1. The 3 concentric zones of thermal injury in burn woundsJackson's description of three concentric zones of thermal injury in the burn wound provides a practical basis for discussing the local burn injury. The central area of the burn wound, which is closest to the heat source, is characterized by coagulation of the cells and is termed the zone of coagulation. Severity of the injury from the surface to the depth of the wound decreases in all directions from the central point of injury. Extending concentrically from the central zone of coagulation lies a labile area of injured cells that, under the most ideal circumstances, have the potential to survive.In this zone, designated by Jackson as the zone of stasis, the progressive injury that results from dermal ischemia occurs. Before the mechanism of progressive dermal ischemia was understood, cells in the zone of stasis routinely progressed to necrosis within 24 to 48 hours after the burn. Finally, lying father peripherally to the zone of statis is the zone of hyperemia, which has sustained only minimal injury. Cells h mis zone normally recover over a period of 7 to 10 days unless they are subjected to some additional insult

2. 1st degree burnThe superficial or first-degree burn is characterized by the classic signs of inflammation: pain, heat, swelling, and redness. Within a few days, the outer layer of injured cells peels away from the totally healed subjacent skin with no residual scarring.

3. 2nd degree burnThe superficial partial-thickness injury is characterized by blister formation. Spontaneous breaking or debridement of the blisters results in weeping of fluid from the burn surface. Because the basal layers of the dermal portion of the skin are uninjured, regeneration of the superficial injured layers is prompt. Barring secondary infection or subsequent insult, these bums usually heal in 14 to 17 days.The deep partial-thickness bum reflects a more severe injury and is often indistinguishable from a full-thickness or third-degree bum. Such a wound includes a great deal of only marginally viable tissue. The injury to the dermis, however, is not complete, and under optimal conditions survival of the remaining dermis and associated epidermal appendages is possible. Deep partial-thickness wounds may heal spontaneously, although healing may require 3 to 4 weeks. On the other hand, these wounds may deepen with progressive der¬mal ischemia and can convert to full-thickness necrosis. If healing does occur, the resultant epitheliuim is often of poor quality and does not hold up to repeated minor trauma. Hypertrophic scar formation is also a frequent sequela of me deep partiaJ-diiekness injury. These wounds have the most treatment options.

4. 3rd degree burns3rd degree burns, or full thickness,the skin is totally destroyed through the entire thickness of the dermis/ Such wounds cannot heal spontaneously. Restoration of the integrity of the skin over such a wound can be acomplished only by ingrowth of epithelium from the margins or by grafting skin from non burned areas

5. Systemic response to injury, GI

The gastrointestinal tract function is altered as a result of thermal injury. The initial response is severe splanchnic vasoconstriction, causing an ileus similar to that occurring with other major trauma. If unrecognized acute gastric dilatation can occur, leading to regurgitation and aspiration. 

Gastroduodenal ulceration is a frequent occurrence in a patient with bums, although this sequela is not always clinically evident This ulceration is not a result of absolute hyperacidity. Nonetheless, patients in whom gastrodnodenal injury develops within 72 hrs of the bum have higher basal acid outputs than do patients without gastro-intestinal injury. Gastrin levels are not increased in thermal trauma and no correlation exists between serum gastrin levels and gastric acid in patients with burns. The pathophysiology of ulceration, therefore, appears to be a relative hyperacidity combined with a mucosal barrier problem or cytotoxicity as a result of mediator release. 

The hepatobiliary system also can be altered in thermal trauma. These changes may be tbe result of hypovolemia or hypoxia (or both) and circulating toxic waste products requiring clearance. During the shock period, to compensate hipovolemia, cutaneous and intestinal vasoconstriction occur.If the patient is not well hidrated, this vasoconstriction lead to ileus and mucosal necrosis, with smallulcerations. This is an open gate for bacteria migration into the blood and bacteriemia. From the blood, bacteria can reach burned necrotic tissue, an excellent grow medium, and capilar network of lung, liver, brain, bone with abcess formation. So, we understand why a burned patient became contaminated and infected, from the inside, even if he/she is very well treated locally, in a sterile cubicle.Liver biopsy findings have shown cloudy swelling as carry as 3 hrs after burn. This swellingprogresses to hepatocellular necrosis, vacuolization, and fatty degeneration.

6. Major burns injuries:- burns of more than 25% TBSA (20% TBS A in children younger than 10 years and adults older than 40 years);- full-thickness burns of 10% TBSA or greater;- all burns involving the face, eyes, ears, hands, feel, or perineum- electric burns- chemical bums- All burn injuries complicated by inhalation injury or major trauma.- burns combined with other type of lesions

7. Moderate burn injuries:Mixed partial and full thickness injuries of :15 to 25 % TBSA in adults10 to 29 % TBSA in children and adults over 40 yrs oldless than 10 % full thickness burns that do not present serious threat of functional on cosmetic impairement of face eyes ears hands feet or perineum

8. Minor burns injuries:Burns of less than 15% TBSA (10% children/elders)with 2% full thickness full injuryWithout cosmetic/functional risk to face eyes ears hands feet / perineum.

9. Initial emergency care in burns:ED treatment depends on triage of burns. if minor burns,can be treated in ambulatory. moderate major burns requires hospitalisation or require sending to another fully staffed/equipped burnt centre. staff in ed must inform receiving facvilities of treatment given in initial emergency care so that it does not complicate later definitive treatment

After triage:Relief of respiratory distressprevention of shocksensurance of perfusion

1.if acute respiratory distress :because of eschar in ant and post thoracical wall, do escharectomy if eschar presentintubation of oedema is preset on epiglottis and larynxnasotracheal tube preferredif present severe fascial lesions/fail chest, then trachesostomy with low presurre cuff recommended.inhalation of co- another cause of respiratory distress, adimnister 100% oxygen

2.Large bore needle insertion/plastic catherisation in the peripheral or central vein preferably than unburnt skin for treatment of impending vascular collapse. leave skin open to prevent infection. watch for thrombophlebitis in case of cathether.

3.infusion of buffered electrolyte solution at rapid rate

4.Give heparin as bolurs, 5000 u at 4 hrs IV to prevent hypercoagulation and haemoconcentration

5. Insert urinary cathether to monitor urine output n record it

6.maintain perfusion to all tissues - remove rings bracelets % constrictive clothing, can develop oedema in peripheral

7.elevation of extremities above right heart to reduce oedema

8. after evaluation of respiratory status and status of shock, relief pain and anxiety, small down of analgesics IV

9. Reflux ileus is present due to splanchic vasoconstriction, with greater 20%, insert a nasograstric tube for gastric decompression and maintain tilll ileus resolves(24 hours)

10. Local burn wound management:Cool burn wound within first 30 mins.

release eschar of limbs and chest.

Cooling not only prevents deepening but actually increases wqound perfusion, cooling decreases oedema, in distant unburnt areas of the body, prevents histamine from mast cells within the wound

Escharectomy : allow wound drainage & skin retraction. This improvwe skin vascularity and prevent deepening of lesions.

11. Etiological classification of burns:Physical factors : hot - solids liquids steamflameelectricity - electrocution electric flame lighteningChemical burns - acids alkalis salts tar cementfriction burnsexplosionsmoke inhalationcombined lesionshigh pression injectionfrostbite

Knowledge of the etiological agent and time of exposure helpful in determining the depth of the injury

Scald burns tend to be more superficial

Chemical and electric burns tend to be deep

Superficial burns - erythema and thin watery blisters.

Deep burns - thick walled steam blisters & dry, leathery eschar

12. Burns Mortality Index: A.Baux indexPrognostic index = age + % bunted surface area- Result > 100 equivalent to 100% mortality- Result 75-100 equivalent 60% mortality- Result < 75 equivalent to 30% mortality- Result < 50 equivalent to 0% mortality The end result depends of the combined lesions or high risk factors, which add 25 points: Previous organ lesions Smoke inhalation (close space injury).Prognostic index = age + % burned surface area + 25 points

B.TTM indexWe consider that, apart of age, burned surface area and associated lesions, we may add risk points depending of the level of care:0 - specialized Burns Unit10%- Plastic surgery unit in University Clinic15%- County Hospital20%- Local Hospital

Determine the extent of the burned surface by careful observation, and graphically record it. This step is important not only for diagnosis and treatment but also for prognosis and statistical analysis. Record the extent of injury in terms of percent TBSA involved. For a rough estimate for the purposes of triage, use the rule of nines. Make a more accurate assessment by carefully mapping the involved areas on a specialized Lund and Browder chart.

13. Burned surface estimation:This is done by determining the extent of burned surface base on the rules of 9. For a more accurate information, we can use the chart which takes into account the difference in age group.

Rule of 9 for adult :Head 9%Arms 9%Torso (front) 9%Torso (back) 9%Genital 1% Legs 18%

For children : Head 19%Arms 9%Front 18%Back 18%Genital 1%Leags 13%

Evaluation of depth of tissue and extent of injury is necessary to know the volume of tissue destroyed. The depth is difficult to estimate even tough many test has been proposed. E.g use of dyes, infrared photography.

14. Flame burns:This result form ignition of clothing by electric sparks or arcing. Flame burns may occur with true electirc or arc burns.

Patient care involve :Initial stabilisationEarly fasciotomyManage edema by continuous debridement as further demarcation occurs.

15. contact burns:Refers to a type of skin damage from electric injury. These are at points of current entry and exit from the body.

16. Electric injury:It is a devastating form of thermal injury. It can be divided into low or hig tension injuries. The dividing line veing 1000 volts. Thermal injuuryt associated with electricity are : electrocution, electric flame, lightnening.

Low voltage injuries mimic thermal burns. Their inujry are on the surface n extend into the tissues. High voltage injuries consists of varying degrees of cutaneous burn n hidden destruction in the deeper tissues. In this kind of injury resuslt progressive tissue necrosis.

Extent of injury depends on : type of circuit, voltage of circuit, body resistance, amperage thru tissue, pathway of current n duration of contact.

