WOUND
DEFINITION
Wound is a break or discontinuity in the integrity of skin or tissues. It can be a simple wound or a complex wound.
Wound is simply a disruption of any tissues—soft tissue or bone or internal organs. Ulcer is disruption or break in the continuity of any lining—may be skin, mucous membrane or others. Ulcer is one of the types of wounds. There may be disruption of the structure and function.
CLASSIFICATION (RANK AND WAKEFIELD)
- Tidy woundsThey are wounds of surgical incisions and caused by sharp objects.Usually primary suturing is done. Healing is by primary intention.
- Untidy woundsThey are:
- Crushed
- Tear
- Avulsion
- Devitalized injury
- Vascular injury
- Multiple irregular wounds
- Burns, etc.
Fracture may be present.
Wound dehiscence, infection, delayed healing are common.
Liberal excision of devitalized tissue and allowing to heal by secondary intention is the management.
OTHER CLASSIFICATION
- Clean incised wound
- Lacerated woundWound edge is devitalized, crushed and wide. It is treated by wound excision and delayed primary suturing. Scar formed is wide and prone for hypertrophic scar formation (Figs 1.3A and B)
- Bruising, contusion.
- Closed blunt injury.
- Puncture wounds and bites.
- Abrasion (Fig. 1.6)It is superficial, and is due to shearing of skin in which surface is rubbed off. It heals by epithelialization.
- Traction and avulsion and degloving injury (Fig. 1.7).
- Crush injuryIt is caused by war wounds, road traffic accidents, and tourniquet.It leads on to:
- Compartment syndrome
- Muscle ischemia
- Gangrene, loss of tissue.
- War wounds and gunshot injuries.
- Injuries to bones and joints may be open or closed.
- Injuries to nerves, either clean cut or crush.
- Injuries to arteries and veins (major vessels).
- Injury to internal organs may be penetrating or non-penetrating (blunt) injuries (Figs 1.8A and B)
CLASSIFICATION OF SURGICAL WOUNDS
- Clean wound
- Herniorrhaphy
- Excisions
- Surgeries of the brain, joints, heart transplant.
- Infective rate is less than 2% (Fig. 1.9).
- Clean contaminated wound
- Appendicectomy (Fig. 1.10).
- Bowel surgeries.
- Gallbladder, biliary and pancreatic surgeries.
- Infective rate is up to 30%—high.
- Contaminated wound (Fig. 1.11)
- Acute abdominal conditions.
- Open fresh accidental wounds.
- Dirty infected wound (Fig. 1.12)
- Abscess drainage.
- Pyocele.
- Empyema gallbladder.
- Fecal peritonitis.
Wound may be
- ▸ Closed wound like contusion, abrasion or laceration.
- ▸ Open wound like incised, lacerated, penetrating or crush injury.
WOUND HEALING
Wound healing is complex method to achieve anatomical and functional integrity of disrupted tissue by various components like neutrophils, macrophages, lymphocytes, fibroblasts, collagen; in an organized staged pathways—hemostasis → inflammation → proliferation → matrix synthesis (collagen and proteoglycan ground substance) → maturation → remodeling → epithelialization → wound contraction (by myofibroblasts).5
Stages
- ▸ Stage of inflammation.
- ▸ Stage of granulation tissue formation and organization. Here as the result of fibroblastic activity, synthesis of collagen and ground substance occurs.
- ▸ Stage of epithelialization—it occurs in 48 hours.
- ▸ Stage of wound contraction and connective tissue formation.
- ▸ Stage of scar formation and resorption.
- ▸ Stage of maturation.
Phases of Wound Healing
Inflammatory Phase (Lag/Substrate/Exudative)
It begins immediately after wound formation lasting for 4-6 days (Rubor, calor, tumour, door and loss of function—features of inflammation will develop). Macrophages secrete fibroblastic growth factor, which enhances angiogenesis. Polymorphonuclear leukocytes appear after 48 hours, which secrete inflammatory mediators and bacterial oxygen derived free radicals. Factors involved are—platelet derived growth factor (PDGF), epidermal growth factor (EGF), transforming growth factor (TGF), interleukins, tumor necrosis factor (TNF), prostaglandins, collagenase and elastase.
Proliferative Phase
It begins within 7 days and lasts for 6 weeks. Here, collagen and glycosamines are produced by fibroblasts. Hydroxyproline and hydroxylysine are synthesized by enzymes using iron, alpha ketoglutarate and vitamin C. About 50% of strength is achieved in 30 days.
Remodeling Phase (Maturation phase)
It begins within 6 weeks and lasts for 2 years. There is maturation of collagen by cross-linking which is responsible for tensile strength of the scar.
Management of Wounds
- ▸ Wound is inspected and classified as per the type of wound.
- ▸ If it is in the vital area, then:
- The airway should be maintained.
- The bleeding if present should be controlled.
- Intravenous fluids are started.
- Oxygen, if required may be given.
- Deeper communicating injuries and fractures, etc. should be looked for.
