Thursday, June 29, 2017

91 to 19 at ..91 to 19? Inversión de la edad ? anything is possible these days

Por favor, compruebe si tiene osteoporosis
¿Cómo puede un 91- 19 huir de los hombres jóvenes?
Puede tener problemas óseos

Please check if you have osteoporosis
How can a 91- 19 flee from young men?
You may have bone problems :-)

91 to 19? Inversión de la edad ??... cuidado de la piel, acné y pigmento Skin Care, Acne & Pigment

91 a 19? Gloria Vanderbilt
Entremos en la máquina del tiempo
Imagina que no hay edad,
Ante nosotros sólo jóvenes
91 to 19? Gloria Vanderbilt
Let's enter the time machine
Imagine that there is no age,
Before us only young people☺️

Wednesday, June 28, 2017

Thanks to all of you in the USA who participated in our new Cyber Online Aesthetic Consults

Always one INNOVATION ahead..that is what drives us at

As pioneers in this field of  cyber aesthetic consults with a Board Certified specialist in Aesthetic Med Miami , we are glad to serve you guys! There are lots of satisfied clients. Some of you prefer our cyber clients even as you buy our products. Some prefer consults alone. 
You can now " buy" our $20 consults online at  This does not include our products.
Satisfied clients have consulted with us and bought the products for $ 80-120 each time and continue to use our brand of skincare.
Just click on the link below and after you pay by paypal or your card, please e mail and mail a clear picture of your face in good lighting. The global consultant will do an assessment and suggest the best treatment option.Thanks again.
Bona Lotha
Board Certified
American Academy of Aesthetic Medicine (Miami)

Thanks to all of you in the USA who participated in our new cyber online aesthetic consults .It is a pleasure to answer your queries and suggest the best treatment options for  your facial skin type. Thanks for using smilemakernyc skin care products. We appreciate your questions and your business.
We will continue to add new and innovative products over the years.

whatsapp aesthetic medicine consultations for US clients
a. Those who want to purchase our skincare products and need a free whatsapp consultation please contact Namgyal Dorjee at his mobile 917-698-0069
b. send a clear frontal image of your face so that our Miami Aesthetic Medicine Board Certified cyber consultant can suggest a treatment option. The Aesthetic Medicine Board is run by world leaders in Beverly Hills CA and Ranchos Palos Verdes CA.

You can learn more about our global surgery/plastic surgery/aesthetic medicine specialist at his blogsite: 
(trained in N Delhi,Singapore,Taipei,USA) (over 1.2 million views across the US and elsewhere)

This offer is valid only in the USA and Nagaland, India/other India for now. The consultation is free ONLY for those who buy the products.
c. Others can get a cyber consultation by e mailing and making a paypal payment of $20 to for a face rejuvenation and treatment consultation and advice on treatment options
Several of you in the USA ,Nagaland India/other India have bought our skincare products in the last few years and have seen the benefits for your skin. We are glad to serve you better in future.

Sunday, June 25, 2017

Your sun reactive skin type this summer

Also known as the Fitzpatrick skin types 1 to 6

Types 3-4 are prone to post inflammatory hyperpigmentation and melesma (fair Asians) wheras darker types have more problems with melesma and post infammatory hyperpigmentation. Skin conditioning is needed to prevent complications before lasers and  deeper peels.

1.white,always burns ,never tans
2 white, usually burns,tans with difficulty
3 white, sometimes mild burn,tan average 
4 moderate brown-rarely burn,tan with 
5 dark brown, very rarely burn,tan very
6 black, no burn,always tans

Perforator based V-Y advancement flap-lesson

Plastic Surgery Topic Discussion

Perforator based V-Y advancement flaps for lower limb defects 
 How to do it sessions

Fasciocutaneous flaps were first described in 1981 by Ponten,but improvements were made in the 90s by various surgeons ;the V-Y flap was known as early as 1848(Blasius)
The improved flaps are based on perforator and fascial feeder vessels and cutaneous nerves
Main advantage over the traditional skin graft :primary closure of defect with intact sensation,better cosmetic result and early mobilisation of the patient

