Download Lacerations Epidermis The epidermis is the outer layer of skin. The

Lacerations
Epidermis
The epidermis is the outer layer of skin. The thickness of the epidermis varies in different types of
skin. It is the thinnest on the eyelids at .05 mm and the thickest on the palms and soles at 1.5 mm.
The epidermis contains 5 layers. From bottom to top the layers are named:
stratum basale (Bottom layer is formed of column shaped cells, in this layer cells divide and
push already formed cellsinto higher layers)

stratum spinosum
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stratum granulosum
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stratum licidum
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stratum corneum (Top layer is made of dead cells and shed every 2 weeks)
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Specialized Epidermal Cells
There are three types of specialized cells in the epidermis.
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The melanocyte produces pigment (melanin)
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The Langerhans' cell is the frontline defense of the immune system in the skin
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The Merkel's cell's function is not clearly known
Dermis
The dermis also varies in thickness depending on the location of the skin. It is .3 mm on the eyelid
and 3.0 mm on the back. The dermis is composed of three types of tissue that are present
throughout - not in layers. The types of tissue are:

collagen
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elastic tissue
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reticular fibers
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The two layers of the dermis are the papillary and reticular layers.
The upper, papillary layer, contains a thin arrangement of collagen fibres.

The lower, reticular layer, is thicker and made of thick collagen fibres that are arranged
parallel to the surface of the skin.
Specialized Dermal Cells
The dermis contains many specialized cells and structures.

The hair follicles are situated here with the erector pili muscle that attaches to each follicle.
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Sebaceous (oil) glands and apocrine (scent) glands are associated with the follicle.
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This layer also contains eccrine (sweat) glands, but they are not associated with hair follicles.
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Blood vessels and nerves course through this layer. The nerves transmit sensations of pain,
itch, and temperature.
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There are also specialized nerve cells called Meissner's and Vater-Pacini corpuscles that
transmit the sensations of touch and pressure.
Subcutaneous Tissue
The subcutaneous tissue is a layer of fat and connective tissue that houses larger blood vessels and
nerves. This layer is important is the regulation of temperature of the skin itself and the body.
History
Where and when the injury occurred?
Mechanism of injury – Is there possibility of an underlying injury, retained FB, or bite?
Size and location of the wound
Sensory function and vascular integrity
Tetanus status?
Contributory past medical history: allergies, bleeding diathesis, medications, etc
Objectives
Restore function
Produce optimum cosmesis
Avoid infection
Haemostasis
Improve healing time
If possible have a painless wound repair
C. ED Assessment
Examine wound adequately – You must see the bottom of the wound.
Most times anesthesia is required before adequate inspection can occur; achieve hemostasis with
direct pressure, and or, vasoconstrictors.
Decide how you the wound should be closed or whether you will close it at all if the wound is dirty,
contaminated, or may have a retained foreign body decide to how you will approach the laceration.
You may need to obtain radiographs (to rule out fractures or foreign bodies), or other studies.
Ideal closure of a wound is within 12-18 hrs (some wounds have been closed at 24-72 hrs. after they
have occurred). If the location or type of injury has a low risk of infection, it may be closed later than
if it is an area that has a high risk. Areas that are important cosmetically may be closed later if there
is a low risk of infection. Generally, after 24 hours wounds should not be sutured. The extremities
probably should not be sutured if over 16 hours because of the high infection rates
Wound Management
Initial
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
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
management
Apply pressure to control bleeding.
Irrigate the wound thoroughly with normal saline to remove dirt and bacteria.
Consider need for tetanus immunisation and human tetanus immunoglobulin.
Consider the risk of rabies in anyone who has sustained a bite or scratch from a dog or cat
whilst abroad.

Consider referral to accident and emergency or plastic surgery.
Wound closure

Primary closure with sutures is not generally recommended for non-facial bite wounds,
especially deep punctures, bites to the hand, and clinically infected wounds or steristrips to
prevent scarring and improve cosmetic outcome.
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Delayed primary closure (after 3-5 days) is advisable for bites to the hand, bites with
extensive crush injury, wounds needing a considerable amount of debridement, and wounds
more than 6 hours old.

