Wednesday, February 27, 2008

Wounds

Epidemiology of wounds

  • The most frequently involved body locations are the face, scalp, fingers, and hands.
  • ~50% of traumatic lacerations seen in the ED are sustained form blunt objects.
  • Children have different wound epidemiologic characteristics: wounds are more likely to be located on the head which are linear, shorter, less contaminated, and more often caused by blunt trauma, compared with the wounds of adults.

Types of wounds

  1. Contusion:

    • Bump or swelling arising quickly following a blow.
    • The surface of the skin is intact but small blood vessels are damaged →
      bruising that is red at first and turns blue and finally to black.

  2. Haematoma:

    • Severe injury → blood vessels are damaged → escape of blood into tissues.
    • Haematomas can be subcutaneous, in between the deeper tissues, or in the deeper tissues.
    • Pressure can build up if the area is surrounded by fascial tissue → compression of blood vessels in that compartment.
    • Mostly the haematomas get resolved.

  3. Abrasion:

    • Superficial layers of the skin are torn or scoured when the skin gets in contact with a
      rough surface e.g. road.
    • Multiple bleeding points and sensitive nerve endings are exposed. Dust and dirt gets into the tissues.

  4. Degloving injuries:

    • Shearing forces can detach the skin from the underlying structure without damage to them.
    • The skin may be lost completely or may be attached at one end to form a flap.
    • In physiological degloving the skin remains intact but it is separated from the deeper structures
      e.g. when tissues are drawn into the rollers of a machine or under the tyres of a motor vehicle.
    • The affected part is insensitive to painful stimulus, lacks capillary circulation and
      is pale in colour.

  5. Incised wounds:

    • Results from sharp cutting edges of knifes, glass or metal.
    • The wound is near the subcutaneous fat and tissues may pout through.
    • Bleeding will be profuse initially → large risk from haemorrhage.
    • Contamination is relatively uncommon.

  6. Lacerations:

    • Irregular untidy wounds resulting from crushing or tearing forces.
    • The laceration is surrounded by abrasion or contusion. The skin edges of the laceration are irregular may be blue or pale indicating devitalisation.
    • Bleeding may not be heavy, as the blood vessels are not cleanly cut like in incised wounds.
    • Underlying muscles may be damaged.
    • Contamination is heavy and may result in infection.
    • Foreign material may be embedded.

  7. Puncture wounds:

    • Results from stabbing action by a thin long weapon, instrument,
      object or missile/bullet where the depth of the wound is longer than the length
      of the object.
    • Damage to deeper structures and organs is high and contamination leads to infection.
    • A penetrating wound is when the puncture wound has no exit.
    • A perforating wound is a puncture wound with an entry and exit.

  8. Hydraulic injection injuries:

    • Caused by striking of the skin & injection by liquid from hydraulic systems under very high pressure e.g. water, oil or grease.
    • Large volumes may be injected.
    • The entry wound is very small & sometimes difficult to identify.

  9. Bites:

    • Bites can be from animals, humans, insects or reptiles.
    • Infection is one of the major risks due to mixed organisms in the mouth which gets deeply implanted into the deeper tissues.
    • Tetanus is always possible in animal bites.
    • Reptile and insect bites are usually small & punctures on the skin can be easily identified.

Wound & healing pathophysiology

Acute traumatic wounds are caused by shear, compressive, or tensile forces, which vertically separate the epithelium and dermis.
  • Shear forces are produced by sharp objects that cut through the skin. The amount of energy required to cut through the skin with a sharp object is relatively low and directed to a very small area
    → little energy is deposited into the surrounding tissue → minimal cell damage. Typically, the resultant wound has straight edges, little contamination, and heals with a good result.

  • Compressive and tensile forces are produced when a blunt object impacts the skin at right and oblique angles, respectively. In contrast to shear forces, the amount of energy deposited from compressive and tensile injuries is larger
    disruption of the microvasculature. The devitalized tissue creates an anaerobic environment, which impairs the ability of leukocytes to function and supports
    bacterial proliferation. Compressive wounds tend to be stellate or complex, with ragged or shredded edges. Tensile wounds tend to be triangular or produce a flap.

The stages of wound healing are described as: haemostasis, inflammation, epithelialisation, angiogenesis, fibroplasia, contraction, and scar maturation.

  1. Haemostasis is initiated at the time of injury.

    • Tissue and vascular smooth muscle contraction → compression of small bleeding vessels.
    • Activation of platelets and the coagulation cascade → fibrin clot within the lumens of the severed vessels and within the exposed wound.

  2. Inflammation

    • Stimulated by chemotactic factors released by activated platelets and the complement cascade.
    • Neutrophils and macrophages phagocytose dead tissue, foreign material, and bacteria, providing physiologic debridement and preventing infection.
    • Initially attracts neutrophils followed by macrophages.
      • Neutrophils perform this function for the first 72 hr after injury.
      • Macrophages perform this task for up to 30 days after a traumatic wound.

  3. Epithelialisation reaches a peak about 24 hr after the injury as the inflammatory response stimulates cell division in the stratum basal. Epithelial cells migrate across a closed traumatic wound during the first 24 to 48 h, making the wound impervious to water. Eschar and surface debris impede this process.

  4. Angiogenesis is vital to wound repair. New vessel growth is detectable at 72 hr and peaks in 7-10 days, accounting for the often-marked erythema seen at this time. As the
    wound matures vascularity decreases nearly back to baseline at 30 days.

  5. Fibroplasia, with collagen synthesis, reaches a peak by 7 days and essentially replaces the inflammatory mass in the wound by 3 weeks. At the same time of ↑ collagen synthesis, hydrolysis and breakdown of old and damaged collagen is also taking place. At 7-10 days is the vulnerable time when the balance between collagen synthesis and breakdown is most tenuous and unwanted wound separation occurs.