Anatomical concepts
3 main arteries of the leg,posterior tibial,anterior tibial and peroneal artery give out several perforators which pierce the deep fascia to enter the suprafascial plane
The flaps are based on direct perforators from the main vessels,perforators from the muscle and upon fascial feeder vessels

The V-Y flap

Flap planned around perforator vessels
Perforator vessels identified by a hand –held Doppler probe
Cutaneous nerve supply identified and preserved

Summary of operative technique
1.location of perforators by Doppler
2. explore one margin to locate perforators
3.after locating suitable perforators,free them for some distance from the fascia and muscle to get extra length
4.insert the flap and leave a drain for 24 hrs
Post op bed rest with leg elevation for 48hrs;discharge pt on the 5th day

Suggested reading

1. A Hayashi, Step ladder V-Y advancement flap for postero planter heel ulcer:BJPS,1997,50:657-661
2. V.Venkat,D Mohan Perforator based V-Y adv flaps in the leg: :BJPS,1998,51,431-435
3. NS Niranjan, Price Fascial feeder and perforator based V-Y flaps in lower limb defects: BJPS 2000:53-679-689
4. GA Georgeu,The horn shaped f-c flap in cutaneopus malignancy of the leg:BJPS 2004,57,66-76

Thursday, June 22, 2017

Considerations in global surgery outreach: Burns Trauma management in conflict zones

this is a presentation on management of burns patients and how to avoid complications by early intervention: very useful for  trauma,accident and emergency centres in conflict zones where I worked for over 17 years

Plastic Surgery Topic Discussion
Advances in the treatment of Burns 2006

1. Pathophysiology
Thermal injury coagulation necrosis of skin and subcutaneous tissues.
Tissues around the area of coagulation moderate degree of vascular injury that causes a decrease in tissue perfusion.
The zone of stasis can progress to a partial or full thickness injury due to the release of local mediators such as arachidonic acid, oxidants, and cytokines produced by the burn wound.
arteriolar and venous dilatation followed by platelet aggregation which causes vascular stasis.
Thromboxane A2 (TX A 2) is found in high concentrations in burn wounds and is thought to contribute to the decreased blood flow in the zone of stasis. TXA2 increases platelet aggregation and neutrophil migration in the wound microcirculation.
Cytokines found in burn injuries are tumor necrosis factor, interleukin 1,2,4,6,8,12 and interferon gamma.
Tumor necrosis factor is involved in neutrophil sequestration.Neutrophils are the central mediators of the micro vascular injury responsible for the extension of burn injury in the zone of stasis.
Cytokines also activate other classes of inflammatory mediators potentiating their actions.
Burn wound colonization and gut bacterial translocation produce circulatory endotoxin that is a potent activator of primed macrophages and neutrophils that release large amounts of antioxidants,arachidonic acid metabolites and proteases, causing further local and systemic inflammation and tissue damage.

TABLE : Burn depth categories
First (superficial) Flash flame, ultraviolet (sunburn) Dry, no blisters, no or minimal edema Erythematous Painful
Second (partial thickness) Contact with hot liquids or solids, flash flame to clothing, direct flame, chemical, ultraviolet Moist blebs, blisters Mottled white to pink, cherry red Very painful
Third (full thickness) Contact with hot liquids or solids, flame, chemical, electrical Dry with leathery eschar until debridement; charred vessels visible under eschar Mixed white, waxy, pearly; dark, khaki, mahogany; charred Little or no pain; hair pulls out easily
Fourth (involves underlying structure) Prolonged contact with flame, electrical Same as with third degree, possibly with exposed bone, muscle, or tendon

2. Lund and Browder chart
The classic “Rule of Nines” has been shown to be potentially quite inaccurate in establishing the extent of burn injury.
The Lund and Browder chart is easy to use, corrected for age, and more accurate, and it provides a permanent medical record of the initial injury. (Fig. )
On initial evaluation, estimation of the burn depth is of less significance than its extent. Only partial and full thickness burn (not superficial or first degree burn) should be included in quantitating the extent of burns.