Tissue resistance progressiveley increase from nerves to blood vessel, muscle, skin, fat and bone. Bones have the greatest resistance n will so generate the greates amount of heat according to the joule effect. J= I2RTMost current preferentially travels along the lines of lesser resistance. Vessels are injured but not immediately thrombosed. The progressive muscular necrosis is due the vascular leasions leasing to delayed artereial occlusin n progressive ischemic necrois. Elevated levels of arachidonic acid in areas of greatest heat production. Prolongued elevation of thromboxane causes microvascular ischemia and leads to progressive necrosis.

Clinically 3 types of skin dmaage results. Contact burn : at points of entry n exit of currentArc burns : caused by current exiting n reentering adjacents partsThermal burns : caused by ignition of clothing by heat generated due to current passing in body.

Clincial evaluation:Establish airway patencyAssess chest expansion n uniformity in bretahingEvaluate circulationFind out if patient fell down or was projected over a distanceInitial recording of burn degree – may be difficult as much injured tissues hidden beneath uninjured tissue.Fluid loss will be in excess to that predictedSignificant blood lossExtensive destruction of boneLab: hemoglobinemia, increase level of circulating chromoproteins due to release of myoglobin from muscle.Both Hb and myoglobin may be present in urine and if not detected can precipitate n cause renal failure.Creatininine n creatinine phosphokinase increasesECG finding – for dysarythmis. Monitor for 24 hrs.X ray to rule out – pneumothorax, lumbar, thoracric injury

Masangemet :CPR at injury siteECG abnormality – correct dysarythmiaFluid requirements more than predicted values. Begin with balanced salt soluiton about 4ml/kg/TBSA%Maintain urine ouptut 200ml/24hr200 mEq soidum bicarbonate – urine alkalinisation to prevent pigment precipitaitonHepariv 5000IU 3hrly I.VPenicillin 2 million 6hr n gnetamycine 80mg 12hrs – Most frequent cause of death after electric injury is systemic infection. Sepesis arises form : necrotic muscle mass, bacterial invasion and perforation of GI tract.Mafenide acetate – to comabt infection with clostridia.

Operative treatment :Always necessary in siginifacnt electric injury.Remove necrotic tissue and repalce with viable tissue.Life threatening injury n limb threatening problems should be operative manage and definitive wound closure be delayed till progressive injury is complete.Escharotomy and fasciotomy – edema appear under uninjured skinDecompression of nerves as major nerves are susceptioble to increase pressure in close compartemnetDebridemnet of necrotic materialObserver muslce at time of fasciotomy to detmermine its viability. Assess muscle ability to contract n bleed. After derbridement of non viable tissue – wound closure.Flaps may be necessary.Amputaution may be required.Bone can be slavaged thru vascular flap.Laparatomy to check state of intraabdominal orgarn.

Post op :Extensive rehabilitation – can be single or multiple amputeeSpinal cord symptom - progressive muscular atrophy, amytrophic lateral sclerosisPerpipheral nerve lesison – histophathology – perivascualr hemorage, demyelination with vacuolisation, neuronal deathProgressive onset of cataract.

17. Chemical burns:In such burns, surgeon must address for local n systemic toxicity when treating chemical burns. Chemical agents burn by the following : oxidation, reduction, corrosion, protoplasmic poisoning, ischemic concomitant of vesicant activity.

Oxidizing agent cause damage because they become oxidized on contact with body tissuse. Its reaction n byproducs cause further toxicity with continued absorption. E.g chromic acidReducing agent produce protein denaturation by binding free electron in tissue protein. HCL.Corrosive agent net effect is eschar formation n a shallow indolent ulcer. Phenols.Protoplasmic poison – form salt with proteins or by binding or inhibiting calcium n nothe inorganic ions necessary for tissue viability n function.Vesicant agents : produce ischemia with anoxic necrois at site of contact.Desicant causage damage related to dehydration by cretaing excessive heat in tissueAcid n alkali – alkali cuases more dmage than acid. Acid tend to cause coagulation necrosis with precipiation of protein. Alkali tend to prodiuce liquesfaction necrosis allowing more diffusion of alkali deeper into tissues.

Tissue damage is dependent on :Concentration of agent, quantity of agent, duration n manner oof skin contact, extent of penetration into body tissues, mechanism of action.

Identify agent involved. Wear protective gloves or clothing then remove staurated clothing n irrigate the injury. Dnt forget progressive nature of injury. Reassess extent of unjurty at frequent intervals during initial irrigation to evaluate for progression of size n depth of injury.

Management Treatment of systemic n localised manifestationDetermine apropriate antidoteIngestion injury suggest inhalation injury.First aid: remove saturated clohting n irrigate with copiuos amount of water.Do not neutralise agents as neutralisation process generates heat n futhers tissue necrosisEstimate size of injury If less than 20% TBSA inject 10% calcium gluconate at a dose 0.5ml/cm2.

Molten tar/ asphalt : is a scald burn. Cool molten material with cold water. Cleanse gently with soap n water n dress with petroleum based ointment. Gradual separation of tar n spontaneus healing of burn occur. Reassess burn injury after all tar removal.

18. Acute Skin Failure Syndrome:1. Loss of skin surface2. Hyper metabolism3. Loss of integrative functions with: A. increased sensitivity to environmental changes (temperature, humidity, microbial flora) B. neuropsychic disorders (the absence of the normal, and presence of pathologic stimulus) C. Major disturbances in the intentai medium because all the organs lose the system of material, energetic and informational exchange with the environment and their activity is subordinated to the metabolic effort of skin recovery.

In superficial burns, multiple organs disturbance begins immediately post injury and if the Acute Skin Failure Syndrome is not treated, the Multisystem and Organ Failure Syndrome occurs.

For these reasons, in burns, which usually are a mixture of deep and superficial skin loss in different proportions an active approach is required:1. Early wound closure or organ prosthesis until recovery using biological dressing or semi permeable membrane;2. General support of the hyper metabolic effort by adequate nutrition;3. Organism protection against the loss of the integrative functions of the skin by:a. Controlling the external environment and maintenance of favorable levels oftemperature, humidity, microbial flora;b. Gaining informational equilibrium through release of pain and recovery, with priority ofthe zones, rich in exteroceptors: hands, face, perineum.c. Supporting the effort for the rebalance, in the internal medium, of digestive, excretory,respiratory, cardiovascular and immune systems activities (prevention of septic complications).

19. IV flkuid therapy – principles:Is requires for burns more than 20% TBSA or in any patient showing signs of shockSecure a no. 16 or 18 cannucal in an adequate vein.Insert indwelling urianry catherterEstimate 24hr fluid needs thur parkland formular = 4ml Ringer lactacte x wight/kg x % TBSAGive one half in first 8hr from first time of injuryOne fourth in second 8hrOne fourth in third 8hrAdjust infusion rate to obtain 1ml/hr/kg body weight.

20. Mainteance of peripheral circulation in burns:Remove all rings or braceleteObserver extrmity for clinicla signs of imparied circulation : cyanosis, delayed capillary refilling, prorgessive neurological signsPerform echarotomy if circulation impaired : midlater or midmedail line of limb inciusion. Incision must cross the involved joints. Incise only to depth that allows cut edges of eschar to separate.Fasciotomy only when injury involces subfascial tissue or perfusion abnormalities persist.

21. Initial burn wound card:Cleanse n debride ( leave blisters intact)Cover burns with sry sterile dressingIf patient is to be retained, beign topical therapy of choice – silver sulfadiazine.

22. Admit to hospital the following burns:Critical : second degree bruns of more 3% TBSA or third degree burns of face hands feet or of more than 10%TBSAComplicated burns : respiratory tract injury, major soft tissue injury, fractuiresElectrical I jureisModerate : second degree burn of 15% TBSA or third degree burn of lexx than 10% TBSASuspected child abuse.

23. Patient management for minor burns:Minor burns are treated in ambulatory settubf by the physicicna. Minor burn do not requires wound dressing or antimicrobial agentsCool the burnPain may be manage with oral or topical analgesucs or antiinflamatory agents.

24. Goals of Fluid Replacement Therapy: Fluid resuscitation of the patient with burns initially seems confusing. Historically, physicians have successfully used a variety of resuscitation regimens in the early care of even extremely injured patients. Pruitt stated that "the goal of burned patient fluid resuscitation is the maintenance of vital organ functions at the least immediate or delayed physiologic cost."Meeting this goal provides the objectives for fluid resuscitation. The weight of the patient and the percent TBSA injured provide initial guidelines to the amount and rate of fluid replacement, because the amount of edema fluid lost depends on these two parameters.

Goals of fluid replacement therapy are to maintain:1.Urine volume around 50ml/hr2.Sensorium - clear and lucid3.Pulse rate - less than 120 per minute4.Blood pressure - normal to high-normal5.Central venous pressure - less than 5 cm of water6.Lack of nausea and ileus.

25. Fluid replacement in the first 24hrs after injury:The weight of the patient and the % TBSA injured provide initial guidelines to the amount and rate of fluid replacement, because the amount of edema fluid lost depends on these parameters. To determine the resuscitative fluid replacement, recall that the greatest fluid loss occurs during the first 8-12 hrs after burn and the loss continues more lsowly during next 12-16 hrs. Because of

the capillary permeabilitity, colloid replacement or blood transfusion seems to be of no benefit in the immediate period after burn.Therefore, Na and water appear to be the elements that are lost to the circulation in proportionate amounts, Na and water are the key factors in resuscitation for the first 24 hrs. To compensate the loss of fluid from the vascular compartment, the patient must receive Na and water at a rate exceeding 4ml/kg/% TBSA for the first 24 hours. By approx 24 hours, capillary integrity returns and Starlings hypothesis appears to be restored. At that time, colloid can be used to replete plasma volume.No colloid solutions (blood plasma or plasma expander), no glucose in water.

