burns ppt surgery detailed explanation

1. BURNS
1. CAUSES
2. CLASSIFICATION
3. CLINICAL FEATURES
4. 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
•

4. 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

5. METABOLIC POISONING
1. 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

6. 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

7. 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

8. 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

9. • 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

10. 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

11. IMMEDIATE CARE OF THE BURN PATIENT
• PREHOSPITAL CARE
• HOSPITAL CARE
• POST HOSPITAL CARE

12. PREHOSPITAL CARE
1. ENSURE RESCUER SAFETY
IN HOUSE FIRES AND ELECTRICAL AND CHEMICAL BURNS
2. STOP THE BURNING PROCESS
STOP, DROP AND ROLL
3. CHECK FOR OTHER INJURIES
ABC RAPID SECONDARY SURVEY.. HED /SPINE INJURIES IN EXPLOSIONS
4. 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

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

14. 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

15. • 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

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

17. 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

18. • 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

19. 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

20. • 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

21. • 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

22. 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

23. • 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

24. • 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

25. 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

26. 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

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

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

29. SUPERFICIAL PARTIAL THICKNESS WOUNDS
AND MIXED DEPTH WOUNDS
1. WILL HEAL ALMOST IRRESPECTIVE OF DRESSING
2. 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

30. • 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)

31. • 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)

32. • 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

33. 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

34. 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

35. 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

36. • 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

37. 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

38. 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