C……….Decrease Riboflavin

Creatinine

Increased Urinary creatinine

Blood

Increase in Polymorphs Decrease in Lymphocytes, Oesinophils Hypercoagubility states

Body Weight

Decreases

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Change in Immune response

Cytokine mediated response: Cell to cell mediation Immune cell production, proliferation and survival Regulation between proinflammatory & antinflammatory Chemotaxis to the site of the injury and promotes wound healing Hemodynamic instability with tackycardia vasodialation ( Septic

shock) Fever & leukocytosis ( Systemic inflammatory response syndrome) Cachexia

Indothelial cell mediators Intracellular mediators

Metabolic Response to Trauma- Fourth year Lecture- 1423-1424

Methods to Minimize the Metabolic Response

1. Replace blood and fluid losses

2. Maintain Oxygenation

3. Give adequate nutrition

4. Provide Analgesia

5. Avoid Hypothermia