3. Patient Management
Initial intravenous access should be established to handle fluid resuscitation requirements (up to two liters per hour). Intravenous access can be performed through burned tissue if necessary for adequate volume delivery.
 A Foley catheter should be inserted and urine output should be measured hourly. Intravenous fluid (lactated Ringer’s) adjusted to maintain a urine output of 30 to 50 cc’s per hour in an adult and 0.5–1 cc/kg/hr in a child.
Burns of over 20% to 25% TBSA are associated with a paralytic ileus. A nasogastric tube should be inserted and placed to suction to maintain gastric decompression.
Analgesics and sedatives can be given as needed, but should be given intravenously only: intramuscular absorption is erratic. Small doses should be used, titrated to clinical response. The tetanus immunization status of the burned patient should be determined and brought up to date. The patient must be kept warm during transfer using warm intravenous fluids, warm gases if the patient is intubated, and adequate coverings.
 No topical agents should be applied. The burn wounds should be covered with a clean dressing sheet. Hypothermia is a frequent and often serious problem in these patients. The patient’s core temperature should be monitored continually.

Goal of Fluid Resuscitation
Support the patient through the initial 24-48 hr of hypovolemia due to the sequestration of fluid resulting from the burn injury.
The most commonly used and easily available crystalloid for resuscitation is lactated Ringers.
lactated Ringers solution 4 ml/kg/% burn. One half of the calculated fluid requirement is given in the first 8 hrs and the remaining half given over the next 16 hours. This is the cheapest and most cost effective formula and many hospitals can easily afford the cost.
Fluid replacement and adequacy of resuscitation must be closely monitored:
a urine output of 0.5 to 1 ml/kg/hr is a good indicator of vital organ perfusion ( severely burned patients need cardio respiratory monitoring)
Protein should be started at 8–12 hours after injury using crystalloid or nonprotein colloid in the first 8 hours. The most massive fluid shifts occur in that period.
Heat-fixed proteins .Albumin is the most oncotically active of the protein solutions and is associated with no disease transmission. Fresh-frozen plasma contains the entire osmotic load of the plasma in addition to all the clotting factors normally present- concern about disease transmission has made this a less attractive choice.
Te precise amount of protein needed is not defined- requirements are greater in patients with >50% burns, older patients, and patients with significant inhalation injuries. In these situations, protein has been shown to decrease edema and to increase hemodynamic stability
maintains blood volume better than crystalloid alone.

TABLE . Thermal injury fluid resuscitation (modified Parkland formula)
 Day 1:(hour 0-24)
Lactated Ringer’s Solution
Total volume for 24 hr = 4cc/Kg/%burn
Give 1/2 of total volume in 1st 8hr
Give 1/2 of total volume in 2nd 16hrAdjust infusion rate as necessary to keep urine output:Adults: 30-50 cc/hr Children: 1.0 cc/Kg/Hr
Day 2: Hours 25-48
Change lactated Ringer’s to D5W and adjust based on urine output as above.
Begin colloid infusion: 5% Albumin at
0.3-1.0 cc/Kg/% burn /16 =cc 5% albumin/hr. Do not vary based on urine output.
Day 3: (hours 49+)
Change to maintenance IV or begin po intake and/or enteral feedings.
For patients with burns >40% to 50% or in the presence of significant inhalation injury or previously existing cardiorespiratory disease, consider beginning colloid earlier (hour 8-24) and continuing through day 2.

