Burns are a serious public health problem. A burn is defined as an injury to the skin or other organic tissue primarily caused by heat or due to radiation, radioactivity, electricity, friction or contact with chemicals

1. A COMPARATIVE STUDY ON EFFICACY OF TOPICAL
PHENYTOIN AND SILVER SULPHADIAZINE IN PATIENTS
WITH 20 TO 30% BURNS

2. INTRODUCTION
Burns are a serious public health problem. A burn is defined as an
injury to the skin or other organic tissue primarily caused by heat or
due to radiation, radioactivity, electricity, friction or contact with
chemicals. Heat burns occur when some or all of the different layers of
cells in the skin are destroyed by a hot liquid (scald), a hot solid
(contact burn) or a flame (flame burn). Skin injuries due to ultraviolet
radiation, radioactivity, electricity or chemicals, as well as respiratory
damage resulting from smoke inhalation, are also considered as burns.

3. Pathophysiology of Burn Injury
• The skin, which is the largest organ of the human body, provides a staunch
barrier in the transfer of energy to deeper tissues, thus confining much of
the injury to this layer. Once the inciting focus is removed, however, the
response of local tissues can lead to injury in the deeper layers. The area of
cutaneous or superficial injury has been divided into three zones:
• Zone of coagulation, the necrotic area of burn where cells have been
disrupted. This tissue is irreversibly damaged at the time of injury.
• Zone of stasis, the area immediately surrounding the necrotic zone
has a moderate degree of insult with decreased tissue perfusion.
Depending on the wound environment, can either survive or go on to
coagulative necrosis.
• Zone of hyperaemia, associated with vascular damage and vessel
leakage.

5. Systemic Changes
Severe burns are typically followed by a period of
stress, inflammation, and hypermetabolism,
characterized by a hyperdynamic circulatory response
with increased body temperature, glycolysis,
proteolysis, lipolysis, and futile substrate cycling.

6. Complement causes the degranulation of mast cells which causes accumulation of
neutrophils and their degranulation, with the release of large quantities of free radicals and
proteases. Mast cells also release primary cytokines such as tumour necrosis factor alpha (TNF-
a). These act as chemotactic agents to inflammatory cells and cause the subsequent release of
many secondary cytokines. These inflammatory factors alter the permeability of blood vessels
such that intravascular fluid escapes. The increase in permeability is such that large protein
molecules can also now escape with ease. The damaged collagen and these extravasated proteins
increase the oncotic pressure within the burned tissue, further increasing the flow of water from
the intravascular to the extravascular space

7. CLASSIFICATION BY DEPTH
• 1. Superficial
• 2.Partial-thickness
• Superficial partial thickness
• Deep partial thickness
• 3. Full-thickness

8. 1.Superficial or epidermal burns involve only the epidermal layer of skin.
They do not blister but are painful, dry, red, and blanch with pressure.
2.(a)
Superficial partial thickness burns characteristically form blisters
within 24 hours between the epidermis and dermis. They are
painful, red, and weeping and blanch with pressure
2.(b)
Deep partial thickness burns damage hair follicles and glandular
tissue. They are painful to pressure only, almost always blister
(easily unroofed), are wet or waxy dry, and have variable mottled
colorization from patchy cheesy white to red . They do not blanch
with pressure

9. Full-thickness
These burns extend through and destroy all layers of the dermis and often injure the
underlying subcutaneous tissue. Burn eschar, the dead and denatured dermis, is usually
intact.
Full-thickness burns are usually anesthetic or hypo-aesthetic. Skin appearance can
vary from waxy white to leathery gray to charred and black. The skin is dry and inelastic
and does not blanch with pressure. Hairs can easily be pulled from hair follicles. Vesicles
and blisters do not develop.
Fourth-degree burns are deep and potentially life-threatening injuries that extend
through the skin into underlying soft tissue and can involve muscle and/or bone.

