BURNS
Epidemiology  Incidence varies between cultures Majority in children are scalds Adolescents experimenting
Epidemiology Flame burns in adults Most electrical & chemical burns in adults Mental diseases , epilepsy, alcohol & drug abuse
On arrival burn case treated as trauma ABC Soot ,charring around nose – think of inhalation injury
Assessment of burns area Wallace’s rule of nine Adult >20% ,child >10%  needs IVF i/v access for analgesia
Prognosis  Percentage body surface area burned Age & percentage add together to a score of 100 , considered fatal
Assessment of burn depth Temperature of burning agent Mode of transmission of heat Duration of contact
Skin anatomy Epidermis waterproof Replaced from the basal layer Dermis-thicker  strength & integrity Contains the adnexal structures
Superficial burns   Epidermal burns Heal by epithelialisation alone Red & painful Blisters not present
Superficial burns superficial dermal Blistered Painful Heal by epithelialisation in 14 days
Deep burns Adnexal structures lost Heal by second intention  scarring
Deep burns Blistered Blotchy red appearance No capillary return on pressure Absent sensation to pin prick
Full thickness burns White/ charred appearance No sensation Charred layer consists of denatured contracted dermis - eschar
Pathophysiology Injuries to skin Injury to airway & lungs Inflammation & circulatory changes Other effects
Injuries to skin MC organ affected is skin Area affected Depth
Inhalational injury Hot gases cause injury to upper airway Stridor, hoarseness, cough, resp. obstruction CO causes chemical burn dr shabeel’s presentations
Injury to airway & lungs damage airway & lungs Airway injury suspected in face & neck burns Person trapped in burning vehicles,house , plane etc
Injury to airway Burns above larynx Below larynx Metabolic poisoning Inhalational injury Mechanical block on rib movement
Above larynx Hot gases burn nose , mouth, tongue , palate & larynx Linings start swelling May block the airway
Below larynx Rare as heat is absorbed in supra glotic area But steam has a large latent heat of evaporation Epithelium swells & detaches This cast block the airway dr shabeel’s presentations
Metabolic poisoning CO –product of incomplete combustion Affinity 240 times than Hb for O2 Blocks transport of O2 Carboxy Hb > 10% is dangerous Need pure O2 >24 hrs Death occurs with 60%
Another metabolic toxin is hydrogen cyanide Metabolic acidosis by blocking mitochondrial respiration
Inhalation  Caused by minute particles within smoke Stick to moist lining alveoli Chemical pneumonitis
Intense edema Decreasing gaseous exchange Bacterial pneumonia
Mechanical block on rib movement Burned skin – thick & stiff Stop movement of ribs Common in large full thickness burn across the chest
Inflammation & circulatory changes Burned skin activate a web inflammatory cascades Pain - Release of neuro peptides & activation of compliments Hageman s factor – protease driven cascades
Inflammation & circulatory changes Compliments – degranulation of mast cells Coats the proteins burned Attracts neutrophils – degranulate – free radicals & proteases
Inflammation & circulatory changes Mast cells release primary cytokines – TNF alfa Secondary cytokines Alter the permeability of vessels
Inflammation & circulatory changes Large protien molecules escape Oncotic pressure again increases More flow of water into extra vascular space
Inflammation & circulatory changes Water ,solutes, proteins – ECF Occurs in first 36 hrs 10-15% burns – shock >25% loss occurs in remote vessels
Other effects Immune system & infection Changes in intestine Peripheral circulation
Immune system & infection Inflammatory changes affect immune system CMI  reduced in large burns Bacterial & fungal infection
Changes in intestine Micro vascular damage & ischemia of gut mucosa Motility & absorption affected Failure to enteral feeding Translocation of gut bacteria
Septicemia  Abdominal compartment syndrome- mucosal swelling, stasis, peritoneal edema Splinting of diaphragm
Peripheral circulation Full thickness burns- coagulation of collagen Elasticity of skin lost Circumferential burn of the limb act as tourniquet
Regional problems  Circulation  May affect the limb circulation Not by direct damage to main vessel edema -  venous obstruction Muscle compartment syndrome
Effects of burn injury Local  Regional  Systemic
Local effects Tissue damage Inflammation Infection
Tissue damage Heating  -> cell rupture / necrosis Cells of periphery injured Denaturation of collagen
Tissue damage Capillaries thrombosed in severe cases Increased damage in less severe case Tissues become edematous
Inflammation  Marked response Erythema in least burned areas Neurovascular response like Lewis triple response
