Key Steps
1. Make linear incision under minimal tension.
2. Running suture with knot at each end.
3. Reinforce with Steri-strips or tissue glue.

1. Bury subcuticular sutures running horizontal sutures.
2. This technique is useful for wounds that are under minimal tension and in which cosmetic results are important.
3. It is possible to close deeper wounds with deep sutures of subcutaneous sutures first.
4. Begin with a knot beyond one apex of the incision, using polypropylenecoated nylon suture.
5. Place the needle through the skin to emerge in the wound.

6. Run the suture, taking horizontal bites through the superficial papillary dermis, alternating sides so that the exit point of one side matches the entry point of the other.
7. Keep the suture under minimal tension.
8. Emerge at the other end beyond the apex and place a second knot.
9. Reinforce the wound with Steri-strips or tissue glue.
• Low-tension to moderate-tension wound closures that follow skin lines or wounds partially closed by deep sutures to support the skin closure

• Wound closures where external suture punctures would be cosmetically unfavorable
• Wounds that require prolonged support for optimal closure.
• Knots requiring significant tension or sutures applied for hemostasis


Key Steps
1. Cleanse digit with antiseptic.
2. Inject local anesthesia without epinephrine.
3. Inject at 9 to 10 o’clock and at 2 to 3 o’clock.
4. Secondary injections.

1. Perform digital blocks by injecting plain lidocaine alongside the base of the digit from 9 to 10 o’clock and from 2 to 3 o’clock to anesthetize the digital nerves.
2. Approximately 1 ml of lidocaine is sufficient to provide adequate anesthesia.
3. In some patients, injecting lidocaine toward the palmar surface may be necessary to obtain complete anesthesia of the digit.
4. In some instances, as with nail removal, a simple tourniquet from a latex drain may be used to minimize bleeding in the field and retain the injected anesthesia agent in vascular digits.

• Need for local anesthetic that encompasses the digit                                                                                                                    • Ingrown nail removal
• Drainage of felon or paronychia
• Management of fracture of phalanx
• Use of epinephrine in the anesthetic is contraindicated
• Patient with hypotension or sepsis leading to peripheral vasoconstriction
• Coagulation defect (either medication related, congenital, or acquired),

Vulvar Cancer

Vulvar cancer is an abnormal cell proliferation arising on the vulva and exhibiting malignant potential. The majority are of squamous cell origin; however, other types include adenocarcinoma, basal cell carcinoma, sarcoma, and

INCIDENCE: 2.2 cases per 100,000 persons
PREVALENCE: Vulvar cancer is uncommon. It comprises 4% of malignancies of the female genital tract. It is the fourth most common gynecologic malignancy.
MEAN AGE AT DIAGNOSIS: Predominantly a disease of menopause. Mean age at diagnosis is 65 yr.

• Vulvar pruritus or pain is present.
• May produce a malodorous discharge or present as bleeding.
• Raised lesion that may have fleshy , ulcerated, leukoplakic, or warty appearance; may have multifocal lesions.
• Lesions are usually located on labia majora but may be seen on labia minora, clitoris, and perineum.
• The lymph nodes of groin may be palpable.
• The exact etiology is unknown.
• Vulvar intraepithelial neoplasia has been reported in 20% to 30% of invasive squamous cell carcinoma of the vulva, but the malignant potential is unknown.
• Human papillomavirus is found in 30% to 50% of vulvar carcinoma, but its exact role is unclear.
• Chronic pruritus, wetness, industrial wastes, arsenicals, hygienic agents, and vulvar dystrophies have been implicated as causative agents.
• Vulvar cancer in younger women is more directly dependent on HPV infection, vulvar dysplasia, and tobacco use.

• Lymphogranuloma inguinale
• Tuberculosis
• Vulvar dystrophies
• Vulvar atrophy
• Paget’s disease

• Treatment is individualized depending on the stage of the tumor. Fig. 1-1014 describes a treatment algorithm for management of patients with vulvar cancer.
• Stage I tumors with <1 mm stromal invasion are treated with complete local excision
without groin node dissection. Imiquimod 5% cream, a topical immune response modulator, is also effective in the treatment of vulvar intraepithelial neoplasia.
• Stage II tumors require radical vulvectomy with bilateral groin node dissection.
• Advanced-stage disease may require the addition of radiation and chemotherapy to the surgical regimen.