- ▸ If it is an incised wound, then primary suturing is done after thorough cleaning.
- ▸ If it is a lacerated wound then the wound is excised and primary suturing is done.
- ▸ If it is a crushed or devitalized wound, there will be edema and tension in the wound. Wound debridement is done by excising all the devitalized tissues and the edema is allowed to subside in 5–6 days. Then, delayed primary suturing is done.
- ▸ If it is a deep devitalized wound, after wound debridement, it is allowed to granulate completely. Later, if the wound is small, secondary suturing is done. If the wound is large, a split skin graft (Thiersch graft) is used to cover the defect (Fig. 1.13).
- ▸ In a wound with tension, fasciotomy is done so as to prevent the development of compartment syndrome.
- ▸ Vascular or nerve injuries are dealt with accordingly. Vessels are sutured with 6-zero polypropylene nonabsorbable suture material. If the nerves are having clean-cut wounds it can be sutured primarily with polypropylene 6-zero or 7-zero suture material. If there is difficulty in identifying cut ends of nerves or if the cut ends of nerves are crushed then a marker stitch using silk is placed at the site and later secondary repair of the nerves are done.
- ▸ Internal injuries have to be dealt accordingly (intracranial by craniotomy, intrathoracic by intercostal tube drainage, intra-abdominal by laparotomy). Fractured bones also should be identified and properly dealt with.
- ▸ Antibiotics, fluid and electrolyte balance, blood transfusion, tetanus toxoid or antitetanus globulin injection (ATG).
Fig. 1.13: Degloving injury, thigh and leg. It is extensive and needs regular dressing, debridement and later skin grafting
Wound Debridement (Wound toilet, or wound excision) is liberal excision of all devitalized tissues at regular intervals (of 48–72 hours) until healthy, bleeding, vascular tidy wound is created.
PROBLEMS WITH WOUND HEALING
- ▸ Wound infection is common in devitalized deep difficult wounds. Diabetes, immunosuppression, cytotoxic drugs, anemia, malnutrition, malignancy increases the chances of wound infection.
- ▸ Wound dehiscence is common in all above said adverse factors. Wound suddenly gives away with pain causing copious serosanguineous discharge. After laparotomy when done especially as an emergency procedure as in trauma, acute abdomen and also in malignancy, 7abdominal closed wound may burst in 5–7 days. Usually, all layers of abdomen give away causing discharge, occasionally bowel will extrude out. It needs emergency closure of the abdominal wound using specialized sutures or retention sutures.
- ▸ Hypertrophic scar or keloid formation due to altered collagen synthesis in the wound-healing process. Collagen synthesis is increased three times in hypertrophic scar and 20 times in keloid.
- ▸ Deeper wound will cause specified problems like paresthesia, ischemia, paralysis, etc.
COMPARTMENT SYNDROME
- ▸ It is common in calf and forearm.
- ▸ Closed injury causes hematoma leading to increased pressure.
- ▸ It is often associated with fracture, which compresses the major vessel further aggravating the ischemia causing pallor, pulseless, pain, paresthesia, diffuse swelling and cold limb.
- ▸ If allowed to progress, it may eventually lead on to gangrene or chronic ischemic contracture with deformed, disabled limb.
- ▸ Muscle necrosis releases myoglobulin, which is excreted in the urine damaging kidneys leading into renal failure.
Treatment
- ▸ These patients require longitudinal lengthy, deep incisions i.e. fasciotomies to relieve the pressure and prevent compression (Fig. 1.14).
- ▸ Antibiotics.
- ▸ Bladder catheterization.
- ▸ Mannitol or diuretics to create diuresis so as to flush the kidney.
- ▸ Fresh blood transfusion.
- ▸ Hyperbaric oxygen.
CRUSH SYNDROME
It is due to crushing of muscles causing extravasation of blood and release of myohemoglobin into the circulation, leading to acute tubular necrosis and acute renal failure.
Causes
- ▸ Earthquakes
- ▸ Mining and industrial accidents
- ▸ Air crash
- ▸ Tourniquet.
Initially tension increases in the muscle compartment commonly in the limb, which itself impedes the circulation and increases the ischemic damage. In 3 days, urine gets discolored and scanty. Patient becomes restless, apathy and delirious with onset of uremia. Crush syndrome is often life-threatening.
Note: Crush injury of small area my not cause crush syndrome (Fig. 1.15).
Treatment
- ▸ Tension in the muscle compartment is relieved by placing multiple, parallel, deep incisions in the limb so as to prevent further damage.
- ▸ Rheomacrodex, or Mannitol is given to improve the urine output by improving the renal function.
- ▸ Alkalization of the urine is done using sodium citrate or sodium bicarbonate.
- ▸ Hemodialysis is done sometimes as a life saving procedure.
- ▸ Other measures:
- Bladder catheterization
- Oxygen therapy
- Antibiotics
- Blood transfusion.