26. Fluid replacement in the next 24- 48 hrs:After the cardiac output returns to normal levels at 24 hours, a plasma gap remains, this gap amounts to approx. 0.35 to 0.5 ml/kg/% TBSA burn.By 30 hours, both cardiac output and plasma volume should be returned to normal values and effective resuscitation completed. Further administration of Na further aggravates the edema. So from 30 hrs, until GI peristalsis returns, the physician can give free water to maintain a normal serum sodium level and cover the obligatory insensible losses. On the basis of these considerations, effect acute resuscitation by beginning infusion of a buffered balanced salt solution at a rate exceeding 4 ml/kg/hr. The amount of crystalloid (ringer) solution should be initially 4ml/kg/% TBSA- Parkland formula, in the first 24 hours after the injury time. Half of this amount should be given in the first 8 hours starting from the injury moment and the other half in the remaining 16 hours. Usually continue with this solution for 2 hours and at that time replace half of the Ringer solution with dextrose water.In the child weighing 10 kg or less, the maintenance fluid requirements are often greater tan those required for burn loss replacement, Therefore, calculate the maintenance fluid requirements by using 100ml/kg of a fluid containing 3 mEq of Na per 100 ml and 2 mEq of K per 100 ml. this amount in addition to the 2 ml of crystalloid per kg of body weight per percent TBSA whish is required to replace the loss of fluid because of thermal injury itself. Therefore, replace one fourth of the infants burn fluid loss with plasma.Summary: approx ½ of fluid given first day, colloid given as needed to maintain plasma volume, evaporative losses equals 2-5l/day for a 40-70% TBSA. Liquids by mouth can be given as tolerated.

27. Fluid replacement from 48hrs to ten days:Full liquid by mouth, advancing to a high calorie, high calorie diet. Package cells to maintain hematocrit above 30 %. Colloid as needed. Vitamins are replaced at 2-3 times daily minimum requirements.

28. Considerations in Fluid replacement therapy:Clinical observation rather than the ability to fulfill an arbitrary formula is the most important measure. Patient should have a clear lucid sensorium, a heart rate of les than 120b/min and a hematocrit of less than 40 % Urine output of 1 ml/kg/hour in adult and 1.2ml/kg/hr in child. Can be adjusted to 2 ml/kg/hr in patients with severe muscle damage and an increased solute load or downward in the elderly patient whose normal glomerular filtration rate is decreased because of the loss of nephrons with aging. Increase or decrease fluid input accordingly. Use catheters to monitor the CVP in burns greater than 30 % TBSA. Because of total body capillary leak and the tendency for recurrent and brief episodes of left ventricular failure, the pressures obtained with these monitors reflect the volume situation and cardiac performance.1.water loss due to evaporation begins at 36-48 hrs. A TBSA 50 % require 3-5 l/day.2.at 48hr-10 days, mobilization of the burn wound edema occurs. Lab values and clinical signs may be deceptive. A massive fluid dieresis may occur. Usually high cardiac output and

tachycardia, progressive profound microangyopathic anemia with time that should be corrected with packed RBC.3.Perforn hourly urine output and serial determinations of arterial bloof gasses and acid base changes.4.More fluid required by inhalation injuries associated with severe mechanical trauma and large burns with delays in initiation therapy.Potassium losses should be evaluated and replaced.5. Use of digitalis is controversial as it may be toxic.

29. Nutrition in burns:Nutrition important because of accelerated rate of tissue breakdown. Patient with extensive burn should receive nothing enteraly in the first 24 hours to prevent ileus, nausea and vomiting. On the second day, start enteral nutrition. Milk. 200-250 ml, at 3 -4 hr, may help prevent Curlings ulcer. Diet increased as toleratedso that 50-80 calories and 2-4 g/kg/day of protein is consumed by 7 days after injury. Supplemental tube feedings at night and between meals may be necessary in achieving ideal high protein high calorie meal. Nonvolitional nutrition (total parenteral alimentation) may be instituted in burn patients as hyperosmolar solutions delivered by CV cathether if intra abdominal problems such as severe nausea, vomiting or stress ulceration do not allow intake. Frquent nutritional assessment with daly weighting of the patient is indicated to monitor progress. Glucose is the best source of nonprotein calories, minimises nitrogen loss.Also needs fat.GOodwin recommends 2-4% of D.E.R be provided as lineolic acid.Vitamins ADEK and BC given. Sutherland and Batchelor: Need= 3 g (0.48g N)/1% BSA + 1g (0.16gN)/kg corpCAloric need: 25kcal/kg corp + 40 kcal/%BSa.

30. Systemic Antibiotics in Burns:Antibiotic coverage should be limited to specific bacterial infections, as determined by culture and sensitivity. Septicaemia is unlikely the first three days after a burn, except as caused by beta-hemolytic streptococci. Many burn doctors prefer to cover their patients with aqueous penicillin, 600.000 units IV twice daily, to prevent beta-hemolytic streptococcal infections during the first four to five days. Surface cultures of the wounds should be made at the time of admission and at regular intervals thereafter. Antibiotics should be stopped by the fifth day or given only when there is evidence of infection, based upon the culture and sensitivity results. Use of broad-spectrum antibiotics should be avoided unless specific infections are to be treated.

31.H. Nasogastric tube is inserted and attached to suction for nausea, vomiting, ordistention or for greaterthan 25% TBSA bums.

I. Analgesic medications are given in small doses IV as needed (Morphine 3 to 5 mgevery 2 to 3 hr pm).

J. Tetanus prophylaxis according to immunization status: tetanus toxoid, 0.5 ml, and tetanus immune globulin, human, 250 units, should be given for unimmunized patients.

31. Initial Burn Wound Management:Depending on the severity of the injuries, the care of burned patients may be simple or complex. A first degree bum may require first aid only, whereas a critical bum can take 6 to 12 months of intensive hospital care followed by two to three years of multiple-staged reconstructive surgical procedures.

The goal of this chapter is to include basic patient care principles and practice of burn care. Physicians should understand the initial bum assessment, inpatient hospital care, and outpatient wound management.

I. Initial care of burn patientsA. - Stop further injury1. Extinguish and remove burning clothing.2. For chemical bumsa. Immediate removal of all contaminated clothing.b. Prolonged irrigation of eyes.c. Copious water lavage.

3. Reduce temperature of injured tissues with cold water lavages or soaks for 10 to 20 min,avoiding hypothermia.

B. - Maintain airway and ventilation1 . Provide humidified oxygen by mask.2. Provide endotracheal intubation and mechanical ventilation when required. Check fora. Associated trauma to neck or chest wall.b. Acute upper airway edema associated with inhalation injury.

C. - Provide cardiopulmonary resuscitation if indicated.- Check heart beat and pulses.D. - History1. Time and circumstances of injury.2. Preexisting illnesses.3. Medications.4. AllergiesFig. 1. The rule of nines is helpful for initial estimation of the extent of burned body area.

E. Physical examination1. Estimate extent and depth of burn wound.a. Rule of nines for adults (see Fig 1)b. Guide to evaluate degree of injury (see Table 1 )2. Examine airway for signs of inhalation injury:

a. Singed vibrissae.b. Carbonaceous material.c. Edema or inflammatory changes.3.- Examine for associated injuries, such as fractures. 4.- Weigh the patient.F. Intravenous fluid therapy is required for burns over more an 20% of body or in any patient showing signs of shock

Second-degreeThird-degreeFirst-degree Burn Burn

Criteria Burn (Partial Thickness) (Full Thickness)Cause Sunburn Spill scalds, . flashes of flameImmersion scalds; flame, electricity, chemicalsColor Pink or reel Pink or mottled red Pearly white, brown, or charredSurface Uniform, no vesicles Vesicles or weeping Dry •Pinprick PresentPresentAbsent

Time Heals Heals in 2-6 weeks Produces granu¬lating wounds; requires grafting

Table 1. A guide for evaluating degree of burn injur)'1. Secure no. 16 or no. 18 plastic cannula in an adequate vein.2. Insert indwelling urinary catheter.3. Estimate first 24-hr Ringer lactat fluid needs, in ml, according to Parkland formula:

4 x Kg x %TBSAa. Give: one half in first 8 hr from time of injury; one-fourth in second 8 hr; one-fourth in third 8 hr.b. Adjust infusion rate to obtain 30 to 50 ml/hr urine output in patients over 30 kg inweight and 1 ml/hr/kg body weight in patients less than 30 kg (Fig.2)

G. Maintain peripheral circulation1. Remove all rings and bracelets.2. Observe extremity burns for the following clinical signs of impaired circulation:a. Cyanosis.b. Delayed capillary refilling.c. Progressive neurological signs such as paresthesia and deep tissue pain.3. Perform escharotomy if circulation is impaired (see Fig.3).a. Anesthesia is unnecessary.b. Midlateral and/or midmedial line of limb incision.c. Incision must cross the involved joints.d. Incise only to depth that allows cut edges of eschar to separate. In electrical bumis important to incise also the deep muscular fascia!

4. Fasciotomy is needed only when injury involves subfascial tissues and/or perfusionabnormalities persist.

32. Open treatment in burns:Method of treatment. A decision is made as to the method of treatment, i.e., open or

closed, and the topical agent of choice (see Table 26-2). In general, occlusive dressings are beneficial to the severely burned patient because they decrease evaporative water loss, decrease caloric loss, and increase patient comfort.

a. Open treatment. Areas routinely treated openly are the face, ears, and perineum.Meticulous but minimal debridement, topical antibacterial agents such as silver sulfadiazine and/ or saline soaks are required.

33. Closed treatment in burns: b. Closed treatment. Bums involving joints require splinting in posiUon ot tunction,as shown in I-ig. 26-4 for hand position, and daily full range-of-motion exercises. In splintingthe hand, the four required positions are: Wrist dorsiflexion, Metacarpo phalangeal jointflexion, Interphalangeal joint extension, and Abduction of the thumb.

The most important element is dorsiflexion of the wnst in the splint as much as possible.

34. Topical antibacterial agents:Topical antibacterial therapy is utilized forthe control of burn wound sepsis. It is not utilized routinely in small bum wounds where sepsis is no threat.

It is important to remember that topical antibacterial therapy does not sterilize the bum wound.Topical agents reduce the number of bacteria present, and it is to be hoped, the incidence ofinvasive infection. Topical antibacterial therapy must be altered according to the needs of the patientas judged by the patient's clinical responses and the bum wound bacterial population. The agent must exhibit antibacterial activity against the major wound pathogens to be effective against proliferating organisms in a bum wound.