Severe – cytokines Phagocytose necrotic cells Damaged tissues separate by de sloughing in 3 wks
Infection  Damaged tissue – nidus of infection Colonization in 24 – 48 hrs Bacteremia is a common cause of fatality
Systemic effects Fluid loss Multiple organ failure Inhalational injury Systemic complications
Fluid loss External loss Internal loss as edema Mediated by cytokines
Management  Immediate care Assessment of burn wound Fluid resuscitation Treatment of burn wound
Immediate care Pre hospital  Hospital care
Pre hospital Ensure rescuer safety – house fire , chemical , electrical Stop the burning process – stop, drop & roll Check for other injuries Cool the burn wound
Pre hospital Cool the burn wound – minimum 10mts to an hour Oxygen elevate
Hospital care Airway  Breathing Circulation Disability  Exposure with environmental control Fluid resuscitation
Major determinants of outcome Percentage area Depth Inhalational injury
Criteria for admission Inhalational injury Fluid resuscitation Needing surgery Suspicion of non accidental cause Extremes of age Associated potential sequelae
Airway  Burned airway causes obstruction Endo tracheal tube for 48 hours Symptoms of laryngeal edema appear late
Airway  Intubation will be difficult after symptoms appear Crico thyroidotomy needed in late diagnosis Recognition of potentially burned airway
Breathing  Inhalational injury Thermal burns to lower airway Metabolic poisoning Mechanical block to rib movement
Inhalational injury Observe anyone trapped in a fire  Presence of soot in nose & oro pharynx Chest x-ray  -  patchy consolidation
Clinical features Progressive increase in resp effort & rate Rising pulse , anxiety , confusion Decreasing oxygen saturation
Treatment  Secure the airway Physiotherapy, nebulisation, warm humidified oxygen Monitor the progress IPPV for severe cases
Burns of lower airway Steam injury Supportive management Like inhalational injury
Metabolic poisoning Fire within a closed space Altered consciousness ABG
Metabolic acidosis High inspired O2 for 24 hrs if >10% Displacement from Hb
Mechanical block to rib movement Eschar on the chest CO2 retention & high inspiratory pressure if ventilated escharotomy
Assessment of burn wound Size  depth
Size  Formally assessed in a controlled environment Allows areas to be exposed & any soot / debris to be washed off Do not cause hypothermia
Patients whole hand – 1% of TBSA Lund & Browder chart Wallace rule of nine - approximate
Depth  Superficial partial thickness Deep partial thickness Full thickness
Fluid resuscitation Maintain the intravascular volume Needed in a child with > 10% 15% in adults
If oral water should not be salt free Stress hormones – anti diuresis Hypo natremia & water intoxication
Resuscitation volume – area burned Maximum loss in 8hrs Lasts 24 – 36 hrs
Fluids  Ringer lactate / Hartmans Human albumin solution / FFP Hypertonic saline
Parkland formula % burns  x body wt x 4 Half in first 8hrs Half over next 16 hrs
Maintanance fluid given for children as DNS 100ml/kg for 24 hrs for 10Kg 50ml/kg for next 10 kg 20ml/kg for each Kg over 20Kg
Monitoring  Key is urine output 0.5 -1 ml /kg body wt / hr If output low increase the infusion rate by 50% Should not be over resuscitated
Monitoring Acid base balance Hematocrit measurement CVP monitoring
Treatment of burn wound Eshcarotomy Full thickness Superficial partial
Eshcarotomy Circumferential full thickness burns of limbs Incised in mid axial line to avoid nerves Management of burn wound same
Full thickness 1% silver sulphadiazine Silver nitrate solution 0.5% Mefenide acetate Serum nitrate
1% silver sulphadiazine Broad spectrum prophylaxis Pseudomona  MRSA
Silver nitrate solution 0.5% Highly effective – pseudomonas Poor against some gram negative aerobes Needs change every 2 -4 hr Black staining
Mefenide acetate Popular in USA Painful 5% solution Metabolic acidosis
Serum nitrate Hard effect on the burned skin Especially in elderly Reduces the CMI suppression
Superficial burns Honey Boiled potato peel Synthetic biological dressings

Burns

  • 1.
  • 2.
    Epidemiology Incidencevaries between cultures Majority in children are scalds Adolescents experimenting
  • 3.
    Epidemiology Flame burnsin adults Most electrical & chemical burns in adults Mental diseases , epilepsy, alcohol & drug abuse
  • 4.
    On arrival burncase treated as trauma ABC Soot ,charring around nose – think of inhalation injury
  • 5.
    Assessment of burnsarea Wallace’s rule of nine Adult >20% ,child >10% needs IVF i/v access for analgesia
  • 6.
    Prognosis Percentagebody surface area burned Age & percentage add together to a score of 100 , considered fatal
  • 7.
    Assessment of burndepth Temperature of burning agent Mode of transmission of heat Duration of contact
  • 8.
