Edema and Related Medical Conditions

Torsemide - Demadex Part Two

2009-10-17T07:01:00.000-07:00

Torsemide - Demadex Part Two

Warnings

Hepatic Disease With Cirrhosis and Ascites

DEMADEX should be used with caution in patients with hepatic disease with cirrhosis and ascites, since sudden alterations of fluid and electrolyte balance may precipitate hepatic coma. In these patients, diuresis with DEMADEX (or any other diuretic) is best initiated in the hospital. To prevent hypokalemia andmetabolic alkalosis, an aldosterone antagonist or potassium-sparing drug should be used concomitantly with DEMADEX.

Ototoxicity

Tinnitus and hearing loss (usually reversible) have been observed after rapidintravenous injection of other loop diuretics and have also been observed after oral DEMADEX. It is not certain that these events were attributable to DEMADEX. Ototoxicity has also been seen in animal studies when very highplasma levels of torsemide were induced. Administered intravenously, DEMADEX should be injected slowly over 2 minutes, and single doses should not exceed 200 mg.

Volume and Electrolyte Depletion

Patients receiving diuretics should be observed for clinical evidence of electrolyte imbalance, hypovolemia, or prerenal azotemia. Symptoms of these disturbances may include one or more of the following: dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps,muscular fatigue, hypotension, oliguria, tachycardia, nausea, and vomiting. Excessive diuresis may cause dehydration, blood-volume reduction, and possibly thrombosis and embolism, especially in elderly patients. In patients who develop fluid and electrolyte imbalances, hypovolemia, or prerenal azotemia, the observed laboratory changes may include hyper- or hyponatremia, hyper- orhypochloremia, hyper- or hypokalemia, acid-base abnormalities, and increasedblood urea nitrogen (BUN). If any of these occur, DEMADEX should be discontinued until the situation is corrected; DEMADEX may be restarted at a lower dose.

In controlled studies in the United States, DEMADEX was administered tohypertensive patients at doses of 5 mg or 10 mg daily. After 6 weeks at these doses, the mean decrease in serum potassium was approximately 0.1 mEq/L. The percentage of patients who had a serum potassium level below 3.5 mEq/L at any time during the studies was essentially the same in patients who received DEMADEX (1.5%) as in those who received placebo (3%). In patients followed for 1 year, there was no further change in mean serum potassium levels. In patients with congestive heart failure, hepatic cirrhosis, or renal disease treated with DEMADEX at doses higher than those studied in United Statesantihypertensive trials, hypokalemia was observed with greater frequency, in a dose-related manner.

In patients with cardiovascular disease, especially those receiving digitalis glycosides, diuretic-induced hypokalemia may be a risk factor for the development of arrhythmias. The risk of hypokalemia is greatest in patients with cirrhosis of the liver, in patients experiencing a brisk diuresis, in patients who are receiving inadequate oral intake of electrolytes, and in patients receiving concomitant therapy with corticosteroids or ACTH.

Periodic monitoring of serum potassium and other electrolytes is advised in patients treated with DEMADEX.

Precautions

Laboratory Values

Potassium: See WARNINGS.

Calcium

Single doses of DEMADEX increased the urinary excretion of calcium by normal subjects, but serum calcium levels were slightly increased in 4- to 6- weekhypertension trials. In a long-term study of patients with congestive heart failure, the average 1-year change in serum calcium was a decrease of 0.10 mg/dL (0.02 mmol/L). Among 426 patients treated with DEMADEX for an average of 11 months, hypocalcemia was not reported as an adverse event.

Magnesium

Single doses of DEMADEX caused healthy volunteers to increase their urinary excretion of magnesium, but serum magnesium levels were slightly increased in 4- to 6-week hypertension trials. In long-term hypertension studies, the average 1-year change in serum magnesium was an increase of 0.03 mg/dL (0.01 mmol/L). Among 426 patients treated with DEMADEX for an average of 11 months, one case of hypomagnesemia (1.3 mg/dL [0.53 mmol/L]) was reported as an adverse event.

In a long-term clinical study of DEMADEX in patients with congestive heartfailure, the estimated annual change in serum magnesium was an increase of 0.2 mg/dL (0.08 mmol/L), but these data are confounded by the fact that many of these patients received magnesium supplements. In a 4-week study in which magnesium supplementation was not given, the rate of occurrence of serum magnesium levels below 1.7 mg/dL (0.70 mmol/L) was 6% and 9% in the groups receiving 5 mg and 10 mg of DEMADEX, respectively.

Blood Urea Nitrogen (BUN), Creatinine and Uric Acid

DEMADEX produces small dose-related increases in each of these laboratory values. In hypertensive patients who received 10 mg of DEMADEX daily for 6 weeks, the mean increase in blood urea nitrogen was 1.8 mg/dL (0.6 mmol/L), the mean increase in serum creatinine was 0.05 mg/dL (4 mmol/L), and the mean increase in serum uric acid was 1.2 mg/dL (70 mmol/L). Little further change occurred with long-term treatment, and all changes reversed when treatment was discontinued.

Symptomatic gout has been reported in patients receiving DEMADEX, but itsincidence has been similar to that seen in patients receiving placebo.

