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Burns Pathophysiology

• Hypovolaemia is low blood volume
• Cytokines and inflammatory mediators lead to fluid leaking from blood capillaries, causing oedema
• Loss of electrolytes (potassium, sodium, albumin) contributes to hypovolaemia
• Loss of blood volume results in reduced oxygen-carrying capacity, leading to lactic acid buildup and metabolic acidosis
• Heart rate increases to compensate for oxygen loss and maintain cardiac output

Peripheral and Splanchnic Vasoconstriction

• Stress response releases noradrenaline and catecholamines, causing vasoconstriction in limbs, intestines, and stomach
• Vasoconstriction redirects blood to major organs like the brain, lungs, and heart
• Vasoconstriction in peripherals can lead to low tissue perfusion and hypoxia
• Vasoconstriction in splanchnic regions affects drug metabolism
• Low blood pressure is due to hypovolaemia and fluid loss
• Vasodilation happens in essential organs (brain, heart, lungs) to maximize perfusion

Metabolic Changes

• Severe burns trigger cytokine and inflammatory mediator release, increasing heart rate, oxygen consumption, and metabolism (hypermetabolism)
• Catabolism is the breakdown of muscle and fat to provide nutrients and energy
• Muscle breakdown leads to protein loss and hypermetabolism
• Hypermetabolism increases the demand for ATP and oxygen-enriched blood
• Respiratory rate increases to meet oxygen demand and expel excess carbon dioxide from hypermetabolism

Metabolic Acidosis and Insulin Resistance

• Metabolic Acidosis happens when anaerobic metabolism creates lactic acid buildup due to insufficient oxygen
• Catecholamines interfere with insulin binding, causing insulin resistance and increased glucose production (hyperglycaemia)
• Faulty insulin leads to increased glucose in the bloodstream
• The liver produces glucose from glycogen stores, amino acids, lipids, and lactate (gluconeogenesis)
• Catecholamines and cortisol prevent the liver from stopping glucose production
• Hyperglycaemia results from decreased glucose uptake due to insulin resistance
• Hypothermia results from loss of thermoregulators in the dermis
• The lethal triad includes hypovolaemia, metabolic acidosis, and hypothermia, ultimately leading to death

Burns Treatment

• Assess Airway: Airway compromise due to swelling possible by burns on the face or neck
• Breathing: Administer oxygen in respiratory distress, especially with inhalation injury
• Circulation: Ensure adequate tissue perfusion by assessing Blood Pressure and Heart Rate
• Establish IV access for fluids and monitor for shock (hypotension, and low urine output)
• Burn injuries result in fluid loss from capillary leak and increased blood vessel permeability, leading to hypovolemia
• Parkland formula helps calculate fluid requirements in burn patients
• Crystalloid fluids - Hartmanns, are typically used for fluid resuscitation in the early stages of a burn
• Colloids, such as gelofusion can be used later to help maintain volume
• Monitor fluid status using Urine output (0.5-1 mL/kg/hr in adults)
• Early enteral feeding delivers nutrition, helps wound healing, and maintains gut integrity improving immune function and reduces infection

Anaphylaxis Pathophysiology

• Grade 1: Local Reaction (Redness, swelling)
• Grade 2: Mild-Moderate Reaction (Vomiting, abdominal pain, flushing, angioedema)
• Grade 3: Severe Systemic Reaction (Systemic with -/+ cardiovascular or respiratory response: wheezing, stridor, low blood pressure, cardiac arrest)
• Allergic Antibody: Immunoglobulin E (IgE)
• Exposure to allergen (i.e, dust) occurs when White blood cells mature into plasma cells and generate specific IgE against allergen
• IgE circulates and binds to tissue mast cells with IgE receptors
• Mast cells hold histamine and are now sensitized to allergen
• Exposure to allergen binds to mast cells for release of inflammatory mediators such as histamine, prostaglandin and cytokines
• Histamine results in vasodilation (low BP), vascular permeability (oedema, hives), and smooth muscle contraction (bronchoconstriction) coughing/wheezing
• Prostaglandins contribute to inflammation and bronchoconstriction
• Cytokines stimulate IgE production and mast cell response, increasing inflammation and enhancing allergic response
• Stroke Volume X Heart Rate = Cardiac Output
• Cardiac Output X Systemic Vascular Resistance = Blood Pressure
• Histamine release results in vascular permeability, loss of blood volume, loss of oxygen carrying capacity, & increased respiratory rate
• Histamine and Prostaglandin create Bronchoconstriction = More resistance breathing, use of accessory muscles = Lack of oxygen diffusion
• Prostaglandins increase swelling and airway oedema with Mucus Production via Goblet cells, increasing respiratory distress
• Tachyapnea is for lack of oxygen. Excess CO2 in blood, inadequate gas exchange results in Respiratory Acidosis
• Hypoperfusion and Hypovolaemia causes Myocardial Damage and Ventricular Dysfunction
• Respiratory acidosis, hypotension, hypoxia, hypovolaemia cardiac arrhythmias lead to cardiac arrest
• Rash results from vascular permeability

