Metabolic Response to Trauma, Shock, Fluid, & Blood Transfusion PDF

General Surgery for 3072 Metabolic response to injury Shock Blood Transfusion Dr. Mohammed Mansour MBBS, MSc, MD, BDS, FRACDS(OMS) Metabolic response to injury *Factors which initiate the metabolic response to injury are: - Fluid loss (volume depletion) - Afferent nerve (pain) stimuli - Bacteria and...

General Surgery for 3072 Metabolic response to injury Shock Blood Transfusion Dr. Mohammed Mansour MBBS, MSc, MD, BDS, FRACDS(OMS) Metabolic response to injury *Factors which initiate the metabolic response to injury are: - Fluid loss (volume depletion) - Afferent nerve (pain) stimuli - Bacteria and endotoxin - The pro-inflammatory cytokine response - Activated neutrophils and monocytes Metabolic response to injury *Factors which modify the metabolic response to injury are: - The severity of injury - Co-existing disease (e.g. cancer, renal failure) - Infection - Nutritional status - Ambient temperature - Anaesthesia and drugs - Miscellaneous factors (complications) Changes occurring during the metabolic response to injury Tachycardia and pyrexia lasting for 24-48 hours Retention of sodium and water for 2-3 days secondary to aldosterone and ADH secretion Increased energy expenditure Increased glucose turnover Changes occurring during the metabolic response to injury Breakdown of skeletal muscle to provide amino acids for gluconeogenesis and hepatic synthesis of other proteins Breakdown of adipose tissue as principle energy source after trauma Hypercoagulability (with increased risk of thromboembolism) or hypocoagulability. Urinary changes during the metabolic response to injury Oliguria in response to ADH secretion Low urinary sodium excretion due to renal retention of sodium in response to aldosterone secretion Increased urinary excretion of potassium. (This should be seen as a 'beneficial' attempt to avoid hyperkalaemia given that tissue injury releases intracellular potassium, as does the mobilization of intracellular water. The renal excretion of potassium also facilitates renal retention of sodium) Increased urinary excretion of nitrogen reflects breakdown of muscle protein; each gram of urinary nitrogen is equivalent to 6 g of muscle protein and 30 g of skeletal muscle Tissue response to injury Shock Definition: Acute circulatory failure with inadequate tissue perfusion causing cellular hypoxia Types of Shock Four principal categories:  Hypovolaemic  Vasodilatory (Anaphylaxis, Septic, Neurogenic)  Cardiogenic  Obstructive Hypovolaemic shock Low venous return leads to low cardiac output. Causes: Haemorrhage is a common cause of hypovolaemia,. Loss of gastrointestinal fluid may result from vomiting and diarrhoea. Trauma and infection increase capillary permeability, with local sequestration of fluid and oedema. Burns lead to direct loss of fluid from the burned surface and tissue fluid sequestration. Iatrogenic surgical factors contribute to hypovolaemia (e.g poor fluid prescription, slow or tissued intravenous infusion, inappropriate use of diuretics, mechanical bowel preparation, fasting before anaesthesia, insensible fluid losses during prolonged operations and ongoing fluid loss from dissected areas for some hours after surgery). Cardiogenic shock Primary impairment of cardiac function may result from: AMI Myocardial ischaemia Acute arrhythmias Acute cardiomyopathy Acute valvular lesions (caused by aortic dissection or trauma) Myocardial contusion. Obstructive shock Secondary impairment can result from obstruction to cardiac output, eg cardiac tamponade producing constriction of the heart, tension pneumothorax or major pulmonary embolism with obstruction to right ventricular outflow. http://www.youtube.com/watch?v=QwgfuDegC5Y http://www.youtube.com/watch?v=PQHNDuYRViY In all shock states, myocardial performance is affected adversely by reduced coronary arterial perfusion and in some cases by circulating myocardial depressant substances (eg septic shock). Neurogenic factors True neurogenic shock follows spinal transaction or brainstem injury with loss of sympathetic outflow beneath the level of injury and consequent vasodilation. The rapid increase in size of the vascular bed, including venous capacitance vessels, leads to reduced venous return and reduced cardiac output. There is often a relative bradycardia. Anaphylaxis Anaphylactic reactions are mediated by immuglobulin E (IgE) antibodies causing massive degranulation of mast cells in sensitised individuals. Activation of mast cells releases histamine and seretonin; with systemic kinin activation, this leads to rapid vasodilation, a fall in systemic vascular resistance, hypotension, severe bronchospasm, hypoxia and hypercapnia. Prompt treatment with oxygen fluids, adrenaline, hydrocortisone and an antihistamine is required. Stop giving the trigger substance! Septic shock In septic shock, the patient becomes hypotensive and the tissues are perfused inadequately as a result of organisms, toxins or inflammatory mediators. Common sources of sepsis include the abdomen, chest, soft tissues, wounds, urine and intravascular lines (central or peripheral) or other medical implants. http://www.youtube.com/watch?v=HQXgldR _LEA Signs of decreased tissue perfusion (shock) Cool peripheries Poor filling of peripheral veins Increased respiratory rate Capillary refill time prolonged (>2 s) Poor signal on pulse oximeter Poor urine output Restlessness or decreased conscious level Metabolic acidosis or elevated lactate Treatment of Shock Resuscitate Diagnose Treat underlying cause Resuscitate Fluids Oxygen If cardiogenic and obstructive shocks excluded: - Bolus 10ml/kg crystalloid or 20ml/kg if hypotensive - Oxygen 12-15l/min until blood gases or oxygen saturations are available Blood Transfusion Whole blood Red cell concentrate Supplemented red cells Platelet concentrates Fresh Frozen Plasma (FFP) Cryoprecipitate Human albumin Factor VIII and IX concentrates Human immunoglobulin Whole blood Donated whole blood is drawn into 60-100 ml of an anticoagulant (citrate)nutrient (phosphate, dextrose and adenine) solution in which it can be stored for up to 30 days at 4 +/- 20C Changes in the red cells do occur during storage and the haemostatic properties