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Thrombophlebitis, Superficial

Last = Updated: April 10, 2002
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Synonyms and related = keywords:=20 superficial vein thrombophlebitis

  AUTHOR INFORMATION=20 Section 1 of = 9   =20
Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography
Author: Craig = Feied, MD,=20 FACEP, FAAEM, Director of Informatics, = Department of=20 Emergency Medicine, Washington Hospital Center; Clinical = Associate=20 Professor, Department of Emergency Medicine, George = Washington Univ;=20 Director, National Center = for=20 Emergency Medicine Informatics

Coauthor(s): Jonathan A=20 Handler, MD, Director of Informatics, Assistant = Professor, Department of Emergency Medicine, Northwestern = Memorial=20 Hospital

Craig Feied, MD, FACEP, FAAEM, is a member of the = following=20 medical societies: American = Academy=20 of Emergency Medicine, American=20 College of Emergency Physicians, American College of=20 Phlebology, American College=20 of Physicians, American=20 Medical Association, American=20 Medical Informatics Association, Medical Society of the = District of=20 Columbia, Society for = Academic=20 Emergency Medicine, and Undersea=20 and Hyperbaric Medical Society

Editor(s): Samuel M Keim, MD, Program = Director,=20 Associate Professor, Department of Surgery, Division of = Emergency=20 Medicine, University of Arizona Health Sciences Center;=20 Francisco Talavera, PharmD, PhD, Senior = Pharmacy=20 Editor, Pharmacy, eMedicine; Eddy Lang, MDCM, CCFP = (EM),=20 CSPQ, Assistant Professor, Department of Family = Medicine,=20 McGill University; Consulting Staff, Department of Emergency = Medicine, The Sir Mortimer B Davis-Jewish General Hospital;=20 John Halamka, MD, Chief Information = Officer,=20 CareGroup Healthcare System, Assistant Professor of = Medicine,=20 Department of Emergency Medicine, Beth Israel Deaconess = Medical=20 Center; Assistant Professor of Medicine, Harvard Medical = School; and=20 Charles V Pollack, Jr, MD, MA, Associate = Professor,=20 Department of Emergency Medicine, University of Pennsylvania = College=20 of Medicine; Chairman, Department of Emergency Medicine,=20 Pennsylvania Hospital

Background:=20 Superficial vein thrombophlebitis may occur spontaneously = or as a=20 complication of medical or surgical interventions. Sterile=20 thrombophlebitis limited to the superficial veins rarely is life=20 threatening, but a thorough diagnostic evaluation is mandatory = because=20 many patients with superficial phlebitis also have occult deep = vein=20 thrombosis (DVT), which carries very high rates of morbidity and=20 mortality.=20

Phlebitis should be assumed to involve the deep veins until = proven=20 otherwise, because superficial vein thrombophlebitis and deep vein = thrombophlebitis share the same pathophysiology, pathogenesis, and = risk=20 factors.=20

Superficial thrombophlebitis often progresses through = perforating veins=20 to involve the adjacent deep veins. In the case of spontaneous=20 thrombophlebitis, a superficial phlebitis at one location may be=20 accompanied by occult deep vein thrombosis in noncontiguous veins = in the=20 same leg or even in the contralateral leg. This occurs because=20 hypercoagulable states tend to produce thrombosis simultaneously = at=20 multiple sites in both the superficial and deep venous systems. A=20 surprising number of patients with clinically apparent superficial = phlebitis subsequently die from a pulmonary embolism (PE). Autopsy = studies=20 in these patients have demonstrated that the site of deep vein = thrombosis=20 often is not contiguous with the site of superficial phlebitis.=20

Clinical examination alone cannot distinguish purely = superficial=20 thrombophlebitis from phlebitis that has both superficial and deep = vein=20 components. When superficial and deep vein thrombosis coexist, the = superficial veins usually are tender and inflamed, while the deep=20 component most often is clinically silent. Duplex ultrasound = identifies=20 deep vein thrombosis in approximately 30% of patients with obvious = superficial thrombophlebitis who have no clinical evidence of deep = system=20 involvement, and continued surveillance reveals occult deep vein = extension=20 in 45% of cases. In hospitalized patients with superficial = phlebitis, 10%=20 eventually have a recognized diagnosis of PE, and 20% of those PEs = are=20 fatal.=20

Every effort should be made to prevent superficial phlebitis = from=20 progressing to involve the deep veins, because damage to deep vein = valves=20 leads to chronic deep venous insufficiency (often referred to as=20 postphlebitic syndrome) as well as to recurrent PE and a risk of = death.

Pathophysiology: Microscopic thrombosis is a = normal=20 part of the dynamic balance of hemostasis. In 1846, the great = German=20 pathologist Virchow recognized that if this dynamic balance is = altered by=20 venous stasis, abnormal coagulability, or vessel wall injuries,=20 microthrombi may propagate to form macroscopic thrombi.=20

In the absence of a triggering event, neither venous stasis nor = abnormal coagulability alone causes clinically important = thrombosis, but=20 vascular endothelial injury does reliably cause thrombus = formation. The=20 initiating injury triggers an inflammatory response that results = in=20 immediate platelet adhesion at the site of injury. Further = platelet=20 aggregation is mediated by thromboxane A2 and by thrombin. = Platelet=20 aggregation due to thromboxane A2 is inhibited reversibly by = nonsteroidal=20 anti-inflammatory agents and irreversibly by aspirin, but=20 thrombin-mediated platelet aggregation is unaffected by aspirin = and=20 nonsteroidals. This is why aspirin and nonsteroidal = anti-inflammatories=20 are somewhat effective in preventing arterial thrombosis, = including stroke=20 and myocardial infarction, but they are not very effective in = preventing=20 or treating venous thrombophlebitis.

Frequency:

  • In the US: Superficial thrombophlebitis is = so=20 common and so often ignored that obtaining valid estimates of = its=20 frequency is very difficult. Purely superficial thrombophlebitis = often=20 appears clinically obvious, but the clinical diagnosis of=20 thrombophlebitis is accurate only 50% of the time, even if the = patient=20 has classical symptoms.=20

    One third of patients in a medical intensive care unit = develop=20 thrombophlebitis that eventually progresses to the deep veins.=20 Approximately 40% of patients admitted and placed on bedrest for = acute=20 myocardial infarction develop superficial phlebitis that = progresses to=20 DVT. The lifetime incidence of superficial thrombophlebitis in = patients=20 with untreated varicose veins has been estimated at 20-50%, with = unrecognized associated deep vein thrombosis in up to 45% of = patients.=20 This appears to be the mechanism responsible for a 3-fold = increased=20 incidence of DVT in patients with superficial varicosities.=20

    The true incidence of DVT (with or without associated = superficial=20 thrombophlebitis) is also unknown. The incidence has been = estimated as=20 approximately 3 million cases per year, but this number cannot = be=20 considered reliable.