The recent introduction of topical antimicrobial sensitivity testing, basedon in vitro activity, allows selection of the most appropriate agent. The bacterial population of anypatient's bum wounds may change several times throughout the hospital course. Sensitivity testingallows the treating physician to keep current with the changing flora and to use the most appropriatetopical agent.Silver sulfadiazine (Silvadene) or Betadine Helafoam solution are generally preferred initially. When topical therapy fails to control the bum wound flora and sepsis threatens, the treating physician should consider alternate modes of therapy, including changing the antibiotic on the basis of culture results.

35. Primary burn wound excision:The greatest success of cxcisional therapy-has been in cases where areas of full thickness bum injury were totally removed down to deep fasciaand followed by immediat coverage with autografts, homografts, or both. This mode of therapy isgenerally limited to 15% to 20% TBSA injuries and can be utilized by physicians who are familiarwith its techniques. It is clear that in properly selected cases immediate excision and grafting canshorten the hospital stay, and can produce good functional and acceptable cosmetic, resultsThis technique is generally employed early after burning (within 72 hr), but successful cases have been reported after a week's delay. The carbon dioxide laser scalpel is finding increasing application in excisional burn wound therapy.

36. Tangential excision & grafting:A bleeding layer is reached. The wound is covered with expanded meshed skin graft.An alternative to full-thickness burn wound excision is tangential or sequential excision of the nonviable portion of the burn wound. This technique is based on Jackson's description of concentric zones of injury. The idea is to remove the nonviable zone of coagulation. If this sequential excision is only in a deep partial-thickness wound, the technique is also called an intradermal debridement.Although sequential layered excision offers no advantages in the treatment of large full-thickness burns, it does allow early removal of nonviable tissue while preserving deep dermal viable tissue in deep partial-thickness injuries. The important feature of this technique is that immediate wound closure is important after excision. Because the excision exposes the zone of stasis, desiccation must be prevented. The surgeon can perform a temporary wound closure to prevent dehydration and allow the wound to close permanently by epithelialization.

Tangential excision is the immediate grafting of a sequentially excised partial thickness wound. Objective analysis of tangential excision data indicates that the interval between injur}' and

permanent wound closure is regularly shortened with this technique. It is a treatment for specific bum wounds, such as deep dermal burns, mixed with areas in which some dermal base remains for skin-graft placement and should not be considered a universal replacement of conventional wound treatment. The investing fascia should be excised, as an unsatisfactory wound bed unable to accept skin grafts results. Indeed, only a small percentage of burns can be successfully treated with tangential excision.

On the second to fifth day, the patient is taken to the operating room, where excision is performed with a guarded skin graft or dermatome down to viable tissue that will accept an immediate split-thickness skin graft. The burned areas must be excised to viable bleeding tissue and covered with split-thickness skin grafts, or the exposed dermal tissue will become necrotic. This technique has occasionally been used in bums of 60% TBSA or greater.

37. MESHED GRAFTS:Meshing involves cutting slits into a sheet graft and stretching it to open up the holes before it is transplanted.Advantages of mesh grafts over sheet grafts:-meshed grafts will cover a larger area with less morbidity to the patient-a meshed graft can adapt its contour to it an irregular recipient bed-blood and exudates can drain freely through the slits-only a small area of the graft will be jeopardized in the event of localized bacterial contamination-a meshed graft provides multiple independent areas for potential re-epithelializationDisadvantages- significant surface of the wound is left uncovered and must heal by secondary intention and that the cosmetic result of reconstruction with an expanded meshed skin graft is not ideal.

38. CHEMICAL INJURIES –Mechanism of tissue damage:Chemical agents burn by the following mechanism: oxidation, reduction, corrosion, protoplasmatic poisoning and the ischemic concomitants of vesicant activity.Oxidizing agents usually cause damage as they become oxidized on contact with body tissue. Often the reaction and its byproducts amount for further toxicity with continued absorption. Commonly encountered oxidizing agents are chromic acid, sodium hypochlorite(chlorox) and potassium permanganate.Reducing agents act somewhat similarly and produce protein denaturation by binding free electrons in tissue proteins. Eg, alkyl mercuric agents, hydrochloric acid and nitric acid.Corrosive agents act in many ways and are so termed because of degree of denaturization exerted on tissue protein. Their net effect is eschar formation and a shallow indolent ulcer. Eg: phenols and cresols, white phosphorus, dichromate salts, sodium metals and the lyes.Protoplasmic poisons produce their effect by forming salts with proteins or by binding or inhibiting calcium or other inorganic ions necessary for tissue viability and functions. Eg: alkaloidal acids, acetic acid, formic acid and metabolic competitors or inhibitors including oxalic acid and hydrofluoric acids.Vesicant agents produce ischemia with anoxic at the site of contact. Eg: cantharides (Spanish fly), dimethyl sulfoxide, mustard gas, and lewisite. Also a subgroup of agents are desiccants. They produce their deleterious effects by causing damage related to dehydration, by creating excessive heat in the tissue or both. Eg: sulfuric acid and muriatic acid.Chemical burns can also be classified as acid or alkali.A strong acid has a pH of less than 2. A better predictor than pH alone is the amount of alkali needed to raise the pH of an acid to neutrality.

Alkalis capable of producing tissues damage usually have a pH of 11.5 or greater. On a volume –to volume basis, alkalis usually can cause more tissue damage than acids. This difference occurs because acids tend to cause coagulation necrosis with precipitation of protein, while alkalis tend to produce liquefaction necrosis, allowing more diffusion of the alkali deeper into the tissue.

39. First aid in chemical burns:OXIDISING AGENTSChromic acid (common use-metal cleansing), (cleansing and dilution-water)Potassium permanganate(common use-disinfectants, bleach deodorizers), (cleansing and dilution-wateR)Sodium hypochlorite(chlorox)- common use: industrial lab, cleansing and dilution- water Nitric acid-same as aboveCORROSIVESPhenols, common use- deodorants, sanitizers, disinfectants, cleansing and diluation- ethyl alcoholWhite phosphorus- common use- warefare incendiary, C&d-water and debride particles, special therapy-irritage with 1% copper sulphateLyres- common use- industrial cleansingPotassium hydroxide – washing powder, drain cleanrs, pant removers, c&d-waterSodium hydroxide-same as aboveAmmonium hydroxide, common use- urine sugar reagent tabletsLithium hydroxide, barium hydroxide and calcium hydroxide same as aboveLime, common use- agriculture (soil alkalinisation), c&d brush offProtoplasmic poisons:Strong acides-(tungtic,picric,tannic,sulfosalicylic,cresylic,tricloroacetic,formic), oxalic acid, hydrofluoric acid, hydrochloric acid- common use: etching , metal cleansing, cleasing and dilution- waterSpecial therapies: oxalic-1V calcium, hydrofluoric-SC calcium, hydrochloric-glucanate 10%

Irrigation with water constitutes immediate first aid for 20-30mins and thereafter for a period of 2-12h. up to 48h for burns in eye. No agent found superior to water. Irrigation of 6h for acids and superior for alkalis. Alkalis longer because of bonding of alkalis to tissue proteins. Irrigation until patient notices a decrease of pain,burning or stinging. Measurement of pH of skin surface helpful.Do not neutralize because of heat prdution and furers tissue necrosis. Exception hydrouoric acid as it is the strongest inorganic acid.Use of dilute bicarbonate helpful. After irrigation, put aqueous benzalkonium (zephiran) helps to precipitate any residual fluoride and reduce pain. Apply topical salve incorporating magnesium hydroxide and magnesium sulphate in water soluble base.For burns covering less than 20% TBSA, inject soln of 10% calcium glucanate into burn and its imeediate periphery at a dose of approx. 0.5ml/cm square. Also addition of mosit compresses with use of 50:50 dilution of Ca glucanate and dimethyl sulfoxide for 24h.Molten tar or asphalt has no toxicity from absorption and essentially constitutes a scald burn.. cooling with cold water, gently cleanse would with soap and water and dress it with a petrolatum base ointment. Change dressing at intervals. Gradual separation of tar and spontaneous healing will occur. When all tar gone, reassess and see if surgery needed.Lead toxicity- urine level > 150p.g in 24h. administer either dimercaprol (BAI in oil) or ethylenediaminete acetic acid for 5 days. Followed by 10 to 14 day cou of penicillamine. Debridement after cleasning all burns and dressing. Topical antimicrobials used.

40. ELECTRIC INJURIES:Is a unique and thoroughly devastating form of thermal trauma. Divided into high and low tension injuries as determinded by the voltage responsible for the damage. Dividing line is 1000 volts. US- 60Hz per second.Low voltage- mimic thermal burns and have zones of injury from surface extending to tissue.High voltage- varying degrees of cutaneous burn combined with hidden destruction of deeper tissues. Results in progressive tissue necrosis, like crush trauma.PATHOPHYZTissue destruction caused by contact with high voltage electricity is basically a thermal injury.Heat production in joules, J= I(squared) RT, I-current intensity, R-tissue resistance, T-tiem of contact.Tissue resistance increases from nerve to blood vessels, muscle, skin,fat and finally bone.Tissue damage as result of electric injury is thermal injury. Elevated levels of arachidonic acid metabolites in areas of greatest heat production. Prolonged elevation of thromboxane plays key role in progressive microvascular ischemia, leading to progressive necrosis. Therapy block of production of thromboxane successful in prociding tissue salvage.3 types of skin damage-Contact burns at points of current entry and exit from bodyArc burns caused by current exiting and reentering adjacent part of body parts in close proximity.Thermal burns from ignition of clothing because of degree of heat generated by current passing thru body. CLINICAL EVALUATIONHistory of event important. Determine site of injury to know voltage. Home: 110-220 volts. Industrial or powerline-high tension.Find out if patient suffered from cardiac arrest at injury scene, or lost consciousness. Amnesia or partial amnesia often occurs. If patient was thrown from a height after contacting electric source. Severe trauma common. Examination: assess airway patency, chest expansion and uniformity of breath sounds bilaterally…pneumothorax common in high tension injuries. Evaluate circulation, cardiac rate and rhythm and ECG. Ensure peripheral circulation and need for escharotomy or fasciotomy. Assess mental and neurologic status. Type of aphasia exists (loss of ability of produce or comprehend language). Rapid neurologic exam to check for focal motor and sensory deficts.Then record degree burn.Fluid loss will be in excess. In severe, death of large volumes of muscles occurs leading to gracures or chest or abdominal trauma. After high voltage injury, 15% patients develop bone sequestration.Lesions: hemiplegia, aphasia, cerebellar dysfunction, epilepsy, physiologic spinal cord transaction, nausea, vomiting and prolonged paralytic ileus.Hemoglobinemia may appear after injury due to lysis of rbc.release of myoglobin from destroyed muscles may increase levels of chromoproteins. Hb and myoglobin may be present in urine.Creatinine and creatine phosphokinase are elevated. Cardiac muscle damage will result in increase of cardiac enzyme like GOT and lactate hydrogenase. Monitor heart 24hr after injury…ECG.MANAGEMENT Immediate at scene of injury- CPR. If initial ECG abnormal, continue monitoring with pharmacologic treatment of any dysrhythmia. Nasogastric suction for 24-48 hr.Adequate fluid to support the intravascular volume. Fluid requirement exceed anything predicted by formulas. Balanced salt soln abt 4ml/kg% TBSA burn. Maintain urine output at 200ml/h or 2ml/kg/h to dilute pigements in urine flow.

