Trauma/Burns Flashcards
1
Q
What is the definition of massive transfusion in paediatrics?
A
- Massive transfusion =
- Transfusion of more than 50% of total blood volume in 3hrs.
- Transfusion of more than 100% of total blood volume in 24 hours.
- Loss of > 10% of blood volume per hour, despite blood transfusion
2
Q
What is the blood volume (mL/Kg) of a premature neonate, term neonate, infant, older child?
A
Premature neonate = 100mL/kg
Term neonate = 90mL/kg
Infant = 80mL/kg
Older child = 70-80mL/kg
3
Q
What are Jones’ zones of injury?
A
-
Zone of coagulation:
- Irreversible damage and tissue loss secondary to protein coagulation and loss of cell membrane integrity → release of inflammatory mediators.
-
Zone of stasis:
- Potentially reversible damage with appropriate first aid and resuscitation.
- Burn and inflammation affects microvasculature → endothelial injury→ platelet aggregation/thrombus, neutrophil adherence, release of inflammatory mediators + fibrin deposition → vasoconstriction.
-
Zone of hyperaemia:
- Area of increased perfusion secondary to inflammatory mediated vasodilation.
- Not usually associated with irreversible injury.
4
Q
What are the local and general effects of thermal injury (essay)?
A
-
Local response to thermal injury:
- Initial burn injury (zone of coagulation) - irreversible damage and release of toxic inflammatory mediators (oxidants, proteases) → potentiate tissue damage + further release of inflammatory mediators.
- Activation of compliment factors → activation of neutrophils → production of cytotoxic reactive oxygen species + histamine → vasodilation.
- Inflammatory mediators → oedema → exacerbated by loss of cell membrane integrity and disruption of collagen cross linking → compromises osmotic and hydrostatic pressure gradients → local oedema.
- Inflammation, oedema, hypoperfusion → mediators of burn wound progression.
-
Systemic response to thermal injury:
- Tissue destruction and local response → massive systemic release of inflammatory mediators (thromboxane A2, bradykinins, interleukins, catecholamines, activated compliment) → systemic inflammation.
- Local and systemic increased capillary permeability → plasma loss → decreased circulating volume.
- Decreased circulating volume → decreased venous return → decreased CO.
- Decreased CO → decreased renal perfusion → decreased GFR (exacerbated by RAAS response) → oliguria and ATN.
- Decreased CO → decreased splanchnic perfusion → transient mesenteric ischaemia → decreased gut motility and malabsorption.
- GIT = increased permeability to macromolecules following burns → translocation +/- sepsis.
- Global decrease in immune function (cutaneous anergy, decreased macrophage production, reduction in cytotoxic T cells, impaired neutrophil function → increased risk of infectious complications
- Tissue destruction and local response → massive systemic release of inflammatory mediators (thromboxane A2, bradykinins, interleukins, catecholamines, activated compliment) → systemic inflammation.
5
Q
Describe the 3 phases of wound healing/scar formation.
A
- Inflammatory Phase
- Proliferative Phase
- Remodelling Phase
-
Inflammatory phase:
- Characterised by increased capillary permeability → oedema, plus mobilisation of neutrophils and monocytes to phagocytose dead tissue.
-
Proliferative phase:
- Re-epithelialisation
-
Remodelling phase:
- Maturation of graft or scar - fibrous structural proteins (mainly collagen and elastin) are laid down around the epithelial, endothelial and smooth muscle cells as an extracellular matrix.
- Later the extracellular matrix remodels into scar tissue and fibroblasts become myofibroblasts → scar contraction.
6
Q
Which cells are responsible for scar contraction?
A
ANSWER: Myofibroblasts
Scars form when collagen and elastin are laid down around as extracellular matrix (around endothelial, epithelial and smooth muscle cells).
Scar contraction occurs when the extracellular matrix remodels and fibroblasts become myofibroblasts (fibroblasts develop interconnections to assemble actin and myosin that act to contract the wound as myofibroblasts).
7
Q
Describe the mechanism of injury of the three components of inhalation injury.
A
Three components of inhalation injury: systemic intoxication, upper airway burns and bronchopulmonary injuries.
-
Upper airway burns -
- Heated air affects the upper airway predominantly (reflex glottic closure prevents lower airway burn and hot air cools).
-
Bronchopulmonary injury -
- Inhaled smoke and toxins results in injury to the lower airways.