KELOID (LIKE A CLAW)
- ▸ Keloid is common in blacks. Common in females. Common in Negroes.
- ▸ Genetically predisposed. Often familial.
- ▸ There is defect in maturation and stabilization of collagen fibrils.
- ▸ Keloid continues to grow even after 6 months, may be for many years.
- ▸ It extends into adjacent normal skin.
- ▸ It is brownish black in color, painful, tender and sometimes hyperesthetic.
Figs 1.16A to C: Keloid in shoulder and arm area; keloid in ear. Note the keloid at sternum, which is commonest site
Sites
Common over sternum. Other sites are upper arm, chest wall, and lower neck in front (Figs 1.16A to C and 1.17A).
Differential diagnosis: Hypertrophic scar.
Treatment
Controversial.
Modes of treatment
- ▸ Steroid injection—Triamcinolone is given intrakeloidally, at regular intervals, may be once in 7–10 days, of 6–8 injections.
- ▸ Steroid injection → Excision → Steroid injection.
- ▸ Methotrexate and vitamin A therapy into the keloid.
- ▸ Intralesional excision retaining the scar margin which may prevent recurrence. It is ideal and better than just excision.
Recurrence rate is very high
Note: Excision and primary suturing has got high recurrence rate; hence it is not usually practiced.
HYPERTROPHIC SCAR
- ▸ Occurs anywhere in the body (Fig. 1.17B).
- ▸ Not genetically predisposed. Not familial.
- ▸ Growth usually limits up to 6 months.
- ▸ It is limited to scar tissue only. It will not extend to the normal skin.
- ▸ It is pale brown in color, not painful, non-tender.
- ▸ Often, self-limiting also. It responds very well for steroid injection.
- ▸ Recurrence is uncommon.
Complication
- ▸ Repeated breakdown of the scar often occurs causing infection and pain.
- ▸ After repeated breakdown it may turn into Marjolin's ulcer.
It is controlled by pressure garments or often revision excision of scar and closure, if required with skin graft.
SINUS (FIG. 1.19)
- ▸ “Sinus” means “hollow” or “a bay” (Latin).
- ▸ It is a blind track lined by granulation tissue leading from an epithelial surface into the surrounding tissues.
- ▸ Sinus sprouts outside and it does not have a floor clinically.
- ▸ Discharge can be seen on the mouth of the sinus.
Causes of Sinus
- ▸ Congenital: Preauricular sinus.
- ▸ Acquired: Chronic osteomyelitis of bone causing bone spicules and discharge to come out of the sinus opening. Median mental sinus in the mentum in lower jaw is due to tooth infection. Pilonidal sinus is due to entering of hairs in the interbuttock cleft over the sacrum. Madura foot in the foot and leg is due to Nocardia Madurai fungal infection causing multiple discharging sinuses. Tuberculous sinus is eventual outcome of cold abscess in neck, groin, etc. discharging cheesy, caseating, yellowish material.
FISTULA (FIG. 1.20)
- ▸ It is an abnormal communication between the lumen of one viscus to another or the body surface or between the vessels.
- ▸ Fistula means “flute” or “a pipe or tube”.
Causes of Fistula
- ▸ Branchial fistula in neck.
- ▸ Orocutaneous fistula in advanced carcinoma cheek.
- ▸ Tracheo-esophageal fistula.
- ▸ Postoperative gastrointestinal fistula (Fig. 1.21).
- ▸ Rectovesical fistula.
- ▸ Fistula-in-ano.
Fistula can be
- ▸ External: Here fistula communicates from skin to hollow viscus inside. Examples – parotid fistula, thyroglossal fistula, branchial fistula.
- ▸ Internal: Here fistula develops between two hollow viscera. Colovesical fistula, aortoenteric fistula.
Fistula also can be
- ▸ Congenital—Branchial/tracheoesophageal fistula.
- ▸ Acquired—Thyroglossal fistula, fistula-in-ano, etc.
Types of Sinus/Fistula
Congenital | Acquired |
|---|---|
Preauricular sinus | Ruptured abscess |
Branchial fistula | Tuberculosis—common |
Tracheoesophageal fistula | Actinomycosis |
Congenital AV fistula | Chronic osteomyelitis Fistula-in-ano Acquired AV fistula Median mental sinus |
Clinical Features
- ▸ Discharge from the opening of sinus. No floor.
- ▸ Raised indurated edge, indurated base, non-mobile.
- ▸ Often sprouting granulation tissue is seen over the sinus opening.
Investigations (Fig. 1.22)
- ▸ Fistulogram/sinusogram using ultrafluid lipidol or water-soluble iodine dye.
- ▸ Discharge for culture and sensitivity, AFB, cytology, staining.
- ▸ Biopsy from the edge, chest X-ray, ESR.
Treatment
- ▸ The cause is treated—sequestrectomy, foreign body removal, control of tuberculosis.
- ▸ Excision of sinus or fistulas. Always specimen should be sent for histology.