200Meq of sodium bicarbonate then adjust doses according to blood bicarbonate level after tests.urine alkalization prevents pigement precipitation.Heparine administration with 5000 iu at every 3 hours.Peniciline 2 milion at 6h and gentamicine 80mg at 12h to prevent infectins of dead tissues. Cause of death after burn: systemic infection, sepsis can arise from necrotic muscle mass, bacterial invasion from associated thermal burn or perforations of gastrointestinal tract.Mafenide acetate is good for wounds-penetrates to deep levels and antibacterial choice for clostridium oraganisms.

41. OPERATIVE TECHNIQUE:Injury is worst in periosseous tissue, some degree of necrotic tissue exists.surgeon must remove and replace tissue or reconstruct with viable tissue.Definitive management:Immediate excision within 12h of injuryDelay primary excision and reconstruction 4 to 7 days after injuryDelayed reconstruction after complete healing by ondary intentionImmediate splint after burn in an attempt to allow healing without deformities.

Because the injured cells are most heavily concentrated in the periosseous core in a high voltage injury, edema will occur beneath wht appears clinically to be injured skin. Therefore escharotomy and fasciotomy will be necessary soon after injury. Major nerves are susceptible to increased pressure in closed compartments, escharotomy or fasciotomy alone not sufficient to decompress nerves in the arm.therefore decompression of the medial and ulnar nerves as an emergency procedure in high voltage injury of hands.Debridement of obviously necrotic tissue as early as possible. Soon after patient’s admission alongside with escharotomies , fasciotomies and nerve decompressions. In low voltage, perform debridement in a layered or sequential tangential technique. Asses the muscle..ability to bleed and contract.After completing debridement of nonviable tissue, proceed with wound closure. Cover exposed normal or minimal damaged tissue to avoid damage by desiccation.Skin grafts will suffice.Amputations may be required. It is delayed until limb threatening to cause a lot of sepsis.Intreperitoneal injuries common, solved by laparotomy. Exteriorization or resection may be indicated.Manage fracture from falls or injuries operatively after removing necrotic tissue.POST OPERATIVE CARESimilar to thermal burns patient. More extensive if has single or multiple amputee. Long term follow up because complications often result for some time after injury.Earlier complications include myocardial damage, arterial mural necrosis and rupture ad occult injuries to abdominal viscera. Cardiac dysrythmias or ECG changes exist initially in 10-30% of cases. Right bundle branch block, supraventricular tachycardia, and focal ectopic dysrhythmias can occur late.Special cord symptoms similar to progressive muscular atrophy, amyorophic lateral sclerosis or transverse myelitis may occur. Peripheral nerve lesions can appear up to 3 years after injury.Privascular hemorrhage, demyelination with vacuolization, reactive gliosis and neuronal death. Slow progressive onset of cataracts. Can often be delayed for several years. Blurred vision beings abt 6 months after injury. 30% of patients affected.

42. Electric flame burns: Flames result from ignition of clothing by electric sparks or arcing and cause the typical flame burn injury. Flame burns may occur together with true electric or arc burns.

Patient care for electric burn victims consists of initial stabilization, followed by early fasciotomy when swelling is severe and by excision of obviously necrotic tissues. The progressive necrosis secondary to vascular thrombosis and edema is managed by continued debridement as further demarcation occurs. Electric injuries stimulate crush injuries, a factor that should be considered in the overall patient care plan. After complete debridement, amputation may be indicated.Specific adverse long-term effects of electric injuries include ECG changes, cataract formation, and spinal cord damage, which may develop from a few days to two years after injury.When abdominal injuries occur, sub mucosal hemorrhage and interstitial intestinal necrosis is possible. Vascular effects of electric burn injuries include delayed hemorrhage from large blood vessels and progressive vascular profusion problems as a result of fibrosis and fibro muscular abnormalities.

43. Lightning Injuries: Electric burns have occurred throughout the ages. Until the late eighteenth century, lightning was the sole cause. The first electric shock recorded occurred in Holland in 1746 when two Dutch physicists accidentally discharged a Leyden jar and the current went through their bodies. Early experimental studies in 1884 demonstrated changes in the cardiovascular and central nervous systems. As human beings learned to produce electricity, the number of electric injuries rapidly increasedAn electric injury is a unique and thoroughly devastating form of thermal trauma. Clinicians arbitrarily divide electric injuries into high- and low-tension injuries as determined by the voltage responsible for the damage. The dividing line is 1000 volts. All current in the United States is 60 Hz or cycles per second. Low-voltage injuries mimic thermal burns and have zones of injury from the surface extending into the tissue. High-voltage injuries comprise varying degrees of cutaneous burn combined with "hidden" destruction of the deeper tissues. The high-voltage injury results in progressive tissue necrosis, somewhat resembling the injury of crush trauma.

Pathophysiology:The tissue destruction caused by contact with highvoltage electricity is basically a thermal injury.Passage of electric current through a solid conductor results in conversion of electric energy into heat, the Jouleeffect. Ohm's law and the Joule effect enable determination of the amount of heat. Ohm's Law states that thevoltage (V) divided by the resistance ® determines the current traveling through tissue. Heat production injoules is proportional to the power dissipated multiplied by the duration of contact and is expressed by thefollowing equation: J = PRTJ = heat production,1 = current intensity,R = tissue resistance, andT = time of contact.The extent of injury depends on the type of current, the pathway of flow, the local tissue resistance, and the duration of contact.Researchers have postulated several theories to explain the pathologic changes that occur after electric injury. The first emphasizes the differences in tissue resistance to current flow. Tissue resistance progressively increases from nerve to blood vessels, muscle, skin, fat, and, finally, bone. Bone, having the greatest resistance, generates the most heat according to the Joule effect. This resistance would cause greater necrosis in the deep periosseous tissues.

Most of the current, however, would preferentially travel along the lines of lesser resistance, particularly the blood vessels. These vessels are injured but not immediately thrombosed.This theory attributes the progressive muscular necrosis to these vascular lesions leading to delayed arterial occlusion and progressive ischemic necrosis. Progressive small vessel thrombosis could convert these areas of patchy necrosis into complete tissue loss.Tissue damage as a result of electric current is a thermal injury, producing elevated levels of arachidonic acid metabolites in areas of greatest heat production. The prolonged elevation of thromboxane plays a key role in the progressive microvascular ischemia in electrically injured tissues, leading to progressive necrosis. Therapy to block the production of thromboxane was successful in providing tissue salvage. Clinically, three types of skin damage may result from electric injury:- contact burns at points of current entry and exit from the body,- arc burns caused by current exiting and reentering adjacent parts or body parts in close proximity,- thermal burns from ignition of clothing because of the degree of heat generated by the current pass¬ing through the body.

Clinical evaluation:The history of the traumatic event is very useful in evaluating patients with electric injury. Determine the site where the injury occurred to help approximate the voltage. Injuries in the home probably equate to 110 to 220 volts. Industrial injuries or powerline injuries are usually high tension; the information is usually readily available from co-workers or superintendents. Find out whether the patient suffered a cardiac arrest at the injury scene. Cardiac arrest frequently occurs. Similarly, determine whether the patient lost consciousness. The patient will often have amnesia or partial amnesia about the electric insult. Also find out whether the patient was thrown a distance or fell from a height after contacting the electric source. Severe trauma is commonly associated with electric injury.Begin the physical examination by establishing airway patency, and assess chest expansion and uniformity of breath sounds bilaterally. Pneumothorax is not uncommon in hightension injuries. Next, evaluate circulation. Examine cardiac rate and rhythm, and consider electrocardiographic monitoring. Ensure peripheral circulation, and determine the need for escharotomy or fasciotomy. Muscle compartmental pressures may be an adjunct in making this determination.

44. GI complications in burns:The gastrointestinal tract function is altered as a result of thermal injury. The initial response is severe splanchnic vasoconstriction, causing an ileus similar to that occurring with other major trauma. If unrecognized, acute gastric dilatation can occur, leading to regurgitation and aspiration. Gastroduodenal ulceration is a frequent occurrence in a patient with burns, although this sequela is not always clinically evident. This ulceration is not a result of absolute hyperacidity. Nonetheless, patients in whom gastroduodenal injury develops within 72 hours of the burn have higher basal acid outputs than do patients without gastro¬intestinal injury. Gastrin levels are not increased in thermal trauma and no correlation exists between serum gastrin levels and gastric acid in patients with burns.The pathophysiology of ulceration, therefore, appears to be a relative hyperacidity combined with a mucosal barrier problem or cytotoxicity as a result of mediator release. The hepatobiliary system also can be altered in thermal trauma. These changes may be the result of hypovolemia or hypoxia (or both) and circulating toxic waste products requiring clearance.During the shock period, to compensate hipovolemia, cutaneous and intestinal vasoconstriction occur. If the patient is not well hidrated, this vasoconstriction lead to ileus and mucosal necrosis, with small ulcerations. This is an open gate for bacteria migration into the blood and bacteriemia.