Cover with a sterile, non-adhesive dressing to protect the wound.
Antibiotic prophylaxis
o
Facial injuries; puncture wounds (particularly likely with cat bites); wounds
requiring surgical debridement; wounds involving joints, tendons, ligaments, or
suspected fractures.
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Wounds that have undergone primary closure.
o
People who are at risk of serious wound infection complications, e.g. those who are
diabetic, cirrhotic, asplenic, or immunosuppressed.
o
People with a prosthetic valve or who have suffered a bite proximal to prosthetic
joints.
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The choice of antibiotic is the same as for treatment of established infection.
Treatment of established infection
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Most infections resulting from bites are polymicrobial, often including anaerobes.
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Infected dog bites often contain multiple species of bacteria, including Pasteurella
canis,Pasteurella multocida, Staphylococcus aureus, other staphylococci, streptococci, and
anaerobic bacteria.
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Co-amoxiclav is recommended as first-line treatment for mild to moderate infections
following a dog, cat, or human bite.6
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If the person is allergic to penicillin, first-line treatment is doxycycline plus metronidazole.6
Hepatitis B, Hepatitis C, and HIV
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Blood-borne viruses are potentially transmissible by a human bite if the skin is broken.
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There are some cases reported where hepatitis C has been transmitted through bites.
Although there is no prophylaxis available, serological testing and follow up should be
arranged. If there is any suggestion of risk, hepatitis B immunoglobulin and hepatitis B
vaccine, and/or the use of antiretroviral drugs following exposure to HIV infection.
Anesthesia
Topicals – LET(Lidocaine, Epinephrine, Tetracaine) Topicals are most effective when used in smaller
lacerations(<7cm) on highly vascularised areas like the scalp and face. They have been shown to be
as effective on the face and scalp as infiltration with lidocaine.
Coagulation is a complex process by which blood forms clots. It is an important part
of haemostasis, wherein a damaged blood vessel wall is covered by a platelet and fibrin-containing
clot to stop bleeding and begin repair of the damaged vessel.
Platelet activation
Damage to blood vessel walls exposes subendothelium proteins, most notably von Willebrand
factor (vWF), present under the endothelium. Underlying vWF is exposed to white blood cells and
recruits Factor VIII, collagen, and other clotting factors. Circulating platelets bind to collagen with
surface collagen-specific glycoprotein Ia/IIa receptors. Additional circulating proteins vWF link
platelets glycoprotein Ib/IX/V and the collagen fibrils and adhesions activate the platelets.
Activated platelets release granules containing ADP, serotonin, platelet-activating
factor (PAF), vWF, platelet factor 4, and thromboxane A2 (TXA2), which, in turn, activate additional
platelets.A Gq-linked protein receptor cascade is activated, resulting in increased calcium
concentration in the platelets' cytosol which encourages the release of many molecule that increase
the fibrinogen binding affinity.
The coagulation cascade
There are 2 pathways that lead to fibrin formation; the contact activation pathway (intrinsic and
primary pathway), and the tissue factor pathway (extrinsic pathway). The pathways are a series of
reactions, in which a zymogen (inactive enzyme precursor) of a serine protease and
its glycoprotein co-factor are activated to become active components that then catalyze the next
reaction in the cascade, ultimately resulting in cross-linked fibrin.
The coagulation factors are generally serine proteases (enzymes). There are some exceptions. For
example, FVIII and FV are glycoproteins, and Factor XIII is atransglutaminase. Serine proteases act
by cleaving other proteins at specific sites. The coagulation factors circulate as inactive zymogens.
The coagulation cascade is classically divided into three pathways. The tissue factor and contact
activation pathways both activate the "final common pathway" of factor X, thrombin and fibrin.
Cofactors
Calcium and phospholipid (a platelet membrane constituent) are required for the tenase and
prothrombinase complexes to function.
Vitamin K is an essential factor that adds glutamic acid residues on factors II, VII, IX and X and is
pharmacologically important as a target for anticoagulant drugs such as warfarin by inhibiting
maturation of clotting factors.
Regulators
There are 5 regulatory mechanisms, abnormalities can lead to an increased tendency toward
thrombosis, Protein C, Antithrombin,Tissue factor pathway inhibitor, Plasmin and Prostacyclin.
Antisepsis
Prevention of infection by inhibiting or arresting the growth and multiplication of germs (infectious agents).
Antisepsis implies scrupulously clean and free of all living microorganisms.
For practical help on wound management and healing. Visit:
http://famona.tripod.com/ent/cummings/cumm022.pdf
Bacteriology of Infected Wounds
Wound contamination: the presence of non-replicating organisms in the wound.
Wound colonization: the presence of replicating microorganisms adherent to the wound in the
absence of injury to the host.
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Most of these organisms are normal skin flora such as Staphylococcus epidermidis, other
coagulase negative Staph., Corynebacterium sp., Brevibacterium sp., Proprionibacterium
acnes, Pityrosporum sp..
Wound Infection: the presence of replicating microorganisms within a wound that cause host injury.

