BURNS.pptx surgery detailed explanation with causes and surgical treatment

burns ppt surgery detailed explanation

1. BURNS CAUSES CLASSIFICATION CLINICAL FEATURES MANAGEMENT

2. CAUSES CHILDREN  SCALDS ACCIDENTS WITH KETTLES,PANS,HOT DRINKS, BATH WATER ADOLESCENTS YOUNG MALES EXPERIMENTING WITH MATCHES AND FLAMMABLE LIQUIDS ADULTS  FLAME BURNS > SCALDS: ELECTRICAL AND CHEMICAL INJURIES ASSOCIATED CONDITIONS LIKE MENTAL DISEASE, EPILEPSY, DRUG ABUSE IN 80% OF PATIENTS ADMITTED WITH BURNS

3. INJURIES TO THE AIRWAY AND LUNGS PHYSICAL BURN INJURY TO THE AIRWAY ABOVE THE LARYNX Hot gases physically burn the nose, mouth, tongue, palate and larynx once burned  lining swells After few hours may block the airway PHYSICAL INJURY TO THE AIRWAY BELOW THE LARYNX Very rare as heat exchange mechanisms in the supraglottic airway usually safely absorb the heat from hot air Steam has a large latent heat of evaporation and can cause thermal damage to the Lower Airway Respiratory epithelium rapidly swells and detaches from bronchial tree It creates casts, which can block the upper airway

4. METABOLIC POISONING CARBON MONOOXIDE POISONING  PRODUCT OF INCOMPLETE COMBUSTION CAUSES ALTERED CONSCIOUSNESS CO BINDS TO Hb WITH AN AFFINITY 240 TIMES GREATER THAN O2 SO BLOCKS TRANSPORT OF OXYGEN CONCENTRATIONS > 10% DANGEROUS, TREAT WITH PURE O2 FOR MORE THAN 24 HOURS CONCENTRATIONS > 60%  DEATH 2. HYDROGEN CYANIDE CAUSES METABOLIC ACIDOSIS BY INTERFERING WITH MITOCHONDRIAL RESPIRATION

5. INHALATIONAL INJURY CAUSED BY MINUTE PARTICLES WITHIN THICK SMOKE CARRIED DOWN TO LUNG PARENCHYMA STICK TO MOIST LINING, CAUSING AN INTENSE REACTION IN THE ALVEOLI  CHEMICAL PNEUMONITIS CAUSES OEDEMA WITHIN ALVEOLAR SACS AND DECREASING GASEOUS EXCHANGE + BACTERIAL PNEUMONIA

6. MECHANICAL BLOCK ON RIB MOVEMENT BURNED SKIN  THICK AND STIFF PHYSICALLY STOPS THE RIBS MOVEMENT IN CASES OF LARGE FULL THICKNESS BURNS ACROSS THE CHEST

7. INFLAMMATION AND CIRCULATORY CHANGES BURNED SKIN  ACTIVATES A WEB OF INFLAMMATORY CASCADES RELEASE OF NEUROPEPTIDES AND ACTIVATION OF COMPLEMENT ARE INITIATED BY STIMULATION OF NERVE FIBRES AND ALTERATION OF PROTEINS BY HEAT ACTIVATION OF Hageman Factor initiates protease driven cascades, altering arachidonic acid, thrombin and kallikrein pathways CELLULAR LEVEL complement causes degranulation of mast cells and coats the proteins altered by the burn It attracts Neutrophils degranulates  release free radicals and proteases further damage MAST CELLS release primary cytokines(TNF alfa ) chemotactic agents to inflammatory cells  release of secondary cytokines alter permeability of blood vessels large proteins escape intravascular fluid escapes Damaged collagen and extravasated proteins increase oncotic pressure within the burned tissue further fluid escape

8. Net flow of water, solutes and proteins It does not include red blood cells If burn 10-15% TBSA  it can cause circulatory shock If burn >25% of TBSA, the inflammatory reaction causes fluid loss in vessels remote from the burn injury