of the blood decline. Platelets are non-functional after exposure to 40C, there are no functional granulocytes, and concentrations of the labile factors V and VIII decrease quickly in the first week of storage. The blood is not sterilized so that whole blood transfusion can transmit organisms not detected by donor screening. There are few situations where plasma, proteins and red cells are all needed. Whole blood is an inefficient means of giving haemostatic factors and can cause cardiac failure when used in patients with chronic anaemia. It is indicated when rapid large volume transfusion is needed as in patients who have suffered major trauma. Transfused blood must be ABO and Rh compatible with the recipient. Red cell concentrate This concentrate is prepared from a unit of donated blood by removing most of the plasma to leave a haematocrit of 65-75% and final volume of about 300 ml. Packed cells are ideal for use in chronic anaemic patients, and can be given with colloid crystalloid solutions in acute blood loss. The risk of infection, storage considerations and administration safeguards are those which apply to whole blood. Supplemented red cells These are concentrates to which saline, adenine and glucose have been added to give a haematocrit, 55-65% and final volume of 300 ml. The resulting solution has better flow characteristics than concentrated cells but must be used with care in large volume transfusions and renal failure. Platelet concentrates Some 50-60 ml of platelets can be produced from unit of whole blood by centrifugation. The resulting unit can be stored on an agitator for 5 days at 20-240C. An adult is usually given 4-6 of these units, and once pooled the platelets must be used in 4 hours. Platelet concentrates are not sterile and carry a greater infection risk than whole blood as each transfusion exposes the recipient to the blood of 4-6 donors. Bacterial contamination is also more likely as platelets cannot be refrigerated. Five platelet donations should raise the platelet count by 20-40,000 x 109/1. Fresh Frozen Plasma (FFP) Some 200-300 ml of plasma can be removed within 6 hours of donation from a unit of whole blood and stored frozen at -300C. FFP contains albumin, immunoglobulins and all of the coagulation factors. Like whole blood it carries an infection risk although the risk of cell-borne infection (e.g. CMV infection) is reduced. FFP can be stored at -300C for a year and is thawed to 370C before issue. FFP must be ABO compatible with the recipient and should be given within 4 hours of thawing. The average adult dose is 3-4 units. FFP is used when there are multiple coagulation defects (e.g. disseminated intravascular coagulation (DIC)), for single factor replacement when a heattreated product is not available, and when there has been an overdose of the anticoagulant warfarin (bleeding and an international normalized ratio (INR) >4.5). Cryoprecipitate A single unit of cryoprecipitate can be removed from one unit of FFP after controlled thawing. After resuspension in 10-20 ml plasma, the cryoprecipitate is frozen once more to -300C. It contains fibrinogen, factor VIII and fibronectin, and can be stored for up to a year. Cryoprecipitate carries the same basic risk of transmitting infection as FFP, but as an adult dose is normally 10 units, the recipient is exposed to material from 10 donors. ABO compatibility is achieved whenever possible, and the product is infused as soon as possible after thawing. It is used when fibrinogen levels are low, in bleeding associated with uraemia, and in some cases of von Willebrand's disease. Human albumin Albumin is prepared by fractionation of large pools of donated plasma. The final product is pasteurized at 600C for 10 hours and carries no risk of transmitting viral infection. There are no compatibility requirements. A 4.5% and 20% solution are available. Are used to maintain plasma albumin levels in burns, and are sometimes used in acute blood volume replacement, although crystalloid or nonplasma colloid solution are usually just as effective. Factor VIII and IX concentrates Purified factor VIII and IX concentrates (containing some factor II and X) are prepared from large pools of plasma. Virus inactivation processes now mean that these products should not transmit HIV I and II or hepatitis B and C, but this may not apply to heat resistant viruses which have no lipid envelope (e.g. hepatitis A). The concentrates are used to treat factor VIII and IX deficiency. Factor IX concentrates which include other vitamin K-dependent factors may also be used in warfarin overdose. Care must be taken in patients with liver disease as this therapy may be thrombogenic. Human immunoglobulin Immunoglobulin (90% IgG) is prepared from fractionation of large pools of plasma from unselected donors or from individuals known to have high levels of specific antibodies. There is no risk of transmitting hepatitis or HIV. Pretransfusion testing Type and screen determines ABO, Rh(D) status and antibody screen. The sample is then normally held for 7 days thereafter. Compatible blood can be available within 10-15 minutes if needed. Cross-matching involves typing and screening followed by direct testing of the patient's serum for compatibility with red cells of units to be transfused: normally takes 1 hour. Cross-matched units are held for 48 hours. The process has to be repeated if any of the reserved blood is used and further transfusion is deemed necessary. Emergency cross-matching means rapid ABO and Rh typing with release of 'compatible' blood after checking ABO compatibility and while the antibody screen continues. Infection and Transfusion of Blood and Blood products Risk of infection still exists although it has declined with greater awareness of risks, improved screening, better methods of decontamination, and more judicious use of blood and blood products. Risk of viral transmission (hepatitis B, C and HIV) has diminished with routine screening but virus infection may escape detection in the early stages when levels of antigen or antibody are still low. CMV infection is transmitted by white blood cells. CMV-negative blood is used to avoid transmitting infection to transplant recipients and premature infants.