Mortality/Morbidity: Adverse outcomes from=20 thrombophlebitis are common, particularly when the process extends = to=20 involve the deep venous system.=20

  • Recanalization of thrombosed veins results in a valveless = channel,=20 leading to a prolonged venous circulation time and often to = chronically=20 elevated ambulatory venous pressure within the legs. Elevated = venous=20 pressures and delayed clearance of venous blood from the legs = produces a=20 clinical postphlebitic syndrome of chronic pain, edema,=20 hyperpigmentation, ulceration, and a high risk of recurrent=20 thrombophlebitis and PE.
  • Valvular damage from phlebitis is equally important at any = level in=20 the leg. Isolated calf vein thrombophlebitis results in clinical = postphlebitic syndrome in 20-40% of cases. Valvular incompetence = isolated to popliteal venous segments produces signs and = symptoms of=20 severe chronic venous insufficiency in more than 60% of cases, = with=20 elevated ambulatory venous pressures averaging 72 mm = Hg.
  • In the Framingham study population, PE was an autopsy-proven = principal or contributing cause of death in 16% of cases. Other = autopsy=20 studies have revealed evidence of prior venous thrombosis in up = to 60%=20 of all patients who undergo autopsy.

Sex:

  • Pregnancy and the puerperium are recognized risk factors for = phlebitis. High-dose estrogen therapy is also a risk factor, but = no=20 intrinsic sex-linked preferential risk exists for the = disease.
  • The likelihood of thrombophlebitis is increased through most = of=20 pregnancy and for approximately 6 weeks after delivery. This is = partly=20 due to increased platelet stickiness and partly due to reduced=20 fibrinolytic activity.
  • Case-controlled and cohort studies based on clinical signs = and=20 symptoms of thrombosis suggest that, by taking high-estrogen = oral=20 contraceptives, a woman may increase her risk of thrombosis by a = factor=20 of 3-12 times, although the absolute risk remains low. Newer = low-dose=20 oral contraceptives are associated with a much lower risk of=20 thrombophlebitis, although the absolute risk has not been well=20 quantified.

Age: Age is not an independent risk factor for = phlebitis, but the incidence of other recognized risk factors = increases=20 with age, leading to an overall increased risk with increasing = age.

  INTRODUCTION = Section 2 of = 9   
Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography

History:

  • Patients with superficial thrombophlebitis often give a = history of a=20 gradual onset of localized tenderness, followed by the = appearance of an=20 area of erythema along the path of a superficial vein. There may = be a=20 history of local trauma, prior similar episodes, varicose veins, = prolonged travel, or enforced stasis. The patient should be = asked about=20 risk factors for hypercoagulability, but the absence of = identifiable=20 risk factors has no prognostic value.
  • Occasionally, a spurious history of sudden onset of pain is = given. A=20 true sudden onset of pain suggests some other etiology for the = symptoms.=20 Similarly, patients occasionally report the recent sudden = development of=20 venous ulcers, stasis changes, and other conditions that, upon=20 inspection, obviously have been present for many months or=20 years.

Physical:

  • Inspection: Visual appearance is not a reliable guide to = peripheral=20 venous condition, because the clinical findings of venous = disease are=20 common to many other entities. Swelling may result from acute = venous=20 obstruction (as in deep vein thrombosis) or from deep or = superficial=20 venous reflux, or it may be caused by an unrelated disease = condition=20 such as hepatic insufficiency, renal failure, cardiac = decompensation,=20 infection, trauma, or environmental effects. Lymphedema may be = primary=20 or it may be secondary to overproduction of lymph due to severe = venous=20 hypertension.
    • Normal veins are distended visibly at the foot, ankle, and = occasionally in the popliteal fossa, but not in the rest of = the leg.=20 Normal veins may be visible as a blue subdermal reticular = pattern, but=20 dilated superficial leg veins above the ankle usually are = evidence of=20 venous pathology.
    • Darkened, discolored, stained skin or nonhealing ulcers = are=20 typical signs of chronic venous stasis, particularly along the = medial=20 ankle and the medial lower leg. Chronic varicosities or=20 telangiectasias also may be observed.
    • Acute deep venous obstruction may cause the sudden = appearance of=20 new vessels, large or small, that have become dilated to serve = as a=20 bypass pathway. New varices and telangiectasias often appear = during=20 pregnancy, principally due to hormonal changes that make the = vein wall=20 and valves more pliable. Although hormonally mediated = varicosities of=20 pregnancy are common, the sudden appearance of dilated = varicosities=20 during pregnancy still warrants evaluation for acute deep vein = thrombosis, which is also common in pregnancy.
  • Palpation: Palpation of a painful or tender area may reveal = a firm,=20 thickened, thrombosed vein. Palpable thrombosed vessels are = virtually=20 always superficial, but combined deep and superficial venous = thrombosis=20 is very common.
    • A thrombosed popliteal vein sometimes may be palpated in = the=20 popliteal fossa and a thrombosed common femoral vein sometimes = may be=20 palpated at the groin. These must not be mistaken for = superficial=20 vessels.
    • Palpation helps to distinguish varices of recent onset = from=20 chronic varices. New varices lie on the surface of the = underlying=20 tissue, but chronically dilated vessels erode channels into = underlying=20 muscle or bone, creating deep boggy pockets in calf muscle and = palpable notches in the bone of the anterior = tibia.
    • If the patient is kept standing for a few minutes, = palpation=20 reveals other superficial veins that cannot be seen. The = greater=20 saphenous vein becomes palpable in most patients after a few = minutes=20 of standing, but other normal superficial veins above the foot = cannot=20 be detected by palpation, even after prolonged = standing.
    • Palpation also may reveal fascial defects along the course = of a=20 varicosity. These defects are sites through which perforating = veins=20 may pass, carrying blood between the superficial and deep = venous=20 systems. Arteries and nerves often accompany perforating veins = as they=20 pass through these fascial defects.
  • Percussion: Perthes percussive test is a classic maneuver = that is=20 useful to test whether venous segments are interconnected. With = the=20 patient in a standing position, a vein segment is tapped at one = location=20 while an examining hand feels for a pulse wave at another = location.=20 Propagation of a palpable pulse wave suggests that a = fluid-filled vessel=20 with open or incompetent valves connects the two = locations.
    • A pulse wave may be propagated after prolonged standing in = the=20 absence of true pathology, because prolonged standing causes = even=20 normal veins to become distended and normal valves to float=20 open.
    • Perthes test is most valuable when a bulging varicosity in = the=20 lower leg has no obvious connection with a varicosity in the = upper=20 thigh. A palpable pulse wave propagation between the two = vessels is=20 proof positive of the existence of an unseen = connection.
  • Trendelenburg test: The Trendelenburg test is a classic = physical=20 examination maneuver that helps to distinguish superficial = venous reflux=20 from incompetence of the deep vein valves.
    • The leg is elevated until all superficial veins have = collapsed,=20 and the point of suspected reflux from the deep system is = occluded by=20 manual compression or by a tourniquet. The patient is then = asked to=20 stand, and the distal varicosity is observed for refilling. If = the=20 distal varicosity remains mostly empty, the reflux pathway is=20 principally through the peripheral varicosity that has been=20 occluded.
    • Inability to prevent rapid filling of the varicosity = despite=20 manual occlusion of the suspected high point of reflux = suggests that=20 another reflux pathway is involved.
    • Rapid refilling of calf varices despite occlusion of the = proximal=20 trunk suggests deep system reflux or failure of the valves of = multiple=20 perforating veins.