From the blood, bacteria can reach burned necrotic tissue, an excellent grow medium, and capilar network of lung, liver; brain, bone, with abcess formation. So, we understand why a burned patient became contaminated and infected, from the inside, even if he/she is very well treated locally, in a sterile cubicle.Liver biopsy findings have shown cloudy swelling as early as 3 hours after burn. This swelling progresses to hepatocellular necrosis, vacuolization, and fatty degeneration.With time, however, these changes show repair. Also, every liver function test has been shown to be abnormal at some time during the course of a severe burn. Biliary tract stasis occurs, and the normal bile salt ratios change, leading to the formation of sludge in the gallbladder.Numerous metabolic and neuroendocrine changes occur throughout the course of injury and recovery. Some of these result primarily from the low flow rate of hypovolemia. Others, however, occur when perfusion and tissue oxygenation are adequate.

45. Infections in Burns:The complication of sepsis in the patient with burns arise from multiple causes. Because health in the patient with burns clearly is associated with the maintenance of a bacterial equilibrium in the wound, the surgeon should aim treatment from admission at maintaining this balance.As discussed in earlier sections, the treatment of burn wound infection starts on admission and can be divided into two phases: attempts to boost the host defense and preventionand treatment of the numeric increase in bacteria. All tients should undergo this treatment, as discussed in the noperative care of the patient.Only when the patient is clinically septic or when bacterial counts exceed 105 bacteria per gram of tissue on biopsy findings is burn wound sepsis established. Then additional measures should be instituted as follows. First change topical antibacterials if the in vitro susceptibility test findings suggest that a more appropriate antibacterial is available.While attempting to reestablish the normal bacterial equilibrium of the burn wound with the use of the topical antibacterials, do not forget that the necrotic avascular tissue enriches the wound as a culture medium. Therefore physical removal of necrotic debris must take the form of early total excision of the burn wound, intradermal or tangential debridement, or daily meticulous cleansing of the loosening eschar.Removal of this necrotic tissue becomes a therapeutic imperative if the bacterial balance is shifted in favor of the bacteria, with greater than 109 organisms per gram of tissue. As this eschar is being removed, close the wound either temporarily or permanently, as discussed previously.If the treatment of the burn wound is not effective in controlling bacterial proliferation, sepsis from the wound may invade the systemic circulation. The earliest sign of invasion is at the interface of subeschar and uninjured tissue. Diagnose this by histologic examination of a biopsy specimen of the burn wound and the adjacent normal tissue.Once systemic sepsis exists, institute support for the entire patient. Start hemodynamic support, because inereased capillary permeability will occur, often causing vascular collapse. The resultant pulmonary edema and respiratory distress may require intubation of the patient and ventilatory support.Maintain nutrition during septic episodes. Undernutrition can markedly influence several parameters of host defense, including the ability of neutrophils to ingest and kill bacteria, the synthesis of specific antibody to an antigenic challenge, the synthesis of opsonic components of the complement system, delayed hypersensitivity responses, and vascular reactivity.Providing adequate nutritional requirements to meet the increased demands can reduce these effects, increased protein is especially needed to convert the immunologic defects. For best results in reversing the immune defects nutrition should be given by the enteral route. We found markedly worse results with intravenous alimentation in comparison with administration of the same nutritional formula by means of the intestinal tract.

Closely monitor the blood antibiotic levels, because proper levels are difficult to be maintained in the hypermetabolic patient with burns.Vaccination, or active immunization, has been tried in many trials. Munster, however, has pointed out that active immunization with vaccines requires that the vaccine be started before infection becomes a threat. This timing is not always clinically feasible. Also, a constantly changing spectrum of pathogenic organisms is dominant in patients with burns. This spectrum requires any successful vaccine to be polyvalent.Authors in the literature have recommended the use of human gamma globulin in children for many years. Intramuscular doses of 1 ml/lkg on days 1, 3, and 5 after burn are suggested. Intravenous IgG has had some initial success, and Munster has cautiously recommended its use in infection-prone patients with burns whose admission serum IgG concentration is less than 300 mg/dl. Another type of passive immunization is plasma exchange therapy. This exchange removes any circulating toxic factors and replenishes immune factors in fresh-frozen plasma.'The initial bacterial danger is beta-hemolytic streptococci. The rich vascularity of the inflammatory phase, edema, and neutralization of the bactericidal defense mechanisms of sebum render the burn wound prone to streptococcal invasion. Administration of penicillin for systemic effect does not reduce the overall incidence of burn wound sepsis, but prophylactic administration of penicillin can prevent streptococcal infection.Although topical antibacterials may be antistreptococcal, most patients with burns should receive intravenous penicillin during the edema phase of 48 to 72 hours. Then penicillin therapy should be discontinued to reduce the chance of the emergence of resistant organisms. This procedure seems particularly efficacious in patients who are not receiving topical antibacterial treatment. The alternative choice in the patient allergic to penicillin appears to be erythromycin, rather than broadspectrum coverage.Another potential and serious invader of the burn wound is Clostridium tetani. Because clinical tetanus is a recognied complication of even minor partial-thickness burns, the physician should follow the recommendations for tetanus immunoprophylaxis set by the Health Ministry.Nonviable burned tissue is not only a site for anaerobic bacterial growth, but this tissue also has a role in generalized suppression of host immune responses. Therefore early excision of tissue appears to be the most expeditious means of avoiding suppression. Results of clinical studies have shown that early burn wound excision, and grafting may improve lymphocyte function.The prevention of infection thus involves maintaining an equilibrium between the ever-present bacteria and a host resistance. Therefore the surgeon aims early care of the burn wound toward preventing the numeric proliferation of bacteria.In mixed full- and partial-thickness burn injuries, early colonization occurs within the lumen of hair follicles and glands. In uniform full-thickness injuries, colonization may not begin until the eschar begins to crack and open at 12 to 14 days after burn. Lodgment and growth of bacteria to numbers less than \05 bacteria per gram of tissue are compatible with the survival and healing of the deep dermal elements of partial-thickness injuries. When bacterial counts exceed 105 bacteria per gram of tissue, bacteria spread from the follicles, and colonization occurs along the dermal-subcutaneous junction. Perivascular colonization is accompanied by thrombosis, vascular occlusion, and necrosis of any remaining viable elements.The partial thickness burn injury then converts to a full-thickness loss as a result of ischemia and bacterial autolysis. When growth of bacteria exceeds 10 bacteria per gram of tissue, this constitutes burn wound sepsis, and lOx to I09 Pseudomonas organisms per gram of tissue appear in lethal injuries. Autopsy examinations often fail to identify any metastatic organisms, and blood cultures before death are frequently negative for microorganisms. Thus burn wound sepsis as a result of infection will) pseudomonas can be lethal without the spread of viable organisms outside the burn wound itself.

Concentrations of 109 bacteria per gram of tissue may deliver sufficient byproducts or toxins to the body to produce the picture of gram-negative sepsis or endotoxemia and death.A direct linear relationship, both experimentally and clinically among the amount of devitalized tissue, the level of bacterial growth, and the mortality rate, has been described. Study findings on the pathophysiology of burn wound sepsis indicate that most bacteria in the wound originate from endogenous sources within the skin. Bacteria can also arise from exogenous sources.In a recent study by Meggers et al. organisms recovered in cultures of material from the hands of burn unit personnel were not the same as those in biopsy specimens of wounds in patients with burns, suggesting that exogenous transmission is less important than self-contamination.Regardless of the source of the bacteria, quantitative cultures of biopsy specimens have been a useful guide to management of burn wound sepsis. Wound biopsy specimens for culture and microscopic examination are very important. The mere presence of bacteria is not as critical as the quantitative level of bacterial growth.Recently, McManus demonstrated that histologic examination of tissue is also important to determine the depth of invasion of the bacteria. When quantitative bacterial screening techniques show 103 or fewer bacteria per gram of tissue, the examiner can be confident that burn wound sepsis is absent. When more than 105 bacteria per gram of tissue are present, however, only the potential for invasive infection exists. In these cases histologic examination allows de onstration of viable organisms invading unburned tissue subjacent or adjacent to the burn wound. Invasive sepsis with systemic signs of septicemia occurs only when this test shows positive findings, demonstrating bacteria invading unburned tissue.Septicaemias usually result in the first days alter the injury, due to bacteremia from intestinal tract. If hypovolemia is not correctly treated, intestinal vasoconstriction occur, with ileus, mucosal necrosis and bacteria migration through the wall in the blood. Bacteremia with intestinal origin is the main cause of wound contamination and septicemia.If septicaemia occur one week later after the injury, wound contamination or, catheter contamination are the most frecvent causes of this. They are treated by meticulous local wound care and appropriate antibiotics, based on clinical impression and culture and sensitivity reports.Patients with gram-positive septicaemia, such as that caused by staphylococcus, usually have spiking temperature, leukocytosis and toxic delirium. Methicilin, 1 g IM or IV at 4 to 6h, or lincomycin, 600 mg IM or IV at 12h may he beneficial. Gram-negative septicaemia with hypothermia, leukopenia and a clear sensorium can lead quickly to anuria and death before the blood culture report are known. Gentamicin, 3mg/kgand carbenicillin, 4 to 5 g IV / 6 h , are the most effective drugs against Pseudomonas aeruginosa, which is th emost common gram-negative organism in infected burn patients. Sensitivities to organisms vary from hospital to hospital and should be evaluated individually.Several clinical signs are suggestive of a systemic response to sepsis in the burn wound. Abnormal temperatures are common in the patient with burns and may result from a central defect or from the hypermetabolism described in the normal systemic response. Nevertheless, the surgeon must consider hyperthermia or hypothermia as a possible sign of sepsis when the patient's temperature is greater than 39° Cor less than 36, 5° C. Also, the surgeon might consider congestive heart failure in a patient who is not considered to be fluid overloaded and who has no history of heart disease as a sequela of systemic sepsis until proved otherwise.In addition to clinical symptoms and signs, laboratory studies can help diagnose infection in the patient with burns. As mentioned previously, the most important indication is the presence of greater than 10 bacteria per gram of tissue from a biopsy specimen and the histologic determination of bacteria invading viable unburned tissue. Blood cultures may be helpful if they are positive for microorganisms, but lethal burn wound sepsis may occur with no systemic spread of viable organisms into the bloodstream.Kucan found that blood glucose concentration is a helpful guide.

