Burns lecture.pptx77777777777777777777777777777777

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1. Management of skin burns Dr Mohamed Salieu Soh MBChB , BSc (Hons) Chemistry.

2. Lecture outline Introduction Mechanism of injury Aetiology Pathophysiology Principles of management Burn resuscitation Assessment of severity of injury Indications for admission Complications Conclusion

3. Learning objectives Identify how burn injuries occur List the aetiological factors Explain the body response to burn injury Enumerate steps involved in assessing the severity of injury List the steps in the management of burn injury Appreciate the complications of burns and how to avoid them

4. Introduction Burn injury is the coagulative necrosis of the skin. It sometimes affects the underlying tissues in addition and there may be great local and systemic effects. A large burn wound is a major trauma and it could be life threatening.

5. Introduction Burn injury is to a person or group of patients The patient/s is/are part of a family Wider community

6. Mechanism of Injury Burn can be caused by different mechanisms resulting in skin damage Skin damage is proportional to the temperature of the burning agent Length of time of contact Thickness of the skin

7. Aetiology Flame burn Moist heat (scald) Contact burn Electrical burn High voltage (>1000 volts) Low voltage (<1000 volts) Chemical burns Radiation burns Friction burns Frost bite

8. Pathophysiology Thermal injury causes a loss of intravascular plasma volume to the interstitium in the form of edema that accumulates rapidly during the initial 6-8 hours post burn and continues more slowly for the next 16-18 hours These inflammatory responses are mediated by a host of inflammatory mediators which include Cytokines Oxygen free radicals Arachidonic acid derivatives Endotoxins

9. Inflammatory mediators in burns Cytokines These include IL-1 , IL-2 ,IL-6 ,interferon gamma and their effects include Increase in vascular permeability Muscle catabolism Production of anaemia / fever Initiation of wound healing Oxygen radicals These are the super oxides and the hydrogen peroxide and they Alter vascular permeability Cause RBC hemolysis Disrupt interstitial matrix

10. Inflammatory mediators in burns Arachidonic acid metabolites Cyclooxygenase pathway Prostaglandins Vasodilators Pain Erythema Lipooxygenase pathway Leukotrienes C4 , D4 vasoconstrictors

11. Local response Zone of coagulation—This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins. Zone of stasis—The surrounding zone of stasis is characterised by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults such as prolonged hypotension infection or oedema can convert this zone into an area of complete tissue loss. Local respons

12. Local response Zone of hyperaemia —In this outermost zone tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion. These three zones of a burn are three dimensional and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening.

13. Systemic response The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30% of total body surface area. Cardiovascular changes—Capillary permeability is increased, leading to loss of intravascular proteins and fluids into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased, possibly due to release of tumour necrosis factor . These changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end organ hypoperfusion.

14. Systemic response Respiratory changes—Inflammatory mediators cause bronchoconstriction, and in severe burns adult respiratory distress syndrome can occur. Metabolic changes -The basal metabolic rate increases up to three times its original rate. This, coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity. Immunological changes—Non-specific down regulation of the immune response occurs,

15. Burn assessment Full assessment of the burn involves Detailed history Assessment of circumstance of the injury Assessment for inhalation injury Assessment for prognostic factors Social history Examination General Extent of the injury Sites Size Depth

16. Principles of management Prehospital care (First Aid) Remove the person from further damage Douse patient’s clothing if still burning with cool water Pour a lot of cool water of the burn wound Cover the wound with clean wet cloth For chemical injury, Remove patient’s clothing Copious irrigation of wound with water must commence immediately

17. Principles of Management Burn resuscitation follows the ATLS protocol Primary survey A irway maintenance with C spine control B reathing and ventilation C irculation with bleeding control + catheterization D isability (neurological status) E xposure + Environmental control + Burn wound assessment

18. Principles of management Hospital care Resuscitation This takes precedence in the management protocol Follows the ATLS protocol of ensuring a patent AIRWAY , endotracheal intubation may be indicated in patients with inhalation injury or a patient with a significant facial burn and 100% humidified oxygen is administered. BREATHING : In significant CO poisoning, intubation plus ventillatory support may be indicated. The patient may also require hyperbaric oxygen therapy. Where there is significant circumferential burn of the chest with restriction of chest excursion, escharotomy will be necessary

19. Principles of management Resuscitation contd. CIRCULATION : prompt fluid resuscitation through wide bore canulae (14 or 16 G) must be commenced without delay with crystalloids –ringers lactate (or normal saline) The exact fluid requirement is calculated using a guide which takes into consideration the patients’ weight and the severity of injury. Urethral CATHETERISATION is done using a self retaining catheter to monitor the patient’s hourly urine output which should be maintained at 1-2 mls /Kg/hour in children and 0.5-1 ml/Kg/hour in adults

20. Principles of management DISABILITY Assess the patient for other disabilities Fractures Head injury Abdominal / chest injury

21. Principles of management Secondary survey History Biodata Time and place of injury Agent / severity of the injury Assess for possibility of inhalation injury Factors which may suggest inhalation injury include Burn injury in closed environment Significant facial burn Loss of consciousness Cough with carbonaceous sputum Hoarseness of voice Significant facial swelling