    Skin anatomy Epidermiswaterproof Replaced from the basal layer Dermis-thicker strength & integrity Contains the adnexal structures
  • 9.
    Superficial burns Epidermal burns Heal by epithelialisation alone Red & painful Blisters not present
  • 10.
    Superficial burns superficialdermal Blistered Painful Heal by epithelialisation in 14 days
  • 11.
    Deep burns Adnexalstructures lost Heal by second intention scarring
  • 12.
    Deep burns BlisteredBlotchy red appearance No capillary return on pressure Absent sensation to pin prick
  • 13.
    Full thickness burnsWhite/ charred appearance No sensation Charred layer consists of denatured contracted dermis - eschar
  • 14.
    Pathophysiology Injuries toskin Injury to airway & lungs Inflammation & circulatory changes Other effects
  • 15.
    Injuries to skinMC organ affected is skin Area affected Depth
  • 16.
    Inhalational injury Hotgases cause injury to upper airway Stridor, hoarseness, cough, resp. obstruction CO causes chemical burn dr shabeel’s presentations
  • 17.
    Injury to airway& lungs damage airway & lungs Airway injury suspected in face & neck burns Person trapped in burning vehicles,house , plane etc
  • 18.
    Injury to airwayBurns above larynx Below larynx Metabolic poisoning Inhalational injury Mechanical block on rib movement
  • 19.
    Above larynx Hotgases burn nose , mouth, tongue , palate & larynx Linings start swelling May block the airway
  • 20.
    Below larynx Rareas heat is absorbed in supra glotic area But steam has a large latent heat of evaporation Epithelium swells & detaches This cast block the airway dr shabeel’s presentations
  • 21.
    Metabolic poisoning CO–product of incomplete combustion Affinity 240 times than Hb for O2 Blocks transport of O2 Carboxy Hb > 10% is dangerous Need pure O2 >24 hrs Death occurs with 60%
  • 22.
    Another metabolic toxinis hydrogen cyanide Metabolic acidosis by blocking mitochondrial respiration
  • 23.
    Inhalation Causedby minute particles within smoke Stick to moist lining alveoli Chemical pneumonitis
  • 24.
    Intense edema Decreasinggaseous exchange Bacterial pneumonia
  • 25.
    Mechanical block onrib movement Burned skin – thick & stiff Stop movement of ribs Common in large full thickness burn across the chest
  • 26.
    Inflammation & circulatorychanges Burned skin activate a web inflammatory cascades Pain - Release of neuro peptides & activation of compliments Hageman s factor – protease driven cascades
  • 27.
    Inflammation & circulatorychanges Compliments – degranulation of mast cells Coats the proteins burned Attracts neutrophils – degranulate – free radicals & proteases
  • 28.
    Inflammation & circulatorychanges Mast cells release primary cytokines – TNF alfa Secondary cytokines Alter the permeability of vessels
  • 29.
    Inflammation & circulatorychanges Large protien molecules escape Oncotic pressure again increases More flow of water into extra vascular space
  • 30.
    Inflammation & circulatorychanges Water ,solutes, proteins – ECF Occurs in first 36 hrs 10-15% burns – shock >25% loss occurs in remote vessels
  • 31.
    Other effects Immunesystem & infection Changes in intestine Peripheral circulation
  • 32.
    Immune system &infection Inflammatory changes affect immune system CMI reduced in large burns Bacterial & fungal infection
  • 33.
    Changes in intestineMicro vascular damage & ischemia of gut mucosa Motility & absorption affected Failure to enteral feeding Translocation of gut bacteria
  • 34.
    Septicemia Abdominalcompartment syndrome- mucosal swelling, stasis, peritoneal edema Splinting of diaphragm
  • 35.
    Peripheral circulation Fullthickness burns- coagulation of collagen Elasticity of skin lost Circumferential burn of the limb act as tourniquet
  • 36.
    Regional problems Circulation May affect the limb circulation Not by direct damage to main vessel edema - venous obstruction Muscle compartment syndrome
  • 37.
    Effects of burninjury Local Regional Systemic
  • 38.
    Local effects Tissuedamage Inflammation Infection
  • 39.
    Tissue damage Heating -> cell rupture / necrosis Cells of periphery injured Denaturation of collagen
  • 40.
    Tissue damage Capillariesthrombosed in severe cases Increased damage in less severe case Tissues become edematous
  • 41.
    Inflammation Markedresponse Erythema in least burned areas Neurovascular response like Lewis triple response
  • 42.
    Severe – cytokinesPhagocytose necrotic cells Damaged tissues separate by de sloughing in 3 wks
  • 43.