Glucose

Hypertensive patients who received 10 mg of daily DEMADEX experienced a mean increase in serum glucose concentration of 5.5 mg/dL (0.3 mmol/L) after 6 weeks of therapy, with a further increase of 1.8 mg/dL (0.1 mmol/L) during the subsequent year. In long-term studies in diabetics, mean fasting glucose values were not significantly changed from baseline. Cases of hyperglycemia have been reported but are uncommon.

Serum Lipids

In the controlled short-term hypertension studies in the United States, daily doses of 5 mg, 10 mg, and 20 mg of DEMADEX were associated with increases in total plasma cholesterol of 4, 4, and 8 mg/dL (0.10 to 0.20 mmol/L), respectively. The changes subsided during chronic therapy.

In the same short-term hypertension studies, daily doses of 5 mg, 10 mg and 20 mg of DEMADEX were associated with mean increases in plasma triglyceridesof 16, 13 and 71 mg/dL (0.15 to 0.80 mmol/L), respectively.

In long-term studies of 5 mg to 20 mg of DEMADEX daily, no clinically significant differences from baseline lipid values were observed after 1 year of therapy.

Other

In long-term studies in hypertensive patients, DEMADEX has been associated with small mean decreases in hemoglobin, hematocrit, and erythrocyte count and small mean increases in white blood cell count, platelet count, and serumalkaline phosphatase. Although statistically significant, all of these changes were medically inconsequential. No significant trends have been observed in any liver enzyme tests other than alkaline phosphatase.

Carcinogenesis, Mutagenesis and Impairment of Fertility

No overall increase in tumor incidence was found when torsemide was given to rats and mice throughout their lives at doses up to 9 mg/kg/day (rats) and 32 mg/kg/day (mice). On a body-weight basis, these doses are 27 to 96 times a human dose of 20 mg; on a body-surface-area basis, they are 5 to 8 times this dose. In the rat study, the high-dose female group demonstrated renal tubularinjury, interstitial inflammation, and a statistically significant increase in renal adenomas and carcinomas. The tumor incidence in this group was, however, not much higher than the incidence sometimes seen in historical controls. Similar signs of chronic non-neoplastic renal injury have been reported in high-dose animal studies of other diuretics such as furosemide and hydrochlorothiazide.

No mutagenic activity was detected in any of a variety of in vivo and in vitro tests of torsemide and its major human metabolite. The tests included the Ames testin bacteria (with and without metabolic activation), tests for chromosomeaberrations and sister-chromatid exchanges in human lymphocytes, tests for various nuclear anomalies in cells found in hamster and murine bone marrow, tests for unscheduled DNA synthesis in mice and rats, and others.

In doses up to 25 mg/kg/day (75 times a human dose of 20 mg on a body- weight basis; 13 times this dose on a body-surface-area basis), torsemide had no adverse effect on the reproductive performance of male or female rats.

Pregnancy

Pregnancy Category B.

There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide (on a mg/kg basis, this is 15 times a human dose of 20 mg/day; on a mg/m² basis, the animal dose is 10 times the human dose), or in rabbits, treated with 1.6 mg/kg/day (on a mg/kg basis, 5 times the human dose of 20 mg/kg/day; on a mg/m² basis, 1.7 times this dose). Fetal and maternal toxicity(decrease in average body weight, increase in fetal resorption and delayed fetalossification) occurred in rabbits and rats given doses 4 (rabbits) and 5 (rats) times larger. Adequate and well-controlled studies have not been carried out in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.

Labor and Delivery

The effect of DEMADEX on labor and delivery is unknown.

Nursing Mothers

It is not known whether DEMADEX is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when DEMADEX is administered to a nursing woman.

Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

Administration of another loop diuretic to severely premature infants with edemadue to patent ductus arteriosus and hyaline membrane disease has occasionally been associated with renal calcifications, sometimes barely visible on X-ray but sometimes in staghorn form, filling the renal pelves. Some of these calculi have been dissolved, and hypercalciuria has been reported to have decreased, when chlorothiazide has been coadministered along with the loop diuretic. In other premature neonates with hyaline membrane disease, another loop diuretic has been reported to increase the risk of persistent patent ductus arteriosus, possibly through a prostaglandin-E- mediated process. The use of DEMADEX in such patients has not been studied.

Geriatric Use

Of the total number of patients who received DEMADEX in United States clinical studies, 24% were 65 or older while about 4% were 75 or older. No specific age-related differences in effectiveness or safety were observed between younger patients and elderly patients.

rxlist

Overdose

There is no human experience with overdoses of DEMADEX, but the signs and symptoms of overdosage can be anticipated to be those of excessive pharmacologic effect: dehydration, hypovolemia, hypotension, hyponatremia,hypokalemia, hypochloremic alkalosis, and hemoconcentration. Treatment of overdosage should consist of fluid and electrolyte replacement.

Laboratory determinations of serum levels of torsemide and its metabolites are not widely available.

No data are available to suggest physiological maneuvers (eg, maneuvers to change the pH of the urine) that might accelerate elimination of torsemide and its metabolites. Torsemide is not dialyzable, so hemodialysis will not accelerate elimination.

Contraindications

DEMADEX is contraindicated in patients with known hypersensitivity to DEMADEX or to sulfonylureas.

DEMADEX is contraindicated in patients who are anuric.

