Edema and Related Medical Conditions

Comprehensive information on edema, swelling, treatment and medical conditions that can cause edema. For all articles, please click on "Archives"

Tuesday, January 31, 2006

Optic Disc Edema and Papilledema


Patients with optic disc edema may present asymptomatically, but this can vary depending upon the etiology of the nerve swelling. In cases of optic neuropathy due to inflammation, infiltration, ischemia or demyelinization, visual acuity is often significantly diminished. Papilledema, a specific form of disc edema resulting from elevated intracranial pressure, generally exhibits a minimal acuity deficit, but may demonstrate transient visual obscurations associated with postural changes. Patients with papilledema also may report headache, intermittent diplopia, vomiting and/or nausea, and pulsatile tinnitus. Visual field defects vary widely as well.

In general, you may observe an enlarged physiologic blind spot in any form of disc edema which displaces the peripapillary photoreceptors. Arcuate scotomas are also common when the inferior and superior poles of the disc are compromised. Altitudinal defects may be seen in ischemic and demyelinating neuropathies; central and cecocentral scotomas are common in primary optic nerve inflammations and infections. If disc swelling is unilateral and vision is poor, expect to find a relative afferent pupillary defect in the involved eye.

True bilateral papilledema will not present with an afferent pupillary defect. The earliest signs of disc edema include striations within the nerve fiber layer in conjunction with blurring of the superior and inferior margins of the neural rim tissue. The disc itself will, in time, protrude from the retinal surface. In cases of inflammation or papilledema, it may display hyperemia and capillary dilation. In ischemic optic neuropathy, the disc is swollen and elevated, but characteristically pale. In more severe presentations of optic disc edema, the retinal venules become engorged and tortuous, hemorrhages and/or cotton wool spots form in the peripapillary area, and you'll see circumferential retinal microfolds (Paton's lines) in the region surrounding the disc. Chronic disc edema may ultimately result in atrophy of the nerve head, with associated pallor and gliosis of the rim tissue.


Optic disc edema results primarily because of axoplasmic stasis, or slowed cellular conduction along the nerve. When this occurs, intracellular fluids and metabolic by-products accumulate and are eventually regurgitated at the level of the optic nerve head. Mechanical compression, infiltration, infection, inflammatory disease, demyelinating disease, or compromised vascular perfusion to the nerve may all lead to disc edema. Papilledema is not a primary neural inflammation but rather a direct sequela of elevated intracranial pressure. In this disorder, cerebral edema is effectively transmitted along the common meningeal sheaths of the brain and optic nerve producing an engorged, swollen disc. The condition is bilateral in almost all cases. True papilledema is a critical sign of intracranial hypertension, a potentially life-threatening situation.


Management of optic disc edema begins with a correct diagnosis. Most importantly, it is crucial to distinguish between papilledema and the many other forms of optic disc edema, including "masqueraders" such as buried optic disc drusen. Consider the acuity, visual fields, ophthalmoscopy findings and especially the laterality of presentation carefully in the initial work-up. Order or perform a B-scan ultrasound, which is invaluable in differentiating swelling of the nerve head from infiltration by hyaline bodies (drusen).

If the signs indicate an optic neuropathy such as papillitis or anterior ischemic optic neuropathy, management is aimed at treating the underlying disorder. Often, this involves systemic steroids, particularly when the etiology is inflammatory. You must obtain a CT or MRI scan of the brain within 24 hours of any tentative diagnosis of papilledema (i.e., when you suspect that increased intracranial pressure is the cause of the disc edema). These tests may help to identify an intracranial mass lesion, such as tumor, hemorrhage or abscess; in addition, the appearance of the cerebral ventricles may indicate hydrocephalus or pseudotumor cerebri. In the absence of positive radiographic studies, lumbar puncture may yield information regarding meningitis, encephalitis, or spinal cord tumors. Neurological consultation and co-management is obligatory in all cases of intracranial hypertension.

The treatment of papilledema and its underlying causes may be medical or surgical, depending upon the disorder. Neuro-ophthalmologists have attempted surgical therapy of the optic nerve using optic nerve sheath decompression to alleviate fluid retention within the surrounding meninges by creating a small fenestration site within the intraorbital portion of the nerve. While this procedure has yielded some positive results, it is extremely complex work and may fail in up to one-third of all cases.


There are two critical points to remember: (1) Not all swollen optic discs constitute optic disc edema and (2) Not all cases of optic disc edema constitute papilledema. Many benign clinical entities can simulate an edematous nerve head, even to the most experienced practitioners. Malinserted discs, congenitally full discs (seen often in hypermetropes), or especially buried drusen may sometimes be mistaken for optic disc edema, even though all are non-pathological conditions.

By the same token, many primary inflammations of the optic nerve which are treatable and in some cases self-limiting are often misdiagnosed as papilledema, a condition which constitutes a medical emergency to the general practitioner. Take care to distinguish these disorders and initiate or refer for proper management in all cases.

Handbook of Ocular Disease Management

Wednesday, January 25, 2006

Study sheds light on why diabetes drug causes edema

Category: Diabetes News

Article Date: 18 Jun 2005 - 12:00pm (UK)

In related discoveries with far-reaching implications for treating diabetes and understanding hypertension, University of Utah researchers have learned why thiazolidinediones (TZDs), a major anti-diabetes drug, cause edema and also have found a new pathway critical to fluid metabolism. Identification of this pathway may help understand fundamental mechanisms of blood pressure control.

Using knockout-gene technology, the U of U School of Medicine researchers found that when TZD is activating a nuclear receptor, the peroxisome proliferator-activated receptor gamma, in the collecting duct in the kidney, it serves as a mechanism for fluid retention, or edema. The researchers suggest that the distal nephron, for example the collecting duct, is crucial for regulation of sodium balance and blood pressure. The research is published this week in the Proceedings of the National Academy of Sciences online.

The discoveries may point the way to developing different drugs to treat Type II diabetes and open an entirely new area in the study of hypertension, according to Tianxin Yang, M.D., Ph.D., the two-year study's principal investigator, associate professor of internal medicine at the U medical school, and staff physician at the George E. Wahler Veterans Affairs Medical Center in Salt Lake City. An estimated 18 million Americans suffer from diabetes. TZD compounds have been shown to be highly effective in lowering blood glucose and lipid levels and in controlling blood pressure.

"It's almost a perfect drug for diabetes,"

Yang said. But many diabetics who use TZD eventually have to discontinue the drug because it causes edema. About 1 percent of people who take TZD get pulmonary edema and chronic heart failure, both being potentially life-threatening conditions.