Figs 1.23A and B: Fecal fistula with discharging fecal matter through the fistulous wound. Note the tension sutures in one of the pictures
MEDIAN MENTAL SINUS
It is a chronic infective condition, wherein there is infection of roots of one or both lower incisor teeth forming root abscess, which eventually tracks down between two halves of the lower jaw in midline, presenting as discharging sinus on the point of chin in midline (Fig. 1.24).13
Fig. 1.24: Median mental sinus. Note the origin of the sinus from the root/roots of the lower incisor/incisors
Clinical Features
- ▸ Usually painless discharging sinus in the midline on the point of chin.
- ▸ Often infection in incisor may be revealed (in many patients clinically tooth looks normal, even though root is infected invariably).
- ▸ It is often mistaken for infected sebaceous cyst.
- ▸ Osteomyelitis of the mandible is the possible complication.
Differential Diagnosis
- ▸ Infected sebaceous cyst.
- ▸ Tuberculous sinus.
- ▸ Osteomyelitis.
Investigations
- ▸ Dental X-ray is diagnostic (Plain X-ray mandible may not reveal the disease).
- ▸ Discharge study—culture and sensitivity, cytology, AFB.
Treatment
- ▸ Antibiotics after doing discharge study (culture and sensitivity).
- ▸ Lay opening and excision of the sinus track with extraction of incisor tooth/teeth.
ULCER
Definition
An ulcer is a break in the continuity of the covering epithelium, either skin or mucous membrane due to molecular/cell death.
Parts of an Ulcer (Fig. 1.25)
Margin
It may be regular or irregular. It may be rounded or oval.
Edge
Edge is the one, which connects floor of the ulcer to the margin.
Different edges are (Fig. 1.26):
Sloping edge. It is seen in healing ulcer. Its inner part is red because of red, healthy granulation tissue.
Undermined edge is seen in tuberculous ulcer (Fig. 1.27).
Punched out edge is seen in gummatous (syphilitic) ulcer, trophic ulcer and pressure sores. It is due to endarteritis.
Raised and beaded edge (pearly white) is seen in rodent ulcer (BCC).
Everted edge (rolled out edge): It is seen in carcinomatous ulcer.
Floor
It is the one, which is seen. Floor may contain discharge, granulation tissue, or slough.
Base
Base is the one where ulcer rests. It may be bone or soft tissues.
CLASSIFICATION I (CLINICAL)
Spreading ulcer: Here edge is inflamed and edematous.
Healing ulcer (Fig. 1.28): Edge is sloping with healthy pink/red granulation tissue with serous discharge.
Callous ulcer: Floor contains pale unhealthy granulation tissue with indurated edge/base (Fig. 1.29). Ulcer has no tendency to heal. It lasts for many months to years. It is due to callous attitude of the patient (Figs 1.30 and 1.31).
CLASSIFICATION II (PATHOLOGICAL)
Specific Ulcers
- ▸ Tuberculous ulcer (See Fig. 1.26).
- ▸ Syphilitic ulcer: It is punched out, deep ulcer, with ‘wash-leather’ slough in the floor and with indurated base.
- ▸ Actinomycosis.
- ▸ Meleney's ulcer.
Fig. 1.30: Callous ulcer in the leg. Note the slough on the surface of ulcer with no signs of healing
Fig. 1.31: Callous ulcer leg. Note ulcer floor without any granulation tissue. It is due to callous attitude of the patient
Malignant Ulcers
- ▸ Carcinomatous ulcer.
- ▸ Rodent ulcer.
- ▸ Melanotic ulcer.
Nonspecific Ulcers
- ▸ Traumatic ulcer: It may be due to mechanical, physical, chemical injury.
- ▸ Arterial ulcer: Atherosclerosis, TAO.
- ▸ Venous ulcer (gravitational ulcer, post-phlebitic ulcer).
- ▸ Trophic ulcer.
- ▸ Infective ulcers: Pyogenic ulcer.
- ▸ Tropical ulcers: It occurs in tropical countries. It is callous type of ulcer, e.g. Vincent‘s ulcer.
- ▸ Ulcers due to chilblains and frostbite (cryopathic ulcer).
- ▸ Martorell‘s hypertensive ulcer: It occurs due to obliteration of end arteries. It is observed in skin over the back of calf region. Ulcer is severely painful with deep, non-healing ischemic look.
- ▸ Bazin's ulcer: It is seen exclusively in the legs and ankles of young females, as erythematous purplish nodules and non-healing ulcers. It may be due to ischemic (Fig. 1.32)/hypersensitive/tuberculous etiology. It is treated with antituberculous drugs, dressings, vasodilators and often by sympathectomy. It is also called as Erythrocyanosis frigida.
Fig. 1.32: Ischemic ulcer foot is due to poor blood supply due to either, atherosclerosis, TAO, diabetes mellitus
- ▸ Diabetic ulcer.
- ▸ Ulcers due to leukemia, polycythemia, jaundice, collagen diseases, lymphedema.