Blood glucose levels of greater than 130 mg/dl are statistically associated with septicemia from gram-positive organisms, whereas blood glucose levels of less than 110 mg/dl suggest gram-negative septicemia. Other helpful signs are a depressed leukocyte count of less than 4000 cells/mm or a markedly elevated count of more than 30,000 cells/mm. Azotemia without dehydration or obstructive uropathy in the absence of treatment with nephrotoxic drugs might also suggest invasive sepsis.The presence of thrombocytopenia, hypofibrinogenemia, or fibrin-split products in the blood after 24 hours after the burn suggests sepsis. The presence of interstitial pulmonary edema evidenced on a chest radio¬graph must also raise suspicion of sepsis.In addition to the problems with bacteria, as demonstrated by infection with Pseudomonas aeruginosa, burn wounds can be invaded by other microbes such as fungi or viruses. Prominent among these are the Candida species.Predisposition to infection with Candida organisms is provided by the decreased host resistance in the patient with chronic burns and potentiated by the disturbance in the bacial equilibrium resulting from the use of antibiotics. Longstanding indwelling intravascular catheters may provide a port of entry, but more often the portal is the patient's bowel. Sepsis with Candida spp. is heralded by hypothermia, leukopenia, agitation, and, later, vasculitis of the wound with purpura.A definite diagnosis of candidiasis that necessitates systemic therapy is possible if blood cultures remain positive for microorganisms, if with appropriate serologic tests the patient becomes serapositive, if funduscopic evidence of candidal retinitis appears, or if histopathologic examination of biopsy specimens of lung, kidney, or liver reveal Candida species. Unfortunately, such direct evidence of infection is rarely obtainable. Blood culture techniques, either arterial or venous, have a low sensitivity, and cultures are negative for microorganisms in more than half of the cases of autopsy-proved disseminated infection. Because the laboratory tests used to determine if active infection with Candida organisms exists do not have high reliability, a practical approach for defining candidal infections necessitating systemic therapy is to obtain materia! for culture repetitively from multiple sites and to initiate systemic therapy when cultures of material from three or more sites are positive for microorganisms. The term site includes the burn wound, sputum, urine, blood, or scrapings from mucocutaneous lesions.Other mycotic infections occasionally occur in the burn wound, such as those caused by species of Aspergillus, Mucor, and Rhizopus. Clinical manifestations of these infections include edema, induration, tenderness, ulcerations, early separation of the eschar, conversion of the wound to deeper injury, and underlying muscle necrosis. Histologic examination of the excised biopsy specimen is diagnostic.Treatment for these rarer forms of burn waund sepsis includes radical excision of the involved area. Reports of viral burn wound sepsis have been infrequent but alarming. One report of six cases of herpes virus infection included two fatalities. Also, Nash reported cytomegalovirus in patients with burns with disseminated cytomegalic inclusion disease. Most recently, human immunodeficiency virus is appearing more commonly in burn centers. To date no report has been made of recovering the virus directly from the burn wound, although exudate from the burn wound may contain the virus.

46. Skin Grafts: Through the years, a split-thickness graft (STSG) has come to mean a graft taken anywhere within the dermis. By contrast, a full-thickness graft (FTSG) includes the epidermis as well as all of the dermis.Split-thickness skin grafts include a variable amount of dermis, whereas full-thickness grafts are taken with all the dermis.

Thin split-thickness skin grafts "take" under conditions less favorable than required by full-thickness or thicker split-skin grafts, but tend to shrink considerably, pigment abnormally, and are very susceptible to trauma. Unlike split skin, fullthickness skin does not contract much upon grafting and appears to resist trauma better. Because full-thickness skin grafts are thicker than split-thickness grafts, however, their early survival is precarious until the new perfusion system has been established, so that they require a well-vascularized recipient bed.Skin thickness varies according to age and body area. The skin is thin in the first decade of life, after which time it thickens and remains relatively thick until the fourth decade. With aging there is progressive thinning of the dermis, with diminishing sebaceous gland content and loss of elasticity, a process that continues until death. Skin from the eyelid, the postauricular area, the supraclavicular area, the medial aspect of the thigh, and upper extremity is quite thin. Skin from the back and buttocks, on the other hand, is quite thick.It is estimated that 95% of the skin thickness is dermis and its components while the other 5% is epidermis. The subcutaneous tissue lying just below the dermis contains the sweat glands and hair follicles. Sebaceous glands are located actually within the dermis. The blood vessels which supply the skin are superficial to the fascia and are parallel to the skin surface, then branch at right angles, penetrating the subcutaneous tissue. They continue to arborize within the dermis, where the final capillary tufts terminate between the dermal papillae. The more superficially a skin graft is harvested, therefore, the greater the number of blood vessels that are transected.

47. Skin allografts:Homografts have been used for decades to cover granulating and contaminated wounds. They arc variably effective in reducing pain and fever, restoring function, increasing appetite, and controlling fluid loss, mostly by stimulating granulation and promoting wound healing.Allografts remain the most important clinical tool in the management of extensive skin loss. Cadaver skin is a good substitute material except for its antigenicity, limited availability, and susceptibility to infection.Contraindication for accepting potential skin donors: General Absolute Malignancies (excluding primary brain tumours)Serogical evidence of HIV, HCV, HBsAg, TPHA/VDKL SepsisPostmortem time > 24 h (12 h if body is not cooled)Age < 18 yearsDrowningTuberculosis"Slow viral disease''Relative 1DDM/NIDDMHistory of long-term IV drug abuse; alcohol abuseMember of "risk-group" with regard to HIV and other, equally life-threatening, Iransmittable diseases Chronic use of corticosteroids (Auto) intoxication Unknown cause of death Specific Absolute Autoimmune dermatosesGeneralized skin damage (physical, infectious)Systematic collagenoses

Attempts to extend the time" frame in which al lografts can be left in contact with an open wound have served to decrease the amount of allograft that is needed to cover long-term open wounds, and lengthen the interval for regeneration of available donor sites. When applied at the time of grafting, cyclosporin (CsA) increases graft viability through its immunosuppressive action on T suppressor lymphocytes. First-set rejection is prevented, presumably through the suppression of donor-specific T cells, but second-set rejection proceeds normally and subsequentgrafts from another donorwill be rejected.

O'Donoghue and Zarem tested isografts, fresh skin allografts, lyophilized isogafts, and frozen isografts, and found fresh isografts to be generally superior, but fresh allografts and preserved isografts were also effective in promoting healing of the recipient bed. Human allografts have a short shelf-life of two weeks when stored at 4°C, and since periods of demand and availability of allografts do not always coincide, an effective preservation method is highly desirable.Allograft rejection is a function of the immune response of the body to a foreign antigen.Allografts are rejected because of their antigenicity. Graft rejection is commonly believed to be a delayed-type hypersensitivity (DTH) reaction mediated through killer "T" cells. The strength of the rejection is proportional to the degree of genetic disparity between the donor and the host. Because autografts do not elicit an immunologic response, they enjoy a rejection-free course. Even allografts have a good chance of surviving the transplantation procedure if the host has not been previously sensitized to that donor.Current examples of synthetic skin substitutes include both unilaminate and bilaminate membranes. Hydron is a transparent unilaminate membrane formed by alternately spraying polyhydroxyethylmethacrylate powder and liquid polyethylene glycol on the wound. Hydron is easy to apply and repair, can be impregnated with antibiotia for direct and more consistent delivery to the wound bed, and does not need to be changed as often, for increased patient comfort. Adverse effects, in fact, are nil. While valuable as a barrier and vehicle for antimicrobials, Hydron requires a dry bed for adherence and is water soluble, limiting its use to the most superficial, nondraining wounds.Another type of unilaminate skin substitute consists of agar copolymerized with acrylamide. The material is chemically inert, nonallergenic, and transparent. Underlying wound infection can be easily identified, wound discomfort is reduced, and dressing changes are painless. On the minus side, it has low tensile strength and adheres poorly to the bed, making itmore useful as a syntheticwound dressing than as a skin substitute.Bilayered skin substitutes can be composites of biologic and synthetic material or wholly synthetic. The first type may have a collagen matrix ("dermis") covered by a Silastic "epidermis", such as reported by Burke et al.The material is neither inflammatory nor immunogenic, biodegrades at a controlled rate, and has the appropriate pore size and structure to allow cell migration into it and collagen orientation subsequently. It is vascularized within three to five days to form a neodermis, and some time later the Silastic epidermis can be peeled off and the neodermis covered by a thin autograft. This artificial skin is best indicated for immediate closure of excised burn wounds.Biobrane consists of silicone membrane and nylon bonded with dermal collagen peptides. It has been used clinically to resurface split-thicknessgraft donor sites and other open wounds, markedly reducing evaporative water loss and patient discomfort. Because of its semipermeable construction, Biobrane can also be combined with topical antimicrobials such as Silvadene in the management of partial-thickness burns.

48. Skin Tissue Culture:When large areas of full-thickness skins are destroyed, such as, in extensive burn injuries, the available donor-sites for auto grafts are limited. One of the most encouraging approaches to find new sources of skin to replace the missing epithelium is the in vitro culture of human epidemial cells (keratinocytes). The prototype for this concept was Bell's "living skin equivalent'; which is a composite of fibroblast-seeded fibrillar collagen lattice upon which dissociated epidermal cells proliferate.Rhinewald and Green are credited with the first successful in vitro culture technique that led to reproducible epidermal cultures. This technique allowed expansion of a 2 cm2 skin surface area by a factor of 10,000 in three to four weeks. The dermal component of the tissue culture vascularizes rapidly upon application, preventing graft necrosis. Grafts up to 8 x 12 cm are possible provided they have good epidermal covering.