Inhalation injury
 responsible for more deaths than surface burns. 20-80% of burn mortality now results from pulmonary pathology. Confirmed inhalation injury may increase mortality by 30% to 40%.
Carbon monoxide - odorless, tasteless gas impairs tissue oxygenation by preferentially binding to hemoglobin and displacing oxygen from the hemoglobin molecule. affinity for hemoglobin is 210 times that of oxygen;it enters the cell’s cytochrome system and impairs oxygen utilization.
 Direct thermal injury to the lower airway is uncommon because of the great heat-dissipating capacity of the oro- and hypopharynx. The increase in airway, peaks at 18–24 hours postburn and resolves over 4–5 days.
most common and significant component of inhalation injury is the inhalation of products of combustion-Aldehydes, ketones, and organic acids . All cause significant chemical injury to the respiratory tract.
Mucosal ciliary function may be markedly and almost instantaneously depressed, causing marked impairment of secretion clearance.
The chemical injury is most significant in the lower respiratory tract. Severe cases may develop increased capillary permeability and alveolar cell injury that then leads to pulmonary edema and adult respiratory distress syndrome. This carries a mortality of 60% to 70%. With severe damage to the airways and sloughing of the bronchial mucosa, plugging and secondary infection begin to supervene at 72 hours postburn
Diagnosis begins with clinical suspicion. A flame burn occurring in a closed space , singed nasal hairs, facial or oropharyngeal burns, and expectoration of carbonaceous sputum are occasionally seen. Signs of upper respiratory obstruction—such as crowing, stridor, or air hunger—usually signify a significant injury to the hypopharynx/larynx and mandate immediate intubation.
 All patients suspected of having inhalation injury should have arterial blood gases drawn, including determination of CHgb level. CHgb levels >10% are probably significant; levels >50% are associated with death.100%oxygen will decrease the washout time of the carbon monoxide from 250 minutes to 40–50 minutes.
The mainstay of diagnosing inhalation injury to the oropharynx, hypopharynx, larynx, and upper airway is fiberoptic bronchoscopy. Significant findings in the hypopharynx and larynx include vocal cord edema and charring, sloughing, or edema of the hypopharyngeal and upper tracheal mucosa.

Management of inhalation injury
The treatment is supportive only. The primary goal is airway maintenance. An easy intubation at the initial evaluation in the emergency room may become later an impossible situation, with resuscitation fluid and airway edema necessitating emergent tracheostomy. Liberal endotracheal intubation is recommended in the setting of inhalation injury or its suspicion.
 If carbon monoxide poisoning is present, 100% oxygen is given. For the other two components of inhalation injury, treatment is ventilatory support until the mucosal barrier reforms (generally in 7–14 days).
 corticosteroids in inhalation injury :well-controlled, prospective series indicate that these are, in fact, deleterious to survival. Their use is contraindicated.
Meticulous pulmonary toilet is helpful to clear inspissated secretions and soft mucosal plugs. Repeat bronchoscopy, either fiberoptic or rigid, may be necessary to clear the airways. Adequate ventilatory support, with the use of positive end-respiratory pressure (PEEP), if necessary, is mandatory to keep systemic oxygenation in the normal range.
Resuscitation volumes should be carefully controlled. The presence of an inhalation injury, in cardio repsiratory problem pts Swan-Ganz catheterization and invasive monitoring.
no clear evidence that a carefully monitored crystalloid resuscitation is any more detrimental to pulmonary function in the presence of inhalation injury than the combination of crystalloid and colloid.
Documented infections should be aggressively treated with appropriate antibiotics. Empiric therapy early in the patient’s course (3–10 days post-burn) should cover Staphylococcus aureus and gram negative organisms.