- ▸ Cortisol ulcers are due to long time application of cortisol (steroid) creams to certain skin diseases. These ulcers are callous ulcers, last for long time and requires excision with skin grafting.
Note: Maggots may form in ulcer and they eat only dead tissues (Fig. 1.33).
GRANULATION TISSUE
It is proliferation of new capillaries and fibroblasts intermingled with RBC‘s and WBC‘s with thin fibrin cover over it.
Types
Healthy Granulation Tissue
It occurs in a healing ulcer. It has a sloping edge with serous discharge. It bleeds on touch. Skin grafting takes up well with healthy granulation tissue. Streptococci growth in culture should be less than 105/gram of tissue before skin grafting (Figs 1.34A and B)
Figs 1.34A and B: Healthy granulation tissue seen in ulcer bed; it is coverd with split skin graft (SSG)
Unhealthy Granulation Tissue
It is pale with purulent discharge. Its floor is covered with slough. Its edge is inflamed and edematous. It is a spreading ulcer (Fig. 1.35).
Unhealthy, Pale, Flat Granulation Tissue
Exuberant Granulation Tissue (Proud Flesh)
It occurs in a sinus wherein granulation tissue protrudes out of the orifice of the sinus like a proliferating mass. It is commonly associated with a retained foreign body in the sinus cavity.
Pyogenic Granuloma
It is a type of exuberant granulation tissue. Here granulation tissue protrudes out from an infected wound or ulcer bed, presenting as well localized, red swelling, which bleeds on touch (Figs 1.36A and B)
Treatment: Antibiotics, excision and biopsy.
Figs 1.36A and B: Pyogenic granuloma on the face and finger. They present with pain, bleeding and swelling. It needs excision under local anesthesia
Induration in an ulcer is due to carcinoma or due to fibrosis in a long-standing ulcer.
Investigations for an Ulcer
- ▸ Study of discharge: Culture and sensitivity, AFB study, cytology.
- ▸ Edge biopsy: Biopsy is taken from the edge because edge contains multiplying cells. Usually two biopsies are taken. Biopsy from the center may be inadequate because of necrosis.
- ▸ X-ray of the part.
- ▸ FNAC of the lymph node.
- ▸ Chest X-ray, Mantoux test is done in suspected case of tuberculous ulcer (Figs 1.37A and B)
Treatment of an Ulcer
- ▸ Treat the cause like diabetes, anemia, and malnutrition. Often needs blood transfusion.
- ▸ Antibiotics are given depending on the culture and sensitivity.
- ▸ Regular dressings using EUSOL (Edinburgh University Solution containing calcium hydroxide, boric acid, sodium hypochlorite), H2O2, povidone iodine.
- ▸ Wound excision/slough excision/debridement of the wound at regular intervals.
- ▸ Once wound granulates well, split skin grafting is done to cover the defect (Figs 1.38A and B)
- ▸ If there is no adequate blood supply, or if bone is exposed then flap is needed depending on the location of ulcer, either groin flap, pectoralis major flap, etc.
Figs 1.38A and B: Healing ulcers in leg and shoulder area in different patients. Note the healthy granulation tissue with sloping edge
TROPHIC ULCER
It is due to:
- ▸ Impaired nutrition.
- ▸ Defective blood supply.
- ▸ Neurological deficit.
It usually occurs:
- ▸ Over the heel.
- ▸ In relation to heads of metatarsals.
- ▸ Buttocks.
- ▸ Over the ischial tuberosity.
- ▸ Sacrum.
- ▸ Over the shoulder.
- ▸ Occiput.
Because, there is neurological deficit, trophic ulcer is also called as neurogenic ulcer/neuropathic ulcer.
Due to repeated trauma and pressure, it initially begins as callosity which suppurates and gives way through a central hole extending into the deeper plane as perforating ulcer (penetrating ulcer).
Clinical Features
- ▸ Painless ulcer, which is punched out.
- ▸ Ulcer is non-mobile with base formed by underlying bone.
Investigations
Study of discharge, biopsy from the edge, X-ray of the part, X-ray spine, blood sugar.
Treatment
- ▸ Cause should be treated.
- ▸ Nutritional supplements.
- ▸ Rest, antibiotics, slough excision, regular dressings.
- ▸ Once ulcer granulates well, flap cover or skin grafting is done.
- ▸ Excision of the ulcer and skin grafting.
PRESSURE SORE (BEDSORE/DECUBITUS ULCER)
Bedsore/pressure sore is a trophic ulcer with underlying bone as the base.
It is nonmobile, deep, punched out ulcer.
It is common in:
- ▸ Old age.
- ▸ Bedridden individuals.
- ▸ Tetanus.
- ▸ Patients with orthopedic and head injuries.
- ▸ Diabetic.
- ▸ Paraplegic.
- ▸ Comatose.
- ▸ Emaciated patient.
- ▸ Anemia.
- ▸ Prolonged immobilization.