Torsemide - Demadex

2009-10-14T09:42:00.000-07:00

Torsemide - Demadex - Diuretic for Generalized Edema

Part One

One of the most commonly prescribed medicines for

fluid retention (generalized edema/ swelling)

DEMADEX (torsemide) is a diuretic of the pyridine-sulfonylurea class.

DEMADEX is indicated for the treatment of edema associated with congestive heart failure, renal disease, or hepatic disease. Use of torsemide has been found to be effective for the treatment of edema associated with chronic renal failure.Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials.

DEMADEX intravenous injection is indicated when a rapid onset of iuresis is desired or when oral administration is impractical.

DEMADEX is indicated for the treatment of hypertension alone or in combination with other antihypertensive agents.

Dosage and Administration

General

DEMADEX tablets may be given at any time in relation to a meal, as convenient. Special dosage adjustment in the elderly is not necessary.

Because of the high bioavailability of DEMADEX, oral and intravenous doses are therapeutically equivalent, so patients may be switched to and from the intravenous form with no change in dose. DEMADEX intravenous injection should be administered either slowly as a bolus over a period of 2 minutes or administered as a continuous infusion.

If DEMADEX is administered through an IV line, it is recommended that, as with other IV injections, the IV line be flushed with Normal Saline (Sodium Chloride Injection, USP) before and after administration. DEMADEX injection is formulated above pH 8.3. Flushing the line is recommended to avoid the potential for incompatibilities caused by differences in pH which could be indicated by color change, haziness or the formation of a precipitate in the solution.

If DEMADEX is administered as a continuous infusion, stability has been demonstrated through 24 hours at room temperature in plastic containers for the following fluids and concentrations:

200 mg DEMADEX (10 mg/mL) added to:

250 mL Dextrose 5% in water
250 mL 0.9% Sodium Chloride
500 mL 0.45% Sodium Chloride

50 mg DEMADEX (10 mg/mL) added to:

500 mL Dextrose 5% in water
500 mL 0.9% Sodium Chloride
500 mL 0.45% Sodium Chloride

Before administration, the solution of DEMADEX should be visually inspected for discoloration and particulate matter. If either is found, the ampul should not be used.

Congestive Heart Failure

The usual initial dose is 10 mg or 20 mg of once-daily oral or intravenous DEMADEX. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied.

Chronic Renal Failure

The usual initial dose of DEMADEX is 20 mg of once-daily oral or intravenous DEMADEX. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied.

Hepatic Cirrhosis

The usual initial dose is 5 mg or 10 mg of once-daily oral or intravenous DEMADEX, administered together with an aldosterone antaagonist or a potassium-sparing diuretic. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 40 mg have not been adequately studied.

Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials.

Hypertension

The usual initial dose is 5 mg once daily. If the 5 mg dose does not provide adequate reduction in blood pressure within 4 to 6 weeks, the dose may be increased to 10 mg once daily. If the response to 10 mg is insufficient, an additional antihypertensive agent should be added to the treatment regimen.

105 (for 5 mg, 10 mg, 20 mg, or 100 mg, respectively). On the opposite side, the tablet is debossed with 5, 10, 20, or 100 to indicate the dose.

DEMADEX for intravenous injection is supplied in clear ampuls containing 2 mL (20 mg, NDC 0004-0267-06) or 5 mL (50 mg, NDC 0004-0268-06) of a 10 mg/mL sterile solution. The ampuls are supplied in boxes of 10.

Side Effects

At the time of approval, DEMADEX had been evaluated for safety in approximately 4000 subjects: over 800 of these subjects received DEMADEX for at least 6 months, and over 380 were treated for more than 1 year. Among these subjects were 564 who received DEMADEX during United States-based trials in which 274 other subjects received placebo.

The reported side effects of DEMADEX were generally transient, and there was no relationship between side effects and age, sex, race, or duration of therapy. Discontinuation of therapy due to side effects occurred in 3.5% of United States patients treated with DEMADEX and in 4.4% of patients treated with placebo. In studies conducted in the United States and Europe, discontinuation rates due to side effects were 3.0% (38/1250) with DEMADEX and 3.4% (13/380) with furosemide in patients with congestive heart failure, 2.0% (8/409) with DEMADEX and 4.8% (11/230) with furosemide in patients with renal insufficiency, and 7.6% (13/170) with DEMADEX and 0% (0/33) with furosemide in patients withcirrhosis.

The most common reasons for discontinuation of therapy with DEMADEX were (in descending order of frequency) dizziness, headache, nausea, weakness, vomiting, hyperglycemia, excessive urination, hyperuricemia, hypokalemia, excessive thirst, hypovolemia, impotence, esophageal hemorrhage, anddyspepsia. Dropout rates for these adverse events ranged from 0.1% to 0.5%.

The daily doses of DEMADEX used in these trials ranged from 1.25 mg to 20 mg, with most patients receiving 5 mg to 10 mg; the duration of treatment ranged from 1 to 52 days, with a median of 41 days. Of the side effects listed in the table, only "excessive urination" occurred significantly more frequently in patients treated with DEMADEX than in patients treated with placebo. In the placebo-controlled hypertension studies whose design allowed side-effect rates to be attributed to dose, excessive urination was reported by 1% of patients receiving placebo, 4% of those treated with 5 mg of daily DEMADEX, and 15% of those treated with 10 mg. The complaint of excessive urination was generally not reported as an adverse event among patients who received DEMADEX for cardiac, renal, or hepatic failure.

