Nail Fungus: Overview, Causes, Management

Nail fungus, or onychomycosis, is an infection of nails with fungal organisms. More toenails than fingernails are affected. It’s more common in elderly people with poor circulation and diabetics. People often have a fungal foot infection (athlete’s foot), along with toenail fungus.

What Causes Nail Fungus?

The most frequent causes are fungi called dermatophytes. People often pick up and spread the infection at public swimming pools and locker rooms, where they walk around barefoot. Conditions there are warm and damp, which are best for fungi to grow. Fungal infections can also spread in families by sharing towels and footwear. Damage to nails can make it easier to get infected.

What Are the Symptoms of Nail Fungus?

Symptoms include change in nail color to yellow, brown, or white; thicker nails with shape changes; brittle and  flaky nails, with splits and chips; accumulation of fungus and dirt under nails, leading to a bad smell; separation  of nails from toes or fingers; and, rarely, pain.

How Is Nail Fungus Diagnosed?

The doctor makes a diagnosis from an examination of the nails. A scraping of the nail or nail clippings may be taken and sent to a laboratory for study.

How Is Nail Fungus Treated?

Early treatment is best, but getting rid of the fungus may be hard. Untreated, nails may have permanent damage and deformity, leading to problems wearing shoes or walking. Oral antifungal drugs, such as terbinafine, taken for 3 months for toenail fungus and 6 weeks for fingernail fungus are the usual treatment. Some people cannot take these drugs because of their other drugs or medical problems. Antifungal drugs can also be put directly on infected nails (topical treatment) for up to 12 months. These topical drugs don’t usually work very well.

Other treatments, not usually done, include removing the infected nail and scraping the nail to make it less thick. Usually, a foot doctor (podiatrist) does these.

Best Management in Vulvar Cancer

DEFINITION
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
melanoma.

EPIDEMIOLOGY & DEMOGRAPHICS
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.

PHYSICAL FINDINGS & CLINICAL PRESENTATION
• 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.

ETIOLOGY
• 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.

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

NONPHARMACOLOGIC THERAPY
• 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.

Carotid Stenosis

DEFINITION
Carotid stenosis is narrowing of the arterial lumen within the carotid artery that is typically a result of atherosclerosis.

PRESENTATION
Patients with carotid stenosis are often asymptomatic, but many have the presence of a carotid bruit or TIA.

• Carotid bruit: In general, the presence of a carotid bruit is a better indicator of generalized atherosclerosis and as such, is a better predictor of ischemic heart disease than future stroke.
• TIA: Carotid stenosis is classically heralded by ipsilateral transient monocular blindness (amaurosis fugax), contralateral numbness or weakness, contralateral homonymous hemianopsia, aphasia, or syncope (if bilateral
disease is present).


ETIOLOGY
• Atherosclerosis (most common by far)
• Aneurysm
• Arteritis
• Carotid dissection
• Fibromuscular dysplasia
• Postradiation necrosis
• Vasospasm

NONPHARMACOLOGIC THERAPY
Carotid endarterectomy (CEA) and carotid angioplasty and stenting (CAS) are available. CEA—several studies have proved the efficacy of this procedure. The selection of surgical candidates should be guided primarily by the
presence or absence of symptoms and the degree of stenosis.
Asymptomatic patients: Four major trials have investigated the benefit of CEA in an asymptomatic patient with carotid stenosis:
-Carotid Artery Surgery Asymptomatic
-Narrowing Operation vs Aspirin (CASANOVA),
-Veterans Affairs Cooperative Study Group,
-Asymptomatic Carotid Atherosclerosis
-Study (ACAS), and Asymptomatic Carotid
-Surgery Trial (ACST). In addition, a metaanalysis was subsequently performed. Pearls:

Most studies have shown that a benefit from CEA in asymptomatic patients is not seen until 2 yr after surgery.
CEA should be considered in asymptomatic patients only if the perioperative
risk for stroke and death at the given surgical institution is less than 3%. The studies failed to show a benefit in
the presence of contralateral carotid occlusion.
Recommendations for asymptomatic patients with carotid stenosis:
CEA should be considered in patients between the ages of 40 and 75 yr with asymptomatic 60% to 99% stenosis
if their life expectancy is greater than 5 yr and the perioperative stroke and mortality rates are <3%. However,
medical therapy has improved since early trials comparing medical management and revascularization. Stroke rates have fallen to about 1% in medically treated patients over the past decade.

