This ppt describes about the definition,types,pathophysiology,fluid shift in burns,jackson's theory of thermal burns,calculation of TBSA etc in burns

2. SEMINAR ON BURNS
PRESENTED BY,
SIGYMOL JOHN
II ND MSC (N)
D.Y.P.S.O.N

4. Anatomy of skin

5. Anatomy of skin

6. Physiology of skin

7. Definition of burns

8. DEFINITION
 Injury to the body tissues caused by heat, chemicals, radiation, or electricity
 Burns is defined as a wound caused by exogenous agent leading to coagulative
necrosis of the tissue.

9. Types/causes of burns

10. Types of burns
 Thermal
 Chemical
 Smoke/ inhalation injury
 Electric current
 Cold burns
 radiation

11. Thermal burns
 Heat changes the molecular structure of tissues causing denaturation of proteins.
 Extent of burns depends on temperature of the agent, amount of heat, duration of
contact.
 Eg: scalds, flame, flash or contact with hot objects.
 Effect of burns depends on the intensity of energy, duration of exposure and type of
tissue injured.

12. Chemical burns
 Due to Acids (hcl), alkalies or organic compounds
 Alkali burns are more dangerous than acid burns because it’s not neutralized readily
by the body tissues.
 Alkalies adhere to the body tissues causing protein hydrolysis and liquefaction that
occurs when it is neutralized. Alkalies are present in oven, drain cleaners etc.

13. Organic compounds eg:

14. Inhalation injury
 Carbon monoxide poisoning: occurs when victim is trapped inside a burning room.
Co combines with hb after displacing the oxygen and forms carboxy haemoglobin,
causing hypoxia and finally death. Main manifestation is cherry red appearance.
 Injury above the glottis: is due to thermal cause.
c/m : evidence of facial burns, singed nasal hair,
carbonaceous sputum

16. i
 Injury below the glottis : due to chemicals
c/m : pulmonary oedema develops in 12 to 24
hours after burns and is manifested as ards.
Usually gas cools when it reaches the body
temperature and glottis & vocal cord closes to
protect the lungs . Airway swelling and
inflammation can occur in minor cases.

17. Electric current
 Acts directly on the body tissues.
 Current passing through the vital organs are life threatening.
 Effect is called ‘iceberg’ effect because the manifestations are seen under the skin.
 Sometimes it can ignite the clothing of the victim and cause second degree burns too.

20. Classification of burns

22. Based on depth of injury

23. Based on extent of burns
 Lund & browder chart : it is the most reliable method as it considers victim’s age in
proportion to body size area.

24. TBSA CALCULATION

26. Rule of nine
 This method is adequate and easy for initial burns assessment.
 Used for burns with larger surface area.

28. The sage burn diagram
 Is a computerized method used in burns tbsa calculation and provides fluid
resuscitation requirements. SAGE II is a free, on-line, computerized burn
diagramming tool for burn-care professionals.

30. Palm method
 In case of irregular or odd burns area of patients palm is considered as 1% to calculate tbsa.
Calculation is done after the oedema subsides.
 Used for burns < 10% body surface area.

32. Jackson’s theory of thermal wounds
According to Jackson's thermal wound theory, there are three zones of major burn injury,
shaped usually like a bull's-eye.
 Zone of coagulation : area in a burn nearest the heat source that suffers the most damage
evidenced by clotted blood and thrombosed blood vessels.
 Zone of stasis :area surrounding the zone of coagulation characterized by decreased blood
flow.
 Zone of hyperemia : peripheral area around the burn that has an increased blood flow.

34. Jackson’s theory of thermal wounds

35. Pathophysiology of burns

36. MAJOR BURNS
RBC
ANEMIA
METABOLIC RATE
GLUCONEOGENESIS &
GLYCOGENOLYSIS
O2 DEMAND
CATECHOLAMINE RELEASE
VASOCONSTRICTION
ADRENAL GLAND
STIMULATION
ALDOSTERONE
PRODUCTION
NA+ RETENSION
K+ LOSS
RENAL BLOOD
FLOW
SPLEENIC BLOOD
FLOW
GFR
RENAL FAILURE
HEPATO HYPOXIA
LIVER FAILURE
MYOCARDIAL DEPRESSING
FACTOR
MYOCARDIAL
DYSFUNCTION
CO & TISSUE
PERFUSION
ACIDOSIS
H20
LOSS

37. FLUID SHIFT RESULTING IN
HYPOVOLEMIC SHOCK IN BURNS

38. BURNS (THERMAL INJURY)
INFLAMMATION
HISTAMINE RELEASE
VASOCONSTRICT
ION
BP
BLOOD FLOW TO
INJURED PART
CAPILLARY
PERMIABILITY
FLUID LEAKAGE &
OEDEMA
INTRAVASCULAR
FLUID
HYPOVOLEMIC
SHOCK
PROTEIN
LOSS
HYPOVOLEMIA
PLASMA OSMOTIC
PRESSURE

39. Systemic changes
 Cardiac system
decreased cardiac OUTPUT.
Dysrhythmias, b.p changes, hypovolemia,
peripheral circulation due to circumferential
burns
Ischemia paraesthesia
Necrosis
gangrene