- Damaged respiratory epithelium → activation of immune system (release of TXA2, thromboxane C3a and C3b → hypoxia, increased airway resistance, decreased compliance, increased alveolar epithelial permeability, increased pulmonary vascular resistance → respiratory failure.
- Mucociliary elevator destroyed → impaired clearance of airway debris and secretions → bacterial accumulation and infection.
- Inhaled smoke and toxins results in injury to the lower airways.
-
Systemic intoxication -
-
Carbon monoxide shifts the haemoglobin-oxygen dissociation curve to the left (200 times higher affinity to Hb than oxygen).
- Prolonged exposure → hypoxia → cerebral hypoxia → death.
- Hydrogen cyanide causes tissue hypoxia via disruption of the mitochondrial production of ATP → blocks aerobic metabolism.
-
Carbon monoxide shifts the haemoglobin-oxygen dissociation curve to the left (200 times higher affinity to Hb than oxygen).
8
Q
Describe management of inhalation burns in the first 24 hours (essay questions 2020)
A
- All burns should initially be treated as a trauma according to EMST principles.
- Management specific to inhalation injury should aim to address the three components of inhalation injury (upper airway burn, bronchopulmonary injury, systemic intoxication).
- Patients with history or examination concerning for upper airway burns should be considered for early intubation.
- Upper airway burns can be associated with erythema/ulceration and rapidly evolving oedema.
- Once airway secured, consider applying 100% humidified oxygen (to those with history of being trapped in an enclosed space or concerning for carbon monoxide poisoning) - shortens the half life of Hb-MO from 5 hours to 1 hour.
- If history or exam concerning for hydrogen cyanide inhalation, consider hydrocobalamin (binds cyanide and allows excretion via kidney), or thiosulphate (binds cyanide to thiosulphate)
- Management should then proceed to management of bronchopulmonary injury and its consequences
-
Secretions - aggressive chest physio, frequent suctioning, early mobilisation
- Assisted by administration of N-acetylcysteine and nebulised heparin.
- Bronchospasm - inhaled bronchodilators and nebulised adrenaline.
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Secretions - aggressive chest physio, frequent suctioning, early mobilisation
- Patients with history or examination concerning for upper airway burns should be considered for early intubation.
- In addition must consider concurrent administration of analgesia, antibiotics, nutrition and management of associated injuries.
- Management specific to inhalation injury should aim to address the three components of inhalation injury (upper airway burn, bronchopulmonary injury, systemic intoxication).
9
Q
Describe the pathophysiology of caustic ingestion - alkaline
A
- Alkaline ingestion high risk to oesophagus (3 stages of injury)
- Liquefactive necrosis
- Rapid, deep burn (can progress to full thickness), associated with absorption in vessels leading to endothelial injury and vascular thrombosis → impaired perfusion → exacerbating burn.
- Reparative phase (day 5-14)
- Necrotic debris sloughs away and is replaced by granulation tissue and collagen.
- During reparative phase, oesophagus is thin and friable and at high risk of perforation.
- Scar retraction (>2 weeks)
- Injured submucosa and muscularis mucosae (injured oesophageal muscle unable to be repaired or replaced) replaced by fibroblasts → scar and stricture.
- Liquefactive necrosis
- Neutralised by stomach acids.
- Nil gastric injury.
10
Q
What are the mechanisms by which button battery ingestion cause injury?
A
- Leakage of alkaline products → severe and rapid alkaline burn → liquefactive necrosis and erosion.
- Associated with acquired tracheo-oesophageal fistula, aorto-oesophageal fistula.
- Creates low voltage circuit with mucosa → low voltage burn.
- Pressure necrosis
11
Q
Describe the 3 stages of shock
A
- Initial non-progressive stage:
- Reflex compensatory mechanisms are activated and vital organ perfusion is maintained via neuorhumoral mechanisms.
- Baroreceptor reflexes, catecholamine and ADH release plus RAAS activation → tachycardia, vasoconstriction and renal fluid conservation.
- Cerebral and cardiac circulation less sensitive to sympathetic stimulation, therefore retains preferential blood supply.
- Reflex compensatory mechanisms are activated and vital organ perfusion is maintained via neuorhumoral mechanisms.
- Progressive stage:
- Tissue hypoperfusion and onset of worsening circulatory and metabolic derangement (lactic acidosis)
- Widespread tissue hypoxia → intracellular aerobic metabolism replaced by anaerobic glycolysis → lactic acid production.
- Lactic acidosis reduces vasomotor response (arterioles dilate, blood pools in microcirculation (worsens cardiac output and causes endothelial hypoxia → DIC.