Hubbard tank
Classical burn wound care has been performed in a Hubbard tank or some other immersion facility(bath tub). This creates for the patient, a warm, pleasant, antigravity environment, where range of motion can be performed comfortably by physical and occupational therapists. Concern regarding potential cross-contamination has led many burn centers to shower patients on a cart rather than immerse them, especially patients with large, deep burn wounds. This procedure is somewhat more uncomfortable for the patient and must be done more quickly. There is a greater tendency towards hypothermia, even with a high ambient
temperature in the tub room. There are advantages, however, in terms of infection control. Even intubated patients can be debrided and cleansed very adequately in this fashion.
H-2 receptor blockers
Gastrointestinal bleeding was formerly a common complication in burned patients, but it is virtually nonexistent today. Gastric and duodenal mucosal lesions have been shown to occur within 48 hours post injury, and previously led to hemorrhage, ulceration, perforation, and death. The use of effective antacid prophylaxis has solved this problem. In many cases, prophylactic use of a histamine H-2 receptor blocker may make the administration of antacids less important.

Topical antibiotics are present in greatest concentration on the wound surface, where the risk of exogenous contamination is the greatest.
Deep wounds become rapidly colonized in 24 hours by gram positive cocci, and in 3–7 days by gram negative aerobes. Surface colonization will eventually lead (in the untreated wound) to deeper invasion of healthy tissue. It is therefore logical to institute topical antibiotic therapy as soon as possible. Upon their introduction the topical antibiotics immediately decreased burn patient mortality by 50%, when applied effectively.
Silver sulfadiazine: the most frequently used topical agent. It was introduced in the early 1970s . It is supplied in a water-soluble base at a concentration of 1%. This concentration is sufficient to inhibit growth of most sensitive microorganisms in vitro; applied every 12–24 hours and can be used with or without dressings. It is active in vitro against a number of gram positive and gram negative bacteriae. It can form a thin pseudoeschar over the wound 2–3 days after its application. This can confuse the inexperienced examiner attempting to determine wound depth. The pseudoeschar can generally be removed from the wound with gentle debridement. . Leukopenia is not infrequently seen after 2–3 days of treatment with this agent.
Silver Nitrate (0.5% Solution): Silver nitrate solution is not toxic in a 0.5% concentration, but it has a significant antimicrobial effect. It was introduced in 1965 . a broad-spectrum agent; Because of its minimal absorption; markedly hypotonic; leaking of sodium, potassium, from the burn wound- monitoring of serum electrolytes is mandatory. gram-positive and especially gram-negative organisms can reduce the nitrate from this compound to nitrite. Absorption of this nitrite can rarely lead to methemoglobinemia, and occasionally it may necessitate treatment with intravenous methylene blue or other reducing agents. Silver nitrate solution must be used by soaking bulky wet dressings. These must be kept wet every two hours to keep the concentration of the agent at <2%, which is caustic and cytotoxic.
Mafenide. applied every 12 hours; a broad antibacterial spectrum; It has the best eschar penetration , and it also efficiently penetrates cartilage. This makes it an excellent choice for use on burned ears and noses; strong carbonic anhydrase inhibitor and its use results in an alkaline diuresis; acid-base abnormalities when used on >20% of the body surface area. The polyuria induced by the agent can lead to a hyperchloremic metabolic acidosis, which, if then compensated for by hyperventilation, may eventually lead to pulmonary failure.

Bacterial Toxicosis (Toxic Shock Syndrome)
Younger children are predisposed to this disease due to initial low levels of antibodies to Staph Aureus .Occlusive dressings may act as favourable culture media for Staph aureus.When a child with thermal injury suddenly becomes unwell,this condition should be suspected on the fol criteria:
1.fever ( > 102 degree F)
2.diffuse macular erythroderma(rash)
3.desquamation of soles and palms 1-2 weeks after onset of illness
4.hypotension (<90mmHg in adults/orthostatic syncope/< 5th percentile by age for children<16yrs of age)
5.involvement of three or more of the fol organ systems:
 vomiting/diarrhea
b.severe myalgia
c.hyperaemia of mucous membranes (orophayngeal/conjunctiva)
d.renal-blood urea nitrogen > 2 times upper limit of normal, >5 white blood cells per hign power field in the absence of UTI
e.hepatic-Total bil,OT/PT>2 times normal)
f.platelets>100,000 cub. Mm
g. CNS-disorientation alteration in consciousness
Treatment is aggressive and performed in an ICU and includes circulatory support, ventilatory support, appropriate antimicrobial therapy(usually flucloxacillin) iv to stop further staph aur. toxin production.