9. IMMUNE SYSTEM AND INFECTION CELL MEDIATED IMMUNITY IS REDUCED MORE SUSCEPTIBLE TO BACTERIAL AND FUNGAL INFECTIONS SOURCES OF INFECTION  BURN WOUND, LUNG INJURY, CENTRAL VENOUS LINES, TRACHEOSTOMIES OR URINARY CATHETERS CHANGES TO THE INTESTINE: Microvascular damage and ischemia to gut mucosa decreased gut motility and prevent food absorption Enteral feeding is must Failure of enteral feeding in a patient with large burn is a life threatening complication It increases the translocation of gut bacteria source of infection Gut mucosal swelling + gastric stasis + peritoneal oedema  Abdominal compartment syndrome which splints the diaphragm and increases the airway pressures needed for respiration DANGER TO PERIPHERAL CIRCULATION: FULL THICKNESS BURN COLLAGEN FIBRES COAGULATION LOSS OF NORMAL ELASTICITY OF SKIN CIRCUMFERENTIAL FULL THICKNESS BURN TO A LIMB ACTS AS A TOURNIQUET AS LIMB SWELLS LIMB THREATENING ISCHEMIA

10. IMMEDIATE CARE OF THE BURN PATIENT PREHOSPITAL CARE HOSPITAL CARE POST HOSPITAL CARE

11. PREHOSPITAL CARE ENSURE RESCUER SAFETY IN HOUSE FIRES AND ELECTRICAL AND CHEMICAL BURNS STOP THE BURNING PROCESS STOP, DROP AND ROLL CHECK FOR OTHER INJURIES ABC  RAPID SECONDARY SURVEY.. HED /SPINE INJURIES IN EXPLOSIONS COOL THE BURN WOUND PROVIDES ANALGESIA AND SLOWS THE DELAYED MICROVASCULAR DAMAGE COOL FOR MINIMUM 10 MINUTES AND IS EFFECTIVE UP TO 1 HOUR AFTER INJUY PARTICULARLY IMPORTANT FIRST AID STEP IN PARTIAL THICKNESS BURN, ESPECIALLY SCALDS COOL AT 15* C ANDAVOID HYPOTHERMIA 5. GIVE OXYGEN 6. ELEVATE  SITTING POSITION, ELEVATION OF BURNED LIMBS REDUCE SWELLING

12. HOSPITAL CARE AIRWAY CONTROL 2. BREATHING AND VENTILATION CIRCULATION DISABILITY- NEUROLOGICAL STATUS EXPOSURE WITH ENVIRONMENTAL CONTROL FLUID RESUSCITATION DETERMINANTS OF SEVERITY OF BURN INJURY  PERCENTAGE OF TBSA  PRESENCE OF AN INHALATION INJURY  DEPTH OF BURN

13. AIRWAY BURNED AIRWAY  SWELLING OCCLUSION OF AIRWAY TREATMENT SECURE AIRWAY ENDOTRACHEAL TUBE/ CRICOTHYROIDOTOMY USUALLY SWELLING SUBSIDES IN 48 hours SYMPTOMS OF LARYNGEAL OEDEMA CHANGE IN VOICE, STRIDOR,ANXIETY, RSPIRATORY DIFFICULTY{ LATE SYMPTOMS } LATE INTUBATION DIFFICULT/IMPOSSIBLE OWING TO SWELLING EARLY INTUBATION  TREATMENT OF CHOICE BURN TO AIRWAY OCCLUSION  BETWEEN 4 AND 24 HOURS

14. HISTORY AND EARLY SIGNS SYMPTOMS LATE PRESENTATION HISTORY  INHALATION OF HOT GASES IN HOUSE/CAR FIRES EXAMINATION  BLISTERS ON HARD PALATE/BURNED NASAL MUCOSA/LOSS OF ALL HAIR IN NOSE( ANTERIOR HAIRS ARE OFTEN BURNED)/PRESENCE OF DEEP BURNS AROUND MOUTH AND IN NECK

15. BREATHING INHALATIONAL INJURY THERMAL BURN INJURY TO THE LOWER AIRWAY METABOLIC POISONING MECHANICAL BLOCK TO BREATHING