TZD works by activating PPAR-gamma, a receptor that helps sensitize the body to insulin. PPAR is found in muscle, fat, kidney, and heart and controls fatty acid and lipid metabolism. In the kidney, PPAR is found in the collecting duct, a critical site for the control of fluid metabolism.

To test the role of PPAR in edema, Yang created mice that specifically lacked PPAR-gamma in the collecting duct. He then administered TZD to these mice, as well as to a control group that didn't lack PPAR-gamma.

The mice not lacking PPAR-gamma showed about a 10 percent average increase in body weight because of fluid retention. The blood plasma volume of these mice increased by one-third, Yang said. But the mice bred without PPAR-gamma experienced no increase in body weight in response to the drug, according to Yang.

"This tells us that the body weight gain is regulated by PPAR-gamma in the collecting duct," he said. "We also found this drug decreased the sodium excretion in urine, so this could explain the fluid retention."

The mice without PPAR in the collecting ducts incurred no changes in sodium reabsorption, while those with PPAR excreted less sodium through urination. Yang said that the distal nephron, which is usually subject to hormone regulation in the kidney, serves as a key pathway for keeping an accurate amount of sodium in the body.

Hypertension affects one in four U.S. adults and long had been considered a cardiovascular disease. But research now also focuses on the kidneys and the role of the distal nephron in retaining sodium opens a new area for study, he said.

Contact: Phil Sahm



University of Utah Health Sciences Center

Sunday, January 22, 2006

Bone Marrow Edema

Subchondral Bone Marrow Edema in Patients with Degeneration of the Articular Cartilage of the Knee Joint.

Abstract Jan 19 2006 - Radiology Online

Kijowski R, Stanton P, Fine J, De Smet A.

1 Departments of Radiology and Statistics, University of Wisconsin Hospital, Clinical Science Center-E3/311, 600 Highland Ave, Madison, WI 53792-3252.


To retrospectively determine at magnetic resonance (MR) imaging the prevalence of subchondral bone marrow edema beneath arthroscopically proved articular cartilage defects.

Materials and Methods:

The study was performed in compliance with HIPAA regulations, and a waiver of informed consent was obtained from the institutional review board before the study was performed. The study consisted of 132 patients (70 men, 62 women; average age, 53 years) with articular cartilage defects of the knee joint who underwent MR imaging of the knee and subsequent arthroscopic knee surgery. At the time of arthroscopy, each articular cartilage lesion was graded by using the Noyes classification system. MR examinations were retrospectively reviewed to determine the size, depth, and location of subchondral bone marrow edema without knowledge of the arthroscopic findings. Pairwise Fisher exact tests and two-sample t tests were used to correlate MR imaging findings of subchondral bone marrow edema with the arthroscopic grade of articular cartilage degeneration.


Subchondral bone marrow edema was seen beneath 105 (19%) of 554 articular cartilage defects identified at arthroscopy. It was not observed beneath any of the six grade 1 cartilage defects but was observed beneath eight (4.9%) of 163 grade 2A defects, 40 (14.4%) of 278 grade 2B defects, 54 (55.1%) of 98 grade 3A defects, and three (33.3%) of nine grade 3B defects. Subchondral bone marrow edema was also seen beneath four (1.4%) of 238 articular surfaces that appeared normal at arthroscopy. The mean depth and cross-sectional area of subchondral bone marrow edema increased with increasing grade of the articular cartilage lesion.


Higher grades of articular cartilage defects are associated with higher prevalence and greater depth and cross-sectional area of subchondral bone marrow edema.

(c) RSNA, 2006.PMID: 16424243

[PubMed - as supplied by publisher]


[Bone marrow edema of the knee joint.]

Jan 4, 2006

[Article in German]

Breitenseher MJ, Kramer J, Mayerhoefer ME, Aigner N, Hofmann S.

Institut fur Radiologie, Waldviertelklinikum Horn/Osterreich, .

Bone marrow edema of the knee joint is a frequent clinical picture in MR diagnostics. It can be accompanied by symptoms and pain in the joint.

Diseases that are associated with bone marrow edema can be classified into different groups.

Group 1 includes vascular ischemic bone marrow edema with osteonecrosis (synonyms: SONK or Ahlback's disease), osteochondrosis dissecans, and bone marrow edema syndrome.

Group 2 comprises traumatic or mechanical bone marrow edema.

Group 3 encompasses reactive bone marrow edemas such as those occurring in gonarthrosis, postoperative bone marrow edemas, and reactive edemas in tumors or tumorlike diseases.Evidence for bone marrow edema is effectively provided by MRI, but purely morphological MR information is often unspecific so that anamnestic and clinical details are necessary in most cases for definitive disease classification. PMID: 16315067

[PubMed - in process]


Effective and rapid treatment of painful localized transient osteoporosis (bone marrow edema) with intravenous ibandronate.

Dec. 16, 2005

Ringe JD, Dorst A, Faber H.

Medizinische Klinik IV, Klinikum Leverkusen, University of Cologne, 51375 , Leverkusen, Germany, ringe@klinikum-lev.de.

Localized transient osteoporosis (LTO; bone marrow edema syndrome) is a rare disorder of generally unknown etiology that is characterized by acute onset of disabling bone pain.

Treatment options are currently limited and largely ineffective. The locally increased bone turnover and low bone mineral density (BMD) typical of LTO indicate a potential role for bisphosphonate therapy.

Ibandronate, a potent nitrogen-containing bisphosphonate, has proven efficacy in the management of postmenopausal osteoporosis and corticosteroid-induced osteoporosis when administered as a convenient intermittent intravenous (IV) injection with a between-dose interval of 2 or 3 months. In a study of 12 patients with LTO, ibandronate was administered as an initial 4-mg IV dose with a second, optional injection of 2 mg at 3 months. Daily calcium and vitamin D supplements were provided. Pain was measured at baseline and at 1, 2, 3, and 6 months using a visual analog scale (VAS) of 1-10, and BMD was measured at baseline and 6 months. IV ibandronate provided rapid and substantial pain relief. The mean (SD) VAS score decreased from 8.4 (1.3) at baseline to 0.5 (0.7) at 6 months, at which time seven patients had achieved complete pain relief. At 6 months, mean lumbar spine BMD had increased by 4.0% (range -0.8 to 7.7%) in the overall population. IV ibandronate injection affords advantages over currently available oral and IV bisphosphonates and thus offers a promising therapeutic advance in the treatment of LTO.PMID: 16228105

[PubMed - in process]


The relationship of bone marrow edema pattern in the mandibular condyle with joint pain in patients with temporomandibular joint disorders: longitudinal study with MR imaging.