Pain Control
Morphine, given frequently in small intravenous doses titrated to the clinical response of the patient, is an ideal method of pain control in the acute resuscitation period.
Methadone given on a q 8 hr (not prn) basis in doses of 5–10 mg for adults is excellent for most patients when used to treat chronic pain. Supplementation is generally needed for dressing changes, debridement, and some therapy manipulations, but the patients generally remain awake and alert. Methadone takes two to three days to establish a constant blood level with this regimen. Dependency on this drug does develop; it should be gradually tapered and discontinued 7–10 days prior to discharge. In the presence of severe pain even with Methadone, often the addition of an antianxiety agent (e.g., one of the benzodiazepenes) may be of help.

Support of the hyper metabolic response to burn trauma
Severe burns can drive the metabolic rate to twice normal. The body temperature remains elevated for upto two months regardless of the timing of wound closure because of the direct stimulation of the hypothalamus by inflammatory mediators and cytokines.
In large burn injuries cortisol, glucagons and cathecholamines are all markedly elevated.
Cortisol is strongly catabolic and is associated with negative nitrogen and calcium balance and loss of tissue protein and bone mineral. It also stimulates gluconeogenesis, increases proteolysis and sensitizes adipocytes to the action of lipolytic hormones.
Cathecholamines increase the rate of glyconeolysis, hepatic gluconeogenesis, promotes lipolysis and peripheral insulin resistance.
The hyperglycemia is a result of serum glucagons levels that are increased disproportionately to serum insulin levels.
 The elevated levels of glucagons see following burn injury are critical for maintaining an adequate rate of glucose production to meet the patient’s energy requirements, particularly for accelerated wound healing.
Glucose is an important energy source in burn patients. When glucose cannot be adequately supplied, the result is excessive protein catabolism.
Burn patients have difficulty metabolizing glucose when the infusion rate exceeds 4mg/kg/min.
High concentrations of free amino acids result from a significant increase in muscle protein catabolism in severe burn injury. There is an increase in amino acid and protein recycling to allow for the synthesis of collagen for wound healing and of antibodies for resisting infection.
Administration of recombinant growth hormone at the rate of 2mg/kg/day to massively burned children has been shown to accelerate skin graft donor site wound healing, allowing wounds to be closed earlier. Recombinant growth hormone is a potent anabolic agent and has been shown to improve nitrogen balance and increase muscle mass in hyper catabolic burn patients.
Growth hormone improves protein synthesis in muscle as well as improving wound healing in the treatment of severely burned patients.
Post burn hyper metabolism is also characterized by an increase in heart rate and oxygen consumption. Burn patients have high levels of cathecholamines and propanolol (0.5mg/kg/day) in a child with 60% burns will cause only a 20% decrease in heart rate.

Patients with severe burns (>40%) have metabolic rates that are 100-150 % above their basal rate.
These patients have increased energy and protein requirements that must be satisfied in order to prevent impaired wound healing, cellular dysfunction and decreased resistance to infection.
Role of early enteral feeding:
Early enteral feedings within the first 24 hour post burn have been shown to decrease the production of catabolic hormones, improve nitrogen balance, maintain gut mucosal integrity and lower the incidence of diarrhea.
Total parenteral nutrition is limited to supporting patients with severe gastrointestinal dysfunction because it is associated with metabolic and immunological complications.
The exact nutrient requirements of burn patients are not clear but it is accepted that maintenance of energy requirements and replacement of large protein losses are vital.
A formula in wide use today is that described by Curreri. It quantitates the adult daily caloric requirements as 25 calories per kilogram plus 40 calories per percent of burn. For children, the formula is 60 calories per kilogram plus 35 calories per percent of burn. This formula appears to be accurate in assessing moderate-sized burns in young healthy patients. However, caloric requirements are overestimated with this formula in large burns or in the elderly.
Vitamins C and A are necessary co-factors for wound healing and should be supplied in at least normal diet amounts.
Enteral tube feeds:
a. 20% of calories as protein (eggs/ soyabean)
b. 30% as fat
c. 50% as carbohydrate
Age 16-59 25kcal/kg + 40 K cal/% burn
Age over 60 20kcal/kg + 65kcal/%burn
0-12mths 2100kcal/m2 +1000kcal/m2 burn
1-11yr 1800kcal/m2 + 1300kcal/m2 burn
12 and above 1500kcal/m2 + 1500 kcal/m2 burn