16. INHALATIONAL INJURY TIME  IMPORTANT FACTOR OBSERVE FOR SIGNS OF SMOKE INHALATION PRESENCE OF SOOT IN NOSE AND OROPHARYNX CHEST RADIOGRAPH PATCHY CONSOLIDATION CLINICAL FEATURES  INCREASE IN RESPIRATORY EFFORT AND RATE,RISING PULSE, ANXIETY, CONFUSION AND DECREASING OXYGEN SATURATION C/F CAN TAKE UPTO 24 HOURS TO 5 DAYS TO DEVELOP START TREATMENT AS SOON AS INJURY IS SUSPECTED SECURE AIRWAY,PHYSIOTHERAPY,NEBULISERS, WARM HUMIDIFIED OXYGEN PROGRESS MONITORING  RESPIRATORY RATE, BLOOD GAS ANALYSIS IF DETERIORATION CONTINUOUS / INTERMITTENT POSITIVE PRESSURES/ ENDOTRACHEAL INTUBATION

17. THERMAL BURN INJURY TO THE LOWER AIRWAY: WITH STEAM INJURIES MANAGEMENT SUPPORTIVE AND AS INHALATIONAL INJURIES METABOLIC POISONING: FIRE WITHIN CLOSED SPACE+ ALTERED CONSCIOUSNESS MEASURE BLOOD GASES IMMEDIATELY CARBOXYHAEMOGLOBIN LEVELS>10%  TREAT WITH HIGH INSPIRED OXYGEN FOR 24 HOURS MECHANICAL BLOCK TO BREATHING: ESCHAR OF SIGNIFICANT FULL THICKNESS BURN ON CHEST WALL CO2 RETENTION AND HIGH INSPIRATORY PRESSURES IF VENTILATED TREATMENT  ESCHAROTOMY NERVES DESTROYED IN SKIN  PAINLESS

18. ASSESSMENT OF THE BURN WOUND ASSESSING SIZE TEMPERATURE AND TIME DEPENDANT 6 HOURS AT 44*C  IRREVERSIBLE CAHNGES SURFACE TEMPERATUR OF 70*C FOR 1 SECOND EPIDERMAL DESTRUCTION HOT WATER AT 65*C 45sec  FULL THICKNESS BURN 15sec  DEEP PARTIAL THICKNESS BURN 7 sec  SUPERFICIAL PARTIAL THICKNESS BURN ASSESSING DEPTH FROM HISTORY SUPERFICIAL PARTIAL – THICKNESS BURNS DEEP PARTIAL – THICKNESS BURNS FULL – THICKNESS BURNS

19. SUPERFICIAL PARTIAL – THICKNESS BURN: DAMAGE TILL PAPPILARY DERMIS C/F  BLISTERS AND/OR LOSS OF THE EPIDERMIS DERMIS  PINK AND MOIST, CAPILLARY RETURN NORMAL, NO FIXED CAPILLARY STAINING, PINPRICK SENSATION NORMAL HEAL WITHOUT RESIDUAL SCARRING IN 2 WEEKS: TRETMENT NON SURGICAL DEEP PARTIAL – THICKNESS BURN DAMAGE TO DEEPER PARTS OF RETICULAR DERMIS EPIDERMIS IS LOST, DERMIS  LESS MOIST, ABUNDANT FIXED CAPILLARY STAINING AFTER 48 HOURS, COLOUR DOES NOT BLANCH WITH PRESSURE,SENSATION REDUCED, UNABLE TO DISTINGUISH SHARP FROM BLUNT PRESSURE TAKE 3 /MORE WEEKS TO HEAL WITHOUT SURGERY LEAD TO HYPERTROPHIC SCARRING

20. FULL – THICKNESS BURNS WHOLE DERMIS DESTROYED HARD LEATHERY FEEL APPEARANCE  NORMAL SKIN  CHARRED BLACK, DEPENDING ON INTENSITY OF HEAT NO CAPILLARY RETURN THROMBOSED VESSELS UNDER SKIN COMPLETELY ANAESTHETISED WITHOUT PAIN AND BLEEDING