Sites of bedsore are occiput, heel, sacrum (Fig. 1.39), ischium, scapula, greater trochanter, spinous process, elbows, and buttocks.
Predisposing Factors
- ▸ Malnutrition, anemia, sensory loss, pressure, moisture.
- ▸ Incontinence makes skin moist and septic, so five times more prone for pressure sore.
- ▸ Excessive sweating, edema body.
- ▸ Friction due to foreign body, thick bed sheets, hard rough cot.
Superficial bedsores are common (75%). They are painful and heal slowly by itself.
Deep bedsores are painless but covered with slough. It requires antibiotics, grafting or flaps to cover it later.
Treatment
- ▸ Change of positions should always be encouraged.
- ▸ Use of waterbed, ripple bed is advised. Bed should be smooth and free from wrinkles and unevenness. Air rings or air cushions are also useful.
- ▸ Moisture has to be avoided. Skin must be kept clean and dry. It should be washed with soap and water and dried properly. A soothening powder may be beneficial.
- ▸ Ripple bed has an alternate pressure point pad under the bottom sheet of ordinary mattress. It provides regular automatic frequent redistribution of pressure areas. The pad consists of vinyl plastic pad with alternating sets of air cells. To control the air, an air pump is also present.
- ▸ In a patient with urinary incontinence, special silicone bedclothes are used to attain waterproof covering to skin. Indwelling Foley‘s catheter is placed to drain urine. Thorough washing of the back and drying twice daily is essential. Disposable soft inco-pads are used repeatedly as required.
- ▸ Bowker-Davidson special pressure cushions contain foamed cushion with a waterproof polyvinyl chloride bag containing 5 liters of the thixotropic gel.
- ▸ Soaking by urine, sweat, pus, and feces has to be taken care off.
- ▸ Good nursing, regular dressing, good nutrition are necessary.
- ▸ Antibiotics, blood transfusions are very essential.
- ▸ Excision of dead tissue followed by skin grafting or local rotation flaps may have to be done.
DIABETIC ULCER (FIG. 1.40) (DIABETIC FOOT)
Patients with diabetes are more prone for foot problems like cellulitis, abscess formation, gangrene, osteomyelitis of foot. It is due to neuropathy, more susceptibility for infection, clawing of toes, loss of functioning of foot arch, microangiopathy, bacterial resistance, and decreased body immunity.
Sites
- ▸ Foot-plantar aspect—is the commonest site.
- ▸ Upper limb, back, scrotum, perineum.
Diabetic ulcer may be associated with ischemia. Ulcer is spreading and deep.
Investigations
- ▸ Blood sugar both random and fasting.
- ▸ Urine ketone bodies.
- ▸ Discharge for culture and sensitivity.
- ▸ X-ray of the part.
- ▸ Arterial Doppler of the limb.
Treatment
- ▸ Control of diabetes using insulin. Sliding scale insulin is used depending on the color seen in urine test. Human insulin is the preferred type of insulin. When there is ketosis, intravenous insulin is used in normal saline.
- ▸ Antibiotics.
- ▸ Nutritional supplements.
- ▸ Regular cleaning, debridement, dressing.
- ▸ Microcellular (MCR) chappals are used to avoid ulcer formation (Fig. 1.41)
- ▸ Abscess drainage, toe amputation (Ray amputation), below-knee/above-knee amputations (Fig. 1.42).
- ▸ Once granulates, the ulcer is covered with skin graft or flap.
- ▸ Suitable prosthesis to the limb helps the patient to achieve ambulation (Fig. 1.43).
- ▸ Patient is prone for septicemia, ketosis, electrolyte imbalance, silent myocardial infarction and often all these can be fatal.
MELENEY'S ULCER
- ▸ It is commonly seen in postoperative wounds in abdomen and chest wall like empyema drainage or after surgery for peritonitis.
- ▸ It is common over abdomen and thorax. It begins in wound margin and spreads rapidly. It can also occur in other areas of skin.
- ▸ Infection is severe, often with endarteritis of the skin leading to ulcer and destruction.
- ▸ It causes severe toxicity and extensive necrosis of the skin and deeper plane, which often needs debridement, antibiotics and later skin grafting.
TRAUMATIC ULCER
- ▸ Such ulcer occurs after trauma. It may be mechanical—dental ulcer in the margin of the tongue due to tooth injury; physical like by electrical burn; chemical like by alkali injury.
- ▸ Such ulcer is acute, superficial, painful and tender. Secondary infection or poor blood supply of the area makes it chronic and deep.
- ▸ Footballer's ulcer is a traumatic ulcer occurring over the shin of males due to direct knocks on the shin. It is staphylococcal infection with a chronic and deep ulcer.
- ▸ Traumatic ulcers can occur anywhere in the body due to trauma.
- ▸ Trauma causes infection, necrosis, fasciitis, crush injury, endarteritis of the skin leading into formation of large/deep non-healing ulcer.
- ▸ Treatment depends on size and extent of ulcer. Regular dressing, later skin grafting.