Serious adverse events reported in the clinical studies for which a drug relationship could not be excluded were atrial fibrillation, chest pain, diarrhea, digitalis intoxication, gastrointestinal hemorrhage, hyperglycemia, hyperuricemia, hypokalemia, hypotension, hypovolemia, shunt thrombosis, rash,rectal bleeding, syncope, and ventricular tachycardia.

Angioedema has been reported in a patient exposed to DEMADEX who was later found to be allergic to sulfa drugs.

Of the adverse reactions during placebo-controlled trials listed without taking into account assessment of relatedness to drug therapy, arthritis and various other nonspecific musculoskeletal problems were more frequently reported in association with DEMADEX than with placebo, even though gout was somewhat more frequently associated with placebo. These reactions did not increase in frequency or severity with the dose of DEMADEX. One patient in the group treated with DEMADEX withdrew due to myalgia, and one in the placebo group withdrew due to gout.

Drug Interactions

In patients with essential hypertension, DEMADEX has been administered together with beta-blockers, ACE inhibitors, and calcium-channel blockers. In patients with congestive heart failure, DEMADEX has been administered together with digitalis glycosides, ACE inhibitors, and organic nitrates. None of these combined uses was associated with new or unexpected adverse events.

Torsemide does not affect the protein binding of glyburide or of warfarin, theanticoagulant effect of phenprocoumon (a related coumarin derivative), or the pharmacokinetics of digoxin or carvedilol (a vasodilator/beta-blocker). In healthy subjects, coadministration of DEMADEX was associated with significant reduction in the renal clearance of spironolactone, with corresponding increases in the AUC. However, clinical experience indicates that dosage adjustment of either agent is not required.

Because DEMADEX and salicylates compete for secretion by renal tubules, patients receiving high doses of salicylates may experience salicylate toxicity when DEMADEX is concomitantly administered. Also, although possible interactions between torsemide and nonsteroidal anti-inflammatory agents (including aspirin) have not been studied, coadministration of these agents with another loop diuretic (furosemide) has occasionally been associated with renal dysfunction.

The natriuretic effect of DEMADEX (like that of many other diuretics) is partially inhibited by the concomitant administration of indomethacin. This effect has been demonstrated for DEMADEX under conditions of dietary sodium restriction (50 mEq/day) but not in the presence of normal sodium intake (150 mEq/day).

The pharmacokinetic profile and diuretic activity of torsemide are not altered by cimetidine or spironolactone. Coadministration of digoxin is reported to increase the area under the curve for torsemide by 50%, but dose adjustment of DEMADEX is not necessary.

Concomitant use of torsemide and cholestyramine has not been studied in humans but, in a study in animals, coadministration of cholestyramine decreased the absorption of orally administered torsemide. If DEMADEX and cholestyramine are used concomitantly, simultaneous administration is not recommended.

Coadministration of probenecid reduces secretion of DEMADEX into the proximal tubule and thereby decreases the diuretic activity of DEMADEX.

Other diuretics are known to reduce the renal clearance of lithium, inducing a high risk of lithium toxicity, so coadministration of lithium and diuretics should be undertaken with great caution, if at all. Coadministration of lithium and DEMADEX has not been studied.

Other diuretics have been reported to increase the ototoxic potential of aminoglycoside antibiotics and of ethacrynic acid, especially in the presence of impaired renal function. These potential interactions with DEMADEX have not been studied.

RxList

Abdominoscrotal hydrocele with leg edema in a 4-month-old boy

2009-10-14T09:32:00.000-07:00

Abdominoscrotal hydrocele with leg edema in a 4-month-old boy

Prog Urol. 2009 Oct

Faure A, Bouali O, Chaumoitre K, Louka B, Alessandrini P, Merrot T.

Service de chirurgie pédiatrique, hôpital Nord, AP-HM, université de la Méditerranée, chemin des Bourrelly, 13915 Marseille cedex 20, France.

We present a case of a 4-month-old boy with a right abdominoscrotal hydrocele associated to a compression of the femoral triangle, causing an unilateral leg edema. Abdominoscrotal ultrasound revealed a fluid collection with abdominal and scrotal components, communicating through the deep inguinal ring. Sagittal views of magnetic resonance imaging (MRI) showed a dumbbell-shaped hydrocele and the angio-MRI venous sequences confirmed the compression of the right iliac vessels.

Curative treatment was surgical through an inguinal approach and consisted in high ligation of the processus vaginalis and hydrocelectomy. Abdominoscrotal hydrocele is an uncommon pathology, which rarely occurs in pediatric population. This diagnosis should be discussed when a cystic abdominal mass is associated to an ipsilateral scrotal hydrocele. The abdominal component of the hydrocele can result in compression of adjacent structures (iliac vessels, ureter). Surgical treatment is recommended. Epididymal and testicular abnormalities are frequently described, as in our observation, and the effects on the future fertility are unknown.

Elsevier/Science Direct

Feasibility of treatment of lower limb edema with calf muscle pump stimulation in chronic heart failure.

2009-09-28T03:40:00.000-07:00

Feasibility of treatment of lower limb edema with calf muscle pump stimulation in chronic heart failure.