Anemia, Aplastic

DEFINITION
Aplastic anemia is a bone marrow failure syndrome defined by peripheral blood pancytopenia and hypocellular bone marrow.

DEMOGRAPHICS INCIDENCE: The annual incidence of aplastic anemia is 2 cases per million.
PREDOMINANT SEX AND AGE: The incidence has two peaks, with most patients presenting between ages 15 and 25 or after 60 yr.
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Mucosal bleeding, easy bruising, petechiae or heavy menstrual bleeding is seen secondary to thrombocytopenia.
• Fatigue, lassitude, skin pallor, exertional dyspnea, or palpitations are seen secondary to anemia.
• Infection is an uncommon presentation, but neutropenia may lead to fever and sore throat.
• Various physical manifestations like short stature, skeletal or nail changes may be seen in congenital forms of aplastic anemia.

DIFFERENTIAL DIAGNOSIS
• Bone marrow infiltration from lymphoma, carcinoma, myelofibrosis
• Severe infection
• Hypoplastic myelodysplastic syndrome or hypoplastic acute myeloid leukemia in adults
• Hypersplenism
• Hairy cell leukemia
WORKUP
• Diagnostic workup  consists primarily of bone marrow aspiration and biopsy, and laboratory evaluation (CBC and examination of blood film).
• Bone marrow examination generally shows paucity or absence of erythropoietic and myelopoietic precursor cells ; patients with pure red cell aplasia demonstrate only absence of red blood cell (RBC) precursors in the marrow.


LABORATORY TESTS
• CBC reveals pancytopenia .
Macrocytosis and toxic granulation of neutrophils may also be present. Isolated cytopenias may occur in the early stages.
• Reticulocyte count reveals reticulocytopenia.
• Additional initial laboratory evaluation should include Ham test and/or peripheral blood flow cytometry to exclude paroxysmal nocturnal hemoglobinuria and testing for hepatitis C.

NONPHARMACOLOGIC THERAPY
Discontinue any offending drugs or agents.
ACUTE GENERAL Rx
• Aggressive treatment of neutropenic fevers with parenteral broad-spectrum antibiotics.
• Administer platelet and RBC transfusions as needed; however, it is important to avoid transfusions in patients who are candidates for bone marrow transplantation.

CHRONIC Rx
• Allogenic bone marrow transplantation (ABMT) from a human leukocyte antigen (HLA)–matched sibling donor is curative.
• Patients who do not have a matched sibling can be treated with a matched unrelated transplant, but the mortality rate is higher.
• Immunosuppressive therapy with antithymocyte globulin (ATG) is an effective alternate treatment for patients who are not candidates for ABMT.
• Other immunosuppressive agents such as cyclosporin, cyclophosphamide, or corticosteroids also have a role in the treatment of aplastic anemia.
• Androgens such as danazol are effective second-line agents.
• The oral thrombopoietin mimetic eltrombopag can improve hematopoiesis in refractory severe aplastic anemia.

Acne Vulgaris

DEFINITION
Acne vulgaris is a chronic disorder of the pilosebaceous apparatus caused by abnormal desquamation of follicular epithelium leading to obstruction of the pilosebaceous canal, resulting in inflammation and subsequent formation
of papules, pustules, nodules, comedones, and scarring.

PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Open comedones (blackheads), closed comedones (whiteheads)
• Greasiness (oily skin)
• Presence of scars from prior acne cysts
• Various stages of development and severity may be present concomitantly
• Common distribution of acne: face, back, and upper chest
• Inflammatory papules, pustules, and ectatic pores

ETIOLOGY
• Overactivity of the sebaceous glands and blockage in the ducts. The obstruction leads to the formation of comedones, which can become inflamed because of overgrowth of Propionibacterium acnes.
• Exacerbated by environmental factors (hot, humid, tropical climate), medications (e.g., iodine in cough mixtures, hair greases), industrial exposure to halogenated hydrocarbons.

