Varicose

DEFINITION
Veins in the leg are soft, thin-walled tubes that return blood back to the heart. This is accomplished
by the presence of one-way valves and the action of the calf pump. Superficial venous insufficiency develops when venous return is impaired by valvular incompetence, obstruction, or calf muscle pump failure.
Varicose veins, the most common clinical manifestation of chronic venous disease, are bulging (>3 mm in diameter), tortuous conduits. Reticular veins, often called “feeder veins,” are bluish subdermal veins about 1 to 3 mm in diameter that give rise to telangiectasia. Spider veins or telangiectasias are very small (≤1 mm in diameter) thread veins found commonly in clusters on the surface of the skin.

EPIDEMIOLOGY
PREVALENCE: One large U.S. cohort study found the biannual incidence of varicose veins was 3% in women and 2% in men. The prevalence of varicose veins in Western populations was estimated in one study to be
about 25% to 30% in women and 10% to 20% in men.
RISK FACTORS
Gender: female
Genetics: family history of varicose veins Increasing age ,Multiple pregnancies.

CLINICAL PRESENTATION
• Chronic vein disease is the result of the introduction of high pressures into a normal low-pressure superficial venous system.
• This increased pressure or venous hypertension causes superficial veins to distend to such a degree that vein valves fail to close, causing reflux and pooling of blood in surface veins.
• Manifested clinically by two syndromes:
1. Junctional: failure of the terminal valve at the intersection between the saphenous vein trunks and the deep system. If the great saphenous vein is involved, large varicose veins are found mainly above medial knee or calf. When the small saphenous vein is involved, large varicose  veins are found in posterior knee or calf area. If the anterior accessory of great saphenous vein is involved, large varicose veins are found mainly in anterior or lateral thigh.
2. Perforator: failure of valves located in perforating vein. Large varicose veins are found most commonly in medial calf and proximal thigh region.
CLASSIFICATION
Chronic venous disease can now be classified using the Clinical-Etiology-Anatomy- Pathophysiology (CEAP) criteria to allow a precise description of the type of venous disease being discussed and provide an orderly framework for decision making.

ETIOLOGY
• The underlying etiology of varicose veins remains uncertain.
• Important structural changes that occur: failure of vein valve function and vein wall dilation from fragmentation of the muscle layer.
COMPLICATIONS
• Superficial venous thrombophlebitis (SVT): a very common disorder with an incidence of 125,000 new cases per year in the U.S. The most frequent predisposing risk factors are varicose veins. The clinical findings include
the presence of erythema, tenderness, and a palpable cord. Pain, increased warmth, and swelling are also present. Diagnosis is made by ultrasonography, which is useful to identify associated deep vein thrombosis that can
occur in approximately 15% of patients. The location of the SVT determines the course of treatment; if the proximal great saphenous vein (GSV) is involved, a 1-mo course of sion stockings has been found to be more effective than vein ligation. If SVT involves branch varicosities, treatment is usually symptomatic (control of pain).
• Bleeding is a more common complication than traditionally suspected. It is associated with thin-walled ectatic veins known as “blue blebs” that are found predominantly in the medial lower calf and ankle region.                               The best emergency treatment consists of pressure wrapping and not suture ligation, which results in delayed healing of the bleeding site. Sclerotherapy of these veins is the definitive treatment to prevent further bleeding.

DIFFERENTIAL DIAGNOSIS
Other conditions that cause leg pain:
• Stress fracture
• Arthritis hip/knee joint
• Gout
• Degenerative disk disease of lower back
• Intermittent claudication secondary to peripheral arterial disease (PAD)
• Medications such as allopurinol and statins Other conditions that cause leg swelling:
• Cellulitis
• Soft tissue injury to leg/ankle/foot

TREATMENT
CONSERVATIVE THERAPY
• Aerobic exercise regularly for 30 min a day.
• Elevate legs above heart level to reduce swelling.

