1.

The 3 concentric zones of thermal injury in burn wounds

Jackson'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 burn
The 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 burn
The 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 partialthickness wounds may heal spontaneously, although healing may require 3 to 4 weeks. On the
other hand, these wounds may deepen with progressive dermal 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 burns
3rd 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
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 carry as 3 hrs after burn. This swelling
progresses 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 adults
10 to 29 % TBSA in children and adults over 40 yrs old
less 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 injury
Without 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 distress
prevention of shocks
ensurance of perfusion
1.if acute respiratory distress :
because of eschar in ant and post thoracical wall, do escharectomy if eschar present
intubation of oedema is preset on epiglottis and larynx
nasotracheal tube preferred
if 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 steam
flame
electricity - electrocution electric flame lightening
Chemical burns - acids alkalis salts tar cement
friction burns
explosion
smoke inhalation
combined lesions
high pression injection
frostbite
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 index
Prognostic 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 index
We consider that, apart of age, burned surface area and associated lesions, we may add risk
points depending of the level of care:
0specialized Burns Unit
10%- Plastic surgery unit in University Clinic
15%- County Hospital
20%- 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 stabilisation
Early fasciotomy
Manage 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= I2RT
Most 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 current
Arc burns : caused by current exiting n reentering adjacents parts
Thermal burns : caused by ignition of clothing by heat generated due to current passing in body.
Clincial evaluation:
Establish airway patency
Assess chest expansion n uniformity in bretahing
Evaluate circulation
Find out if patient fell down or was projected over a distance
Initial recording of burn degree may be difficult as much injured tissues hidden beneath
uninjured tissue.
Fluid loss will be in excess to that predicted
Significant blood loss
Extensive destruction of bone
Lab: 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 increases
ECG finding for dysarythmis. Monitor for 24 hrs.
X ray to rule out pneumothorax, lumbar, thoracric injury
Masangemet :
CPR at injury site
ECG abnormality correct dysarythmia
Fluid requirements more than predicted values. Begin with balanced salt soluiton about
4ml/kg/TBSA%
Maintain urine ouptut 200ml/24hr
200 mEq soidum bicarbonate urine alkalinisation to prevent pigment precipitaiton
Hepariv 5000IU 3hrly I.V
Penicillin 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 skin
Decompression of nerves as major nerves are susceptioble to increase pressure in close
compartemnet
Debridemnet of necrotic material
Observer 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 amputee
Spinal cord symptom - progressive muscular atrophy, amytrophic lateral sclerosis
Perpipheral nerve lesison histophathology perivascualr hemorage, demyelination with
vacuolisation, neuronal death
Progressive 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 acid
Reducing 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 tissue
Acid 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 manifestation
Determine apropriate antidote
Ingestion 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 necrosis
Estimate 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 surface
2.
Hyper metabolism
3.
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 of
temperature, humidity, microbial flora;
b.
Gaining informational equilibrium through release of pain and recovery, with priority of
the 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 shock
Secure a no. 16 or 18 cannucal in an adequate vein.
Insert indwelling urianry catherter
Estimate 24hr fluid needs thur parkland formular = 4ml Ringer lactacte x wight/kg x % TBSA
Give one half in first 8hr from first time of injury
One fourth in second 8hr
One fourth in third 8hr
Adjust infusion rate to obtain 1ml/hr/kg body weight.

20. Mainteance of peripheral circulation in burns:

Remove all rings or bracelete
Observer extrmity for clinicla signs of imparied circulation : cyanosis, delayed capillary refilling,
prorgessive neurological signs
Perform 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 dressing
If 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%TBSA
Complicated burns : respiratory tract injury, major soft tissue injury, fractuires
Electrical I jureis
Moderate : second degree burn of 15% TBSA or third degree burn of lexx than 10% TBSA
Suspected 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 agents
Cool the burn
Pain 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/hr
2.Sensorium - clear and lucid
3.Pulse rate - less than 120 per minute
4.Blood pressure - normal to high-normal
5.Central venous pressure - less than 5 cm of water
6.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 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 corp
CAloric 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 betahemolytic 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 broadspectrum antibiotics should be avoided unless specific infections are to be treated.
31.
H.
Nasogastric tube is inserted and attached to suction for nausea, vomiting, or
distention or for greaterthan 25% TBSA bums.
I.
Analgesic medications are given in small doses IV as needed (Morphine 3 to 5 mg
every 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 patients
A.
- Stop further injury
1.
Extinguish and remove burning clothing.
2.
For chemical bums
a.
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 ventilation
1 . Provide humidified oxygen by mask.
2. Provide endotracheal intubation and mechanical ventilation when required. Check for
a.
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.
- History
1.
Time and circumstances of injury.
2.
Preexisting illnesses.
3.
Medications.
4. Allergies
Fig. 1. The rule of nines is helpful for initial estimation of the extent of burned body area.
E. Physical examination
1.
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-degree
First-degree Burn Burn
Criteria
Burn (Partial Thickness) (Full Thickness)
Cause Sunburn
Spill scalds, . flashes of flameImmersion scalds; flame, electricity,
chemicals
Color Pink or reel Pink or mottled red Pearly white, brown, or charred
Surface
Uniform, no vesicles Vesicles or weeping Dry
Pinprick
PresentPresentAbsent