Jan 2006

Chiba M, Kumagai M, Fukui N, Echigo S.

Division of Oral Surgery, Department of Oral Medicine and Surgery, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai #980-8575, Japan.


The purpose of this study was to investigate the course of bone marrow edema pattern (decreased signal intensity on T1- or proton-density-weighted images and increased signal intensity on T2-weighted fat-suppressed images) in the mandibular condyle after improvement in clinical symptoms, and to clarify its relationship with temporomandibular joint (TMJ) pain. This study was based on 14 joints of 11 patients (all female, mean age 37.5 years) with TMJ disorders showing condylar bone marrow edema pattern on initial magnetic resonance (MR) images. All joints were re-evaluated clinically and using MR images after relief of joint pain following arthrocentesis combined with non-surgical treatment. The time interval between the initial and follow-up MR images ranged from 14 to 27 months (mean 17 months). Of the 14 joints, 4 joints (28.6%) showed a normal bone marrow signal, whereas 10 joints (71.4%) showed persistent bone marrow edema pattern on follow-up MR images (P = 0.125). Therefore, the reduction in TMJ pain did not correlate with resolution of bone marrow edema pattern in most joints. The results of this study suggest that the bone marrow edema pattern in the mandibular condyle does not always contribute to the occurrence of joint pain in patients with TMJ disorders.PMID: 15964172

[PubMed - in process]


Transient bone marrow oedema of the knee.

Aug 12, 2005

Arjonilla A, Calvo E, Alvarez L, Fernandez Yruegas D.

Department of Radiology, Madrid, Spain.


OBJECTIVE: To evaluate the role of MRI in the diagnosis of transient bone marrow oedema of the knee.

DESIGN: All cases were analysed with plain film and MR. Bone scan was performed to one of them. Laboratory tests were obtained in all 8 cases and core decompression was performed in two cases.

PATIENTS: The study includes 8 patients, 7 men and 1 woman with ages ranging from 33 to 74 years with severe knee pain, tenderness and slightly limited range of motion.

RESULTS AND CONCLUSIONS: Radiographs were unremarkable in terms of osteopenia because they were obtained early in the course of the disease and proved to be of no value in the diagnosis. MR is the imaging modality of choice showing low signal intensity in T1WI and increased signal intensity in T2WI with no joint destruction, fractures, bone death, periostitis or cortical disruption. Bone scan showed increase uptake of the affected area. Laboratory tests were normal. Spontaneous resolution was the rule. It should not be a diagnosis of exclusion and it should be ruled out every time a patient presents with pain and limited range of motion in the absence of history of trauma.

Publication Types:

Evaluation Studies

PMID: 16026695

[PubMed - indexed for MEDLINE]

Saturday, January 14, 2006

COX Inhibition, Hypertension, and Edema Effect

Vibeke Strand, MD
Even if they are mechanistically different, cyclooxygenase-2 (COX-2) inhibitors have effects on hypertension (HTN) similar to those observed with conventional nonsteroidal anti-inflammatory drugs (NSAIDs). According to Pope et al, use of nonselective NSAIDs in treated hypertensive patients, including those taking angiotensin-converting enzyme (ACE) inhibitors and beta-blockers, results in an average unadjusted increase in mean arterial pressure (MAP) ranging from 0.61 mm Hg with aspirin to 6.10 mm Hg with naproxen. After adjusting for dietary salt intake, the effect ranged from an increase of just over 3.5 mm Hg for naproxen and indomethacin to a decrease in MAP with sulindac, aspirin, and ibuprofen.1 This is a common problem in the osteoarthritis (OA) population. Singh et al report that 40% of the 24.3 million people in the US with OA have HTN.2

All coxibs induce salt and water retention and destabilization of blood pressure (BP), as do conventional NSAIDs. Additionally, there is a dose-related effect with rofecoxib at doses between 12.5 mg and 50 mg (with a markedly increased percentage of patients with BP elevation at the 50-mg dose). There are also dose-related increases with valdecoxib at 40 mg and 80 mg. Bensen et al3 report that 2.7% of rheumatoid arthritis (RA) patients taking 40 mg/day of valdecoxib develop HTN.

In the Celecoxib Rofecoxib Efficacy and Safety in Comorbidities Evaluation Trial (CRESCENT),4 rofecoxib significantly increased 24-hour BP during and at landmarks after 6 weeks of therapy, while celecoxib and naproxen did not, as determined by ambulatory BP measurements. While reductions in OA symptoms were similar across all groups, patients taking rofecoxib had a mean 4 mm Hg increase in 24-hour systolic BP. Patients taking rofecoxib also had increases in pulse pressure. The mean change in 24-hour ambulatory systolic BP from baseline to week 6 between rofecoxib and celecoxib was 3.78 mm Hg and 3.85 mm Hg between rofecoxib and naproxen. There were no significant differences between celecoxib and naproxen. Moreover, the percentage of patients who developed HTN in the study was higher for people taking rofecoxib than celecoxib. In CRESCENT, patients using rofecoxib, but not celecoxib or conventional NSAIDs, had an increased rate of edema (23.3% versus 18.0%), while the rates for celecoxib and conventional NSAIDs were 17.5% and 18.2%, respectively. The adjusted risk of edema was significantly increased for rofecoxib compared with celecoxib.

The Celexcoxib Long-term Arthritis Safety Study (CLASS), the Vioxx Gastrointestinal Outcome Research (VIGOR) trial, and the Therapeutic Arthritis Research and Gastrointestinal Event Trial (TARGET) all suggest that COX-2 inhibitors can increase BP. In CLASS, there was a relatively low, non-dose-dependent incidence of HTN with celecoxib when compared with diclofenac and ibuprofen.

In a 6-week, randomized, double-blind study of edema and HTN during treatment with rofecoxib 25 mg daily and celecoxib 200 mg daily in OA patients with HTN, Whelton et al5 found that edema and BP destabilization (systolic pressure increase) were more common in patients receiving rofecoxib than celecoxib.

NSAID use is not associated with incident congestive heart failure (CHF); however, once CHF is present, there is a substantial increase in risk with NSAID use, according to Feenstra et al.6 Nevertheless, compared with HTN there is markedly less data with regard to CHF and edema. In one study by Mamdani et al,7 patients taking rofecoxib and nonselective NSAIDs (but not celecoxib) had an increased risk of hospital admission for CHF relative to non-NSAID users. Compared with celecoxib users, admission was significantly more likely in users of nonselective NSAIDs and rofecoxib. Risk of admission for rofecoxib users was higher than for nonselective NSAID users. Of patients who had not been admitted to a hospital in the past 3 years, only rofecoxib users were at increased risk of subsequent admission relative to controls.