Primarily pathogens are of concern here. Examples include; Staphylococcus aureus, Betahemolytic Streptococcus (S. pyogenes, S. agalactiae), E. coli, Proteus, Klebsiella, anaerobes,
Pseudomonas, Acinetobacter, Stenotrophomonas (Xanthomonas).
The microbial flora in wounds appear to change over time.
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Early acute wound; Normal skin flora predominate. E.g. S. aureus, and Beta-hemolytic
Streptococcus soon follow. (Group B Streptococcus and S. aureus are common organisms
found in diabetic foot ulcers)
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After about 4 weeks
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Facultative anaerobic gram negative rods will colonize the wound.
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Most common ones= Proteus, E. coli, and Klebsiella.
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As the wound deteriorates deeper structures are affected. Anaerobes become more
common. Oftentimes infections are polymicrobial (4-5).
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Long-term chronic wounds oftentimes contain more anaerobes than aerobes.Aerobic gramnegative rods also infect wounds late in the course of chronic wound degeneration. Usually
acquired from exogenous sources; bath and foot water. Ex. Pseudomonas, Acinetobacter,
Stenotrophomonas (Xanthomonas).
Organisms like Pseudomonas are not very invasive unless the patient is highly compromised (ex.
Erythema gangrenosum in neutropenic patients). These organisms are associated with marked
wound deterioration due to endotoxin, enzymes, and exotoxins. As the wounds go deeper and
become more complex they can infect the underlying muscles and bone causing osteomyelitis.
Coliforms and anaerobes are associated with osteomyelitis in these patients. You also see
Staphylococcus aureus.
Wound depth can result in different
diseases:
In summary: early chronic wounds contain mostly gram-positive organisms. Wounds of several
months duration with deep structure involvement will have on average 4-5 microbial pathogens,
including anaerobes (see more gram-negative organisms).
Tetanus
Tetanus is a serious, acute (severe but short-lived) condition that is caused by infection with a
bacterium known as Clostridium tetani. Clostridium tetani bacterium is commonly found in the
environment, often in soil, dust and manure.
The incubation period for a tetanus infection (the time between getting the infection and the onset
of symptoms) is 4 to 21 days. The average incubation time is 10 days.
The tetanus bacteria usually enter the body through a wound or cut in the skin, they multiply and
release a neurotoxin called tetanospasmin. It can spread through the bloodstream, blocking the
nerve signals from the spinal cord to the muscle causing muscle spasms and rigidity throughout the
body, particularly in the neck, face and jaw (lockjaw).Tetanus is a notifiable condition. Tetanus
vaccination is in the National Immunisation schedule at 2,3,4 months, then at pre-school age (3 ½ - 5
years) and 13 – 18 years.
Necrotising fasciitis
Necrotising fasciitis is an insidiously advancing soft tissue infection characterised by widespread
fascial necrosis. Most often associated with S. pyogenes (group A beta-haemolytic streptococci)
infection but most infections are polymicrobial, with both anaerobic and aerobic bacteria frequently
present. Organisms spread from the subcutaneous tissue along the superficial and deep fascial
planes.
Clinical Presentation
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Patients may present with skin vesicles, bullae, oedema, crepitus, erythema, and fever.7
Differential diagnosis
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Cellulitis
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Erysipelas
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Erythema induratum
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Pyoderma gangrenosum
Investigations
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Blood tests: leucocytosis, acidosis, altered coagulation profile, hypoalbuminaemia, abnormal
renal function.3
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X-ray: soft tissue gas.
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MRI or CT delineation of the extent of infection may be useful in directing rapid surgical
debridement.
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Excisional deep skin biopsy
Management
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The primary treatment is early and aggressive debridement of involved skin, subcutaneous
fat and fascia.
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The role of hyperbaric oxygen is controversial but has been shown to improve survival and
limb salvage.
Drugs
 Intravenous immunoglobulin may be a useful adjunct in severe streptococcal infections.
 Combination therapy with 2 or 3 antibiotics. Ampicillin and gentamicin are useful for aerobic
infection (usually gram-negative organisms). Clindamycin or metronidazole have been
used against anaerobes. Clindamycin with a beta-lactam antibiotic has been used against
group A streptococcal infections.