21. FLUID RESUSCITATION PRINCIPLE MAINTAIN INTRAVSACULAR VOLUMETO PROVIDE SUFFICIENT CIRCULATION TO ESSENTIAL AND NON ESSENTIAL ORGANS I/V RESUSCITATION : CHILD IF BURN>10% TBSA, ADULT IF >15% TBSA ORAL RESUSCITATION  WATER + SALT STRESS DIURESIS IN FIRST 24 HOURS DUE TO STRESS HORMONES HYPONATREMIA AND WATER INTOXICATION CAN BE FATAL GIVE ORAL REHYDRATION WITH A SOLUTION AS DIORYLATE RESUSCITATION VOLUME  CONSTANT IN PROPORTION TO AREA OF BODY BURNED FLUID LOSS MAXIMUM IN FIRST 8 HOURS AND SLOWSBY 24-36 HOURS 3 TYPES OF FLUID – RINGER LACTATE OR HATMAN SOLUTION, HUMAN ALBUMIN OR FFP, HYPERTONIC SALINE

22. PARKLAND FORMULA:- CALCULATE FLUID REPLACEMENT IN FIRST 24 HOURS TBSA * WEIGHT(kg) * 4 = VOLUME(Ml) HALF IN FIRST 8 HOURS AND NEXT HALF IN NEXT 16 HOURS CRYSTALLOID RESUSCITATION: RINGER’S LACTATE – MOST COMMONLY USED IN CHILDREN MAINTENANCE FLUID MUST BE GIVEN  DEXTROSE- SALINE 100ml/kg for 24 hours for first 10 kg 50ml/kg for next 10 kg 20ml/kg for 24 hours for each kilogram over 20 kg body weight HYPERTONIC SALINE: IT PRODUCES HYPEROSMOLARITY AND HYPERNATREMIA IT REDUCES SHIFT OF INTRACELLULAR WATER INTO EXTRACELLULAR SPACE. ADVANTAGES: LESS TISSUE OEDEMA AND RESULTANT DECREASE IN ESCHAROTOMIES AND INTUBATIONS

23. COLLOID RESUSCITATION: HUMAN ALBUMIN SOLUTION(HAS) PLASMA PROTEINS RESPONSIBLE FOR INWARD ONCOTIC PRESSURE WHICH COUNTERACTS THE OUTWARD CAPILLARY HYDROSTATIC PRESSURE WITHOUT PROTEINS, PLASMA VOLUME IS NOT MAINTAINED AS THERE IS OEDEMA PROTEINS SHOULD BE GIVEN AFTER THE FIRST 12hours OF BURN BECAUSE BEFORE THIS TIME MASSIVE FLUID SHIFTS CAUSE PROTEIN TO LEAK OUT OF CELLS COLLOID BASED FORMULA:- MUIR AND BARCLAY FORMULA 0.5 * % OF TBSA * WEIGHT= ONE PORTION PERIODS OF4/4/4, 6/6 AND 12 HOURS RESPECTIVELY ONE PORTION TO BE GIVEN IN EACH PERIOD

24. MONITORING OF RESUSCITATION TARGET URINE OUTPUT  0.5 – 1.0ml/kg body weight/hour IF UO BELOW 0.5ml/ kgbw / hr THEN INCREASE INFUSION RATE BY 50% IF UO INADEQUATE + HYPOPERFUSION(RESTLESSNESS+TACHYCARDIA,COOL PERIPHERIES AND HIGH HAEMATOCRIT) THEN BOLUS 10ml/kg body weight DO NOT OVER RESUSCITATE / UO > 2ml/ kgbw / hr  DECREASE RATE OF INFUSION ABG ANALYSIS HAEMATOCRIT

25. TREATING THE BURN WOUND ESCHAROTOMY CIRCUMFERENTIAL FULL THICKNESS BURNS TO LIMBS INCISE THE WHOLE LENGTH OF FULL – THICKNESS BURN IN MID AXIAL LINE, AVOIDING MAJOR NERVES BLOOD LOSS MUST BE REPLACED MANAGEMENT OF BURN WOUND SAME IRRESPECTIVE OF THE SIZE OF THE INJURY CLEAN THE BURN, ASSESS SIZE AND DEPTH OF BURN FULL-THICKNESS/DEEP PARTIAL-THICKNESS BURNS  OPERATIVE TREATMENT + DRESSING WITH ANTIBACTERIAL DRESSING