Moreover, two epidemiologic studies in the Netherlands showed an increased incidence of CHF, and new-onset CHF, with NSAIDs versus patients taking diuretics. In a study by Garcia Rodriguez and Hernandez-Diaz,8 the estimated adjusted relative risk of heart failure associated with prescription of NSAIDs was 1.6. The relative risk was greater during the first month of therapy and was independent of treatment indication. Further, the relative risk was 1.9 among patients with a prior history of HTN, diabetes, or renal failure and 1.3 among individuals without these conditions. In TARGET, CHF occurred with similar frequency among lumiracoxib users (0.24%) and NSAID users (0.34%), respectively.9

BP and edema effects differ among the medications. With rofecoxib, greater frequencies of edema and increased BP are observed in patients with HTN versus celecoxib. Moreover, there is an increase in BP among OA patients with treated HTN compared with celecoxib and naproxen. There is no dose-related increase in HTN, edema, or CHF with celecoxib. Celecoxib has a more modest effect on HTN, edema, and CHF than rofecoxib (even in OA patients receiving antihypertensives). It is not yet known whether BP is the surrogate marker for an increase in CV events; however, such events are rare and must be considered in the context of the risk/benefit profile of these agents.

Key Points

HTN among OA patients is a significant problem

All coxibs result in salt and water retention and destabilization of BP, as do conventional NSAIDs
BP and edema effects differ among the medications; for example, edema and increase in BP are seen in rofecoxib-treated patients with HTN versus celecoxib; there are also dose-related increases with valdecoxib at 40 mg and 80 mg

CV events are rare and must be considered in the context of the risk/benefit profile of these agents


Pope JE, Anderson JJ, Felson DT. A meta-analysis of the effects of nonsteroidal anti-inflammatory drugs on blood pressure. Arch Intern Med. 1993;153:477-484.

Singh G, Miller JD, Lee FH, Pettitt D, Russell MW. Prevalence of cardiovascular disease risk factors among US adults with self-reported osteoarthritis: data from the Third National Health and Nutrition Examination Survey. Am J Manag Care. 2002;8(suppl 15):S383-S391.

Bensen W, Weaver A, Espinoza L, et al. Efficacy and safety of valdecoxib in treating the signs and symptoms of rheumatoid arthritis: a randomized, controlled comparison with placebo and naproxen. Rheumatology (Oxford). 2002;41:1008-1010.

Sowers JR, White WB, Pitt B, et al; Celecoxib Rofecoxib Efficacy and Safety in Comorbidities Evaluation Trial (CRESCENT) Investigators. The effects of cyclooxygenase-2 inhibitors and nonsteroidal anti-inflammatory therapy on 24-hour blood pressure in patients with hypertension, osteoarthritis, and type 2 diabetes mellitus. Arch Intern Med. 2005;165:161-168.
Whelton A, Fort JG, Puma JA, Normandin D, Bello AE, Verburg KM; SUCCESS VI Study Group. Cyclooxygenase-2-specific inhibitors and cardiorenal function: a randomized, controlled trial of celecoxib and rofecoxib in older hypertensive osteoarthritis patients. Am J Ther. 2001;8:85-95.

Feenstra J, Heerdink ER, Grobbee DE, Stricker BH. Association of nonsteroidal anti-inflammatory drugs with first occurrence of heart failure and with relapsing heart failure: the Rotterdam Study. Arch Intern Med. 2002;162:265-270.

Mamdani M, Juurlink DN, Lee DS, et al. Cyclo-oxygenase-2 inhibitors versus non-selective non-steroidal anti-inflammatory drugs and congestive heart failure outcomes in elderly patients: a population-based cohort study. Lancet. 2004;363:1751-1756.

Garcia Rodriguez LA, Hernandez-Diaz S. Nonsteroidal anti-inflammatory drugs as a trigger of clinical heart failure. Epidemiology. 2003;14:240-246.

Farkouh ME, Kirshner H, Harrington RA, et al; TARGET Study Group. Comparison of lumiracoxib with naproxen and ibuprofen in the Therapeutic Arthritis Research and Gastrointestinal Event Trial (TARGET), cardiovascular outcomes: randomised controlled trial. Lancet. 2004;364:675-684.

Foundation for Better Health Care

Thursday, January 12, 2006

Chandler's Syndrome and Corneal Edema


Dystrophia Endothelialis Cornea
Iris Atrophy with Corneal Edema and Glaucoma

Disorder Subdivisions


General Discussion

Chandler's syndrome (CS) is a rare eye disorder in which the single layer of cells lining the interior of the cornea proliferates, causing the drying up of the iris, corneal swelling, and unusually high pressure in the eye (glaucoma). CS is one of three syndromes affecting the eyes (progressive iris atrophy and Cogan-Reese syndrome are the other two) that make up the iridocorneal endothelial syndrome. Chandler’s syndrome affects females more often than males and usually presents sometime during middle age. Most often the condition affects one eye only but if it is not treated, with time, the second eye may become involved. The combination of high pressure within the eye (glaucoma) and leaking of fluid through the cellular membrane can result in reduced vision with pain..


National Association for Visually Handicapped, 22 West 21st StreetNew York, NY 10010,USATel: 2128893141, Fax: 2127272931
Email: staff@navh.org

Schepens Eye Research Institute 20 Staniford StreetBoston, MA 02114-2500, Tel: (617)912-0100, Fax: (617)523-3463
Email: geninfo@vision.eri.harvard.edu

National Association for Parents of Children with Visual Impairments (NAPVI) P.O. Box 317 Watertown, MA 02472, Tel: (617)972-7441, Fax: (617)972-7444, Tel: (800)562-6265
Email: napvi@perkins.org

Prevent Blindness America 500 East Remington Road, Schaumberg, IL 60173, Tel: (847)843-2020, Fax: (847)843-8458, Tel: (800)331-2020
Email: info@preventblindness.org

NIH/National Eye Institute Building 31 Rm 6A3231 Center Dr MSC 2510, Bethesda, MD 20892-2510, United States, Tel: 3014965248, Fax: 3014021065
Email: 2020@nei.nih.gov

Monday, January 09, 2006

FDA Warning for 2 Diabetes Drugs - Regarding Macular Edema

Rare Reports of Worsening Diabetic Eye Complications With Avandia and Avandamet
Miranda HittiWebMD Medical News

Jan. 5, 2006 -- The FDA and drug company GlaxoSmithKline are alerting doctors about reports of new or worsening diabetic eye complications in patients with diabetes taking the drugs Avandia or Avandamet.