Time Heals Heals in 2-6 weeks

Produces granulating 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 %TBSA
a.
Give: one half in first 8 hr from time of injury; one-fourth in second 8 hr; onefourth in third 8 hr.
b.
Adjust infusion rate to obtain 30 to 50 ml/hr urine output in patients over 30 kg in
weight and 1 ml/hr/kg body weight in patients less than 30 kg (Fig.2)
G. Maintain peripheral circulation
1.
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 bum
is important to incise also the deep muscular fascia!
4.
Fasciotomy is needed only when injury involves subfascial tissues and/or perfusion
abnormalities 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 splinting
the hand, the four required positions are: Wrist dorsiflexion, Metacarpo phalangeal joint
flexion, 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 for
the 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 of
invasive infection. Topical antibacterial therapy must be altered according to the needs of the
patient
as 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, based
on in vitro activity, allows selection of the most appropriate agent. The bacterial population of
any
patient's bum wounds may change several times throughout the hospital course. Sensitivity
testing
allows the treating physician to keep current with the changing flora and to use the most
appropriate
topical 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 therapyhas been in cases where areas of full thickness bum injury were totally removed down to deep
fascia
and followed by immediat coverage with autografts, homografts, or both. This mode of therapy
is
generally limited to 15% to 20% TBSA injuries and can be utilized by physicians who are
familiar
with its techniques. It is clear that in properly selected cases immediate excision and grafting can
shorten the hospital stay, and can produce good functional and acceptable cosmetic, results
This 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-epithelialization
Disadvantages- 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 AGENTS
Chromic 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 above
CORROSIVES
Phenols, common use- deodorants, sanitizers, disinfectants, cleansing and diluation- ethyl
alcohol
White phosphorus- common use- warefare incendiary, C&d-water and debride particles, special
therapy-irritage with 1% copper sulphate
Lyres- common use- industrial cleansing
Potassium hydroxide washing powder, drain cleanrs, pant removers, c&d-water
Sodium hydroxide-same as above
Ammonium hydroxide, common use- urine sugar reagent tablets
Lithium hydroxide, barium hydroxide and calcium hydroxide same as above
Lime, common use- agriculture (soil alkalinisation), c&d brush off
Protoplasmic poisons:
Strong acides-(tungtic,picric,tannic,sulfosalicylic,cresylic,tricloroacetic,formic), oxalic acid,
hydrofluoric acid, hydrochloric acid- common use: etching , metal cleansing, cleasing and
dilution- water
Special 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.
PATHOPHYZ
Tissue 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 damageContact burns at points of current entry and exit from body
Arc 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 EVALUATION
History 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
bilaterallypneumothorax 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 injuryECG.
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 injury
Delay primary excision and reconstruction 4 to 7 days after injury
Delayed reconstruction after complete healing by ondary intention
Immediate 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 patients 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 CARE
Similar 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
increased
An 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 highvoltage 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 Joule
effect. Ohm's law and the Joule effect enable determination of the amount of heat. Ohm's Law
states that the
voltage (V) divided by the resistance determines the current traveling through tissue. Heat
production in
joules is proportional to the power dissipated multiplied by the duration of contact and is
expressed by the
following equation: J = PRT
J = heat production,
1 = current intensity,
R = tissue resistance, and
T = 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 passing 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 gastrointestinal 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 dermalsubcutaneous 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 gramnegative 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 radiograph 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 fullthickness 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 Sepsis
Postmortem time > 24 h (12 h if body is not cooled)
Age < 18 years
Drowning
Tuberculosis
"Slow viral disease''
Relative
1DDM/NIDDM
History of long-term IV drug abuse; alcohol abuse
Member 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 dermatoses
Generalized 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 4C, 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 layers

The 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.