burns ppt.pptx

etiology and pathopysiology of burns

1. Burns –Thermal, Chemical, Electrical burns and Pathophysiology of Burns -by Ranjita Hegde

2. Burn Defined as a wound caused by exogenous agent leading to coagulative necrosis of the tissue

3. History Fabrigus Hildanicus in his book De- Combustionibus first described classification Parre distinguished between 2nd and 3rd degree burn Richard Wiseman 1676 : Splintage in burns Edward Kentish 1796: Pressure dressings to relief pain Earle 1799: Means to reduce effect of burn -Ice usage Wallace 1949: open dressing for face Lister 1875: boric+ carbolic acid for dressing Bradford Cannon : Skin grafting as main treatment line

4. Types of Burn Injury Thermal Scald Flame Flash Contact Cold burn - Frostbite Inhalational burn Electric Low tension High tension Lightning. Chemical : alkali and acid Radiation

5. 66 % of all burns - at home, The MCCs are flame and scald burns. Alcohol Scald burns MC in children < 5 years Child abuse. The survival rate for all burns is 94.6%, But for at-risk populations, in communities lacking medical, legal, and public health resources, survival can be nearly impossible

6. Classification of Burn Injury Severity of injury is determined by Depth of burn Extent of burn Location of burn Patient risk factors

7. Depth of Burn In the past, burns were defined by degrees: First-degree, second-degree, third and fourth degree burns Burns now classified according to depth of skin destruction: Partial-thickness burn Full-thickness burn Superficial partial thickness - Involves the epidermis –1st degree Deep partial thickness - Involves the dermis -2 nd degree Full thickness - Involves fat, muscle, bone-3 rd and 4 th degree

8. Evaluation of extent of burn surface: Superficial burns are not included in the calculation. Only partial or full thickness burns are included. 1. Lund and Browder chart 2. Palm method 3. Rule of 9 4. Berkow’s percentages chart

9. Rule of 9

10. RULE OF PALMS A burn equivalent to the size of the patient’s hand is equal to 1% body surface area (BSA).

11. Thermal Burns Caused by flame, flash, scald, or contact with hot objects Most common type of burn Heat changes molecular structure of tissue causing denaturation of proteins Extent of burns damage depends on Temperature of agent Amount of heat Duration of contact

12. Smoke Inhalation Injuries Result from inhalation of hot air or noxious chemicals Cause damage to respiratory tract Important determinant of mortality in fire victims CO poisoning CO is produced by the incomplete combustion of burning materials Inhaled CO displaces oxygen

13. Chemical Burns Acids Form a thick, insoluble mass where they contact tissue. Coagulation necrosis Limits burn damage Alkalis Destroy cell membrane through liquefaction necrosis Deeper tissue penetration and deeper burns Most commonly caused by acids Tissue destruction may continue for up to 72 hrs after injury

14. Electrical Burns Result from coagulation necrosis caused by intense heat generated from an electrical current May result from direct damage to nerves and vessels causing tissue anoxia and death Severity of injury depends on the amount of voltage, tissue resistance, current pathways, surface area, and on the length of time of the flow Greatest heat occurs at the points of resistance , Longer the contact, the greater the potential of injury , Smaller the point of contact, the more concentrated the energy Electrical sparks may ignite the patient’s clothing, causing a combination of thermal and electrical injury

15. BEST WORST CONDUCTORS NERVE BLOODVESSELS MUSCLE SKIN TENDON FAT BONE

16. CONTACT BURN Due to close contact POINT OF ENTRY : Raised Blister containing GAS or FLUID POINT OF EXIT: Punctured or lacerated Wound SPARK BURN Due to poor or intermittent contact Dry Pitted Lesion Surround by Yellow Parchment Scab FLASH BURN Due to without actual contact with very high voltage, more then 1000 volts.

17. Local whitening Zone of hyperemia Chain of blisters Dried and wrinkled skin Scorched and blackened skin. Explosively splitting of clothes.