Causes: The most important clinically = identifiable=20 risk factors for thrombophlebitis are a prior history of = superficial=20 phlebitis, deep vein thrombosis, or pulmonary embolism. Other = extremely=20 common risk markers include recent surgery or pregnancy, prolonged = immobilization, or underlying malignancy. Other recognized markers = of risk=20 for venous thromboembolic disease are listed here.

  • AIDS (lupus anticoagulant)
  • Antithrombin III deficiency
  • Beh=E7et disease
  • Blood type A
  • Burns
  • Catheters (indwelling venous infusion catheters)
  • Chemotherapy
  • Congestive heart failure
  • Drug abuse (intravenous [IV] drugs)
  • Drug-induced lupus anticoagulant
  • DVT in the past
  • Estrogen replacements (high dose only)
  • Fibrinogen abnormality
  • Fractures
  • Hemolytic anemias
  • Heparin-associated thrombocytopenia
  • Homocystinuria
  • Hyperlipidemias=20

  • Immobilization=20

  • Malignancy=20

  • Myocardial infarction=20

  • Obesity=20

  • Old age=20

  • Oral contraceptives
  • PE in the past=20

  • Phenothiazines=20

  • Plasminogen abnormality=20

  • Plasminogen activator abnormality=20

  • Polycythemia
  • Postoperative=20

  • Postpartum period=20

  • Pregnancy=20

  • Protein C deficiency=20

  • Protein S deficiency=20

  • Resistance to activated protein C=20

  • Systemic lupus erythematosus=20

  • Thrombocytosis=20

  • Trauma=20

  • Ulcerative colitis=20

  • Varicose veins=20

  • Venography=20

  • Venous pacemakers=20

  • Venous stasis=20

  • Warfarin (first few days of therapy)
  CLINICAL = Section 3 of = 9   
Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography

Cellulitis =
Deep Venous = Thrombosis=20 and Thrombophlebitis
Thrombophlebitis,=20 Septic


Other Problems to be Considered:

The clinical diagnosis of superficial phlebitis is moderately = reliable,=20 but the key question of whether the deep system is involved simply = cannot=20 be answered without definitive testing. Many other problems can = masquerade=20 as thrombophlebitis of the deep and superficial systems, including = the=20 following:

Baker cyst
Chronic venous=20 = insufficiency
Hematomata
Lipodermatosclerosis
Lymphangitis
Ly= mphedema
Neuritis
Postphlebitic=20 syndrome
Ruptured medial head of the = gastrocnemius
Soft-tissue=20 injury
Varicosities

  DIFFERENTIALS = Section 4 of = 9    3D"Click
Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography
Quick Find
Author=20 Information
Introduction
Cli= nical
Differentials
Worku= p
Tr= eatment
M= edication
Miscellaneous
Bibliography

Click=20 for related images.

Related Articles
Cellulitis=20

Deep Venous=20 Thrombosis and Thrombophlebitis

Thrombophlebitis,=20 Septic


Continuing Education =
CME available for this topic. = Click here=20 to take this=20 = CME.

Patient Education
Click here for patient education.=20


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Lab Studies:

  • Blood tests rarely are helpful in the diagnosis of venous=20 thrombophlebitis, but they can be very helpful in identifying = risk=20 factors for further progression or recurrence in patients who do = have=20 superficial or deep phlebitis.
    • The prothrombin time (PT) and activated partial = thromboplastin=20 time (aPTT) are not useful in the diagnostic evaluation of = patients=20 with suspected superficial or deep thrombophlebitis. Most = patients=20 with thrombophlebitis have a normal PT and aPTT, and active=20 thrombophlebitis is not uncommon in patients with a = therapeutically=20 elevated INR due to warfarin therapy.
    • A low white blood cell (WBC) count lowers the likelihood = of an=20 infectious process and raises the likelihood of phlebitis. An = elevated=20 WBC count is nonspecific because both normal and elevated WBC = counts=20 are common in patients with thrombophlebitis. Chronic venous=20 insufficiency (venous congestion due to reflux) and = superficial or=20 deep vein thrombosis can mimic leg cellulitis very closely, = and true=20 cellulitis (with an elevated WBC count) is a frequent = complication of=20 both diseases.
  • D-dimer is a unique degradation product produced by = plasmin-mediated=20 proteolysis of cross-linked fibrin. D-dimer is measured by latex = agglutination or by an enzyme-linked immunosorbent assay (ELISA) = test=20 whose result is considered positive if the level is greater than = 500=20 ng/mL.
    • At the present time, D-dimer is not sensitive or specific = enough=20 to change the course of diagnostic evaluation or treatment for = patients with suspected superficial or deep thrombophlebitis = or PE.=20 Complex theoretical algorithms that attempt to combine = unreliable=20 D-dimer results with unreliable guesses at clinical likelihood = are not=20 useful in guiding the workup of a live patient with signs or = symptoms=20 suggestive of DVT or PE.
    • The latex agglutination test (various trade names) is = completely=20 unreliable, with a sensitivity of only 50-60% for DVT and=20 PE.
    • The ELISA test is more sensitive than the latex = agglutination=20 test, but in a population with a PE prevalence of 50%, the = negative=20 predictive value of the test is still only 79%. Under the best = of=20 circumstances the D-dimer study misses 10% of the patients = with=20 positive pulmonary angiograms, while only 30% of those with a = positive=20 D-dimer have a positive angiogram.
  • Several common hypercoagulable states can be identified = through=20 laboratory studies. These tests should be ordered for every = patient with=20 phlebitis. They can have a profound impact on the treatment plan = and the=20 frequency of follow-up examinations.
    • Resistance to activated protein C (most often due to = factor V=20 Leyden)
    • Protein C deficiency
    • Protein S deficiency
    • Antithrombin III deficiency
    • Antiphospholipid antibodies
    • Lupus anticoagulant