Eur J Cardiovasc Nurs. 2009 Aug 31

Pierce C, McLeod KJ.

Decker School of Nursing, Binghamton University, United States; Department of Bioengineering, Binghamton University, United States.

BACKGROUND: Persons with chronic heart failure may exhibit a decrease in functional ability related to lower extremity edema in spite of optimal diuretic therapy and salt restrictions.

AIM: The aim of this pilot prospective clinical study was to test the feasibility of using exogenous calf muscle pump stimulation to decrease lower leg edema and thus improve functional status and quality of life.

METHODS: Six subjects entered into this study and agreed to use the intervention 30min/day for one month. DXA was used to assess lower extremity composition.

RESULTS: Device use averaged approximately 1h/day and resulted in a reduction in the lean mass of the legs of 0.5kg (range=0.08-1.0L; p=0.03). Linear regression analysis of reduction of lower limb edema against daily usage suggests that increased utilization of calf muscle pump stimulation was associated with increased water losses, although this trend was not significant (R(2)=0.4, p=0.18).

CONCLUSION: This pilot indicates that exogenous calf muscle pump stimulation could be a useful and safe addition to the patients' treatment regimes, but further studies testing a more typical population with heart failure is warranted.

Science Direct

Mesoglycan

2009-09-28T03:35:00.000-07:00

Mesoglycan

Description

Mesoglycan is a mucopolysaccharide complex that is extracted from calf aorta or synthetically created and taken in pill or capsule form as a dietary supplement. Mucopolysaccharides are long molecular chains of sugar. They are used by the body in the building of connective tissues, such as cartilage, tendons, and ligaments. The substance is related to the blood-thinning drug heparin, and the supplements glucosamine and chondroitin. Both are used to treat joint pain and arthritis.

What other names is Mesoglycan known by?

Aortic Glycosaminoglycans, Aortic GAGs, Glycosaminoglycans, Heparinoid Fraction, Heparinoids, Mucopolysaccharide, Sulfomucopolysaccharide.

What is Mesoglycan?

Mesoglycan is a substance obtained from cow lung or blood vessels (aorta), or pig intestine.

Possibly Effective for...

Treating poor circulation that can lead to varicose veins and other conditions.
Treating leg ulcers.
Reducing blood levels of certain fats called triglycerides.
Reducing pain when walking in people with a disease called peripheral arterial disease.
Improving thinking and quality of life in people with limited blood flow to the brain (cerebrovascular disease).

Possibly Ineffective for...

Preventing blood clots in the legs and lungs (deep vein thrombosis and pulmonary embolism).
Treating stroke.

Insufficient Evidence to Rate Effectiveness for...

Hemorrhoids, atherosclerosis (a type of heart disease), inflammation of blood vessels (vasculitis), and other conditions.

rxlist.com

Pharmacological treatment of mechanical edema: a randomized controlled trial about the effects of mesoglycan.

2009-09-28T03:29:00.000-07:00

Pharmacological treatment of mechanical edema: a randomized controlled trial about the effects of mesoglycan.

Eur J Phys Rehabil Med. 2009 Mar

Recovery and Rehabilitation Agency, University Hospital of Careggi, Florence, Italy

AIM: Mechanical edema (MO) is frequently found in a lot of the lower extremities' orthopedic diseases. In absence of deep vein thrombosis, MO is caused by the change in the dynamics of calf muscle pump with venous hypertension and by the change in capillary permeability which offsets the extra-vascular fluid balance resulting in edema formation. The correct treatment includes specific training for musculo-skeletal and gait recovery, together with medical treatment focused on venous endothelium. Little information is available about pharmacological treatment of this condition. Some studies suggest the efficacy of mesoglycan in venous pathology. Aim of this study was to evaluate the clinical efficacy of the pharmacological treatment (mesoglycan 50 mg p.o., twice a day) in patients affected by MO.

METHODS: Forty-four patients with MO, aged 20-89 years, were randomized in two treatment groups: specific physiotherapy (Fkt) alone or physiotherapy plus mesoglycan 50 mg twice a day, per os. The patients were evaluated before treatment (t0), and after 1 month of treatment (t1), measuring ankle joint range of motion (degrees), calf circumference and malleolar circumference (cm), pain Borg CR10 Scale and adapted lymphedema Weiss Scale. Statistical analysis was performed by the Pearson's c2 test and the Mann-Whitney-Wilcoxon test.

RESULTS: At the final evaluation of the objective and subjective parameters, the mesoglycan effect combined to the Fkt provided statistical differences on nearly all the parameters in comparison with the patients randomised to Fkt alone.

CONCLUSIONS: The present study suggest that mesoglycan treatment (50 mg p.o., twice a day) can improve the recovery of MO, and it is well tolerated by the patients. Specific physiotherapy remains the first treatment for the recovery of both muscular pump and correct walking, but the optimal treatment of MO seems to be a synergic approach, including both pharmacological and mobilization programs.

Minerva Medica

Efficacy of intravitreal bevacizumab (Avastin) for short-term treatment of diabetic macular edema.

2009-09-21T23:11:00.000-07:00

Efficacy of intravitreal bevacizumab (Avastin) for short-term treatment of diabetic macular edema.
Nagasawa T, Naito T, Matsushita S, Sato H, Katome T, Shiota H.
Department of Ophthalmology, Institute of Health Biosciences, the University of Tokushima Graduate School, Tokushima, Japan.