DIFFERENTIAL DIAGNOSIS
• Gram-negative folliculitis
• Staphylococcal pyoderma
• Acne rosacea
• Drug eruption
• Sebaceous hyperplasia
• Angiofibromas, basal cell carcinomas, osteoma cutis
• Occupational exposures to oils or grease
• Steroid acne

• Hidradenitis suppurativa
• Perioral dermatitis
• Pseudofolliculitis barbae
• Miliaria
• Seborrheic dermatitis

TREATMENT
NONPHARMACOLOGIC THERAPY
Blue light (ClearLight therapy system) can be used for treatment of moderate inflammatory acne vulgaris. Light in the violet/blue range can cause bacterial death by a photoreaction in which porphyrins react with oxygen to generate
reactive oxygen species, which damage the cell membranes of P. acnes. Treatment usually consists of 15-min exposures twice weekly for 4 wk.

Typhoid Fever

DEFINITION
Typhoid fever is a systemic infection caused by Salmonella typhi.

PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Incubation period of a few days to several wk.
• Usual manifestations:
1. Prolonged fever
2. Myalgias
3. Headache
4. Cough
5. Sore throat
6. Malaise
7. Anorexia, at times with abdominal pain and hepatosplenomegaly
8. Diarrhea or constipation may occur early in the course of illness
9. Rose spots, which are faint, maculopapular, blanching lesions, may sometimes be seen on the chest or abdomen
• In the untreated patient, fever may last 1 to 2 mo. The main complication of untreated disease is GI bleeding as a result of perforation from ulceration of Peyer’s patches in the ileum. Mental status changes and shock
are rare complications. The relapse rate is approximately 10%.

ETIOLOGY
• Salmonella typhi
• S. paratyphi
• S. typhi or S. paratyphi found only in humans
• Acquisition of disease by ingestion of food or water contaminated by other humans
• In the U.S. most cases are acquired either during foreign travel or by ingestion of food prepared by chronic carriers, many of whom acquired the organism outside of the U.S.

DIFFERENTIAL DIAGNOSIS
• Malaria
• Tuberculosis
• Brucellosis
• Amebic liver abscess

LABORATORY TESTS
• Neutropenia is common.
• Transaminitis is possible.
• Culture:
1. Blood
2. Body fluids
3. Biopsy specimens

TREATMENT
ACUTE GENERAL Rx
• If not acquired in Asia: ciprofloxacin 400 mg IV q12h or levofloxacin 750 mg PO/IV q24h for 7-10 days
• If acquired in Asia: ceftriaxone 2 g IV daily for 7-14 days
• Dexamethasone, 3 mg/kg IV initially, followed by 1 mg/kg IV q6h for 8 doses for patients with septic shock or typhoid meningitis with antibiotic therapy
CHRONIC Rx
• Carrier states possible
• More common in age >60 yr and in people with gallstones
• Usual site of colonization: gallbladder
• Treatment in those with persistently positive stool cultures and in food handlers.

• Suggested regimens for eradication of carrier state
1. Ciprofloxacin 500 mg PO bid for 4 wk
2. SMX/TMP 1 to 2 tabs PO bid for 6 wk (if susceptible)
3. Amoxicillin, 2 g PO q8h for 6 wk (if susceptible)
• Cholecystectomy possibly required in carriers with gallstones who fail medical therapy.

SUBCUTICULAR RUNNING STITCHES

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.

INSTRUCTIONS
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.
INDICATIONS
• 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.
CONTRAINDICATIONS
• Knots requiring significant tension or sutures applied for hemostasis

DIGITAL BLOCK

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.

INSTRUCTIONS
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.

INDICATIONS
• Need for local anesthetic that encompasses the digit                                                                                                                    • Ingrown nail removal
• Drainage of felon or paronychia
• Management of fracture of phalanx
CONTRAINDICATIONS
• 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),
relative

Vulvar Cancer

DEFINITION
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
melanoma.

EPIDEMIOLOGY & DEMOGRAPHICS
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.

PHYSICAL FINDINGS & CLINICAL PRESENTATION
• 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.
ETIOLOGY
• 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.

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

NONPHARMACOLOGIC THERAPY
• 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

DEFINITION
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.

LABORATORY TESTS
• 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.

TREATMENT
NONPHARMACOLOGIC THERAPY
• 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.

GENERAL Rx
• 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.