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.

Abscess, Breast

DEFINITION
Breast abscess is an acute inflammatory process resulting in the formation of a collection of purulent material in breast tissue. Typically there is painful erythematous mass formation in the breast, occasionally draining through the overlying skin or nipple duct.

PHYSICAL FINDINGS & CLINICAL PRESENTATION
Painful erythematous induration involving breast and leading to fluctuant abscess
ETIOLOGY
• Lactational abscess: milk stasis and bacterial infection leading to mastitis and then abscess, with Staphylococcus aureus the most common causative agent
• Subareolar abscess:
1. Central ducts involved, with obstructive nipple duct changes leading to bacterial infection

2. Cultured organisms mixed, including anaerobes, staphylococci, streptococci, and others.

DIFFERENTIAL DIAGNOSIS
• Inflammatory carcinoma
• Advanced carcinoma with erythema, edema, and/or ulceration
• Tuberculous abscess (rare in the United States)
• Hidradenitis of breast skin
• Sebaceous cyst with infection
WORKUP
• Clinical examination
• If abscess suspected, referral to surgeon for incision, drainage, and biopsy
LABORATORY TESTS
• Perform culture and sensitivity test of abscess contents.
• If mammogram or ultrasound is required but prevented by discomfort, perform after treatment and subsequent resolution of abscess.

TREATMENT
NONPHARMACOLOGIC THERAPY
• Established abscess: incision and drainage
• Biopsy of abscess cavity wall to exclude carcinoma
ACUTE GENERAL RX
• Antibiotics: generally staphylococci in lactational abscess. Recommended initial antibiotic therapy is nafcillin or oxacillin 2 g q4h IV or cefazolin 1 g q8h IV for 10 to 14 days. Alternative includes vancomycin 1 g IV q12h.
• If acute mastitis is identified and treated early without the development of an abscess, resolution without drainage is possible.

• Subareolar abscess: broad-spectrum antibiotic treatment (e.g., cephalexin 500 mg PO qid or cefazolin 1 g q8h IV for 10 to 14 days for more severe infection) and drainage are needed to control acute phase. If abscess
is odoriferous, consider anaerobes as most likely etiology and add metronidazole 500 mg PO/IV tid.
CHRONIC RX
Further surgical treatment for recurrences or fistula.

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.