The complication, called macula edema, results from fragile and leaking blood vessels in the eye and can lead to blurry vision; it affects the part of the eye where sharp, straight-ahead vision occurs. If you notice any changes in your vision, such as blurred vision, decreased color sensitivity, or a change in the ability to see in the dark, let your doctor know.
Avandia and Avandamet are made by GlaxoSmithKline and contain the drug rosiglitazone. They are used to treat type 2 diabetes. Avandamet also contains a second drug called metformin.

A GlaxoSmithKline letter sent to doctors makes these points:

The reports are "very rare."

Most patients also reported swelling in their legs and feet (peripheral edema) at the same time.
In some cases the macula edema stopped or improved when patients stopped taking the drugs.
In one case, macula edema stopped when the drug's dose was reduced.
Worldwide, more than 5 million people have taken Avandia and 769,000 have taken Avandamet, states the GlaxoSmithKline letter, which is posted on the FDA's web site.

Diabetes and Swelling

Diabetes can cause swelling, including swelling or edema of the back layer of the eyes. This layer contains blood vessels that can become damaged and fragile as a complication of long-standing diabetes.

Macula edema also can be related to poor control of blood sugar, high blood pressure, and abnormal cholesterol levels.

Diabetic retinopathy is a result of high blood sugar. If you have diabetic retinopathy, at first you may notice no changes to your vision. However, it can cause severe vision loss or blindness, if untreated. Diabetic retinopathy damages tiny blood vessels in the retina, which senses light and is located at the back of the eye.

People with diabetes are advised to get eye exams at least once a year from an ophthalmologist, regardless of any drugs they take.

Thursday, January 05, 2006

Macular Edema

Cystoid Macular Edema

Also referred to as:

Macular Edema

Macular Swelling

Cystoid macular edema (CME) is a swelling of the macula which most commonly presents after routine, uncomplicated cataract surgery. The condition presents with decreased visual acuity, most commonly 4 to 12 weeks following surgery. Sometimes the condition presents as early as a few days, or as late as many months, after surgery.

The eye usually looks good on examination and a fluorescein angiogram is required to confirm the diagnosis. The fluorescein angiogram shows leakage of fluid in the macula indicating the edema (swelling). A fluorescein angiogram is an extraordinarily safe, in-office procedure, in which fluorescein dye is given IV or sometimes orally followed by retinal photography. X-rays are not used in a fluorescein angiogram, though this is a common misconception.

Patients diagnosed with CME are usually started, or re-started, on steroidal or non-steroidal anti-inflammatory eye-drop medications. Some ophthalmologists also prefer to give a steroid injection adjacent to the eye or underneath the outer layers of the eye. Patients are usually followed every few weeks until resolution. The majority of patients will recover excellent acuity though a small percentage may have permanently reduced vision.

Other conditions associated with spontaneous development of CME include diabetic retinopathy, uveitis or iritis, retinitis pigmentosa, and other inflammatory syndromes.

Related Conditions

Anterior Uveitis
Branch Retinal Artery Occlusion
Branch Retinal Vein Occlusion
Diabetic Retinopathy
Retinitis Pigmentosa

Related Eye Procedures

There are no related Eye Procedures

Related Specialties

Cataract / General

Related Tests

Visual acuity



Diabetic Macular Edema

Diabetes is the most common cause of blindness among working-aged people, and all people living with the disease should monitor their eye health carefully. Over time, diabetes can lead to diabetic retinopathy, which is damage to the blood vessels in the retina. As this damage continues, blood vessels in the retina begin to leak fluid.

This, in turn, can lead to a condition known as diabetic macular edema, or DME, where fluid accumulates in the macula. Patients with DME typically experience blurred vision which may progress to blindness.

Diabetic Macular Edema (DME) affects up to 10% of all patients with diabetes1

Up to 75,000 new cases occur every year1

Up to 30% of patients with DME will experience moderate visual loss (doubling of the visual angle)1

There are two kinds of DME:

Focal DME is caused by tiny abnormalities in blood vessels, known as microaneurysms. These leaking microaneurysms can lead to vision loss.

Diffuse DME is caused by widening (dilation) of retinal capillaries (extremely thin, narrow blood vessels) throughout the back of the eye.

What are the Symptoms of DME?

All patients who suffer from diabetes have a risk of developing DME. The symptoms of DME can include:

Blurred vision
Double vision
Floaters (small black dots or lines made up of cellular debris seen "floating" across the front of the eye) These floaters may temporarily interfere with vision. They are also linked with other eye diseases.

What Causes DME?

DME is linked with the following:

The degree of diabetic retinopathy (problems with blood vessels in the retina related to diabetes)
The length of time a patient has had diabetes
The type of diabetes each patient has (the milder the diabetes, the lower the incidence of DME)
Severe hypertension (high blood pressure)
Fluid retention
Hypoalbuminemia (low protein in body fluids)
Hyperlipidemia (high levels of fats in the blood)

Many of these conditions can make DME worse, but when they are treated and controlled, DME may get better.

How is DME Treated?

Laser treatment for focal DME:

Focal laser treatment may be used to treat focal DME.

The goal of treatment is to close leaking microaneurysms to help maintain current vision and reduce progressive visual loss.

The laser light is absorbed by the blood inside the microaneurysms using green and yellow wavelengths.

Confirm closure at the end of the treatment session, and retreat if necessary.

Laser treatment for diffuse DME :

Grid laser treatment is used to treat diffuse DME.

The goal of treatment is to produce a mild to moderately intense retinal burn to help maintain current vision and reduce progressive visual loss.

A fluorescein angiogram may guide treatment.

Three months after treatment the patient should be rechecked to make sure that the DME is responding to therapy.

Realistic Expectations:

In 3-6 months, expect retinal thickening and hard exudates (concentrated areas of protein) to start to improve.

The excess fluid that leads to edema (swelling) will begin to reabsorb into the surrounding tissues.

Eventually the bodily substances that create the hard exudates will be reabsorbed as well. Be aware that as the swelling begins to improve, hard exudates may increase temporarily in the eye. This is a sign of improvement, and the exudates will soon disappear.

The reality is: even after successful treatment, some people do not experience improved vision. However, if vision remains stable, continued treatment could be beneficial.