18. FLASH BURN Charring of tissues with carbonisation is common. Brownish discoloration of skin. Crocodile skin – multiple spark burns over large areas of skin

19. LIGHTENING A natural electric discharge in the atmosphere is called lightning or lightning flash. It is electric discharge from cloud to earth. Lightning has 100-1000 million volts. Charred body and skin Burns Arborescent marking due to passage of current through blood vessels. (Branches of tree) Megnitisation of metallic articles e.g rings, spectacle frames, keys, watches etc. due to tremendous heat. Cardiac failure. , Rupture of tympanic membrane. , Bone fractures. , Torn clothes

20. Cold Thermal Injury Frostbite : Exposure to dry cold. The exposed parts such as ears, nose, fingers and toes may show localized effects. Lesions (blisters) may superficial involving skin and subcutaneous tissue. Necrosis of tissues. Temp is usually below 0C.

21. Pathophysiology of Burns Temp : 40° to 44° C (104° to 111.2° F) - Enzymes malfunction - Proteins denature - Cellular pumps fail. > 44° C (111.2° F) the damage occurs faster than the cell’s repair mechanism can function.

22. Jackson burn model ZONE OF COAGULATION • The first of three zones. • The cell death is complete. • Area nearest to the heat source. ZONE OF STASIS • cells are viable. • If untreated thrombosis and vasoconstriction Necrosis. ZONE OF HYPEREMIA. • Minimal cellular injury • Predominant vasodilation. • These cells usually recover.

23. Pathophysiology of Burns Fluid shift Period of inflammatory response Vessels adjacent to burn injury dilate : increased capillary hydrostatic pressure & capillary permeability Continous leak of plasma from intravascular space into interstitial space Associated imbalances of fluids ,electrolytes & acid –base occur Hemoconcentration Last 24-36 hrs

24. Metabolic - Hypermetabolic state Increased oxygen & calorie requirements Increase in core body temperature Immunologic Loss of protective barrier - Increased risk of infection Suppression of humoral & cell mediated immune responses

25. ACUTE PHASE Clinical Shock External loss of plasma Loss of circulating red cells Burn edema

26. Body’s response to burns Emergent Phase (stage 1) - - Pain response - Catecholamine release - Tachycardia, tachypnea , Mild hypertension Fluid Shift Phase (stage 2 ) Length 18-24 hrs Begins after emergent phase (reaches peak in 6-8 hrs) Damaged cells initiate inflammatory response ( Increased blood flow to cells, Shift of fluid from intravascular to extravascular space )

27. Hypermetabolic Phase ( stage 3) Last for days to weeks Large increase in body’s need for nutrient as it repairs itself Resolution Phase( stage 4) Scar formation General rehabilitation & progression to normal function

28. PRIMARY BURN MANAGEMENT Safe from the scene Stop the burning process Consider burn patient as a multiple trauma patient untill determined otherwise Perform ABCDE assessment Initiate cooling (Thermal) : Avoid hypothermia Flush chemicals off (Chemical) High flow oxygen Calculate TBSA ( Evaluate injury depth, Evaluate injury severity) Expose and examine : Remove constricting clothing and jewellery

29. Airway Signs of airway burn/inhalation injury : stridor, hoarseness, black sputum, respiratory distress, singed nasal hairs or facial swelling Sign of oropharyngeal burn : soot in mouth, intraoral oedema and erythema Significant neck burn If above present, consider early intubation If suspicion of airway burns or carbon monoxide intoxication apply high flow oxygen Protect the cervical spine with immobilisation if there is associated trauma Breathing Full thickness and/or circumferential chest burns may require escharotomy to permit chest expansion

30. Circulation If early shock is present, consider causes other than the burn IV fluid resuscitation  as required IV or IO access (preferably 2 points of access) For circumferential burns check peripheral perfusion and need for escharotomy Disability If altered conscious state, consider airway support Assess neurovascular status if limb involved Exposure – Expose whole body - remove clothing and log roll to visualise posterior surfaces,Use Lund & Browder Chart.