The Burn Wound
Early excision and wound closure in large burns has been shown to decrease mortality. Once the wound is excised rapid closure is essential. In massive burns over 50% closure is achieved with autograft, allograft, or synthetic wound coverings. Alternatives include the use of boiled potato peels which are cheap and easily available.
Dermagraft which is Biobrane populated with neonatal fibroblasts is one currently available cover.
Dermal replacements like Integra (collagen and chondroitin sulfate with a sialistic cover) and Alloderm (de-epithialized pathogen free cadaver skin) are also used in some centres. The main disadvantages of these newer treatments in poor countries are the high costs, complex dressing requirements and lower rates of take compared to conventional autografts.
Once complete closure of the burn wound is achieved the treatment emphasis shifts from wound management to rehabilitation.
Burn scars are kept moist with emollients to prevent dry scaly regions that are prone to breakdown and infection.
Better control of burn scar can be obtained by applying pressure garments to healed skin grafts as well as deep second degree burns.
The routine use of pressure garments appears to reorient collagen so that scars are smoother, flatter and mature more rapidly.
The post burn depigmented skin can be treated with dermabrasion upto the level of the dermis and the raw surface grafted with a thin skin graft7.
Early splinting in combination with pressure garments also reduces the formation of joint contractures that limit rehabilitation.

Circumferential burns and the leathery eschar they produce can be a life- or limb-threatening problem in the chest and extremities:can cause a decrease in chest wall excursion sufficient to result in respiratory embarrassment;in the limbs,cause compartment syndromes and/or distal ischemia and necrosis. Signs of impending circulatory or respiratory compromise from constricting eschar must be recognized and treated
escharotomies should be performed bilaterally in the anterior axillary lines, using an electrocautery current or scalpel to incise the full length and depth of the eschar. When adequate, obvious release of the underlying soft tissues will be noted. Bleeding may be brisk but can generally be controlled with direct pressure or topical hemostatic agents.
In the extremities, pulses in the fingers and toes can be assessed using a Doppler apparatus. In the absence of this instrument, a large (16-gauge) needle can be used to prick the fingers and toes. Slow or absent bleeding is indicative of diminished or absent arterial inflow. Rapid dark bleeding indicates partial or complete venous occlusion, immediate escharotomies should be performed on the affected extremity; an oxygen saturation of <95 percent also correlates with the need for emergent escharotomy.

Extremity escharotomies
performed in the mid-lateral lines of the affected extremity, taking care in the arm to avoid the ulnar nerve posterior to the medial epicondyle, and in the lower extremity to avoid the common peroneal nerve posterior to the fibular head. It is essential that the escharotomy be extended through the entire length and depth of the eschar. Underlying soft tissue release indicates adequate incision. If the fingers are severely burned, digital escharotomies should be performed along their mid-lateral lines, preferably on the ulnar aspects of the second, third, and fourth digits and the radial aspect of the fifth. This procedure minimizes scars on the primary working surfaces of the fingers.
Escharotomy of the thumb is best performed along the mid-lateral radial aspect. The thenar and hypothenar muscle compartments are often involved in severe hand burn injuries. Eschar and, if necessary, fascia over these compartments should be incised. In deep hand burns, dorsal escharotomies with interosseous compartment fasciotomies should also be performed. Opening the dorsal interosseous fascia in this way will minimize the possibility of late ischemic intrinsic contracture.
In the extremities, eschar should be released until perfusion is restored to the distal parts.
With deep thermal injury to the muscles or electrical injury, escharotomies should be combined with formal fasciotomies in affected muscle compartments. In a severely burned limb, the decision to proceed with a formal fasciotomy is often difficult. However, the consequences of compartment syndrome are much more devastating to the patient’s long-term rehabilitation than unnecessary fasciotomy. Therefore, we recommend liberal indications for fasciotomy in deep extremity thermal burns.