• Flex ankles frequently at work and during air travel or long car travel.
• Maintain proper weight.
• Graduated compression stockings (below knee) to alleviate symptoms in patients who are not candidates or do not desire to undergo treatment of their varicose veins.
SCLEROTHERAPY
• Small- to medium-sized varicose veins such as spider veins and reticular varices in the absence of reflux in saphenous trunks are best treated with liquid sclerotherapy.
• The three principal sclerosants used in the U.S. are hypertonic saline, sodium tetradecylsulfate, and the newly FDA-approved solution, polidocanol.
• These agents are injected into vessels using 27-gauge or 30-gauge needles at concentrations of 23.4%, 0.1%, or 0.5%, respectively, causing injury to the endothelium with the resultant disappearance of the vein over period of time (usually 8-12 wk).
AMBULATORY PHLEBECTOMY
• A procedure in which large varicose vein branches are removed with special hook instruments through a small puncture— incisions are made with an 18-gauge needle or No. 11 blade
• Performed safely under local anesthesia in an office setting and offers excellent cosmetic results and relief of symptoms
• Most commonly performed in conjunction with endovenous ablation procedures

ENDOVENOUS ABLATION
• Ablation of diseased saphenous vein trunks, large incompetent tributaries, or perforating veins can be achieved by using:
1. Radiofrequency energy
2. Laser energy
3. Ultrasound-guided foam sclerotherapy.
• The first two accomplish thermal injury to the vein in situ via an intraluminal catheter or bare-tipped laser wire. Chemical ablation uses a solution (polidocanol or sodium tetradecyl sulfate) that is injected directly into the
vein in the form of foam.
• Endovenous ablation can be performed in an office setting using local anesthesia. Patients can return to their normal daily activities immediately.
• The efficacy of these endovenous ablation procedures has been borne out by numerous published reports with occlusion rates over 95% and reflux free rates over 5-yr follow-up of 86%. A recent trial comparing ultrasoundguided
foam sclerotherapy and endovenous laser ablation revealed that quality of life measures were generally similar among the study groups, with the exception of a slightly worse disease-specific quality of life in the foam group than in the surgery group. Both treatments had similar efficacy, but complications were less frequent after laser treatment
and ablation rates were lower after foam treatment.

Abdominal Aortic Aneurysm (AAA)

An abdominal aortic aneurysm (AAA) is a focal full-thickness dilation of the abdominal aortic artery to at least 1.5 times the diameter measured at the level of the renal arteries, or exceeding the normal diameter of the abdominal aorta by 50%.

Risk factors for AAA are similar to other atherosclerotic cardiovascular diseases. They include age, smoking, male gender, family history, hypertension, hyperlipidemia, peripheral vascular disease, and aneurysm of other large vessels.

CAUSES

_ Unknown and likely multifactorial

1/. Degenerative

  • The most common association is atherosclerosis.
  • Tobacco use

2/. Inherited

The nature of the genetic disorder is unclear but may be linked to alpha-1-antitrypsin deficiency or X-linked mutation. Connective tissue disorders, such as Marfan’s syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA.

3/. Inflammatory

4/. Infection, mycotic: syphilis, Salmonella.

NATURAL HISTORY

The risk of aneurysmal rupture is largely influenced by aneurysm size, rate of expansion, and sex. Other factors associated with increased risk for rupture include continued smoking, uncontrolled hypertension, and increased wall stress.

CLINICAL

_ Most aneurysms are asymptomatic and incidentally discovered on imaging studies; however, symptomatic aneurysms are at an increased risk for rupture.

_ Symptomatic patients may present with abdominal, back, flank, or groin pain.

_ A pulsatile epigastric mass that may or may not be tender may be present.

_ Abdominal pain radiating to the back, flank, and groin.

_ Abdominal bruits can be present in case of renal or visceral arterial stenosis.

_ Rupture classically presents as a triad of abdominal or back pain, hypotension, and a pulsatile abdominal mass in 50% of patients.