  6. Wound contraction occurs over the next several months. Contraction significantly modifies the cosmetic appearance of treated wounds.

  7. Scar remodeling also occurs over the next several months. Remodeling is such a powerful process that, at the time of suture removal, it is impossible to predict the ultimate appearance of wounds.

Wound management

Triaging wounds

Unless airway and breathing are compromised or there is active bleeding from the wound edge, acute traumatic wounds are evaluated and treated after other life-or limb-threatening conditions have been evaluated and managed.

Haemostasis may be required and is best done by local pressure.

Sometimes, wound repair must be delayed to address other issues. In this case, fresh wounds should be covered by saline-moistened gauze to prevent drying. Encircling clothing, rings, and jewelry should be removed as soon as possible to reduce the potential for damaging
oedema and contamination.

Physical Examination

  • Neurologic function should be assessed by evaluating distal sensory and motor function.

  • Absent distal pulses and capillary refill indicate a vascular injury, but their presence does not exclude one.

  • Tendon function should be performed for each one in isolation, where possible.

  • Underlying and adjacent structures should be carefully inspected.

  • Things specific to particular sites:
    • Areas with excellent vascular supply and a low incidence of infection include the scalp, face, neck, and trunk.
    • Lacerations on the extremities are at increased risk of infection, and those on the feet and hands are at greatest risk.
    • Lacerations on the hands can damage tendons, nerves, and joints important for normal function. Lacerations over joints may penetrate into the joint capsule and are at risk for hypertrophic scar formation. Any laceration over the metacarpophalangeal joint is suspicious for a clenched-fist injury.
    • Lacerations in the perineum have a high likelihood for contamination.

  • Wound characteristics are important to note.
    • Large wounds, both in length and width (gaping), are at increased risk of infection.
    • Wounds with flaps, stellate shape, complex arrangement, avulsed tissue, jagged edges, or deep penetration are at increased risk of infection.
    • Lacerations heal with best results when the long axis of a laceration is
      in the direction of the maximal skin tension.

  • Wounds that usually require consultation:
    • Wounds involving the tarsal plate of the eyelid or lacrimal duct.
    • Wounds involving an open fracture or joint space.
    • Wounds associated with multiple traumas that need surgical admission.
    • Wounds of the face that require extensive plastic reconstruction.
    • Wounds associated with amputation.
    • Wounds associated with loss of function.
    • Wounds that involve tendons, nerves, or vessels.
    • Wounds that involve a significant loss of epidermis.

Types of healing

The three types of clinical wound healing depend on the timing and method by which wound closure is achieved.
  1. Primary closure (healing by primary intention) is performed with sutures, staples, or adhesives at the time of initial evaluation.

  2. Secondary closure (healing by secondary intention) is where the wound is allowed to granulate and fill in with eventual epithelialization with only cleaning and minimal debridement.

  3. Tertiary closure (delayed primary closure) is where the wound is initially cleaned, debrided, and observed for a period of time (typically 4 or 5 days) before closure.

Mode of closure

There are 2 types:
  1. Primary closure - closure of wound by approximation of the wound edges via sutures, staples or skin tape.
  2. Secondary closure - use of non-native tissue (e.g. skin grafts, skin flaps) to achieve closure.

Skin grafts

  • Skin grafting can provide wound cover in large raw areas that cannot be closed by direct closure.
  • Skin grafts can be:
    • Split-thickness skin grafts (STSG) - include two skin layers: the full epidermis and part of the derm.
    • Full-thickness skin grafts (FTSG) - consists of both the epidermis and complete dermis.
  • The advantage of STSG includes less tissue use. That offers a higher percentage rate of graft survival and it minimizes the donor site damage.
  • The one disadvantage, of STSG, is that it tends to contract more than full-thickness skin grafts → poorer cosmetic effect when compared to full-thickness grafts.
  • Skin should not be grafted over bare bone, tendon, cartilage, major vessels or an irradiated area.

Skin flaps

  • Skin flaps are an advanced form of skin grafting.
  • Skin flaps are usually used when the area requiring reconstruction lacks the blood supply needed to support a skin graft. All the tissues that are used to restructure these wounds must carry their own blood supply.
  • In skin flap surgery, skin, along with underlying fat, blood vessels and sometimes muscle, is moved from a healthy part of the body to the injured site.
  • Local or distant flaps are preferred to skin grafting if:
    • the wound bed is not very vascular

    • bare tendons or nerves are exposed

    • the wound is over a bony prominence

    • radiotherapy or repeat surgery is contemplated

    • better cosmetic effect is required.

References

Thursday, February 21, 2008

List of antibodies & autoimmune diseases

This list is from a handypost by Graham at Over My Med Body!. I'm only duplicating his list below in case his site ever disappears:

AntibodyDisease
Anti-Basement MembraneGoodpasture’s Syndrome
Anti-Centromere, Anti-Scl 70Scleroderma (CREST)
Anti-ds DNALupus/SLE
Anti-epithelial cellPemphigus Vulgaris
Anti-gliadinCeliac Disease
Anti-histoneDrug-induced SLE
Anti-IgG, Anti-RF, Anti-CCPRheumatoid Arthritis
AntimitochondrialPrimary Biliary Cirrhosis
Anti-neutrophilVasculitis
Anti-plateletITP
Anti-cholinesteraseMyasthenia Gravis
Anti-endomyesialCeliac Disease
Anti-Jo 1poly or dermatomyositis
Anti-SSA, Anti-SSBSj√∂gren’s Syndrome