A useful procedure for burn contractures-the running Y-V plasty

Scar contracture is a common burn sequelae which may develop after infection, skin grafts, or secondary intention healing in deep burns.
Scar lengthening can be achieved by the running Y-V plasty design without the need for undermining and transposition of flaps.
the skin lateral to the scar should be lax (pinch bet thumb and finger to test laxity-you should be able to do this easily)
The lateral margin of the scar is marked and the zig –zag line is drawn from one end to another; the angles are about 60-90 degrees
The stem of the Y is marked at the tip of each V flap and is about 1/3rd to ½ the length of the V flaps
After superficial incisions down to the dermis the entire flaps are incised and reconstructed;hemostasis is secured with the bipolar cautery
After removal of the stitches, pressure garments are applied and worn for at least 3 mths.


important to begin rehabilitative efforts as soon as possible after injury.
General rehabilitative goals are to limit or prevent loss of motion, prevent or minimize anatomic deformity, prevent loss of body weight (especially muscle mass), and return the patient to work and activity as early and completely as possible.
 program of rehabilitation as early as possible, preferably on the day of injury: active motion by the patient ; If active movement is not achievable, passive movement frequently as possible. Standing and walking should be performed frequently, unless there is a specific contraindication; proper positioning is absolutely crucial to prevent development of contractures and joint stiffness. Attention should be given to unburned as well as burned areas.
The only therapy of lasting benefit is active movement by the patient. This should be the ultimate goal of all therapeutic interventions.
hand splinting when active motion is not feasible or at night in the protected position is essential to prevent ligament shortening;often quite difficult or impossible to reverse once it has occurred (Fig. ).
Positioning is important :Flexion contractures of the neck may be caused by sleeping supine with a pillow under the head. They can lead to deformities of the lower face and can be reduced by keeping the neck extended during the periods of rest by placing a pillow under the neck.
In the upper extremities, the patient should be encouraged to rest with the shoulders abducted to between 80–90 degrees, the elbows fully extended and the hands and wrists splinted in the protected position.
During sleep, appropriate positioning of the lower extremities is much easier than for the upper extremities. Supine positioning will usually maintain the hips and knees in an extended posture. One area of concern is the position of the feet. - keep the foot and ankle in a neutral position and prevent development of an equinus deformity. Compulsive attention must be given to the fit and use of these splints.
Splinting is also important after skin grafting. can avoid previously common secondary deformities: easier to prevent these than to treat them operatively after they have occurred.

Suggested reading

 1. Advances in burns treatment:JK Rose ,Burns Vol 23sup1,19-27 ‘97
 2. Running Y-V plasty for burn contractures :CS Lai,SD Lin Burns 21:6,458:95
 3. Burns management: Grabb and Smith Pl Surg 5th Edn(Lippincott) 
 4. Toxic shock syndrome in paediatric burn cases: AP Brown, Burns 29(2003) 733-738
 5. Review of burns of the hand and upper limb: M Smith ,Burns (98) 493-505 
 6. Integra in acute burns: AR Fitton, BJPS 2001:54-208-212
 7. CO2 laser dermabrasion/ skin graft for the depigmented burn scar PRS 105:1973,2000

* PRP may play a major role in early burns treatment and wound healing in the near future