Imaging Studies:

  • Proper diagnosis of venous system disease often requires = both=20 functional and anatomic information about the venous=20 circulation.
    • The functional tests (discussed below) are extremely = useful as=20 measures of whole-leg or regional venous function, but = functional=20 tests can detect only regionally significant reflux or a = significant=20 impediment to venous outflow.
    • Anatomic imaging of the venous system can detect small = amounts of=20 local and regional reflux as well as obstructing and = nonobstructing=20 thrombus. Unfortunately, anatomic imaging often fails to = identify=20 important functional deficits.
    • A combination of functional and semi-anatomic or anatomic=20 techniques allows a complete understanding of most venous = system=20 pathology.
  • All patients with superficial phlebitis must undergo a = complete=20 workup including an anatomic imaging test to rule out DVT, = because=20 determining from clinical examination whether the process has = spread to=20 involve the deep veins is impossible.
    • Successful anatomic imaging of the deep venous system = requires a=20 thorough knowledge of venous anatomy and physiology and a = meticulous=20 attention to detail.
    • Anatomic imaging is performed using contrast venography, = B-mode=20 ultrasound, or MRI to produce an actual picture of the deep = vessels=20 and their contents.
    • Venous imaging can reveal thrombi that are functionally = silent,=20 such as small, nonobstructing mural thrombi and free-floating = thrombi=20 that do not disturb flow significantly. Venous imaging also = can=20 identify thrombus that occludes venous collaterals or = accessory veins=20 but does not produce a functional alteration of regional flow = because=20 it poses no major impediment to venous outflow.
  • Duplex ultrasound is the initial diagnostic study of choice = for most=20 patients with signs and symptoms of phlebitis. When phlebitis = reflects=20 an underlying hypercoagulable state, superficial phlebitis in = one area=20 may accompany deep vein thrombosis in another area or even in = the other=20 leg. For this reason, duplex examination should not be limited = to just=20 one leg or to just one area of one leg.
    • Unfortunately, duplex ultrasound is not perfectly = sensitive, and=20 it fails to detect DVT in many patients who are ultimately = proven to=20 have had a DVT.
    • After DVT has been excluded by ultrasound examination, = patients=20 with superficial phlebitis should be monitored carefully with = serial=20 examinations until the phlebitis is resolved. Disease that = initially=20 involves only the superficial veins may progress over time to = involve=20 the deep system.
    • A negative duplex ultrasound scan is reassuring, but it is = not a=20 guarantee of a good outcome. Duplex ultrasound is not 100% = sensitive=20 for deep vein thrombosis, and even when DVT is truly absent, = purely=20 superficial thrombophlebitis can embolize to the lungs in some = cases.
    • Because ultrasound can miss DVT, all patients with = superficial=20 phlebitis who also have chest symptoms (such as pain, = shortness of=20 breath, or cough) should have a chest x-ray and = ventilation-perfusion=20 (V/Q) scan, even if a duplex examination fails to reveal deep = vein=20 thrombosis.
  • Magnetic resonance venography (MRV) is a noninvasive test = that=20 probably is more sensitive and more specific than ultrasound in = the=20 detection of deep venous thrombophlebitis.
    • Unfortunately, MRV is not readily available at many = institutions,=20 and many radiologists are inexperienced in the reading of MRV=20 studies.
    • MRV has a great advantage in the assessment of symptoms = attributed=20 to venous disease, because it can reveal an alternate = diagnosis in 60%=20 of the cases in which primary venous disease is not the=20 culprit.
  • Invasive contrast venography has long been the criterion = standard=20 for evaluation of the venous system, but it has fallen into = disuse in=20 many institutions. The procedure is time-consuming, involves = ionizing=20 radiation, and carries a risk of anaphylactoid reactions to IV=20 contrast.
    • The belief is widespread that as many as 16% of patients = develop=20 new DVT after venography, but careful review suggests that = most of=20 these reports actually represented missed thromboses that = simply=20 continued to grow after being missed.
    • Contrast venography has recently begun to enjoy a = renaissance,=20 largely because it is now used to guide direct transcatheter = infusion=20 of fibrinolytic agents in an increasing number of patients = with deep=20 venous thrombosis.
  • Where definitive testing is not immediately available, the = patient=20 should be presumed to have deep system involvement and should be = fully=20 anticoagulated immediately while awaiting a definitive test=20 result.

Other Tests:

  • Physiologic tests of venous function are very important when = used to=20 assess venous function in both the deep and the superficial = venous=20 systems, but they are of secondary importance in patients with = active=20 phlebitis. These tests can sometimes detect deep system=20 thrombophlebitis, but only when significant obstruction to = outflow has=20 produced significant venous congestion.
    • The criterion standard for functional testing of the lower = extremity venous system is invasive ambulatory venous pressure = (AVP)=20 monitoring. The AVP is measured by placing a catheter into a = dorsal=20 foot vein or a vein of the lower leg and recording the venous = pressure=20 while the patient ambulates and performs other = maneuvers.
    • The most common noninvasive tests are impedance = plethysmography,=20 photoplethysmography (including light reflection rheography = and=20 digital techniques), and pneumoplethysmography (including = quantitative=20 air plethysmography). All of these tests address the same = physiologic=20 functional measures.
    • In each type of functional testing, venous pressure = changes are=20 recorded while the patient walks or raises up on tiptoe or = performs=20 ankle dorsiflexions. The recorded pressure tracings reflect = the=20 functional condition of the venous system.
    • In a normal leg, each pumping cycle lowers the pressure as = blood=20 is pumped inward and upward. Six cycles are usually sufficient = to=20 achieve a maximal reduction in pressure. The pressure normally = rises=20 again slowly as the leg is refilled, reaching a maximum within = 3-5=20 minutes.
    • The physiologic parameters that are measured include the = maximum=20 venous outflow (MVO), calf muscle pump expulsion fraction = (MPEF), and=20 venous refilling time (VRT) of the extremity.
    • The MVO and MPEF are decreased when the deep veins are = occluded=20 significantly. The MPEF also is decreased when primary failure = of the=20 calf muscle pump mechanism occurs. The VRT is shortened when = valvular=20 damage in the deep or superficial veins allows venous blood to = reflux=20 downward into the extremity.
  WORKUP = Section 5 of = 9   
Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography

Emergency Department Care: The critical role = of the=20 emergency department is to make the correct diagnosis of = superficial=20 versus deep thrombophlebitis based not on guesswork but on = objective=20 diagnostic testing.=20

If diagnostic tests show that the deep system is not involved, = a=20 rational approach to the initial treatment of superficial = phlebitis can be=20 based upon the patient's history and risk factors, together with = the=20 results of a detailed ultrasound examination.=20

Recognized causes of venous stasis such as air travel or = extended=20 bedrest are strongly contraindicated in all patients with = phlebitis of any=20 type.

    Consultations:


      TREATMENT = Section 6 of = 9   3D"Click <= IMG=20 height=3D10 alt=3D"Click here to go to the next section in = this topic"=20 src=3D"http://www.emedicine.com/images/next3.gif" width=3D31 = align=3Dmiddle border=3D0>
    Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography

    The goals of therapy for = superficial=20 phlebitis are to prevent progression into the deep venous system = and to=20 hasten the resolution of the inflammatory and thrombotic processes = in=20 areas already involved.

    Drug Category: Fibrinolytic agents = --=20 Fibrinolysis often is indicated for deep vein thrombophlebitis, = but it is=20 indicated only rarely for superficial phlebitis.=20

    The principal indication for fibrinolysis in superficial = phlebitis is=20 greater saphenous phlebitis approaching the saphenofemoral = junction at the=20 groin.=20

    A secondary indication is to prevent postthrombotic sclerosis = and to=20 preserve superficial vessels for use in dialysis and in other rare = cases=20 in which preserving an affected superficial vessel is highly = desirable.=20

    Catheter-directed local infusions of fibrinolytic agents are = safer than=20 systemic fibrinolytic regimens because they use a low dose of the = drug and=20 usually do not produce a systemic lytic state. Several = fibrinolytic agents=20 are currently available for local-regional lysis of thrombus.=20

    Reteplase is a second-generation recombinant tissue-type = plasminogen=20 activator that seems to work more quickly and to have a lower = bleeding=20 risk than the first-generation agent (alteplase).=20

    Alteplase is the first-generation recombinant tissue-type = plasminogen=20 activator. Alteplase is the fibrinolytic agent most familiar to = emergency=20 departments, and it is the lytic agent most often used for the = treatment=20 of coronary artery thrombosis, pulmonary embolism, and acute = stroke.=20

    Urokinase is the fibrinolytic agent most familiar to = interventional=20 radiologists, and the one that has most often been used for septic = phlebitis. At the time of this writing, urokinase is not available = from=20 the manufacturer. Availability of urokinase in the immediate = future is not=20 known. In the meantime, the FDA has encouraged the off-label use = of=20 reteplase and alteplase for local-regional lysis of venous and = arterial=20 thrombus at any location.=20

    Streptokinase is a less expensive alternative that, = unfortunately, is=20 highly antigenic and produces a high incidence of untoward = reactions. This=20 drawback limits the usefulness of streptokinase in the clinical = setting.

      MEDICATION = Section 7 of = 9   
    Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography
    Drug Name
    		 Reteplase (r-PA, = Retavase) --=20 Second-generation recombinant tissue-type plasminogen = activator. As=20 fibrinolytic agent, seems to work faster than its = forerunner,=20 alteplase, and also may be more effective in patients with = larger=20 clot burden. Also has been reported to be more effective = than other=20 agents in lysis of older clot. In patients being treated for = peripheral vascular disease, has been reported to cause = fewer=20 bleeding complications than alteplase.
    Contrast = venography=20 used to guide duration and intensity of therapy.
    For = local=20 lysis of arterial thrombosis (with or without associated = infection),=20 suggested dose is lower (0.5 U/h infusion).
    Adult Dose For thrombosed dialysis = grafts:=20 5-10 U/h bolus by pulse-spray delivery
    For segmental=20 superficial or deep venous thrombus: 1 U/h local/regional = infusion=20 for 18-36 h
    For infected catheter thrombus or fibrin = sleeve:=20 1 U/h for 3 h
    Pediatric Dose Not established
    Contraindications Documented = hypersensitivity;=20 uncontrolled hypertension; recent intracranial surgery;=20 arteriovenous malformation or aneurysm; bleeding diathesis
    Interactions May increase effects of = warfarin,=20 heparin, and aspirin
    Pregnancy C - Safety for use during = pregnancy=20 has not been established.=20
    Precautions Caution in cardiovascular = arrhythmias, hypotension, and perfusion arrhythmias; when = used as=20 infusion for local or regional fibrinolysis, some monitor = fibrinogen=20 levels at 6-h intervals; if systemic fibrinogen levels drop = below=20 100 U, reduce infusion rate by half
    Drug Name
    		 Alteplase (t-PA, = Activase) -- First=20 recombinant tissue plasminogen activator to be released for = clinical=20 use, and agent with which EDs are most = familiar.
    Although=20 best known as fibrinolytic agent used for coronary artery = occlusion=20 and pulmonary embolism, also widely used for treatment of = DVT, for=20 dissolution of catheter-related thrombus, and for re-opening = of=20 occluded central lines and thrombosed dialysis=20 grafts.
    Contrast venography used to guide duration = and=20 intensity of therapy.
    Adult Dose For catheter-directed = treatment of=20 deep vein thrombosis: 5 mg bolus and 1 mg/h infusion for = 12-24=20 h
    For infected catheter thrombus or fibrin sleeve: 1 = mg/h for=20 3 h
    For occluded dialysis grafts: 10 mg bolus = delivered into=20 graft site, repeated q2h for 4 doses prn
    Pediatric Dose Administer as in adults
    Contraindications Documented = hypersensitivity; active=20 internal bleeding; cerebrovascular accident or stroke within = last 2=20 mo; intracranial or intraspinal surgery or trauma; = intracranial=20 hemorrhage on pretreatment evaluation; suspicion of = subarachnoid=20 hemorrhage; intracranial neoplasm; arteriovenous = malformation or=20 aneurysm; bleeding diathesis; severe uncontrolled = hypertension
    Interactions Drugs that alter platelet = function=20 (eg, aspirin, dipyridamole, abciximab) may increase risk of = bleeding=20 prior to, during, or after therapy; may give heparin with = and after=20 to reduce risk of rethrombosis=97either heparin or alteplase = may cause=20 bleeding complications
    Pregnancy C - Safety for use during = pregnancy=20 has not been established.=20
    Precautions Monitor for bleeding, = especially at=20 arterial puncture sites, with coadministration of vitamin K=20 antagonists; control and monitor BP frequently during and = following=20 alteplase administration (when managing acute ischemic = stroke); do=20 not use >0.9 mg/kg to manage acute ischemic stroke; doses = >0.9=20 mg/kg may cause ICH
    Drug = Category:=20 Anticoagulants -- Heparin is essential for = patients with=20 superficial thrombophlebitis that is progressive and for those = with=20 particular risk factors for progression or recurrence. Heparin = should=20 always be used when thrombophlebitis involves the greater = saphenous vein.=20 Heparin is the mainstay of treatment when deep system involvement = is=20 suggested, but anticoagulation alone does not guarantee a = successful=20 outcome. The disease may progress despite full and effective = heparin=20 anticoagulation.=20