Von Willebrand’s Disease

Von Willebrand’s disease is a congenital disorder of hemostasis characterized by defective or deficient von Willebrand factor (vWF). There are several subtypes of von Willebrand’s disease. The most common type (80% of cases) is type I, which is caused by a quantitative decrease in vWF; type IIA and type IIB are results of qualitative
protein abnormalities; and type III is a rare, autosomal recessive disorder characterized by a near-complete quantitative deficiency of vWF. Acquired von Willebrand’s disease is a rare disorder that usually occurs in elderly patients and usually presents with mucocutaneous bleeding abnormalities and no clinically meaningful family history. It is often accompanied by a hematoproliferative or autoimmune disorder. Successful treatment of the associated illness can reverse the clinical and laboratory manifestations.

• Decreased factor VIII coagulant activity
• Decreased vWF antigen or ristocetin cofactor
• Normal platelet number and morphology
• Prolonged bleeding time
• Normal platelet aggregation studies
• Type IIA von Willebrand’s disease can be distinguished from type I by absence of ristocetin cofactor activity and abnormal multimer
• Type IIB von Willebrand’s disease is distinguished from type I by abnormal multimer.

• Avoidance of aspirin and other nonsteroidal anti-inflammatory drugs
• Evaluation for likelihood of bleeding (with measurement of bleeding time) before surgical procedures. When a patient undergoes surgery or receives repeated therapeutic doses of concentrates, factor VIII activity
should be assayed every 12 hr on the day a dose is administered and every 24 hr thereafter.

• The mainstay of treatment in von Willebrand’s disease is the replacement of the deficient protein at the time of spontaneous bleeding or before invasive procedures are performed.
• Desmopressin acetate (DDAVP) is useful to release stored vWF from endothelial cells. It is used to cover minor procedures and traumatic bleeding in mild type I von Willebrand’s disease. Dose is 0.3 mcg/kg in 100 ml of
normal saline solution IV infused >20 min. DDAVP is also available as a nasal spray (dose of 150 mcg spray administered to each nostril) as a preparation for minor surgery and management of minor bleeding episodes.
DDAVP is not effective in type IIA von Willebrand’s disease and is potentially dangerous in type IIB (increased risk of bleeding and thrombocytopenia).
• In patients with severe disease, replacement therapy in the form of cryoprecipitate is the method of choice. The standard dose is 1 bag of cryoprecipitate per 10 kg of body weight.
• Factor VIII concentrate rich in vWF (Humate-P) is useful to correct bleeding abnormalities in type IIA, IIB, and type III von Willebrand’s disease without alloantibodies. Alloantibodies that inactivate vWF and form circulating
immune complexes develop in 15% of patients with type III von Willebrand’s disease who have received multiple transfusions. In these patients, recombinant factor VIII is preferred because autoantibodies can elicit lifethreatening
anaphylactic reactions because of complement activation by immune complexes.


Vitiligo is the acquired loss of epidermal pigmentation that is characterized histologically by the absence of epidermal melanocytes. There are two major forms: nonsegmental (generalized) vitiligo, which accounts for >80% of cases,
and segmental vitiligo, which accounts for 30% of childhood cases.

• Three pathophysiologic theories:
1. Autoimmune theory (i.e., autoantibodies against melanocytes)
2. Neural theory (i.e., neurochemical mediators selectively destroy melanocytes)
3. Self-destructive process in which melanocytes fail to protect themselves against cytotoxic melanin precursors
• Although vitiligo is considered to be an acquired disease, 25% to 30% of cases are familial. The mode of transmission is unknown; the condition seems to be polygenic or autosomal dominant with incomplete penetrance and variable expression.

• Associated disorders:
– Alopecia areata
– Type 1 diabetes mellitus
– Adrenal insufficiency
– Hyperthyroidism and hypothyroidism
– Mucocutaneous candidiasis
– Pernicious anemia
– Polyglandular autoimmune syndromes
– Melanoma

Treatment is indicated primarily for cosmetic purposes when depigmentation causes emotional or social distress. Depigmentation is more noticeable among patients with darker complexions.
• Cosmetic masking agents (e.g., Dermablend, Covermark) or stains (e.g., DY-O-Derm, Vitadye)
• Sunless tanning lotions (e.g., dihydroxyacetone)
• Repigmentation (This is achieved by the activation and migration of melanocytes from hair follicles; therefore, skin with little or no hair responds poorly to treatment.)
• Narrow-band ultraviolet B radiation (This is the preferred treatment for nonsegmental vitiligo. It is given twice weekly [not on successive days] during sessions that last from 5 to 10 min. The best results are achieved on
the face, trunk, and limbs.)