26. FULL- THICKNESS BURNS + DEEP DERMAL WOUNDS DRESSINGS WITH NANOCRYSTALLINE SILVER SILVER SULFADIAZINE CREAM(1%) BROAD SPECTRUM PROPHYLAXIS including Pseudomonas Aeruginosa and MRSA SILVER NITRATE(0.5%) LESS ACTIVE THAN SILVER SULFADIAZINE AGAINST GRAM NEGATIVE BACTERIA NEEDS TO BE CHANGED EVERY 4 HOURS PRODUCESBLACK STAINING OF FURNITURE

27. MAFENIDE ACETATE CREAM USED AS 5% TOPICAL SOLUTION PAINFUL TO APPLY METABOLIC ACIDOSIS SILVER SULFADIAZINE AND CERIUM NITRATE INDUCES STERILE ESCHAR ON BURNED SKIN BOOST CELLMEDIATEC IMMUNITY

28. SUPERFICIAL PARTIAL THICKNESS WOUNDS AND MIXED DEPTH WOUNDS WILL HEAL ALMOST IRRESPECTIVE OF DRESSING DRESSING MUST BE  EASY TO APPLY, NON PAINFUL,REDUCE PAIN, SIMPLE TO MANAGE AND LOCALLY AVAILABLE CHOICE OF DRESSING IS CRUCIAL IN CASE OF BURNS THAT BORDER ON BEING DEEP DERMAL . CHOICE OF DRESSING MAKES DIFFERENCE BETWEEN SCAR / NON SCAR AND OPERATIVE VS NON OPERATIVE HEAVILY CONTAMINATED WOUND CLEAN THE WOUND UNDER GA SILVER SULFADIAZINE DRESSING FOR 2-3 DAYS DRESSING MPRE EFFICIENT IN HEALING AFTER 3-4 DAYS

29. SIMPLEST METHOD  EXPOSURE FOR EXUDATE FREQUENTLY CHANGE LINEN LATER DRY ESCHAR FORMS WHICH THEN SEPARATES AS THE WOUND EPITHELIALISES PAINFUL METHOD AND REQQUIRES INTENSIVE NURSING SUPPORT EX:-WOUNDS ON FACE NEXT METHOD COVER THE WOUND WITH A PERMEABLE WOUND DRESSING( MEFIX OR FIXAMOL) ALLOWS WOUNDS TO DRY WITHOUT ADHERING TO SHEETS AND CLOTHES PLACE A VASELINE IMPREGNATED GAUZE(WITH/WITHOUT ANTISEPTIC – CHLORHEXIDINE)

30. FENESTRATED SILICONE SHEET(MEPITEL) + SWABS TO ABSORB EXUDATE VASELINE GAUZE/SILICONE USED TO PREVENT ADHERENCE OF SWABS AND REDUCES STIFFNESS OF DRY ESCHAR, PREVENTING IT FROM CRACKING EASILY CHANGE SWABS AFTER FIRST 48 HOURS DUE TO SOAKAGE AND THEN LASTS LONGER HYDROCOLLOID DRESSINGS  CHANGE EVERY 3-5 DAYS, PARTICULARLY USEFUL IN MIXED DEPTH BURNS,PROVIDE MOIST ENVIRONMENT GOOD FOR EPITHELIALISATION(DUODERM)

31. BIOLOGICAL, SYNTHETIC (BIOBRANE) AND NATURAL(AMNIOTIC MEMBRANE) DRESSINGS  NEED NOT TO BE CHANGED IDEAL FOR ONE STEP MANAGEMENT OF SUPERFICIAL BURNS, BEING EASY TO APPLY AND COMFORTABLE HOWEVER, THEY WILL BECOME DETACHED IF APPLIED TO DEEP DERMAL WOUNDS AS THE ESCHAR NEEDS TO SEPARATE SO NOT USED IN MIXED – DEPTH WOUNDS EARLY DEBRIDEMENT AND GRAFTING IS THE KEY TO EFFECTIVELY TREATING DEEP PARTIAL AND FULL THICKNESS BURNS