- Widespread hypoxia affects vital organs → decreased LOC, agitation, confusion.
- Irreversible stage:
- cellular and tissue injury so severe that survival impossible desperate correction of haemodynamic defects.
- Due to cellular death and widespread release of lysosomal enzymes → multi organ failure.
- Decreased contractility (excess NO)
- Bacterial translocation from ischaemic and static bowel.
- Ischaemic acute renal failure and ischaemic hepatitis.
- Due to cellular death and widespread release of lysosomal enzymes → multi organ failure.
- cellular and tissue injury so severe that survival impossible desperate correction of haemodynamic defects.
12
Q
What are the lethal triad of trauma? How does trauma contribute to coagulopathy (3)?
A
Lethal triad of trauma - coagulopathy, acidosis, hypothermia
Coagulopathy and trauma:
- Hypothermia → decreased efficiency of the enzymes required for coagulation.
- Severe brain injury → release of large concentrations of procoagulant tissue thromboplastin → DIC → consumptive coagulopathy.
-
Haemorrhage and massive transfusion
- Dilution thrombocytopaenia (most common) - Platelet count < 50 associated with surgical bleeding.
- Dilution of clotting factors
- Transfusion can cause hypothermia
- Storage of blood products containing anticoagulants (citrate) → chelate calcium and inhibit calcium dependent steps of the coagulation cascade.
13
Q
What are the adjuncts that can be used for intraoperative control of bleeding?
A
Devices used in control of intraoperative bleeding
-
Surgical adjuncts:
-
Mechanical
- Tourniquet - appropriate for use on limbs.
- Femstop - applies direct external pressure to femoral artery to stop bleeding - associated with femoral artery puncture (i.e. endoluminal .
-
Chemical/Topical
- Adrenaline soaked gauze
- Fibrin sealants - Tisseal (contains fibrinogen and thrombin, plus factor XIII - stabilises clots).
- Gelatine-thrombin matrices - Floseal (useful for bleeding from capillary beds).
- Oxidised cellulose - Surgicel, Fibrillar (absorb blood and create gel covering over site of injury. Breakdown of cellulose → cellulosic acid → pH mediated vasoconstriction.
-
Mechanical
-
Medical adjuncts:
-
Tranexamic acid; anti-fibrinolytic - inhibits plasminogen activation and provides clot stabilisation.
- Evidence for use in adult trauma, and in orthopaedic procedures (associated with ⅓ reduction in blood loss).
-
Procoagulant factors:
- Cryoprecipitate - contains factors and fibrinogen.
- Prothrombin complex (prothrombinex) - vitamin K dependent clotting factors (useful in reversing coagulopathy associated with the use of anticoagulants.
- Recombinant factor VII (rVIIa)
-
Tranexamic acid; anti-fibrinolytic - inhibits plasminogen activation and provides clot stabilisation.
- Diagnostic adjuncts: thromboelastogram (TEG) - can determine whether deficiency is with platelet or coagulation cascade and direct appropriate therapy.
14
Q
Describe the systemic effects of crush injury to a limb (5)
A
- Crush injury can cause:
- Direct cellular damage → release of intracellular components → hyperkalaemia, hypocalcaemia (secondary to hypophosphataemia), hyperuricaemia
- Hypoperfusion → lactic acidosis
- Muscle damage → elevated CK and myoglobinuria
- Reperfusion injury
- Rhabdomyolysis → acute renal failure
15
Q
What are the triad of injuries associated with seatbelt sign?
A
Chance fracture of the lumbar vertebrae
Isolated jejuno-ileal perforations
Abdominal wall contusions
16
Q
Explain the zones of neck trauma and the management.
A
- Zone 1 - clavicle to cricoid cartilage
- Zone 2 - cricoid cartilage to the angle of the jaw.
- Zone 3 - angle of the mandible to base of skull.
- Anterior triangle - anterior border of SCM to midline.
- Posterior triangle - posterior border of SCM to anterior border of trapezius.
-
Management of penetrating neck injuries - hard signs warrant exploration:
- Hard signs; rapidly expanding/pulsatile haematoma, severe haemorrhage/uncontrollable bleeding, refractor shock, neurological deficit, haemoptysis/haematemesis, subcutaneous emphysema, air bubbling.
- In the absence of hard signs, treat on case by case basis.
- Zones 1 and 3 are very difficult surgical access.
- Zone 2 should be explored if there is injury deep to platysma.