31. Electrical injuries: Risk of dysrhythmias - consider 24 hours ECG monitoring Monitor for elevated CK, urine haemoglobin and myoglobin Chemical burns Personal protective equipment for first aid givers should be worn (gloves, mask, gown, eye protection) Remove contaminated clothing Brush powdered agent off skin Areas in contact with chemical should be irrigated with cool water Irrigate to floor with appropriate drainage so contaminated water does not cause further injury

32. BURN MORTALITY Management is focused to prevent mortality and morbidly Initial 24 hours: Airway burns and respiratory injury hypovolemic shock After 24 hours: infections kidney failure

33. STRATEGY : PLANNING IMPLEMENTATION/INTERVENTIONS

34. Parkland formula Initial 24 hours : Ringer’s lactated (RL) solution 4 ml/kg/% burn for adults and 3 ml/kg/% burn for children. Next 24 hours : Colloids given as 20–60% of calculated plasma volume. No crystalloids. Glucose in water is added in amounts required to maintain a urinary output of 0.5–1 ml/hour in adults and 1 ml/hour in children.

35. Resuscitation formula Modified Parkland formula a. Initial 24 hours : RL 4 ml/kg/% burn (adults) b. Next 24 hours : Begin colloid infusion of 5% albumin 0.3–1 ml/kg/% burn/16 per hour Brooke formula a. Initial 24 hours : RL solution 1.5 ml/kg/% burn plus colloids 0.5 ml/kg/% burn plus 2000 ml glucose in water b. Next 24 hours : RL 0.5 ml/kg/% burn, colloids 0.25 ml/kg/% burn and the same amount of glucose in water as in the first 24 hours Modified Brooke a. Initial 24 hours : No colloids. RL solution 2 ml/kg/% burn in adults and 3 ml/kg/% burn in children b. Next 24 hours : Colloids at 0.3–0.5 ml/kg/% burn and no crystalloids are given. Glucose in water is added in the amounts required to maintain good urinary output.

36. Evans formula (1952) a. First 24 hours : Crystalloids 1 ml/kg/% burn plus colloids at 1 ml/kg/% burn plus 2000 ml glucose in water b. Next 24 hours : Crystalloids at 0.5 ml/kg/% burn, colloids at 0.5 ml/kg/% burn and the same amount of glucose in water as in the first 24 hours. Monafo formula Monafo recommends using a solution containing 250 mEq Na, 150 mEq lactate and 100 mEq Cl. The amount is adjusted according to the urine output. In the following 24 hours, the solution is titrated with 1/3 normal saline according to urinary output.

37. ASSESSING ADEQUACY OF RESUSCITATION Peripheral blood pressure: may be difficult to obtain – often misleading Urine Output: Best indicator unless ARF occurs CVP: Better indicator of fluid status Heart rate: Valuable in early post burn period – should be around 120/min. > HR indicates need for > fluids or pain control

38. NUTRITIONAL SUPPORT Essential for wound healing, graft survival; prevents “at risk” partial thickness injury from converting to full thickness injury. Enteral feeds preferred over TPN – may prevent gut bacterial translocation – early (within 4 hours) institution of enteral feeds may achieve early positive N2 balance – may be precluded by paralytic ileus Hypermetabolic state favors breakdown/use of fat and protein; rate of loss of lean body mass can be slowed by approximating positive nitrogen balance; high protein content of enteral formula therefore favored Curreri Formula: – calories/day=( wt in kg) (25) + (40) (%BSA) : needs periodic recalculation as healing occurs – probably overestimates caloric needs

39. Wound Management Ist degree superficial burn Run cool, not cold, water over the wounded area to reduce pain and swelling Use a mild soap and water to cleanse affected area Apply an antibiotic ointment if there is no opening of the skin Wrap the affected area loosely with sterile gauze to avoid agitation 2 nd degree burns hydrogel dressings,tulle dressings, silversulfadizine ointment 3 rd degree burns Debridement and skin grafting

40. PAIN MANAGEMENT DOC: Morphine Sulfate Dose: Adults: 0.1 – 0.2 mg/kg IVP Children: 0.1 – 0.2 mg/kg/dose IVP / IO Use opiates cautiously in infants who are not mechanically ventilated - Consider role of anxiolytics Anti-inflammatory drugs, paracetamol and dipyrone: These medications may reduce the amount of opioid needed by up to 20-30% and reduce the adverse effects of opioids significantly  . Due to the inhibition of platelet aggregation, the use of NSAIDs should be avoided in situations in which risk of bleeding is a concern (such as severe burn)   . Its use also requires caution in patients with cardiovascular and gastrointestinal diseases .

41. Thankyou