_ Acute blood loss may lead to myocardial infarction; arteriovenous fistulas may present as heart failure; aortoenteric fistulas may present as hematemesis or melena associated with abdominal and back pain.

DIAGNOSIS

_ Abdominal ultrasound

_ CT Scan

_ Magnetic Resonance Angiography (MRA)

MANAGEMENT

_ Acute symptomatic or ruptured AAA can be treated with open surgical or endovascular aneurysm repair (EVAR). The choice is determined by anatomic considerations, operative risks, and availability of regular patient follow-up for EVAR.

Multiple Myeloma is a Malignancy of Plasma Cells

Multiple myeloma is a malignancy of plasma cells characterized by clonal proliferation of malignant plasma cells in the bone marrow, monoclonal protein in the blood or urine, and associated organ dysfunction. Diagnostic criteria require the following:

  1. Presence of 10% plasma cells on examination of the bone marrow (or biopsy of a tissue with monoclonal plasma cells).
  2. Monoclonal protein in the serum or urine. Occasional patients without detectable monoclonal protein are considered to have nonsecretory myeloma.
  3. Evidence of end-organ damage (alcium elevation, enal insufficiency, nemia, or one lesions [CRAB]).

PHYSICAL FINDINGS & CLINICAL

PRESENTATION

The patient usually comes to medical attention because of one or more of the following:

  • Bone pain (58%) (back, thorax) or pathologic fractures (30%) caused by osteolytic lesions
  • Fatigue (32%) or weakness because of anemia from bone marrow infiltration with plasma cells
  • Recurrent infections as a result of impaired neutrophil function and deficiency of normal immunoglobulins
  • Nausea and vomiting caused by constipation and uremia
  • Delirium resulting from hypercalcemia
  • Neurologic complications, such as spinal cord or nerve root compression, blurred vision from hyperviscosity
  • Pallor and generalized weakness from anemia
  • Purpura, epistaxis from thrombocytopenia
  • Evidence of infections from impaired immune system
  • Paresthesias (5%), weight loss (24%)
  • Swelling on ribs, vertebrae, and other bones

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

  • Metastatic carcinoma
  • Lymphoma (B-cell non-Hodgkin lymphoma)
  • Bone neoplasms (e.g., sarcoma)
  • Monoclonal gammopathy of undetermined significance
  • Primary amyloidosis
  • Chronic lymphocytic leukemia
  • Waldenstrom’s macroglobulinemia

LABORATORY TESTS

  • Normochromic, normocytic anemia; rouleaux formation on peripheral smear
  • Hypercalcemia is present in 15% of patients at diagnosis.
  • Elevated blood urea nitrogen, creatinine, uric acid, and total protein
  • Urine protein immunoelectrophoresis: proteinuria from overproduction and secretion of free monoclonal kappa or lambda chains (Bence Jones protein)
  • Serum protein immunoelectrophoresis: tall homogeneous monoclonal spike (M spike) on protein immunoelectrophoresis in approximately 75% of patients; decreased levels of normal immunoglobulins (Ig)

 

  1. The increased immunoglobulins are generally IgG (75%) and IgA (15%).
  2. Approximately 17% of patients have a flat level of immunoglobulins but increased light chains in the urine by lectrophoresis.
  3. A small percentage (,2%) of patients have nonsecreting myeloma (no increase in immunoglobulins and no light chains in the urine) but have other evidence of the disease (e.g., positive bone marrow examination).
  • Reduced ion gap from the positive charge of the M proteins and the frequent presence of hyponatremia in myeloma patients
  • Hyponatremia, serum hyperviscosity (more common with production of IgA)
  • Bone marrow examination: usually demonstrates nests or sheets of plasma cells, which comprise .30% of the bone marrow; 10% are immature
  • Serum beta-2 microglobulin has little diagnostic value; it is useful for prognosis because levels .8 mg/L indicate high tumor ass and aggressive disease.
  • Elevated serum levels of lactate dehydrogenase at the time of diagnosis define a subgroup of myeloma patients with very poor prognosis.
  • Increased interleukin-6 in serum during active stage of myeloma
  • The production of DKK1, an inhibitor of osteoblast differentiation, by myeloma cells is associated with the presence of lytic bone lesions in patients with multiple myeloma.
  • Nearly all patients with myeloma present with abnormal chromosomes identified by fluorescence in situ hybridization (FISH). The Mayo Clinic Stratification of Myeloma, for purposes of therapy, identifies high-risk patients (,25% of patients at diagnosis) as those who have any of the following: FISH deletion 17p, FISH translocation 4;14, FISH translocation 14;16, cytogenetic deletion 13q, cytogenetic hypodiploidy, or plasma cell labeling index 13%.