10. EXTENT OF BURN INJURY
•The head and neck represents 9
percent TBSA
•Each upper limb represents 9
percent TBSA
•Each lower limb represents 18
percent TBSA
•The anterior and posterior trunk
each represent 18 percent TBSA

11. Topical agents in burn wound dressing
• 1. Silver Sulfadiazine is a sulfonamide-based topical agent with antibacterial and
antifungal activity. Silver sulfadiazine may act through a combination of the
activity of silver and sulfadiazine. When this agent interacts with sodium
chloride-containing body fluids, silver ions are released slowly and sustainably
into wounded areas. Ionized silver atoms catalyze the formation of disulfide
bonds leading to protein structural changes and inactivating thiol-containing
enzymes; silver ions may also intercalate DNA thereby interfering with
replication and transcription of bacteria. As a competitive inhibitor of para-
aminobenzoicacid (PABA), sulfadiazine inhibits
bacterial dihydropteroate synthase, thereby resulting in disruption of folic
acid metabolism and ultimately DNA synthesis

12. Silver sulfadiazine cream (SSD 1%) applied and covered with fine mesh gauze is the most
commonly used burn wound dressing . SSD has antimicrobial activity as demonstrated by
decreased colonization of burn wounds. However, there are no well-designed trials to confirm
improved wound healing or a reduced rate of bacterial wound infection. For wounds covering
more than 50 to 60 percent of the total body surface area, SSD does not consistently prevent or
suppress bacterial growth, particularly of gram-negative bacteria.
In addition, there are potential adverse effects
SSD also impedes reepithelialization; as a result, SSD should be stopped when there is
evidence of reepithelialization. SSD and related agents should not be used in women who are
pregnant or breastfeeding or in infants younger than two months old. SSD is also oculotoxic
and should not be used near the eyes.9

13. Topical Phenytoin
• The mechanism by which phenytoin accelerates wound healing is
unknown. Clinical, animal and in vitro studies suggest that phenytoin may
be involved in the healing process by several mechanisms stated below.
• Stimulation of fibroblast by phenytoin causes fibroblast proliferation and
enhancing the formation of granulation tissue. At low phenytoin
concentration and short incubation times (3 hr), phenytoin markedly
enhanced fibroblast cell proliferation.
• Antibacterial effect of topical phenytoin was reported to eliminate
Staphylococcus aureus, Escherichia coli, Klebsiella spp. and Pseudomonas
spp. from wounds within 7-9 days. In a guinea pig model of wound healing,
it was found that phenytoin cleared gram negative organisms from the
wounds more readily than gram-positive bacteria. It is unknown if
phenytoin has intrinsic antibacterial activity, or if the effect of phenytoin on
the bacterial load of wounds may be mediated indirectly by effects on
inflammatory cells and neovascularisation and decreasing wound exudates.

14. Decreasing collagenase activity by reducing collagenase production or secretion or
both not by direct enzyme inhibition, but by decreasing the synthesis centrally via the
pituitary-adrenal axis or by competitive antagonism of the glucocorticoid receptor and
thus promoting deposition of collagen and other connective tissue components.
Analgesic effect and Local pain relief has also been observed with topical phenytoin
therapy, which can be explained by its membrane-stabilizing action; the reduced
inflammatory response may also contribute. Facilitation of nerve regeneration has also been
reported with phenytoin

15. AIMS AND OBJECTIVES
• Objective To assess the efficacy of topical phenytoin dressing
compared to silver sulphadiazine dressing in patients of 20 to 30%
dermal burns.
•

16. Study Method
• A hospital based prospective study in which cases of 20 to 30% burns are taken into
study . The patients are divied into two groups cases and controls. With controls
comprising of 30% of study patients.
•
• Controls: Patients with 20 to 30 % burns who present to hospital and are treated with
silversulfadine 1% ointment daily dressing.
•
• Cases : Patients with 20 to 30 % burns who present to hospital and are treated by
phenytoin dressing. Phenytoin powder will be directly applied to wounds in a thin,
uniform layer and then covered with gauze. If phenytoin powder is unavailable then
phenytoin from tablet diluted with 0.9% normal saline will be used. The dosage of
phenytoin will be calculated as per the surface area of the wound: 0 to 5 cm2—50 mg,
5.1 to 9 cm2—100 mg and 9 to 15 cm2—150 mg.(ie 50mg per 5cm square).
• Both groups of patients shall receive similar antibiotic coverage and iv fluid
management.

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