Bausch & Lomb

Monday, January 02, 2006

Brain Edema

The Blood Brain Barrier (BBB):

The cerebral capillary is the site of the BBB. Interendothelial tight junctions impede the passage of electron-dense markers. Cerebral capillaries lack fenestrations and have tight junctions. They are active in the process of pinocytosis. All these features regulate the passage of highly polar hydrophilic molecules allowing virtually unrestricted passage of lipid-soluble substances. Cerebral capillaries have 2-4X the number of mitochondria as other capillaries. Cerebral capillaries have an array of important enzymes: ATPase, dehydrogenase, monamine oxidase, DOPA decarboxylase, acid and alkaline phosphatase, NAD and others. BBB has both central (cholinergic and aminergic) and peripheral (sympathetic and parasympathetic) innervation.

Areas without a BBB include:

choroid plexus
area postrema
median eminence
pineal body
subforniceal organ
commissural organ
supra-optic crest.

Carrier Mediated BBB Movement:

Glucose and aa's are actively transported as they are not lipid soluble. These substances demonstrate stereospecifity, competitive inhibition and saturation. May be bi- or unidirectional transport. All aa's appear to use the same active transport system (flooded in PKU, aminoaciduria's etc)

Evaluation of BBB function:

Using radio-isotopes or various exclusion dyes can calculate from single pass what Km and Vmax are.In humans BBB integrity determined by:

1. external detection of radionuclide activity with a sodium iodide crystal
2. CT scanning
3. PET scan with rubidium-82



Excess accumulation of water in the intra- and/or extracellular spaces of the brain.


Vasogenic edema: The disruption of the cerebral capillary provides the underlying mechanism for vasogenic edema. The amount of edema is greatest in the white matter (increased water and sodium in the extracellular spaces, decreased potassium); but the same changes may take place in grey matter but less so. The astrocytes become swollen. This type of edema is seen in response to trauma, tumors, focal inflammation, and late stages of cerebral ischemia.

Cytotoxic edema:This is due to the derangement in cellular metabolism resulting in inadequate functioning of the sodium and potassium pump in the glial cell membrane. As a result there is cellular retention of sodium and water. There are swollen astrocytes in grey and white matter. Cytoxotic edema is seen with various intoxications (dinitrophenol, triethyltin, hexachlorophene, isoniazid) and in Reye's syndrome, severe hypothermia, and early ischemia.

Osmotic edema:Normally CSF and ECF osmolality in the brain is slightly greater than that of plasma. When plasma is diluted by SIADH, water intoxication, hemodialysis, there is passage of water down abnormal gradient creating cerebral edema.

Hydrostatic:This form of cerebral edema is seen in acute, malignant hypertension. It is thought to result from direct transmission of pressure to cerebral capillary with transudation of fluid into the ECF.

Pathophysiology of Cerebral Edema:

This is a cascade of events involving loss of the integrity of the BBB, setting up of a vascular hydrostatic gradient, increased tissue pressure, decreased cerebral blood flow, with resulting tissue acidosis. Chemical changes include glutamate, serotonin, components of kallikrein-kininogen-inin, fatty acids


Surgical removal of offending lesion
Control of arterial blood pressure
Corticosteroids - stabilize membranes
Osmotherapy - mannitol (1 g/kg); lasix 0.7 mg per kg; glycerol 1 g/kg
Control of ICP - carbonic anhydrase, DMSO


Harrigan MR, Cerebral salt wasting syndrome. Neurosurgery 38: 152-160, 1996

Toronto Brain Vascular Malformation Group


Cerebral Edmea

Cerebral edema is swelling of the brain which can occur as the result of a head injury, cardiac arrest or from the lack of proper altitude acclimatization.
Edema also occurs when the chemical balance of brain tissue is disturbed and water or fluids flow into the brain cells, making them swell and burst, releasing their
toxic contents into the surrounding tissues. Edema is one cause of general brain tissue swelling and contributes to the secondary injury associated with stroke.
Symptoms of cerebral edema include
headaches, decreased level of consciousness, hallucinations, psychotic behavior, memory loss and coma. If left untreated, it can lead to death (r. Bruce Lee).


Sunday, January 01, 2006

Evaluation and management of peripheral edema

Edema can be treated systematically and comprehensively, based on an understanding of the pathophysiologic mechanisms involved. This approach encourages accurate diagnosis while ensuring safety and cost-effectiveness.

Beth E. Schroth, PA-C

Edema is a palpable swelling produced by expansion of the interstitial fluid volume and is often nonspecific. When massive and generalized, the excess fluid accumulation is called anasarca. A variety of clinical conditions, ranging from the benign to the potentially life threatening, is associated with the development of peripheral edema.

These include common conditions such as heart failure (HF), cirrhosis, and nephrotic syndrome (NS), but edema may also be idiopathic (see Table 1).1 A systematic approach to the patient with edema allows for prompt and cost-effective diagnosis and treatment.1

Anatomy and pathophysiology

Total body water is divided between the intracellular and extracellular spaces. The extracellular space, which comprises about one third of total body water, is composed of the intravascular plasma volume (25%) and the extravascular interstitial spaces (75%).2 According to Starling’s law, the physiologic forces involved in maintaining the balance of water between these two compartments include the gradient between extravascular and intravascular hydrostatic pressures, differences in oncotic pressures within the interstitial space and plasma, and the permeability of the blood vessel wall.3 Fluid and filtered proteins from the interstitial space are collected by the lymphatic system and returned to the vascular compartment. Peripheral edema results from a disturbance in this delicate equilibrium with net filtration out of the vascular space or from impaired return of fluid by lymphatics in the interstitial space.4,5

Alteration of Starling forces plays a central role in the pathophysiology of edema. Increased venous pressure due to central or regional venous obstruction or to an expansion in plasma volume is transmitted to the capillary bed, thereby increasing hydrostatic pressure and predisposing to edema. Conversely, local autoregulation by smooth muscle sphincters on the precapillary (or arterial) side protect the capillary bed from increases in systemic arterial pressure, which explains why hypertensive patients do not have edema despite elevated BP.6,7

An increase in capillary permeability due to vascular injury is a key event in edema formation resulting from local inflammation. Capillary permeability is under the control of cytokines, circulating vasodilatory prostaglandins, and nitric oxide.8 Increase in capillary permeability promotes the development of edema both directly and indirectly by permitting albumin to move into the interstitium, thereby diminishing the oncotic pressure gradient.