40. PULMONARY SYSTEM
 Upper airway : airway swelling, obstruction, copious secretions, stridor, sternal and
intercostal retractions, difficulty in swallowing.
 Lower airway: oedema develops only after 12 to 24 hrs. carbonaceous sputum, singed nasal
hair, horasness, dyspnoea, altered mental status.
 Pneumonia, copd, pulmonary oedema can occur with increased fluid resuscitation.
 RESPIRATORY INSUFFICIENCY can occur AS A SECONDARY
PROCESS.it CAN PROGRESS TO RESPIRATORY FAILURE
AGGRESSIVE PULMONARY TOILET AND OXYGENATION

41.  GASTRO INTESTINAL SYSTEM
 decreased bowel functions.
 paralytic ileus due to sepsis.
 DECREASED GASTRIC MOTILITY ( MAY NEED NG FEEDS )
 CURLING’S ULCER FORMATION ( due to the stress
response causing decreased gastric mucus
secretion & increased gastric acids resulting
from decreased g.i blood flow . Treatment is
administration of h2 receptors & proton pump
inhibitors.

42.  Diarrhea due to supplementary feeding
 Constipation ( side effect of opiods)
 Occult blood in stools.

43.  METABOLIC
HYPERMETABOLIC STATE
INCREASED OXYGEN AND CALORIE REQUIREMENT
INCREASE IN CORE BODY TEMPERATURE
 IMMUNOLOGIC SYSTEM
LOSS OF PROTECTIVE BARRIER
INCREASED RISK OF INFECTION
SUPPRESSION OF HUMORAL AND CELL MEDIATED IMMUNE
RESPONSES ( circulating immunoglobulins)
Dysfunction of wbcs

44. Genitourinary system
Muscle injury
Release of myoglobins
Accumulation in renal tubules
Blocks the tubules and decreases the blood supply
Atn
Renal failure
Initially oliguria occurs that proceeds to fluid diuresis and fluid mobilization.

45. Musculoskeletalsystem
 Pain
 Decreased rom
 Contractures
 Scarring
 Nervous system : is not much involved. Due to severe hypoxia cerebral edema and
neurological manifestations can occur.

46. Contractures from burns

47. Scars from burns

48. Endocrine system
 Stress mediated increased cortisol levels and gluconeogenesis leading to increased
blood glucose levels.
 Increased insulin production and release also takes place but insulin is relatively
insensitive.
 Subsequent hyperglycemia occurs when feeding starts to meet increased calorie
requirement, then insulin infusion is provided and do not decrease the feeds.

49.  Fluid and electrolyte : fluid shift out of intravascular to interstitial space (second
spacing) and also to area with little or no fluids (third spacing) which leads to
oedema.
 b. p, pulse rate, na+ and k+ shift to interstitial space, haematocrit value due to
increased hemo concentration because of fluid loss, electrolytes.

50. PHASES
 ACUTE PHASE
CLINICAL SHOCK
EXTERNAL LOSS OF PLASMA
LOSS OF CIRCULATING RBC
BURN OEDEMA
 SUB ACUTE PHASE
DIURESIS
CLINICAL ANEMIA
ACCELERATED METABOLIC RATE

51. NITROGEN DISEQUILIBRIUM *
BONE AND JOINT CHANGES
ENDOCRINE DISTURBANCES
CHEMICAL AND ELECTROLYTE IMBALANCE
CIRCULATORY DERANGEMENTS
LOSS OF FUNCTION OF SKIN AS AN ORGAN

52. Nitrogen disequilibrium
a study on nitrogen metabolism after burning conducted on experimental animals by E. J.
CLARK, R. A. PETERS, and R. J. ROSSITER showed that after burning, there is a sharp rise in
the blood urea (noticeable within one hour), a slight fall in the total plasma protein, and a
marked fall in the plasma albumin, giving a decrease in the albumin/globulin ratio. There is,
in addition, a rise in the urea output, sharp rise in the creatine excretion, and fall in the
excretion of creatinine.

53. With more severe burns, the increase in creatine and decrease in creatinine becomes more
marked; there is also a suppression of urea elimination during the first day or so after
burning, suggesting some renal impairment. In animals that died as a result of the burning,
this decrease in the elimination of urea and creatinine was marked. Weight changes indicate
that, at first, there was considerable water retention which gradually decreased over a period
of days.

54. BODY’S RESPONSE TO BURNS
• STAGE I ( EMERGENT PHASE )
PAIN RESPONSE
CATECHOLAMINE RELEASE
TACHYCARDIA, TACHYPNEA, MILD HYPERTENSION,MILD
ANXIETY
• STAGE II ( FLUID SHIFT PHASE)
LENGTH 18 – 24 HOURS
BEGINS AFTER EMERGENT PHASE
REACHES PEAK IN 6 – 8 HOURS

55. DAMAGED CELLS INITIATE INFLAMMATORY RESPONSE CAUSING INCREASED
BLOOD FLOW TO CELLS AND SHIFT OF FLUID FROM INTRA VASCULAR TO EXTRA
VASCULAR SPACE LEADING TO MASSIVE OEDEMA.
• STAGE III (HYPERMETABOLIC STATE)
LASTS FOR DAYS TO WEEKS
LARGE INCREASE IN BODY’S NEED FOR NUTRIENTS AS IT
REPAIRS ITSELF.
• STAGE IV (RESOLUTION PHASE)
SCAR FORMATION, GENERAL REHABILITATION & PROGRESSION TO NORMAL
FUNCTION