    Heparin works by activating antithrombin III to slow or prevent = the=20 progression of venous thrombosis. Heparin does not dissolve = existing clot.=20

    Fractionated LMWHs have largely replaced unfractionated heparin = in the=20 treatment of superficial phlebitis. LMWHs offer several distinct=20 advantages over unfractionated heparin: they may be used in the = outpatient=20 setting, they do not require measurement of the aPTT, they produce = more=20 reliable anticoagulation, and they are associated with a lower = risk of=20 bleeding.=20

    When unfractionated heparin is used, an aPTT of at least 1.5 = times the=20 control value is necessary for a therapeutic effect. To achieve = this,=20 unfractionated heparin must be given intravenously in adequate = doses.=20 Low-dose subcutaneous unfractionated heparin should not be used, = as it is=20 not an effective therapy for thrombophlebitis nor an effective = prophylaxis=20 against progression of the disease.=20

    Warfarin should not be used in the acute treatment of = superficial=20 phlebitis, because the early risk of increased thrombogenesis = outweighs=20 any convenience of oral therapy.
    Drug Name
    		 Enoxaparin (Lovenox) -- = First LMWH=20 released in US. Only LMWH now approved by FDA for both = treatment and=20 prophylaxis of DVT.
    Widely used in pregnancy, = although=20 clinical trials not yet available to demonstrate that it is = as safe=20 as unfractionated heparin.
    No utility in checking = aPTT (drug=20 has wide therapeutic window and aPTT does not correlate with = anticoagulant effect).
    Adult Dose Thrombosis: 1 mg/kg SC=20 q12h
    Prophylaxis: 30 mg SC q12h
    Pediatric Dose Not established; = suggested dose is=20 1.6 mg/kg SC bid if <2 months and 1 mg/kg/dose SC bid if = >2=20 months
    Contraindications Documented = hypersensitivity; major=20 bleeding; thrombocytopenia
    Interactions Platelet inhibitors or = oral=20 anticoagulants such as dipyridamole, salicylates, aspirin, = NSAIDs,=20 sulfinpyrazone, and ticlopidine may increase risk of = bleeding
    Pregnancy B - Usually safe but = benefits must=20 outweigh the risks.=20
    Precautions If thromboembolic event = occurs=20 despite LMWH prophylaxis, discontinue drug and initiate = alternate=20 therapy; elevation of hepatic transaminases may occur but is = reversible; heparin-associated thrombocytopenia may occur = with=20 fractionated LMWHs; 1 mg of protamine sulfate reverses = effect of=20 approximately 1 mg of enoxaparin if significant bleeding=20 complications develop
    Drug Name
    		 Heparin (Hep-Lock) -- = Initial bolus=20 used for patients with inflammatory or septic thrombosis = lower than=20 that needed for spontaneous deep vein thrombosis and = pulmonary=20 embolism, because most patients with inflammatory or septic=20 thrombophlebitis do not have underlying hypercoagulability. = Patients=20 with DVT and PE require more aggressive therapy because DVT = is=20 manifestation of active hypercoagulable state.
    Do not = check=20 aPTT until 6 h after initial bolus, as extremely high or low = value=20 during this time should not provoke any action.
    Adult Dose 60 U/kg (max 4000 U) IV = bolus,=20 followed by 12 U/kg/h (max 1000 U/h) maintenance=20 infusion
    After bolus, check aPTT every 6 hours until = stable,=20 and adjust heparin dosing as follows: If APTT low (<1.5 = times=20 control value), rebolus with 4000 U and increase drip by 10% = If aPTT=20 high (>2.5 times control value), decrease drip 10% If = aPTT=20 extremely high (>100 sec), hold heparin drip for 1 h and = decrease=20 drip 10%
    Pediatric Dose Administer as in adults
    Contraindications Documented = hypersensitivity;=20 subacute bacterial endocarditis; active bleeding; history of = heparin-induced thrombocytopenia
    Interactions Digoxin, nicotine, = tetracycline,=20 and antihistamines may decrease effects; NSAIDs, aspirin, = dextran,=20 dipyridamole, and hydroxychloroquine may increase toxicity
    Pregnancy D - Unsafe in pregnancy=20
    Precautions Thromboembolism may occur = due to=20 inadequate dosing; may cause hemorrhagic complications and = can=20 trigger immune thrombotic thrombocytopenia 1-2 wk after = beginning=20 treatment; platelet-consuming disseminated thrombosis = refractory to=20 traditional treatment can be fatal if not recognized quickly = and=20 managed appropriately; if significant bleeding develops, 15 = mg of=20 protamine (infused over 3 min) usually reverses = anticoagulant=20 effect; in neonates, preservative-free heparin recommended = to avoid=20 possible toxicity (ie, gasping syndrome) by benzyl alcohol, = which is=20 used as preservative; caution in severe hypotension and=20 shock
    Drug Category: = Antibiotics=20 -- Antibiotics are not routinely useful in nonseptic = superficial=20 phlebitis. Antibiotics are indicated whenever infection is = suspected to=20 play a role and whenever phlebitis of the greater saphenous vein = above the=20 knee threatens to approach the saphenofemoral junction. The choice = of=20 antibiotics should be guided by blood culture results whenever = possible,=20 but empiric therapy should at a minimum provide coverage for group = A=20 streptococci and for Staphylococcus aureus.=20