The lymphatics play an essential role in reabsorption of interstitial fluid and proteins, returning them to the central circulation. Lymphatic obstruction is an unusual cause of edema (called lymphedema) that is most often seen with nodal enlargement due to malignancy and with surgical removal of lymph nodes, such as during radical mastectomy. In certain disease conditions such as myxedema, the lymphatic system is overwhelmed because of the marked increase in interstitial accumulation of albumin and other proteins.9

Multiple renal and neurohumoral factors control fluid and electrolyte homeostasis. In certain disease states, such as chronic HF and cirrhosis, the neurohumoral cascade that attempts to maintain effective circulating volume becomes maladaptive, leading to a cycle of further sodium and water retention. In chronic edematous states, end-organ resistance to natriuretic peptides inevitably occurs, which explains the sodium retention in these conditions despite high circulating levels of these peptides.10,11

History and physical examination

Use a multisystem approach when evaluating a patient with edema. Of particular importance is excluding major organ system dysfunction, especially cardiac, liver, and renal dysfunction.

Document the location of the edema, its progression, and whether it occurs intermittently or persistently. Analyze these clinical findings in relation to the patient’s medical history of coronary artery disease, renal disease, liver disease, and so forth. Ask questions such as the following:

Do the rings on your fingers get tight?
Have you had to let your belt out?
Have your clothes or shoes gotten too tight?12

Pay special attention to the patient’s medications; several can cause edema, such as NSAIDs, calcium channel blockers, and estrogens.13-16 Assess whether patients who are already taking a diuretic to treat peripheral edema are adhering to their drug regimen.

Also, obtain a thorough dietary history, paying careful attention to the patient’s dietary sodium intake, total daily fluid intake, and adherence to special dietary restrictions (see www.heartfailure.org and www.kidney.org for special dietary instructions for salt and fluid restriction).

The physical examination In addition to the standard physical examination, chart the patient’s weight and note general appearance, paying special attention to the edema with respect to location, symmetry, pitting or nonpitting appearance, tenderness, and associated skin changes, such as ulceration and rubor. Look for ascites. Evaluating the peripheral and central venous systems may shed light on the pathogenesis of edema. Lastly, assess the severity of edema with a method such as the four-point scale (+1, slight, to +4, very marked), the presence of sacral edema, and the height in the case of lower extremity edema.12

Diagnostic testing Order simple, safe, and cost-effective tests, including a chemistry panel and urinalysis to evaluate renal and liver function and albumin levels to assess nutritional status. Consider measuring the thyrotropin level to rule out hypothyroidism. In cases where screening for a cardiac etiology is required, an ECG and chest radiograph may be helpful in assessing cardiac function. When considering diagnostic tests in the context of a potentially long list of etiologies, a comprehensive history and physical examination, along with basic metabolic laboratory tests, can yield an accurate diagnosis in the majority of cases; expensive testing is usually unnecessary.

Differential diagnosis

Many safety factors must be overcome before edema develops. Because the interstitial tissues easily accommodate several liters of fluid, a patient’s weight may increase nearly 10% before pitting edema is evident.1 Also, the gradient favoring filtration must increase by at least 15 mm Hg before edema can be detected.17

Three factors contribute to this protective response. The first is increased lymphatic flow that initially removes the excess filtrate. For example, with pulmonary edema due to HF, the rate of increase in lung liquid accumulation at any given elevation in pulmonary capillary pressure is related to the functional capacity of the lymphatics. Lymphatic functional capacity is influenced by individual factors and the acuteness of the hemodynamic change. With acute rises in pulmonary capillary pressures, the pulmonary lymphatic system does not have an increased capacity to remove fluid; thus, pulmonary edema occurs at pulmonary artery capillary pressures as low as 18 mm Hg. In contrast, patients with chronic HF have an increased lymphatic capacity and do not develop pulmonary edema until much higher pulmonary capillary pressures (greater than 25 mm Hg) are reached.18

The second form of protection is fluid entry into the interstitium that eventually raises the interstitial hydraulic pressure.17 Fluid entry into the interstitium that also lowers the interstitial oncotic pressure, both by dilution and by lymphatic-mediated removal of interstitial proteins, comprises the third protective factor.19

Heart failure Systolic and diastolic dysfunction elevates venous pressure, which in turn increases capillary hydrostatic pressure. Additionally, the low output state activates neurohormonal mechanisms that initially are aimed at restoring adequate arterial perfusion. Eventually, the resulting extravasation of fluid outpaces the ability of the lymphatic system to return fluid to the vascular space, resulting in pitting edema. Right-sided ventricular dysfunction leads to peripheral edema, whereas left-sided ventricular failure (LVF) produces pulmonary edema.7 Although the capacity of the lymphatic system to remove fluid is increased with HF, the lymphatic system will be overwhelmed in acute cases

Constrictive pericarditis/restrictive cardiomyopathy Clinically, these conditions are sometimes indistinguishable from right heart failure (RHF). All these diagnoses may manifest with peripheral edema, elevated jugular venous pressure, hepatic congestion, and ascites. Also, because of its insidious onset, ascites and cardiac cirrhosis resulting in liver dysfunction may ensue and patients may receive a misdiagnosis of primary hepatic cirrhosis.1,20 Conclusive diagnosis may require transthoracic echocardiography, right heart catheterization, and tissue biopsy.1

Nephrotic syndrome NS comprises a group of disorders characterized by severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. The exact mechanism for edema formation is uncertain, although one possibility includes reduced colloid oncotic pressure due to massive kidney protein loss. Loss of circulating volume also triggers neurohormonal mechanisms that perpetuate the edema formation cycle.

The above mechanisms do not appear to explain edema formation in most adult patients; however, salt retention seems to have a substantial effect.21 The reduction in interstitial oncotic pressure has important implications for the role of hypoalbuminemia in edema formation and for the tendency of edema to form at different sites, but whether this plays a primary role in NS is debatable. In the absence of severe hypoalbuminemia, edema in NS and renal disease is primarily due to in-creased renal sodium retention.22,23

Hypoproteinemia Conditions such as acute nutritional deficiency, protein-losing enteropathies, and severe liver disease can lead to hypoproteinemia. Albumin is important for maintaining plasma oncotic pressure; a level below 2 g/dL of plasma often results in generalized edema.1

Cirrhosis Severe hypoalbuminemia with plasma albumin levels less than 2 g/dL can occur when severe liver disease ensues. However, the most important mechanism behind edema formation in cirrhosis may be decreased effective circulating volume secondary to splanchnic vasodilation. This results in a neurohumoral cascade of events leading to sodium and water retention by the kidneys. In this regard, the mechanism of edema in cirrhosis resembles that in HF and NS.24

Drug-induced edema Certain medications can induce edema by enhancing sodium and water reabsorption by the kidneys. Potent vasodilators such as minoxidil and diazoxide are good examples. Other drugs that can cause edema include calcium channel blockers, which lead to capillary leakage due to dilation of the precapillary sphincter,13 and the NSAIDs, which induce edema formation through different mechanisms by inhibiting renal prostaglandin synthesis. They can also exacerbate edema in patients with underlying HF or cirrhosis.14 Antidepressants, estrogens, corticosteroids, and COX-2 inhibitors can also cause peripheral edema.