PURPOSE: To report the efficacy of intravitreal injections of bevacizumab for diabetic macular edema (DME) in the short-term.

DESIGN: Retrospective, noncomparative, interventional case series.

METHODS: Medical records of 20 eyes of 19 patients who underwent intravitreal injections of bevacizumab for persistent diabetic macular edema were reviewed retrospectively. All eyes received intravitreal injections of bevacizumab (1.25 mg/0.05 ml). The clinical course of best-corrected visual acuity (BCVA) using a logarithm of the minimum angle of resolution chart, and averaged foveal retinal thickness using an optical coherence tomography (OCT) were monitored for up to four weeks after the injection.

RESULTS: BCVA at one week improved by two lines or more in six eyes (30%) and in nine eyes (45%) at four weeks. However, no significant improvement in the mean BCVA from baseline was observed at one week (P>0.05) and four weeks (P>0.05). Mean retinal thicknesses (RT) were 411+/-170 mum at baseline, 349+/-102 microm at one week after the injection (P<0.05),>0.05). One week after the injection, significant regression of macular edema was seen. However, recurrence occurred at four weeks. No complications such as severe vision loss, endophthalmitis, or systemic events developed.

CONCLUSION: No changes in BCVA and RT were observed in the short-term observation after the intravitreal injection of bevacizumab for DME.

Journal of Medical Investigation

Metolazone

2009-09-17T05:36:00.001-07:00

Metolazone

GENERIC NAME: METOLAZONE - ORAL (me-TOLE-a-zone)
BRAND NAME(S): Zaroxolyn

One of the old fashion but quite effective diuretics in the treatment of generalized edema is a medicine called metolazone. Presently, after experiencing severe lymphatic failure with bi-lateral lung edema, a history of lymphoma and contending with hereditary lymphedema radiology tests indicate almost no lymphatic flow through the thoracic duct or through the right side lymphatic drainage fields. Clearly, it is a matter of life for me to be able to somehow get rid of the massive amounts of fluid that is collecting in my body.

I must add however, that unless there is a life threatening co-morbidity, lymphedema patients should not be treated with diuretics.

Very recently, my doctor put me on metolazone with incredible results.

What is metolazone?

Metolazone is a thiazide diuretic (water pill) that helps prevent your body from absorbing too much salt, which can cause fluid retention.

Metolazone treats fluid retention (edema) in people with congestive heart failure, or a kidney disorder such as nephrotic syndrome. This medication is also used to treat high blood pressure (hypertension).

Metolazone may also be used for other purposes not listed in this medication guide.

What is the most important information I should know about metolazone?

Do not use this medication if you are unable to urinate, or if you have severe liver disease.

Before using this medication, tell your doctor if you have liver disease, kidney disease, asthma, allergies, gout, diabetes, or an allergy to sulfa drugs.Avoid drinking alcohol, which can increase some of the side effects of metolazone.

Avoid becoming overheated or dehydrated during exercise and in hot weather. Follow your doctor's instructions about the type and amount of liquids you should drink. In some cases, drinking too much liquid can be as unsafe as not drinking enough.

There are many other medicines that can interact with metolazone. Tell your doctor about all the prescription and over-the-counter medications you use. This includes vitamins, minerals, herbal products, and drugs prescribed by other doctors. Do not start using a new medication without telling your doctor. Keep a list with you of all the medicines you use and show this list to any doctor or other healthcare provider who treats you.

If you are being treated for high blood pressure, keep using this medication even if you feel fine.

High blood pressure often has no symptoms.

What should I discuss with my doctor before taking metolazone?

Do not use this medication if you are allergic to metolazone, or if you have:
severe liver disease; or if you are unable to urinate.

If you have certain conditions, you may need a dose adjustment or special tests to safely take this medication. Before using metolazone, tell your doctor if you have:

kidney disease;
liver disease;
gout;
diabetes; or

an allergy to sulfa drugs.FDA pregnancy category B. This medication is not expected to be harmful to an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant during treatment. Metolazone can pass into breast milk and may harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.

How should I take metolazone?

Take this medication exactly as it was prescribed for you. Do not take the medication in larger amounts, or take it for longer than recommended by your doctor. Follow the directions on your prescription label.

Your doctor may occasionally change your dose to make sure you get the best results from this medication.

To be sure this medication is not causing harmful effects, your blood will need to be tested on a regular basis. Do not miss any scheduled appointments.

Your blood and urine may both be tested if you have been vomiting or are dehydrated.

If you need to have any type of surgery, tell the surgeon ahead of time that you are taking metolazone. You may need to stop using the medicine for a short time.

If you are being treated for high blood pressure, keep using this medication even if you feel fine. High blood pressure often has no symptoms.Store the tablets at room temperature away from heat, light, and moisture.

What happens if I miss a dose?

Take the missed dose as soon as you remember. If it is almost time for your next dose, skip the missed dose and take the medicine at the next regularly scheduled time. Do not take extra medicine to make up the missed dose.

What happens if I overdose?

Seek emergency medical attention if you think you have used too much of this medicine.

Overdose symptoms may include nausea, weakness, dizziness, dry mouth, thirst, muscle pain or weakness, feeling light-headed, or fainting.

What should I avoid while taking metolazone?