• Psoralens and sunlight (e.g., PUVAsol)
• Topical mid-potency steroids (e.g., triamcinolone 0.1% or desonide 0.05% cream qd for 3 to 4 mo)
• Topical calcineurin inhibitors for face and neck lesions
• Intralesional steroid injection
• Systemic steroids (e.g., betamethasone 5 mg qd on two consecutive days per wk for 2 to 4 mo)
• Total depigmentation in cases of extensive vitiligo with 20% monobenzyl ether or hydroquinone (This is a permanent procedure, and patients will require lifelong protection from sun exposure.)
• Topical immunomodulators (e.g., tacrolimus, pimecrolimus) (These substances can also induce the repigmentation of vitiliginous skin lesions. However, their potential for systemic immunosuppression or for increasing the risk
of skin or other malignancies remains to be defined.)
• Calcipotriol, which is a synthetic analog of vitamin D3 (This has also been used in combination with ultraviolet light or clobetasol, with limited results.)
• Surgical techniques

Vitamin Deficiency (Hypovitaminosis)

Vitamins are organic compounds that cannot be synthesized by humans but are required as nutrients in minute amounts. Vitamins have several different functions: They may regulate cell growth and differentiation, as catalysts,
as antioxidants, and as co-enzymes. Vitamins are classified as either fat soluble (vitamins A, D, E, K) or water soluble (B group of vitamins and C). Deficiency of most vitamins is rare in Western countries. Certain groups may be prone
to vitamin deficiency, and these are discussed here. Vitamin D deficiency is discussed in a separate topic.

Most of the vitamins are available over the counter individually or in different multivitamin formulations.
Specific vitamins:
• Vitamin A deficiency: treat with oral supplementation 10,000 IU daily.
– Consume vitamin A–rich foods such as liver, beef, carrots, oranges, mangoes.
– 5 servings of fruit and vegetables give enough carotenoids for a day.
• Vitamin K deficiency: treatment depends on the severity of bleeding, administered subcutaneously (SQ) or intramuscularly (IM).

• Vitamin B1 (thiamine) deficiency: give intramuscular thiamine 50 mg for several days.
– If B1 deficiency is suspected and patient needs intravenous glucose, give thiamine first before intravenous glucose. This prevents the development of Korsakoff psychosis.
• Vitamin B12 deficiency: give 1000 mcg IM daily for 7 days, then once a week for 1 month, then once a month indefinitely.
– A potential option is oral supplementation.
• Folic acid deficiency: daily requirement is 400 to 1000 mcg (1 mg) daily.
– Centers for Disease Control and Prevention (CDC) recommend that women of childbearing age take 400 mcg of folic acid daily.


Key Steps
1. Perform neurovascular examination.
2. Insert tape with hemostat.
3. Wind tape proximal to distal.
4. Do not compromise arterial supply.
5. Pull proximal edge to unwind.

1. After careful neurovascular exam demonstrates intact sensation and arterial supply, lubricate the finger .
2. Carefully insert spooled suture, umbilical tape, or dental floss under the palmar aspect of the ring with a hemostat

3. Secure the suture edge to the palm with an adhesive.
4. Proceed to wrap the suture firmly around the finger, starting immediately distal to the ring and moving distally.
5. Wrap the suture tightly enough to compress the edema without producing any arterial compromise .
6. After relubricating the finger and removing the suture, gently unwind the proximal edge of the suture by pulling distally and circumferentially .
7. After removing the ring, repeat the neurovascular exam.

• Distal finger injury with impending swelling of the finger
• Ring finger with signs of vascular compromise due to compression from the ring
• Ring made of conductive or magnetic metal in patient undergoing procedure in which such objects pose a threat to the patient or staff.

• Extensive bony injury or swelling where it is clear that cutting the ring is he only option


Eclampsia is the occurrence of seizures or coma in a woman with preeclampsia, occurring at >20 wk of gestation or <48 hr postpartum. Atypical eclampsia occurs at <20 wk of gestation or as much as 14 days postpartum.