    Infection Damagedtissue – nidus of infection Colonization in 24 – 48 hrs Bacteremia is a common cause of fatality
  • 44.
    Systemic effects Fluidloss Multiple organ failure Inhalational injury Systemic complications
  • 45.
    Fluid loss Externalloss Internal loss as edema Mediated by cytokines
  • 46.
    Management Immediatecare Assessment of burn wound Fluid resuscitation Treatment of burn wound
  • 47.
    Immediate care Prehospital Hospital care
  • 48.
    Pre hospital Ensurerescuer safety – house fire , chemical , electrical Stop the burning process – stop, drop & roll Check for other injuries Cool the burn wound
  • 49.
    Pre hospital Coolthe burn wound – minimum 10mts to an hour Oxygen elevate
  • 50.
    Hospital care Airway Breathing Circulation Disability Exposure with environmental control Fluid resuscitation
  • 51.
    Major determinants ofoutcome Percentage area Depth Inhalational injury
  • 52.
    Criteria for admissionInhalational injury Fluid resuscitation Needing surgery Suspicion of non accidental cause Extremes of age Associated potential sequelae
  • 53.
    Airway Burnedairway causes obstruction Endo tracheal tube for 48 hours Symptoms of laryngeal edema appear late
  • 54.
    Airway Intubationwill be difficult after symptoms appear Crico thyroidotomy needed in late diagnosis Recognition of potentially burned airway
  • 55.
    Breathing Inhalationalinjury Thermal burns to lower airway Metabolic poisoning Mechanical block to rib movement
  • 56.
    Inhalational injury Observeanyone trapped in a fire Presence of soot in nose & oro pharynx Chest x-ray - patchy consolidation
  • 57.
    Clinical features Progressiveincrease in resp effort & rate Rising pulse , anxiety , confusion Decreasing oxygen saturation
  • 58.
    Treatment Securethe airway Physiotherapy, nebulisation, warm humidified oxygen Monitor the progress IPPV for severe cases
  • 59.
    Burns of lowerairway Steam injury Supportive management Like inhalational injury
  • 60.
    Metabolic poisoning Firewithin a closed space Altered consciousness ABG
  • 61.
    Metabolic acidosis Highinspired O2 for 24 hrs if >10% Displacement from Hb
  • 62.
    Mechanical block torib movement Eschar on the chest CO2 retention & high inspiratory pressure if ventilated escharotomy
  • 63.
    Assessment of burnwound Size depth
  • 64.
    Size Formallyassessed in a controlled environment Allows areas to be exposed & any soot / debris to be washed off Do not cause hypothermia
  • 65.
    Patients whole hand– 1% of TBSA Lund & Browder chart Wallace rule of nine - approximate
  • 66.
    Depth Superficialpartial thickness Deep partial thickness Full thickness
  • 67.
    Fluid resuscitation Maintainthe intravascular volume Needed in a child with > 10% 15% in adults
  • 68.
    If oral watershould not be salt free Stress hormones – anti diuresis Hypo natremia & water intoxication
  • 69.
    Resuscitation volume –area burned Maximum loss in 8hrs Lasts 24 – 36 hrs
  • 70.
    Fluids Ringerlactate / Hartmans Human albumin solution / FFP Hypertonic saline
  • 71.
    Parkland formula %burns x body wt x 4 Half in first 8hrs Half over next 16 hrs
  • 72.
    Maintanance fluid givenfor children as DNS 100ml/kg for 24 hrs for 10Kg 50ml/kg for next 10 kg 20ml/kg for each Kg over 20Kg
  • 73.
    Monitoring Keyis urine output 0.5 -1 ml /kg body wt / hr If output low increase the infusion rate by 50% Should not be over resuscitated
  • 74.
    Monitoring Acid basebalance Hematocrit measurement CVP monitoring
  • 75.
    Treatment of burnwound Eshcarotomy Full thickness Superficial partial
  • 76.
    Eshcarotomy Circumferential fullthickness burns of limbs Incised in mid axial line to avoid nerves Management of burn wound same
  • 77.
    Full thickness 1%silver sulphadiazine Silver nitrate solution 0.5% Mefenide acetate Serum nitrate
  • 78.
    1% silver sulphadiazineBroad spectrum prophylaxis Pseudomona MRSA
  • 79.
    Silver nitrate solution0.5% Highly effective – pseudomonas Poor against some gram negative aerobes Needs change every 2 -4 hr Black staining
  • 80.
    Mefenide acetate Popularin USA Painful 5% solution Metabolic acidosis
  • 81.
    Serum nitrate Hardeffect on the burned skin Especially in elderly Reduces the CMI suppression
  • 82.
    Superficial burns HoneyBoiled potato peel Synthetic biological dressings