7 days - keratocites island, 14 days - confluent populations, 21 days - multiple layersThe most obvious clinical application for tissue cultured skin grafts is in patients with bums greater than 50% of the total body surface area. Other major applications for cultured keratinocytes are in the treatment of chronic venous ulcers, in junctional epidermolysis bullosa, and after excision of giant congenital nevi or tattoos.Cell cultures suitable for use as cover are both allograft and auto grafts. Faure note the allogeneic cultured epidermis is thin but multilayered, and a new derma-epidermal basement membrane is synthesized during the first few days after transplantation. Their cell cultures were suitable for use as allograft or auto grafts in permanent wound coverage.A preliminary report suggests that allograft is long-term survivors probably because of absent antigen-presenting cells (Langerhans' cells). More recently, however, studies have come to light indicating that for long-term survival the cells must be autologous. It is unclear whether the implanted tissue survives on its own or serves as a scaffold for replacement by host tissue. Bell found 75% or greater inhibition of wound contraction in 80% of the grafts, with zero rejection.At the present time, tissue-cultured epidermal grafts are being used extensively in burn centers throughout the world. From this mounting experience, the following observations can be made:- It is very expensive: a 4 x 4 cm2 graft costs approximately 300 6.- The material is quite fragile and must be handled very carefully.- Grafts require well-vascularized beds.- It will not tolerate infection- If graft “takes," the material will spread peripherally to join other grafts or surrounding skin. Using the current technique, autologous cultured epidermis can now be reliably obtained in sufficient quantities to be used as graft material for coverage of large wounds. As these shortcomings are overcome, the clinical care of patients with extensive skin losses will be revolutionized, and surgical coverage of difficult integumentary deficits will no longer be limited by the availability of donor sites or the time needed to grow epidermal grafts from autogenous sources.49. Epidermal grafts:The epidermis protects the body from its environment and is our first and most extensive source of contact with the outside world. Nevertheless, epidermis by itself is not a satisfactory cover for wounds because:- it does not effectively inhibit proliferation of underlying granulation tissue- can produce a hypertrophic scar- in the absence of dermis good graft healing is not possible- the epidermis that differentiates on scar tissue is of poor quality.

50. Dermal grafts:Grafts of dermis are either transplanted or implanted. Placed intraperitoneally, dermal grafts form small epithelial cysts that degenerate with time; implanted intrathoracicallym they lose all epithelial elements and no cysts develop.Thompsons remarked that collagen, elastin and reticular fibers in dermal grafts survive relatively unchanged histologically, providing a strong, serviceable source of these materials.Dermal grafts can be used to reinforce vital structures or to fill undesirable spaces with autogenous tissue bulk. They "take" very well even on unfavourable wounds.

51. Graft failures:1. Hematoma formation: the clot isolates the undersurface of the graft from the endothelial buds of the recipient bed so tha revascularisation cannot take place.

2. Infection: can be prevented by carefully preparing the wound bed, and meshing or pie-crusting the graft surface to allow free drainage of the wound exudate.3. Fluid beneath the graft: may cause graft necrosis. Areas rich in lymphatics such as the supraclavicular, inguinal and axillary regions are particularly prone to develop seromas. A light pressure dressing minimise the risk of fluid accumulations under skin grafts.4. Excessive pressure: on a fresh graft, may cause it to die. The applied pressure should never exceed 30 mmHg.5. Gravitational dependency: proper immobilisation of graft is necessary to prevent it from being dislodged from its bed.

52. Frostbite mechanism:Firstly, there is initial peripheral vasoconstriction, with concomitant shunting of the blood from the surface to the core. This is an attempt to preserve heating.If the vasoconstriction time is too long, ischemia lead to anaerobic metabolism with acidosis and oxygen free radicals and inflammatory mediators response like in burns. The primary site of injury appears to be vascular endothelium. By 72 hours after injury and rethawing, a loss of vascular endothelium in the capillary walls and significant fibrin deposition occur. The endothelium may be totally destroyed and the fibrin may saturate the arteriole walls. But the injury appears greatest on the venules where the circulation is slower.The progressive dermal ischemia occuring in frostbite might be caused by the same inflammatory mediators responsible for progressive dermal ischemia in the burn wound. The vasoconstricting, platelet-aggregating and leukocyte-sticking prostanoids are markedly elevated.The edema formation occuring in frostbite is a result of either leakage of proteins caused by release of these PGs and tromboxanes, or white blood cells sticking in the capillaries and increased hydrostatic pressure.

53. Frostbite first aid:Remove constricting or wet clothing from injured parts. Prohibit smoking. Avoid refreezing after the part has been thawed. Minimise direct cellular damage by thawing the part rapidly with imeersion in water warmed to a temperature between 40-42.Morphine is given for pain experienced with thawing. Keep the frozen extremities in the water bath until the skin becomes erythrematous at the most distal parts of the frostbite. This change usually occurs in less than 30 minutes. Administer topical agents to minimise the production of thromboxane by injured cells.Following rapid rewarming, leave the blisters intact.Clean the area with bethadine.Insert dressing gauze in the web spaces, to keep toes separated.Keep toes free, protected by a tent, in a warm atmosphere.Give tetanus prophylaxis if indicated.Give aspirin (or ibuprofen) (blocks further prodcution of PGf2alpha and thromboxane)Elevate the injury to attempt minimise the edema.Give parenteral penicillin to prevent streptococcal invasion.Give heparin 5000 iu every 4 hours iv for 5 days.

54. Frostbite treatment:Because frostbite most frequently involves injuries to the extremities, recommend appropriate physical therapy and occupational therapy. Daily hydrotherapy for active and passive range of motion has proved to be of extreme value in preservation of fucntion.Early surgical intervention has no role in the acute care of frostbite injuries except with ischemia from a constricting eschar infection that cannot be controlled by topical antimicrobials.

Occasionally, decompressing escharectomy incisions are necessary to increase the circulation distal to the injury. If such escharectomies are necessary to decompress digits and facilitate joint motion, incisions along the nondominant transaxial line are best. Ensure that these incisions prevent injury to the underlying structures. If uncontrolled infection exists early, escharectomy may be necessary. Infection, however, is rare with the use of penetrating anitbacterials such as mafenide acetate.

55. Skin Layers:The skin is a highly specialized bilaminate structure that rests on a subcutaneous layer (third layer) of padding. Two layers, the epidermis (outer layer) and the dermis (inner layer) exist, and the thickness of each layer varies in different areas of the body. The skin varies in thickness from 0.5 mm to 6 mm, depending on the part of the body, but it is generally 1, 2 mm thick. The highly cellular epidermis is 0.06 to 0.8 mm thick, and it communicates with the dermis by way of multiple irregular interpapillary ridges and grooves.The outermost layer of the epidermis is the stratum corneum. It is only 10 to 20 urn thick (except on the palms and soles) and is composed of nonviable, relatively dry keratinized cells. The function of this layer is protective.

The innermost layer, the stratum germinativum (or basal layer) contains melanocytes, as well as cells destined for keratin production. These cells are the only proliferating cells within the epidermis. Melanocytes are limited to the basal layer but can transfer melanin, in melanosomes, to the keratinocytes. Between these two layers are keratinocytes in various stages of differentiation.The stratum spinosum (or spinous layers) constitute the bulk of viable cells that are synthesizing keratin and precursor proteins for the cells in the granular layer. The stratum granulosum primarily synthesizes proteins related to the fully keratinized cell.The dermal-epidermal junctions undulate in most areas of the body, increasing surface contact between the two layers to provide resistance of normal skin to shearing.

The dermal-epidermal junction is a complex of structures referred to as the basement membrane zone, which functions as a filter to inhibit or prevent passage of molecules greater than 40 kD. Inflammatory and neoplastic cells, circulating, pemphigus and pemphigoid autoantibodies, immigrant cells, and neurites, however, can penetrate the basement membrane zone. These cells, therefore, must possess some mechanism for disruption of this barrier. The basement membrane zone is frequently the site of immune complex deposition.

The dermis is 20 to 30 times thicker than the epidermis. It contains the nervous, vascular, lymphatic, and supporting structures for the epidermis and harbors the epidermal appendages. The regions of the dermis respond differently because of differences in structural organization and biochemistry, and each responds uniquely to systemic and genetic diseases and environmental assault. The papillary and reticular dermis comprise the two main dermal zones.The dermis contains fibrous and nonflbrous matrix molecules. The fibrous proteins impart bulk, density, and tensile properties to skin and allow for compliance and elasticity. Fibrous glycoproteins in the dermis function in cell-matrix attachment. The nonfibrous matrix molecules form the ground substance that influences the osmotic properties of skin, permits cellular migration in a more fluid milieu, and serves as an integrative, continuous medium for all of the other structural elements.Fibrous elements of the dermis are composed mainly of collagen fibrils and elastic fibers. The collagen in the skin is primarily types I and III in a ratio of about 85% to 15%. Type IV collagen is the major component of the basal lamina zone.

The elastic fibers comprise two components: aligned bundles of microfibrils and a dense elastin matrix. The microfibrils are believed to serve as a template for the elastin matrix.The nonfibrous portion of the dermis is composed of glycosaminoglycans (GAGs) and glycoproteins of the amorphous ground substance. In the skin GAGs comprise hyaluronic acid, dermatan sulfate, and chondroitin 4-sulfate and chondroitin 6-sulfate.jGAGs play a role in cutaneous permeability, allow cellular migration, and influence the polymerization of such fibrous matrix proteins as collagen. GAGs are synthesized by fibroblasts and turned over in phagocytsc vacuoles by macrophages.

The papillary dermis is only slightly thicker than the overlying epidermis. In general, it is separated from the underlying reticular dermis by a harizontal plexus of vessels. This plexus provides the overlying papillary dermis with a rich blood supply. The papillary dermis is more commonly altered in environmental induced skin lesions (actinic damage) than in systemic disease or inherited diseases of connective tissue metabolism.Most of the dermis is the reticular dermis. Epidermal appendages either terminate in the lower levels of the reticular dermis or penetrate even deeper into the subcutaneous tissue. Vessels pierce the dermis, giving off supplying vessels to the hair follicles and sweat glands.The human epidermal appendages include the nails, hair, sebaceous glands (pilosebaceous apparatus), and eccrine and apocrine sweat glands. Few structures of the skin have as much variability as the pilosebaceous structures. The hair type, density, and rate of growth all depend on the body region, sex, age, and race of the person.