Anaphylaxis Treatment

• Immediate IM Bolus of Adrenaline (1:1000) works as Bronchodilator for airway (Beta Response)/Vasoconstrictor for Low Blood Pressure (Alpha Response)
• Adrenaline also decreases Vascular Permeability, which reduces Oedema and Inhibits histamine and Increase Cardiac output- High Flow Oxygen
• High Flow 02 is used treat respiratory distress and allow for gas exchange, treating Respiratory Acidosis and hypoxia
• Crystalloid Fluid Bolus is used to treat Hypovolaemia & Increase Blood Pressure

Local Anaesthetic Systemic Toxicity (LAST) Pathophysiology

• Happens within 10 to 60 mins after administration
• Blocks pain receptors from sending signals to the brain
• Dissolving rates can affect toxicity
• Sodium (Na+) channels are blocked by the LA, interfering with brain signals
• Na+ carries an electrical charge responsible for contraction & impulse
• No Na+ can cause arrhythmias- as it prevents early depolarization
• LAST occurs when LA anaesthetic reaches a level that affects the heart and brain via blood vessel injection, Overdose and vascularised injection

Local Anaesthetic Systemic Toxicity Effects

• LA is absorbed into circulation- Binds to plasma where systemic circulation becomes toxic
• LA inhibits oxidative phosphorylation and creation of ATP = anaerobic metabolism
• Anaerobic Metabolism prevents displaced hydrogen ions from blood = metabolic acidosis
• Reduction in SVR (WHICH NEEDS ATP)
• Vasopressors and Inotropes Ineffective
• Do NOT hyperventilate. It should be in normal ranges until ATP creates excess CO2
• Drugs cross the blood-brain barrier and block nerve impulse signals.
• Initially causes CNS EXCITATION: Fasciculation/ seizures/ numbness around the mouth
• As it worsens, it can cause respiratory depression and apnea, Tinnitus and loss of conciousness
• Blocks ion channels and reduced cardiac conduction leading to BRADYCARDIA, AV BLOCK, PROLONGED PR INTERVAL AND WIDENED QRS
• LA reduces SVR and can lead to reduce cardiac output
• Low Co is often compensated via Tachicardia but it will progress to arrythmia/cardiac arrest

Local Anaesthetic Systemic Toxicity Treatment

• STOP LA ADMINISTRATION
• USE ABC APPROACH to check if the patient spontaneously breathing, their blood pressure and their SPO2 levels (oxygen saturations)
• 20% INTRALIPID FLUID BOLUS (MAX DOSE =12ML/KG) Draws LA out- Increased SV or BP
• Provide access and fluid resuscitation to support low BP
• BENZODIAZEPINES FOR SEIZURES
• CARDIAC ARREST TROLLEY Amiodranone for arrhythmias
• Don't give too much adrenaline as too much can worsen arrythmias; instead, give smaller adrenaline doses

Malignant Hyperthermia Pathophysiology

• A life-threatening reaction to anaesthetic gases and succinylcholine
• Skeletal muscle contracts repetitively, producing heat, excessive CO2 and tachycardia
• Action Potential (for muscle to move)- electrical impulse releases acetylcholine- causes excitement (depolarisation) once it enters receptor
• Depolarisation releases CALCIUM from the sarcoplasmic reticulum - Calcium binds to troponin and contracts muscle fibres
• ATP AND O2 IS USED UP BY STOPPING LIGAMENTS CONTRACTION
• MH: Genetically altered RyR1 Receptors become hypersensitive once triggered which leads to hyperthermia and muscle contraction
• The body continues to try and sheathe resulting in muscle fibres using up O2, creating CO2, causing cell death and rhabdomyolysis (breakdown of muscle tissues)
• Muscle death releases MYOGLOBIN, TROPONIN AND POTASSIUM into the bloodstream, impairing renal blood flow, causing ACUTE KIDNEY INJURY
• HYPERKAELAEMIA occurs as the body tries to excrete excess potassium , which LEADS TO EXTRASYSTOLES ON ECG
• ATP demand increases from muscle contraction leading to Hypercarbia and Respiratory Acidosis
• GA without paralysis equals increased inspiration. Lack of ATP and 02 INHIBITS BODY FROM EXPELLING CO2 EFFECTIVELY
• Excess production of CO2 makes a demanding acidic blood, leading to Hypoxaemia and Tachycardia
• Hyperthermia occurs AFTER TACHYCARDIA AND HYPERCARBIA with an increased temperature every few minutes due to muscle contraction

Malignant Hyperthermia Treatment

• Disconnect from the anaesthetic machine with o2 cylinder whilst considering TIVA
• Replace filters and circuits & add activated charcoal filters
• Maintain 100% FiO2
• Administer DANTROLENE as a Muscle relaxant to stop contraction
• Start COOLING MEASURES
• Administer SODIUM BICARBONATE: TO CORRECT METABOLIC ACIDOSIS if present
• Ensure CATHETER for URINE OUTPUT for measuring levels whilst using Insulin to treat hyperkalaemia (moves potassium back into cells) & calcium gluconate to stabilise arrhythmias