ARTERIAL/ISCHEMIC ULCER (FIG. 1.44)
- ▸ It is common in toes, feet or legs; often can occur in upper limb digits. It is due to poor blood supply following blockage of the digital or medium sized arteries.
- ▸ Atherosclerosis and TAO (thromboangiitis obliterans) are common causes in lower limb.
- ▸ Cervical rib, Raynaud's phenomenon and vasculitis are common causes in upper limb.
- ▸ Ulcer initially occurs after trauma, soon becomes nonhealing, spreading with scanty granulation tissue.
- ▸ Ulcer is very painful, tender and often hyperesthetic. Digits may often be gangrenous. Intermittent claudication, rest pains are common. Other features of ischemia are obvious in the adjacent areas. They are—pallor, dry skin, brittle nail, patchy ulcerations, and loss of hair.
- ▸ Ulcer is usually deep, destructs the deep fascia, exposing tendons, muscles and underlying bone. Dead tendons look pale/greenish with pus over it.
- ▸ Management: Specific investigations like arterial Doppler, angiogram, lipid profile, and blood sugar are done. Treatment is done accordingly—drugs like vasodilators; arterial surgeries may be needed.
CARCINOMATOUS ULCER (EPITHELIOMA, SQUAMOUS CELL CARCINOMA)
- ▸ It arises from prickle cell layer of skin. It may initially begin as a nodule or ulcer; but later forms an ulcerative lesion with rolled out/everted edge. Floor contains necrotic content, unhealthy (tumor) granulation tissue and blood (Fig. 1.45).
- ▸ Ulcer bleeds on touch and is vascular and friable. Induration is felt at the base 23and edge. It is usually circular or irregular in shape. Initially ulcer is mobile but becomes nonmobile once it infiltrates into deeper tissues. The typical foul smell is due to necrotic material, infection and release of polyamides from the tumor cells.
- ▸ Hard, discrete regional lymph nodes are often palpable, initially mobile but later become fixed. Lymph nodes can fungate eventually. Ulcer and lymph nodes are initially painless; but becomes painful and tender once there is deeper infiltration or secondary infection. Systemic spread is rare. It is a locoregional malignant disease.
- ▸ Verrucous carcinoma is exophytic, locally malignant well differentiated squamous cell carcinoma without lymphatic spread.
- ▸ Management: Edge biopsy; FNAC of regional lymph nodes are the investigations. Treated with wide local excision with skin grafting and regional lymph node block dissection.
Fig. 1.45: Squamous cell carcinoma heel. It is proliferative ulcer. Note the raised and everted edge
MARJOLIN'S ULCER (RENE MARJOLIN,1828, PARIS)
- ▸ It is slow growing locally malignant lesion—a very well differentiated squamous cell carcinoma occurring in an unstable scar of long duration.
- ▸ It is commonly seen in chronic venous ulcer scar. Often it is observed in burns scar and scar of previous snake bite. Lesion is ulcerative/proliferative (Fig. 1.46).
- ▸ Edge may be everted or may not be. It is painless as scar does not contain nerve fibrils. It does not spread into lymphatics as scar is devoid of lymphatics. Induration is felt at the edge and base. There is marked fibrosis also.
- ▸ Once lesion spreads into adjacent normal skin, it can spread into regional lymph nodes behaving like squamous cell carcinoma.
- ▸ Managed by edge biopsy and wide local excision and grafting. If large and deep, amputation is needed.
Fig. 1.46: Marjolin's ulcer in a chronic unstable scar (of long duration) in the leg. It does not spread through lymphatics
RODENT ULCER
- ▸ It is ulcerative form of basal cell carcinoma, which is common in face.
- ▸ Ulcer shows central area of dry scab with peripheral raised active and beaded (pearly white) edge. Often floor is pigmented. It erodes into deeper plane like soft tissues, cartilages and bones hence the name—rodent ulcer.
- ▸ As lymphatics are blocked early in the disease by large tumor cells, it does not spread to regional lymph nodes.
- ▸ It is common in face; rarely can it occur over tibia, external genitalia, mucocutaneous junction. It does not occur in mucosa (Fig. 1.47).
- ▸ Management: Edge biopsy, CT scan of the part to see the depth, wide excision.
MELANOTIC ULCER
- ▸ It is ulcerative form of melanoma. It can occur in skin as de novo or in a pre-existing mole. Ulcer is pigmented often with a halo around (Fig. 1.48).
- ▸ Ulcer is rapidly growing, often with satellite nodules and ‘in–transit’ lesions. It is very aggressive skin tumor arising from melanocytes.
- ▸ It spreads rapidly to regional lymph nodes which are pigmented. Blood spread to liver, lungs, brain, and bone is common. It can occur in mucosa, genitalia, and eye. It is a systemic malignant disease.
- ▸ Investigations: Excision biopsy (usually incision biopsy is not done), FNAC lymph node, US abdomen.