Pregnancy The physiologic mechanisms underlying edema in pregnancy include increased plasma volume and sodium retention, possibly secondary to increased antinatriuretic hormones such as aldosterone and desoxycorticosterone. Other causes include decreased plasma protein concentration and increased capillary hy-drostatic pressure late in pregnancy from mechanical compression of the inferior vena cava and iliac veins.25,26

Lymphedema This nonpitting, less common form of edema usually involves a limb and is caused by impaired lymphatic transport, which leads to pathologic accumulation of protein-rich lymphatic fluid in the interstitium. Lymphedema is classified as primary or secondary. Primary lymphedema includes congenital hereditary lymphedema, Meige’s disease, and other rare congenital disorders.27,28 Secondary lymphedema, far more common, is caused by lymph node dissection, radiation, malignant obstruction, and infection. In developed countries, lymph node dissection and radiation are the most common causes of lymphedema.27 In developing countries, lymphatic obstruction from parasitic infection is the most common cause, with filariasis being the most widespread infection worldwide.27

Myxedema Both hypothyroidism and hyperthyroidism can precipitate peripheral edema, but hypothyroidism is a more common cause. Localized edema frequently occurs on the eyelids, face, and dorsum of the hand in these conditions. The mechanism of myxedema is not fully understood. Increased capillary permeability results in the accumulation of proteins and mucopolysaccharides in the interstitium, followed by water and sodium movement. Concomitant expansion in total body water and increased total body sodium then occurs.29-31

Idiopathic edema A poorly understood syndrome of abnormal fluid retention that primarily affects premenopausal women, idiopathic edema includes entities such as cyclical edema, periodic edema, fluid retention syndrome, and orthostatic edema. Key features are periodic episodes of edema in women who have weight changes not clearly related to the menstrual cycle.32 The diagnosis is usually one of exclusion. It is most common in the third and fourth decades and is usually associated with psychological and emotional disturbances and concomitant misuse/abuse of diuretics or laxatives.33,34

Lipedema is commonly mistaken for peripheral edema or lymphedema, but it occurs almost exclusively in young women and characteristically spares the feet. Onset, which is usually insidious, is often apparent shortly after puberty.35

Treatment and follow-up

The treatment of edema consists of reversing the underlying disorder, if possible; hence, an accurate diagnosis is crucial. Dietary sodium and fluid restriction constitute the mainstay of nonpharmacologic treatment. Before using diuretics, the clinician must recognize the hemodynamic consequences of fluid removal. In cases such as pulmonary edema, where edema is life threatening, pursue immediate treatment and rapid fluid removal. Removing excess fluid can proceed more slowly in patients who have less dangerous edematous states.

Use caution to avoid major fluid shifts, hemodynamic instability, and electrolyte disturbances. For example, in patients with NS who undergo excessive and rapid fluid removal through diuretic therapy, concomitant intravascular volume depletion can lead to further kidney damage. In patients with cirrhosis, overzealous fluid removal can cause life-threatening hypokalemia, metabolic alkalosis, and rapid fluid shifts induced by diuretics, as well as hepatic coma or the hepatorenal syndrome. Use a cautious combination of patient education, diet modification, and diuretics when appropriate.1 Consider specialty referral or consultation to deal with underlying causes.

Diuretic therapy Constituting the mainstay of pharmacologic therapy, diuretics include loop, potassium-sparing, and thiazide agents (see Table 2). Loop diuretics, which are usually the most effective, have short plasma half-lives. For example, furosemide has a half-life of 1.5 to 2 hours,36 so several doses per day are required to maintain natriuresis. Since response to each loop diuretic is patient specific, a threshold level of the drug at the site of action must be attained for maximal response. Exceeding this level will not increase diuresis. Because the mechanisms of action are the same, changing to a second loop diuretic will not work if an adequate dosage of the first is not effective.36

Consider adjusting the dosage for renal insufficiency, since larger dosages may be necessary to attain the threshold amount of drug in the tubular fluid.36 The efficacy of diuretics becomes minimal when the glomerular filtration rate is less than 20 mL/min and may be null when it is less than 10 mL/min. Different classes of diuretics work on different nephron sites, so diuretic combinations from different classes may be used. Reducing sodium reabsorption in the distal nephron by adding a thiazide or potassium-sparing diuretic may improve diuresis when loop diuretics alone do not work.
Prevention and patient education Take the time to educate patients about the side effects of their medication. Instruct them to avoid OTC medications since some, including NSAIDs, may cause drug-induced edema.14 When considering patient education, emphasize also that not all patients with edema are alike. A number of Internet sites have information about edema that may be useful (see “Online resources”).

Sodium and fluid restriction Consider referring to a registered dietitian those patients with chronic conditions leading to peripheral edema. A dietitian can assess a patient’s nutritional status, design an individualized diet, and work with a clinician as a part of a comprehensive team approach. Salt restriction is the mainstay of dietary management; the sodium recommended daily allowance (RDA) is 2,400 mg/d, but clinicians usually recommend 2,000 mg/d for most patients with peripheral edema. Remind patients that sodium intake includes table salt as well as salt already present in foods. Instruct them to check food labels for high salt content and to use fresh ingredients in place of canned or processed foods with especially high sodium content. In addition to restricting salt, patients should restrict fluids to a total of 2 liters per day; the water content in foods alone is often enough to achieve this limit.

Lifestyle modification For most patients with peripheral edema, exercise and weight reduction can decrease symptoms and potentiate the effect of dietary and pharmacologic fluid removal. In those with venous stasis, compression stockings increase venous return to the heart and decrease lower extremity edema. Oxygen therapy and/or continuous positive airway pressure are important adjunctive therapies in patients with hypoxia secondary to obstructive pulmonary disease and obstructive sleep apnea leading to pulmonary hypertension.37

Follow-up Most medical conditions leading to peripheral edema are chronic and require long-term follow-up. In these cases, it is particularly important to involve patients in their own health care. Routinely inquire about adherence to medication regimens, and ask patients what they understand about their disease. For the long term, instruct them to monitor their symptoms at home and to chart their weight, an objective way to assess ongoing treatment success or failure.

Journal of American Academy Physcian Asistants