Avoid drinking alcohol, which can increase some of the side effects of metolazone.

Avoid using other medicines that make you light-headed (narcotic pain medication, muscle relaxers, and medicine for seizures). They can add to the side effects of metolazone. Tell your doctor if you regularly use any of these medicines, or any other blood pressure medications.

Avoid becoming overheated or dehydrated during exercise and in hot weather. Follow your doctor's instructions about the type and amount of liquids you should drink. In some cases, drinking too much liquid can be as unsafe as not drinking enough.

Drugs.com

HOW TO USE: Take this medication by mouth with or without food, usually once daily, or as directed by your doctor. The dosage is based on your medical condition and response to therapy. It is best to take this medication early in the day, before 4-6PM, to prevent having to wake up during the night to urinate. Consult your doctor or pharmacist if you have questions about your dosing schedule. Use this medication regularly in order to get the most benefit from it. Remember to use it at the same time each day as directed. It is important to continue taking this medication even if you feel well. Most people with high blood pressure do not feel sick. Do not stop taking this medication without consulting your doctor. It may take up to 3-6 weeks to see a lowering of your blood pressure. Cholestyramine and colestipol can decrease the absorption of metolazone. If you are taking either of these drugs, separate metolazone from cholestyramine by at least 4 hours and from colestipol by at least 2 hours. Different brands of metolazone may not be equal. Do not switch to another brand without your doctor's approval. If your condition persists or worsens, contact your doctor or pharmacist.

SIDE EFFECTS: Dizziness, lightheadedness, headache, blurred vision, loss of appetite, stomach upset, diarrhea, or constipation may occur as your body adjusts to the medication. If any of these effects persist or worsen, notify your doctor or pharmacist promptly. This medication may lead to excessive loss of body water and minerals (including potassium). Tell your doctor immediately if you have any of these unlikely but serious symptoms of dehydration or mineral loss: muscle cramps or weakness, confusion, severe dizziness, unusual dry mouth or thirst, nausea or vomiting, fast/irregular heartbeat, unusual decrease in the amount of urine, fainting, seizures. Tell your doctor immediately if any of these unlikely but serious side effects occur: numbness/tingling of the arms/legs, decreased sexual ability, chest pain. Tell your doctor immediately if any of these highly unlikely but very serious side effects occur: persistent sore throat or fever, easy bleeding or bruising, stomach/abdominal pain, persistent nausea/vomiting, yellowing of eyes/skin. A serious allergic reaction to this drug is unlikely, but seek immediate medical attention if it occurs. Symptoms of a serious allergic reaction include: rash, itching, swelling, severe dizziness, trouble breathing. If you notice other effects not listed above, contact your doctor or pharmacist.

PRECAUTIONS: Before taking metolazone, tell your doctor or pharmacist if you are allergic to it; or to sulfa medications; or if you have any other allergies. This medication should not be used if you have certain medical conditions. Before using this medicine, consult your doctor or pharmacist if you have: severe kidney disease (inability to make urine or anuria). Before using this medication, tell your doctor or pharmacist your medical history, especially of: kidney disease, liver disease, untreated mineral imbalance (e.g., sodium, potassium), gout, lupus. If you have diabetes, metolazone may worsen control of blood glucose levels. Monitor your blood glucose levels regularly and inform your doctor of the results. This drug may reduce the potassium levels in your blood. Ask your doctor about adding potassium to your diet. A potassium supplement may be prescribed by your doctor. This medication may make you more sensitive to the sun. Avoid prolonged sun exposure, tanning booths or sunlamps. Use a sunscreen and wear protective clothing when outdoors. Before having surgery, tell your doctor or dentist that you are taking this medication. This drug may make you dizzy or cause blurred vision; use caution engaging in activities requiring alertness such as driving or using machinery. Limit alcoholic beverages. To minimize dizziness and lightheadedness, get up slowly when rising from a seated or lying position. Caution is advised when using this drug in the elderly because they may be more sensitive to its effects, especially dizziness. Metolazone should be used only when clearly needed during pregnancy. Discuss the risks and benefits with your doctor. This drug passes into breast milk. Consult your doctor before breast-feeding.

DRUG INTERACTIONS: See also the How to Use section. This drug should not be used with the following medications because very serious interactions may occur: cisapride. If you are currently using any of these medications, tell your doctor or pharmacist before starting metolazone. Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbal products you may use, especially of: cholestyramine, colestipol, corticosteroids (e.g., prednisone), diazoxide, digoxin, lithium, nonsteroidal anti-inflammatory drugs (e.g., ibuprofen, indomethacin). Check the labels on all your medicines (e.g., cough-and-cold products, diet aids) because they may contain ingredients that could increase your blood pressure. Ask your pharmacist about the safe use of those products. This product can affect the results of certain lab tests (e.g., parathyroid function tests). Make sure laboratory personnel and your doctors know you use this drug. Do not start or stop any medicine without doctor or pharmacist approval.

MedicineNet.com

Leg edema with deep venous thrombosis-like symptoms as an unusual complication of occult bladder distension and right May-Thurner syndrome in a stroke

2009-06-11T08:36:00.000-07:00

Leg edema with deep venous thrombosis-like symptoms as an unusual complication of occult bladder distension and right May-Thurner syndrome in a stroke patient: a case report.