- ▸ Treatment is wide local excision, regional node block dissection and chemotherapy.
TROPICAL ULCER
- ▸ It is endemic in monsoon hit humid tropics with repeated epidemics but sporadic in subtropics. Trauma or insect bite leads into infection exclusively in the lower part of the leg and foot.
- ▸ It is an acute ulcerative lesion of the skin observed in tropical regions like Africa, India and South America. It is associated with lower socioeconomic group, anemia, and malnutrition and vitamin deficiency.
- ▸ It is commonly caused by Fusobacterium fusiformis (vincent's organisms) and Borrelia vincenti.
- ▸ There are abrasions, redness, papule and pustule formation, acute regional lymphadenitis and severe pain.
- ▸ Pustule bursts in 3 days along with necrobiosis and phagedena causing a spreading painful ulcer with an undermined edge, brownish floor and serosanguineous discharge. Spreading stops in few weeks with ulcer persisting for many months to years. Eventually a chronic, large nonhealing/callous ulcer forms with persistent pain, profuse serosanguineous discharge, extremely unpleasant odor, long existing firmly adherent slough in the floor without any obvious constitutional symptoms. During healing it causes a slight pigmented, parchment like round scar.25
- ▸ Often destruction is progressive without cessation (phagedena) to extend into entire soft tissues of foot and leg inviting amputation. Phagedena (Greek—to eat) is also seen in chancroid and cancrum oris.
- ▸ Occasionally squamous cell carcinoma can develop on it.
- ▸ Treatment—improvement in nutrition, penicillin, metronidazole, Eusol dressing, skin grafting at a later date.
VENOUS ULCER (GRAVITATIONAL ULCER)
- ▸ It is common around ankle (gaiter's zone) due to chronic venous hypertension. It is due to varicose veins (long saphenous vein/short saphenous vein/perforators) or post-phlebitic limb.
- ▸ Postphlebitic limb consists of veins that is been partially recanalized following deep venous thrombosis, which causes increased venous pressure around ankle through perforators. It is called as post-thrombotic ulcer. DVT has to be treated in these patients.
- ▸ Varicose veins are common in females. Fifty percent of venous ulcer is due to varicose veins; 50% are due to postphlebitic limb (previous DVT). Pain, discomfort, pigmentation, dermatitis, lipodermatosclerosis, ulceration, periostitis, ankle-joint ankylosis, talipes equinovarus deformity and Marjolin's ulcer are the problems of varicose veins and later of venous ulcer (Fig. 1.49).
- ▸ Ulcer is initially painful; but once chronicity develops it becomes painless. Ulcer is often vertically oval; commonly located on the medial side; occasionally on lateral side; often on both sides of the ankle; but never above the middle-third of the leg. Floor is covered with pale or often without any granulation tissue. When well granulated, edge is sloping. Induration and tenderness is seen often at the base of an ulcer.
- ▸ Inguinal lymph nodes (vertical group) are often enlarged. Ulcer often attains very large size which is nonhealing, indolent and callous.
- ▸ Ulcer heals on rest and treatment; but reforms again. Scarring is common due to repeated healing and recurrent ulcer formation. This unstable scar of long duration may lead into squamous cell carcinoma (Marjolin's ulcer).
- ▸ Management: Venous Doppler, regular dressing, skin grafting, specific treatment for varicose veins.
Fig. 1.49: Venous ulcer around ankle with skin changes over surrounding area. It is the commonest site of venous ulcer
TUBERCULOUS ULCER (FIG. 1.50)
- ▸ It is due to mycobacterium tuberculosis. It is usually due to cold abscess later forming ulcer in the neck, chest wall, axilla and groin.
26It can also be primary tuberculosis of the skin (commonly in face). Ulcer can be single or multiple; oval or rounded; with undermined edge (due to progression of disease outwards underneath and healing inwards by skin), painful and tender with caseating material on the floor. Ulcer is usually not deep. Regional lymph nodes may be enlarged matted, firm, and nontender.
- ▸ Management: Discharge study for epithelioid cells (modified histiocytes), AFB; edge biopsy, antituberculous drugs.
LUPUS VULGARIS
- ▸ It is cutaneous tuberculosis, which occurs in young age group.
- ▸ Commonly seen on face, starts as typical apple-gelly nodule with congestion of face around. Eventually ulceration occurs with scarring, necrosis and undermined edge.
- ▸ Long standing lupus vulgaris can turn into squamous cell carcinoma.
Investigation
ESR, discharge study, biopsy, chest X-ray.
Treatment
- ▸ Antituberculous drugs.
- ▸ If complete healing does not occur, then excision and skin grafting is required.
ULCER DUE TO CHILBLAINS
It is due to exposure to intense cold causing blisters, ulceration in the feet. These ulcers are superficial. The condition is also called as perniosis.
ULCER DUE TO FROSTBITE
- ▸ It is due to exposure of the part to wet cold below the freezing point.
- ▸ It leads to gangrene of the part. Ulcers, here are always deep.