BURNS -occurs by transfer of energy from a heat source to the body Categories: -thermal (electrical burn) -radiation -chemical-

by an acid or alkaline Classification of burn injury by depth -partial thickness > superficial ( fst degree burn) involves epidermis and a portion of the dermis) erythema, blanching on pressure, pain and mild swealling, no vesicle or blister ex. Sun burn) > deep- fluid filled vesicles that are red, shiny, wet and sever pain, mild to moderate edema -full thickness burn ( 3-4 degree) > dry, waxy, white, leathery or hard skin, visible thrombosed vessels, insensitive to pain and pressure, possible involvement of muscles, tendons and bones (ex. Flame, scaled chemical, electric current) Extent of Burns Determine the TBSA affected by: >rule of nines- considered adequate for an adult burn patient Head- 9 Trunk=9 Whole leg-9 Groin 1 > Lund and browder method- concider to be acucurate ( considers the age of the victim) for infants, 9-adults > palmar method- used for odd or irregular shaped burns ( used for irregular and wied shape burn= one palm area is 1%)
th

NOTE: extent of burn is often revised after edema subsided Tissue destruction -coagulation -protein denaturation -ionization of cellular ontents SYSTEMIC response to bURN injury -release of cytokines and other chemical mediators -changes in blood flow, tissue edema and infection -less than 25% TBSA- local effects -more than 25% TBSA- local and systemic effects INITIAL systemic event: -cytokine and chemical mediators -loss of capillary integrity: shifts of fluid, Na and CHON ( vascular to interstitial spaces) - hemodynamic instability ( CV alterations) ALTERATIONS Cardiovascular -Hypovolemia ( from fluid shifts: vascular to interstitial spaces -causes decreased perfusion and oxygen deliver -decreased cardiac output, dec, BP- onset of Burn shock -SNS stimulation : release of catecholamine can cause problems in o2 since it can cause vasoconstriction and increases pulse rate and decreases cardiac output > Vasoconstriction: increase PR > further decreases cardiac putput

1000 ml in 24 hours Normal 333.3ml fluid loss for For every degree degree rise in temp there is 100 ml loss of water 7-3 shift 8 am 39C=2x 100=200 12 pm 40C=3x300 =500 devided by 2( times temp taken) First 24-36 hours -greates volume of fluid leak -peak: 6-8hrs When capilliaries regain integrity -fluid returns from ICF to intravascular -increase blood volume -imcrease urine output/diuresis -anemia ( due to RBC destruction, surgical intervention ( escharotomy, debriment, wound dressing) -increase hematocrit F/E alteration EDEMA -less than 25% blister -more than 25% systemic edema May resolve in 1-2 days -may obstruct small B.C causes ischemia ( escharotomy- may be performed) Devitalize= dead tissue will be removed through escharotomy //eschar remival Hyponatremia- due to fluid shifts Hyperkalemia- due to damage of the cells ( there is release K) Pulmonary alterations -inhalation I jury- major cause of morbidity and mortality > bronhcoconstriction and chest constrction >Hypoxia- due to increase oxygen consumption ( catechilamines and hypermetabolism) -carbon monoxide poisoning- burning of organic materials ( competes with 02 binding site carbonmonixide binds 250x in hemoglobin than in 02) >indicatiors of pulmonary damage 1) history indicating that the burn occurred in an enclosed area 2)burns of the face/ neck 3) signed nasal hairs 4)hoarseness, sooty sputum 5)labored breathing 6)erythema/blistering of the oral or pharyngeal mucosa =supper heated gas was inhaled ( leading to pulmonary damage) Renal alteration due to decreasd blood flow -free hemoglobin in the urine -myoglobin ( when muscles are damaged)- large molecules both can occlude tubueles -may occlude renal tubules

ATN- acute tubular necrosis And acute renal failure will come in next The body is under stressed whrn there is burn injury -there is shunting of blood in GIT

GIT alterations -paralytic ileus -curlings ulcer ( a GI complication due to burn injury) >occult blood >regurgitation of coffee ground material ( partially digested blood) ffrom the stomach > bloody vomitous Immunologic alterations -imopairment of the production and realease of granulocyte and macrophages -sepsis- also a major cause of morbidity and mortality - asepsis usually is the cause of death Cortisol realease- inhibits the body becomes immunocompromised ( reverse isolation precaution) STAGES OF BURNS: -Hypovolemic stage- begins at the time of burn injured and last for 48-72 hrd >>>due to rapid shift of fluid from the vascular compartments int o the interstitial space due to vasodilation >>>>increase evaporation of insensible fluid loss >>>impaired circularoty status= hemolysis of RBC >>>electrolytes shift- Na and K -To compensate, peripheral vasoconstriction occurs for approx 1-2 Hrs after injury -as compensatory mechanisms fail, the classic pictures of hypovolemic shock I s seen - dehydration -edema of the burned areas -hypoproteniemia -oligurea -metabolic acidosis DIURETIC STAGE- begins about 48-72 hours after the injury >>.capillary membrane integrity returns and fluid shifts back from the interstitial space int o the intravascular space EFFECTS: -increased blood volume -decreased HCT -Na deficit contiunues -hypokalemia Protein continues to be lost in wouns Metabolic acidosis

QUIZ NEXT MEETING!!!!! BURNS RA TANAN