22. Ask for patient’s pre morbid conditions which can significantly affect outcome Asthma Seizure disorder DM Cardiac conditions HIV/AIDS Drug / allergies Tetanus immunization status Previous treatment (pre hospital care)

23. Physical Examination General examination [Head to Toe] Look for signs of inhalation injury Check limbs/trunks for features of compartmental syndrome especially in patients with deep circumferential wounds Examine the integuments for the extent of the burn wound ( depth and surface area)

24. Assessing severity of Burn Size of burn (TBSA) Depth of burn Site of burn Inhalation injury Associated injuries

25. Assessment of burn surface area Rule of the palm Wallace’s rule of Nines Lund and Browder chart

26. Wallace’s Rule of 9s Body site Percentage surface area (%) Head and Neck 9 U pper limbs 9 x 2 Anterior trunk 9 x 2 Posterior trunk 9 x 2 Each lower limb 18 x 2 Perineal area 1 Total 100

27. Assessment of burn wound depth Hyperemia 1 st degree Superficial dermal 2 nd degree Deep dermal 3 rd degree Full thickness 4 th degree

28. Evaluation of burn wound depth superficial Partial thickness-superficial Partial thickness-deep dermal Full thickness Erythema only Erythema with blistering No blistering Whitish base, non blanching Red base, blanches with pressure Red, often with diffuse white patches Thrombosed small vessels often seen on wound Painful- skin pliability maintained Painful- skin pliability maintained Non-painful. skin pliability lost. May involve subjacent structures

29. Superficial Burn (Blister)

30. Inhalation Injury Signs Facial burn Facial oedema Stridor Difficulty with breathing Carbonaceous sputum Wheezing Burned nasal hair Symptoms Cough Anxiety Shortness of breath Headache Hoarse voice Confusion

31. Inhalation Injury

32. Indications for admission Burn wound >10% in children & >15% in adults Patients <2 or >60 years old Burn involving hands, feet, face, perineum, axilla, joints, neck, and other flexural surfaces Patients presenting with other associated injuries such as fractures etc Patients with significant co-morbid factors such as Asthma, Heamoglobinopathy , seizure disorders etc Patients with inhalation injury Deep circumferential burn involving the limbs

33. Fluid resuscitation Various formulae are available for the estimation of the required fluid for resuscitating burn patients. These include Parkland’s formula Muir and Barclay Baxter Warden

34. Parkland’s formula Uses crystalloid –RINGERS LACTATE Volume= 4 X weight (kg) X TBSA Half of the calculated volume is given in the first 8 hours from the time of injury and the remaining half is given in the subsequent 16 hours The volume for the subsequent days is estimated based on the response to the previous day’s fluid

35. Investigations FBC U&E / Creatinine Wound biopsy Grouping and cross matching CXR Arterial blood gases Carboxyheamoglobin level Fiber optic bronchoscopy

36. Other treatment Interdisciplinary care involving the plastic surgeon, anesthesiologist, physician/pediatrician, burn nurses, physiotherapist, occupational therapist , nutritionist, psychiatrist , microbiologist, hematologist etc Drug therapy Analgesia Anti tetanus Anti ulcer Anti coagulation Antibiotics

37. Other treatment Escharotmy / escharectomy Physiotherapy Nutritional rehabilitation Burn wound management The treatment depends on the depth of the wound For superficial partial thickness wounds, wound dressing is done and it is anticipated that the wound will re epithelialize within two weeks Wound dressing may be open or occlusive Common dressing agents include Povidone iodine (5 -10%) , Honey, Silver nitrate (0.5%) , Silver sulphadizine (1%) , Acetic acid (0.5 – 1%) , Maphenide

38. Other treatment Escharotmy / escharectomy Physiotherapy Nutritional rehabilitation Burn wound management The treatment depends on the depth of the wound For superficial partial thickness wounds, wound dressing is done and it is anticipated that the wound will re epithelialize within two weeks Wound dressing may be open or occlusive Common dressing agents include Povidone iodine (5 -10%) , Honey, Silver nitrate (0.5%) , Silver sulphadizine (1%) , Acetic acid (0.5 – 1%) , Maphenide

39. Wound management – Skin grafting Wound excision plus split thickness skin grafting (STSG) is indicated for : Deep dermal wounds Full thickness wounds

40. Escharotomy

41. Complications of Burn injury Major burn injuries may be life threatening because of the significant systemic inflammatory response that could be associated The complications may present early or late some of the early complications may be life threatening while the late complications are usually associated with major deformities

42. Early complications Hypovolaemic shock Acute renal failure ARDS Pneumonia Urinary tract Infection Acute gastric dilatation Paralytic ileus Curlings ulcer Septicemia Depression/delirium Deep venous thrombosis Wound infection Anemia Compartment syndrome Thrombophlebitis

43. Late complications Abnormalities with scar Hypertrophic scar Keloid Dyschromic changes (hypo and hyper pigmentation) Abnormalities with healing Contracture deformities Secondary syndactyly Chronic ulcer Marjolin’s ulcer Pulmonary fibrosis

44. Complications - Burn Contracture