STAGING

Hemolytic-Uremic Syndrome: Definition, Causes , Diagnosis & Treatment

DEFINITION
Hemolytic-uremic syndrome (HUS) refers to an acute syndrome characterized by hemolytic anemia, thrombocytopenia, and severe renal failure .

PHYSICAL FINDINGS AND CLINICAL PRESENTATION
● HUS usually preceded by diarrhea in 90% of cases
● Bloody diarrhea (75%)
● Abdominal pain
● Vomiting
● Fever
● Irritability, lethargy, and seizures (10%)
● Hypertension
● Pallor
● Anuria or oliguria

CAUSE
● Pathologically, it is thought that thrombin generation (probably the result of accelerated thrombogenesis) and inhibition of fibrinolysis lead to renal arteriolar and capillary microthrombi preceding renal injury.
● In children
● E. coli serotype O157:H7 is the leading cause of HUS.
● The infection is acquired by eating undercooked red meat, especially hamburgers.
● Other causes of HUS in children and adults include the following:
● Drugs (e.g., cyclosporine, mitomycin, tacrolimus, ticlopidine, clopidogrel, cisplatin, quinine, penicillin, penicillamine, oral contraceptives, quinine used to treat muscle cramps)
● Infection (Salmonella, Shigella, Yersinia, group A streptococci, Clostridium difficile, Campylobacter, coxsackievirus, rubella, influenza virus, EBV)
● Toxins
● Pregnancy (usually postpartum) and oral contraceptives
● HIV-associated thrombotic microangiopathy
● Pneumococcal infection
● Persons with a relative deficiency in von Willebrand factor–cleaving protease (VMF-CP) are predisposed to nonenteric infection forms of HUS.

DIAGNOSIS
The triad of thrombocytopenia, acute renal failure, and macroangiopathic hemolytic anemia establishes the diagnosis of HUS.
DIFFERENTIAL DIAGNOSIS
The differential is vast, including all causes of bloody and nonbloody diarrhea because the GI symptoms usually precede the triad of HUS.
● Thrombotic thrombocytopenic purpura
● Disseminated intravascular coagulation
● Prosthetic valve hemolysis
● Malignant hypertension
● Vasculitis

LABORATORY TESTS
● CBC with hemoglobin 10 g/dL
● Peripheral smear shows the hallmark microangiopathic hemolytic anemia with schistocytes, burr cells, and helmet cells .
● Thrombocytopenia (platelet counts usually _60,000/mm3)
● Reticulocyte count is high.
● LDH level is elevated.
● Haptoglobin is low.
● Indirect bilirubin is elevated.
● BUN and creatinine are elevated.
● Urinalysis reveals proteinuria, microscopic hematuria, and pyuria.
● Stool cultures for E. coli O157:H7 are positive in over 90% of cases if obtained during the first week of illness. After the first week, only one third are positive.
TREATMENT
● Blood transfusions for severe anemia
● Antibiotics should be avoided and are not indicated for the treatment of E. coli O157:H7.
● Correction of electrolyte abnormalities
● FFP may benefit patients with nonenteric forms of HUS if they are deficient in VMF-CP.