32. ADDITIONAL ASPECTS OF TREATING THE BURNED PATIENT ANALGESIA ACUTE: SMALL SUPERFICIAL  ORAL ANALGESICS, PCM, NSAIDS TOPICAL COOLING LARGE BURNS  I/V OPIATES AVOID I/M INJECTIONS UNPREDICTABLE ABSORPTION NO I/M INJECTION IF BURN>10% TBSA SUBACUTE: LARGE BURNS CONTINUOUS ANALGESIA AS INFUSIONS ANDORA; MORPHINE POWERFUL SHORT ACTING ANALGESIA BEFORE EACH DRESSING ANAESTHETIST MAY BE REQUIRED

33. ENERGY, BALANCE AND NUTRITION BURN PATIENT HAS INCREASED NUTRITION REQUIREMENT IF BURN>20% TBSA  NASGASTRIC TUBE FEED WITHIN 6 HOURS TO REDUCE GUT MUCOSAL DAMAGE BURN INJURIES ARE CATABOLIC IN NATURE CATABOLIC DRIVE WOUND UNHEALED STABLE COVERAGE OF WOUND AND RAPID EXCISION OF THE WOUND KEEP PATIENT WARM

34. MONITORING AND CONTROL OF INFECTION PATIENTS ARE IMMUNOCOMPROMISED LARGE PORTALS OF ENTRY COMPROMISED LOCAL DEFENCES IN LUNGS AND GUT DUE TO OEDEMA PORTAL OF INFECTION  MONITORING LINES AND CATHETERS CONTROL OF INFECTION  HAND WASHING, BACTERIOLOGICAL SURVEILLANCE OF THE WOUND,CATHETER TIPS AND SPUTUM TAKE CULTURES ANTIBIOTICS

35. LARGE BURNS  CORE TEMPERATURE USUALLY RESET BY HYPOTHALAMUS ABOVE 37*C TEMPERATURE >38.5*C SIGNS OF INFECTION RISE OR FALL IN TLC, THROMBOCYTOSIS, INCREASING SIGNS OF CATABOLISM, DECREASING CLINICLA STATUS OF PATIENT

36. NURSING CARE INTEMSIVE NURSING CARE BANDAGED HANDS AND JOINTS NEED COAXING PERSONAL HYGIENE, BATHS AND SHOWERS  VITAL FOR PATIENT’S PHYSIOTHERAPY PHYSIOTHERAPY: ELEVATE, SPLINTAGE AND EXERCISE REDUCE SWELLING AND IMPROVE FINAL OUTCOME PSYCHOLOGICAL: OVERWHELMING EVENT STRETCHES COPING ABILITY, SUSPENDS SENSE OF SAFETY, POST TRAUMATIC REACTIONS USUALLY SELF LIMITING, RECEDING AS PATIENT HEALS

37. SURGERY FOR THE ACUTE BURN WOUND ANY DEEP PARTIAL THICKNESS OR FULL THICKNESS BURNS, EXCEPT LESS THAN 4cm2 NEED SURGERY BURN OF INDETERMINATE DEPTH SHOULD BE REASSESSED AFTER 48HOURS BURNS MAY INITIALLY APPEAR SUPERFICIAL BUT MAY DEEPEN OVER THE TIME DELAYED MICROVASCULAR DAMAGE IS COMMON IN SCALDS ANAESTHETIST NEEDS GOOD CONTROL OF PATIENT WIDE BORE CANULA, BP MONITORING ARTERIAL LINE FOR BP AND CENTRAL VENOUS LINE IF LARGE EXCISION IS THERE LAB – ABG, CLOTTING TIME AND HAEMOGLOBIN LEVELS CORE TEMPERATURE MUST NOT FALL BELOW 36* C S/C ADRENALINE AND TOURNIQUET CONTROL FOR BLOOD LOSS CONTROL