• Seizure begins as facial twitching, then spreads to generalized clonicotonic state, with cessation of respiration followed by a postictal period of amnesia, agitation, and confusion.
• 40% have severe hypertension, 40% have mild to moderate hypertension, and 20% are normotensive.
• Generalized edema with rapid weight gain (>2 lb/wk) may be one of the earliest signs of eclampsia.
• Persistent occipital headache and hyperreflexia with clonus occur in 80% of patients with eclampsia; epigastric pain occurs in 20% of these patients.

• Exact etiology unknown.
• Common pathway relates to abnormalities in autoregulation of cerebral blood flow. This may involve transient vasospasm, ischemia, cerebral hemorrhage, and edema occurring by a mechanism involving hypertensive
encephalopathy, decreased colloid osmotic pressure, and prostaglandin imbalance.

• Proteinuria: severe (49%), mild to moderate (29%), absent (22%)
• HCT: elevated as a result of hemoconcentration
• Platelet count: decreased; LFTs elevated in HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count)
• BUN and creatinine: elevated with renal involvement
• Serum electrolytes, glucose, calcium, toxicology profile: rule out other causes of seizures
• Hyperuricemia: >6.9 mg/dl found in 70% of eclamptics
• ABG: maternal acidemia and hypoxia.
• CT scan or MRI indicated in atypical presentation, suspected intracerebral bleeding, or focal neurologic deficit.
• There are abnormal findings, including cerebral edema, hemorrhage, and infarction, in 50% of patients.

• Airway protection (risk of aspiration)
• Supportive care during acute event
• Maintain airway, adequate oxygenation, and IV access.
• Fetal resuscitation, involving maternal oxygenation, left lateral positioning, and continuous fetal heart rate monitoring, is needed.
• Magnesium sulfate is the drug of choice. Give magnesium sulfate 6 g IV load over 20 min, then 3 g/hr maintenance, for recurrent seizure prophylaxis. If repeated convulsions, may give an additional 2 g IV over 3 to 5 min. Approximately 10% to 15% of patients will have a second seizure after initial loading dose. Check magnesium level 1 hr after loading dose, then q6h (therapeutic range 4 to 6 mg/dl). Antidote for toxicity is calcium gluconate 10 ml of 10% solution. Phenytoin has been used as an alternative in patients in whom magnesium sulfate is contraindicated
(renal insufficiency, heart block, myasthenia gravis, hypoparathyroidism).
• Give sodium amobarbital 250 mg IV over 3 min for persistent seizures.
• Treat blood pressure if >160 mm Hg/110 mm Hg with labetalol 20- to 40-mg IV bolus, hydralazine 10 mg IV, or nifedipine 10 to 20 mg sublingual q20min.
• Evaluate patient for delivery.

• The first priority is stabilization of the mother in terms of adequate oxygenation, hemodynamics, and laboratory abnormalities, such as associated coagulopathies.
• Cervical status and gestational age should be assessed. If unfavorable cervix and <30 wk of gestation, consider C-section; otherwise consider induction.
• Controlled epidural is the anesthesia of choice for labor or C-section.
• Avoid general anesthesia in uncontrolled hypertension to minimize risk of catastrophic cerebral events.

Bedbug Bite

A bedbug’s bite is a wound caused by the penetration of the bedbug mouthpiece into the skin as the insect feeds on blood from vessels or extravasated blood from the damaged surrounding tissue. The saliva of the bedbug contains pharmacologically active substances responsible for a spectrum of undesirable skin reactions depending on the individual. The bugs typically feed during times when an individual is at rest and may feed without being detected.
Typically feedings take 5 to 10 minutes.

• Traditionally, bedbugs were considered more common in poorer areas, but they are now increasingly found in areas of frequent travel.
• Bedbug infestations may spread among multifamily and institutional facilities with shared walls and are consequently difficult to eradicate.
• Reports of bedbug infestations have increased dramatically in the U.S., as well as worldwide, likely because of the decreased use of pesticides and increased international travel.
• Bedbugs are attracted to carbon dioxide gas and warm bodies.
• Bedbugs do not have a preference for specific age groups, ethnicity, or sex.
• Studies have shown increased sensitivity of cutaneous reaction in previous bite victims.