    Superficial phlebitis must not be confused with septic = phlebitis, which=20 can be life threatening. If septic phlebitis is suspected, the = selection=20 of antibiotics is critically important and depends upon the = clinical=20 setting. Antibiotics for septic phlebitis are discussed in the = article Thrombophlebitis, Septic.
    Drug Name
    		 Ceftriaxone (Rocephin) -- = Third-generation cephalosporin with broad-spectrum, = gram-negative=20 activity; lower efficacy against gram-positive organisms; = higher=20 efficacy against resistant organisms. Arrests bacterial = growth by=20 binding to one or more penicillin-binding proteins. When = used for=20 treatment of phlebitis, should be administered IV rather = than=20 IM.
    Effective in superficial phlebitis and bacterial=20 septicemia caused by S aureus, Staphylococcus = epidermidis,=20 Streptococcus pyogenes, Viridans group streptococci, = E=20 coli, Enterobacter cloacae, Streptococcus pneumoniae, = Haemophilus=20 influenzae, Klebsiella oxytoca, Klebsiella pneumoniae, = Proteus=20 mirabilis, Pseudomonas aeruginosa, Morganella morganii, = Serratia=20 marcescens, Acinetobacter calcoaceticus, Bacteroides = fragilis,=20 and various Peptostreptococcus species.
    Adult Dose 1-2 g IV qd or divided = bid; not to=20 exceed 4 g/d
    Pediatric Dose 50-75 mg/kg/d IV divided = q12h; not=20 to exceed 2 g/d
    Contraindications Documented = hypersensitivity
    Interactions Probenecid may increase = levels;=20 ethacrynic acid, furosemide, and aminoglycosides may = increase=20 nephrotoxicity
    Pregnancy B - Usually safe but = benefits must=20 outweigh the risks.=20
    Precautions Adjust dose in renal = impairment;=20 caution in breastfeeding women and allergy to=20 penicillin
    Drug Name
    		 Cephalexin (Keflex, = Biocef, Keftab)=20 -- First-generation cephalosporin that may be used as = adjunctive=20 therapy in superficial phlebitis where infection is possible = but=20 unlikely, and where only likely organisms would be skin = flora,=20 including staphylococci and streptococci.
    Adult Dose 250-1000 mg PO q6h for = 10-14 d; not=20 to exceed 4 g/d
    Pediatric Dose 25-50 mg/kg/d PO q6h; not = to exceed=20 3 g/d
    Contraindications Documented = hypersensitivity
    Interactions Aminoglycosides increase=20 nephrotoxic potential
    Pregnancy B - Usually safe but = benefits must=20 outweigh the risks.=20
    Precautions Adjust dose in renal = impairment;=20 may cause nephrotoxicity or cholestatic = jaundice

    Medical/Legal Pitfalls:

    • Patients who present with clinical evidence of superficial = phlebitis=20 often have deep system involvement that is clinically occult. = Those who=20 lack deep system involvement often progress to develop DVT over = time.=20 The incidence of fatal PE in these patients is not = insignificant. Any=20 chest symptoms, no matter how minor, should be considered = extremely=20 worrisome in a patient with superficial = thrombophlebitis.
    • PE is extremely common, and some cases can be difficult to = diagnose.=20 Unfortunately, many patients with obvious PE that could be = diagnosed=20 easily still go unrecognized because of inadequate diagnostic = evaluation=20 in the ED. Respiratory problems and leg pain are the most common = complaints in patients who are seen alive in the ED and later = die=20 unexpectedly.
    • A small number of often-repeated mistakes in diagnosis and = treatment=20 are responsible for a large proportion of the bad outcomes with = serious=20 legal repercussions.
      • Failure to pursue a definitive workup, attempting instead = to=20 diagnose superficial thrombophlebitis and rule out DVT on = clinical=20 grounds that are known to be unreliable
      • Failure to warn the patient that superficial phlebitis can = progress to the deep veins and that any change in symptoms = warrants=20 immediate re-evaluation
      • Failure to properly diagnose and treat DVT in patients = whose=20 symptoms include any degree of leg pain or objective or = subjective=20 edema
      • Failure to treat superficial phlebitis = appropriately
      • Failure to recognize that DVT below the knee must be taken = as=20 seriously as more proximal DVT. The obsolete practice of = dismissing=20 calf vein thrombosis as though it were benign is absolutely = wrong and=20 has caused the death of many patients. This practice has = resulted in=20 lawsuits against many physicians, including prominent and=20 knowledgeable leaders in the field.
      • Failure to order a V/Q scan when a patient has chest = symptoms in=20 the presence of leg symptoms
      • Failure to start full-dose heparin immediately upon the = diagnosis=20 of DVT or at the first suspicion of PE (before the V/Q=20 scan)

    Special Concerns:

    • Venous thrombophlebitis and PE are common during all = trimesters of=20 pregnancy and for 6-12 weeks after delivery.
    • Superficial varicosities and superficial phlebitis are = common during=20 pregnancy, and associated DVT is also common because of a=20 pregnancy-related reduction in intrinsic plasminogen activator=20 activity.
      • The diagnostic approach should be exactly the same in a = pregnant=20 patient as in a nonpregnant one.
      • Duplex scanning is safe in pregnancy.
      • If indicated, a nuclear perfusion lung scan may be = performed=20 safely in pregnancy.
      • If indicated, heparin may be used in = pregnancy.
      • If indicated, fibrinolytics may be used in = pregnancy.
      • Failure to treat the mother properly is the most common = cause of=20 fetal demise.
      MISCELLANEOUS = Section 8 of = 9   <= IMG=20 height=3D10=20 alt=3D"Click here to go to the previous section in this = topic"=20 src=3D"http://www.emedicine.com/images/back3.gif" width=3D31 = align=3Dmiddle border=3D0>
    Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography

      BIBLIOGRAPHY = Section 9 of = 9   
    Author=20 Information Introduction=20 Cli= nical=20 Differentials=20 Worku= p=20 Tr= eatment=20 M= edication=20 Miscellaneous=20 Bibliography
    NOTE: =
    Medicine is a = constantly=20 changing science and not all therapies are clearly = established. New=20 research changes drug and treatment therapies daily. The = authors,=20 editors, and publisher of this journal have used their best = efforts=20 to provide information that is up-to-date and accurate and = is=20 generally accepted within medical standards at the time of=20 publication. However, as medical science is constantly = changing and=20 human error is always possible, the authors, editors, = and=20 publisher or any other party involved with the publication = of this=20 article do not warrant the information in this article is = accurate=20 or complete, nor are they responsible for omissions or = errors in the=20 article or for the results of using this information. The = reader=20 should confirm the information in this article from other = sources=20 prior to use. In particular, all drug doses, indications, = and=20 contraindications should be confirmed in the package = insert. FULL = DISCLAIMER=20

    Thrombophlebitis,=20 Superficial excerpt

    =A9 Copyright 2003, eMedicine.com, = Inc.

    About=20 Us | Privacy | = Terms=20 of Use | Contact Us | Advertise | Institutional=20 Subscribers
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    3D"eMedicine
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     =0A= =0A= =0A= =0A= =0A= Articles =0A= =0A= Images =0A= =0A= CME =0A= =0A= Patient = Education=0A= =0A= =0A= =0A= Advanced=0A= Search Link=0A= to this site
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    EMERGENCY MEDICINE=0A= - Medical Reference
     
    =0A= =0A= =0A= =0A= =0A= =0A=
    Table of = Contents
    Alphabetical Index of = Topics

    Allergy = And Immunology
    Cardiovascular
    Dermatology
    Ear, Nose, And Throat
    Emergency Medical = Systems
    Endocrine = And Metabolic
    Environmental
    Epidemiology
    Gastrointestinal
    Genitourinary
    Hematology And = Oncology
    Implantable = Devices
    Infectious = Diseases
    International = Emergency Medicine



    Legal Aspects Of = Emergency Medicine
    Managing The = Emergency Department
    Neurology
    Obstetrics And = Gynecology
    Ophthalmology
    Organizations In = Emergency Medicine
    Pediatric
    Psychosocial
    Pulmonary
    Rheumatology
    Special = Aspects Of Emergency Medicine
    Toxicology
    Trauma And = Orthopedics
    Warfare -=0A= Chemical, Biological, Radiological, Nuclear And Explosives
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    =0A=
    =0A= =0A= =0A= =0A= =0A= =0A= =0A=
    =0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A=
    Chief=0A= Editors
      Jonathan = Adler, MD
    Barry Brenner, MD, PhD
    Steven Dronen, MD
    Craig Feied, = MD, FACEP, FAAEM
    William K Mallon, MD
    Robert O'Connor, MD, = MPH
    Scott H Plantz, MD, FAAEM
    Charles V Pollack, Jr, MD, = MA
    Raymond J Roberge, MD, MPH, FAAEM, FACMT
    =0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A=
    Copy=0A= Editors
      Julie = Bohlen
    =0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A=
    CME=0A= Editors
      John = Halamka, MD
    =0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A=
    Pharmacy=0A= Editors
      Robert = Konop, PharmD
    Francisco Talavera, PharmD, PhD
    John T VanDeVoort, = PharmD, DABAT
    		=0A= =0A= =0A= =0A= =0A= =0A= =0A= =0A=
    Medical=0A= Editors
     Roy Alson, = MD, PhD
    Jerry Balentine, DO
    Kirsten Bechtel, MD
    Michael S = Beeson, MD, MBA
    Edward Bessman, MD
    Jeffrey Glenn Bowman, MD, = MS
    David FM Brown, MD
    William Chiang, MD
    Steven A Conrad, MD, = PhD
    Francis Counselman, MD
    Dan Danzl, MD
    Peter MC DeBlieux, = MD
    Daniel J Dire, MD, FACEP, FAAEM
    Michelle Ervin, MD
    Miguel C = Fernandez, MD
    Theodore Gaeta, DO, MPH
    Michael Glick, = DMD
    William Gossman, MD
    Robin R Hemphill, MD
    Fred Henretig, = MD
    Edmond Hooker, MD
    B Zane Horowitz, MD
    David S Howes, = MD
    Eric Kardon, MD
    James E Keany, MD, FACEP
    Samuel M Keim, = MD
    Mark Keim, MD
    Richard S Krause, MD
    Lance W Kreplick, MD, = MMM
    Richard Lavely, MD, JD, MS, MPH
    David C Lee, MD
    James Li, = MD
    William Lober, MD
    Mark Louden, MD, FAAEM
    Robert M McNamara, = MD, FAAEM
    Edward A Michelson, MD
    Jerry L Mothershead, MD
    Jerome = FX Naradzay, MD, FACEP
    Robert Norris, MD
    David A Peak, = MD
    Joseph J Sachter, MD, FACEP
    Joseph A Salomone III,=0A= MD
    Assaad J Sayah, MD
    Mark S Slabinski, MD
    Debra Slapper, = MD
    Dana A Stearns, MD
    Suzanne White, MD
    Garry Wilkes, MD
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    Howard A = Bessen, MD
    Paul Blackburn, DO
    Michael J Burns, MD
    Robert G = Darling, MD
    David Eitel, MD, MBA
    Gino A Farina, MD
    Mark W = Fourre, MD
    Jonathan A Handler, MD
    Fred Harchelroad, MD, = FACMT
    Eugene Hardin, MD
    Robert C Harwood, MD, MPH
    Jon Mark = Hirshon, MD, MPH
    Michael Hodgman, MD
    J Stephen Huff, MD
    Amin = Antoine Kazzi, MD
    Eddy Lang, MDCM, CCFP (EM), CSPQ
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    Eric Legome, MD
    David Levy, DO
    Mark L Plaster, = MD, JD
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    Tom Scaletta, MD
    Gary Setnik, = MD
    Barry J Sheridan, DO
    Richard Sinert, DO
    Jeter (Jay) = Pritchard Taylor III, MD
    James S Walker, DO
    Eric L Weiss, MD, = DTM&H
    Wayne Wolfram, MD, MPH
    Grace M Young, MD
    Mark Zwanger, = MD, MBA


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