• The Cimex lectularius species, also known as the common bedbug, feeds on mammals and birds. Cimex hemipterus is a tropical species that bites mostly humans, and hybrid species of the two insects exist. Both generally feed nocturnally on the blood of sleeping humans. The adult bedbug is wingless and about 5 to 7 mm in length. It has a modified mouthpart for piercing and sucking that usually leaves a bite mark of papular urticarial presentation to exposed areas of skin. Bedbugs have weak appendages for latching on to their hosts and are not usually
transported from person to person.
• The saliva of the bedbug contains nitrophorin that enables vasodilation, an anticoagulant that interferes with production of coagulation factor Xa, a salivary apyrase that inhibits platelet aggregation, and an anesthetic.
Consequently, the host often does not feel the bite until the effects have worn off.

• Workup begins with history and physical for clinical symptoms and environmental findings.
• Victims should carefully scrutinize the bedroom for signs of bedbug infestation. One may encounter fecal smears or flecks of blood on bed linens, inside furniture cracks and crevices, and behind peeling wallpaper.
Bedbugs may travel as far as 20 feet for a meal. Densely infested rooms may also have a distinctive, pungent, soda syrup–like odor.

• Treatment of bites is often not necessary. Bites may self-resolve within a week for milder cases and a few weeks for more severe cases.
• To prevent infection, avoid scratching the area.
• Topical glucocorticoids or systemic antihistamines are appropriate in patients with severe pruritus from the bedbug bite. C Triamcinolone cream 0.1%; apply thin film to affected areas bid C Chlorpheniramine 4 mg PO at bedtime (adults), 2 mg PO at bedtime (children)
• Insecticides may be effective in eradicating the bedbug, but growing resistance has been seen and multi-insecticide therapy is recommended. C Use permethrin spray for clothing and bedsheets or bednets C Diethyltoluamide (DEET): Be wary of toxic levels in children when used at high concentrations.
C Deltamethrin and chlorfenapyr are two common insecticides used.
C Please consult a pest control professional for safe eradication.

Vacuuming is effective in removing bedbugs but does not remove the eggs. Wash bedsheets and clothing in hot water with detergent with at least 20 minutes in a dryer. Bedbugs have a high thermal death point of 45° C and also
may survive at temperatures as low as 7° C. Some companies perform a treatment in which the room is heated above 50° C, which is a lethal temperature for all stages of a bedbug’s life cycle. Coating bedposts with antifriction or
adhesive substances such as petrolatum or duct tape may hinder bedbugs from gaining access to the bed.


Balanitis is an inflammation of the superficial tissues of the penile head (glans penis). If the foreskin (prepuce) is involved, it is called balanoposthitis.

• Itching and tenderness
• Pain, dysuria, and local edema
• Rarely, ulceration and lymph node enlargement
• Severe ulcerations leading to superimposed bacterial infections
• Inability to void: unusual, but a more distressing and serious complication.

• Leukoplakia
• Nummular eczema
• Balanitis xerotica obliterans
• Psoriasis
• Carcinoma of the penis
• Plasma cell balanitis (noninfectious)
• Erythroplasia of Queyrat
• Nodular scabies
• Circinate balanitis (Reiter’s syndrome)

• VDRL for syphilis
• Serum glucose to rule out diabetes
• Wet mount for Trichomonas
• KOH prep for yeast
• Microbial culture to rule out STD


• Maintenance of meticulous hygiene
• Retraction and bathing of prepuce several times a day
• Warm sitz baths to ease edema and erythema                                                                                                                                  • Consideration of circumcision, especially when symptoms are severe or recurrent
• With Foley catheters, strict catheter care strongly advised
• Metronidazole 2 g PO as a single dose or Fluconazole 150 mg PO × 1 or itraconazole 200 mg PO bid × 1 day
• Clotrimazole 1% cream applied topically twice daily to affected areas
• Bacitracin or Neosporin ointment applied topically 4 times daily
• With more severe bacterial superinfection: cephalexin 500 mg PO qid
• Topical corticosteroids added 4 times daily if dermatitis severe
• Patients with suspected urinary tract infections: trimethoprim-sulfa DS twice daily or ciprofloxacin 500 mg PO bid after obtaining appropriate cultures.