Arch Phys Med Rehabil. 2009 May

Im S, Lim SH, Chun HJ, Ko YJ, Yang BW, Kim HW.
Department of Rehabilitation Medicine, Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seocho-ku, Seoul, Republic of Korea.

Overt bladder distension can compress the iliac vessels and result in lower extremity swelling mimicking deep venous thrombosis (DVT). This phenomenon has been reported in patients with bladder outlet obstruction due to prostatism but no report has been made in relation to poststroke urinary retention (UR). The authors experienced a rare case of abrupt leg edema with DVT-like symptoms due to iliac vein compression by an overdistended bladder that had developed after cerebrovascular stroke. A 74-year-old woman with left striatocapsular infarction and situs inversus presented with severe right leg swelling. Imaging studies revealed external compression of the right iliac veins by an overdistended bladder and underlying May-Thurner syndrome (MTS). The presence of situs inversus totalis resulted in the rare clinical finding of a right-sided MTS. The patient's symptoms were largely attributable to external compression of right iliac veins by bladder distension and they resolved completely after prompt bladder drainage. Follow-up imaging findings showed complete regression of right external iliac vein stenosis. This case provides the first description of lower extremity swelling manifest as an unusual complication from UR in a stroke patient. Proper and strict bladder screening with appropriate management should be implemented as important therapeutic components during the rehabilitative management of stroke patients.

Abbreviations: CT, computed tomography; DVT, deep venous thrombosis; MTS, May-Thurner syndrome; UR, urinary retention

Elsevier

A 62-year-old woman with non-pitting leg oedema

2009-06-11T08:31:00.000-07:00

A 62-year-old woman with non-pitting leg oedema
Tidsskr Nor Laegeforen. 2009 Apr 16

Bergersen TK, Mørk C.
kristin.bergersen@rikshospitalet.no

A patient presented with non-pitting lymphoedema of the legs and finger clubbing. A skin biopsy showed epidermal hyperkeratosis and abundant mucinous material (Alcian blue positive) in reticular dermis. Treatment (radioactive iodine) for Grave's disease (with exophthalmus) 20 years ago, raised suspicion of thyroid dermopathy. Together, these three extrathyroidal manifestations of Graves' disease are typical of the EMO syndrome. In addition, the patient had elevated serum concentrations of thyroid-stimulating hormone receptor autoantibodies. Autoimmune mechanisms are involved in the stimulation of fibroblasts and the production of large amounts of mucin. Pretibial myxoedema relates to scars, mechanical factors, and dependent position. Lack of steroid treatment during radioactive iodine therapy and smoking, may have exacerbated the thyroid dermopathy in this case. Awareness of pretibial myxoedema as a late autoimmune manifestation of Graves' disease, may contribute to earlier diagnosis and correct treatment.

Full text Article

.[Article in Portuguese, English]

2009-06-11T08:29:00.000-07:00

Post -tracheal extubation pulmonary oedema - Case report

Castro MD, Chaves P, Canas M, Moedas ML.
Interna de Anestesiologia, Hospital de S. António dos Capuchos, Centro Hospitalar de Lisboa Central - EPE (CHLC - EPE).

Negative pressure pulmonary oedema is an uncommon complication of traqueal extubation ( approximately 0,1%) mostly caused by acute upper airway obs truction. Upper airway obstruction from glottis closure leads to marked inspiratory effort, which generates negative intrathoracic pressure transmitting to pulmonary interstitium, and inducing fluid transudation from pulmonary capillary bed1 -5. We report a case of post- -extubation pulmonary oedema in a fifteen years old patient, submitted to surgery following traumatic amputation of his left leg. We review the pathophysiology, radiological findings, potential risk factors and preventive measures of this post -anaesthetic respiratory complication. Rev Port Pneumol 2009; XV (3): 537-541 Key-words: Post -extubation pulmonary oedema, upper airway obstruction, laryngospasm, intra -thoracic negative pressure.

PMID: 19401801 [PubMed - as supplied by publisher]

Persistent Subcutaneous Oedema and Aseptic Fatty Tissue Necrosis after Using Octenisept(R).

2009-06-08T07:38:00.000-07:00

Persistent Subcutaneous Oedema and Aseptic Fatty Tissue Necrosis after Using Octenisept(R).
Eur J Pediatr Surg. 2009 Jun

Schupp CJ, Holland-Cunz S.
1Division of Pediatric Surgery, University Hospital Heidelberg, Heidelberg, Germany.

INTRODUCTION: Wound management and the prevention and treatment of tissue infections are part of daily routine. Octenisept ((R)) (Schülke & Mayr), an antiseptic with a broad antimicrobiological effect, is widely used for various indications. This paper reports prolonged oedema and tissue swelling after treatment of deep wounds with Octenisept ((R)) in three children.

CASE REPORTS: Three paediatric patients, aged between 2 months and 4 years, were treated with Octenisept ((R)) in different hospitals. One initially presented with an abscess of the gluteal area, two with deep wounds of the cheek following injury with a wooden stick. The wounds were cleaned and washed out with Octenisept ((R)). Adequate drainage was in place at all times.

COMMON FINDINGS: We observed aseptic, non painful subcutaneous tissue swelling and oedema in all three cases after wound lavage with Octenisept ((R)). This occurred shortly after the wound was initially treated and lasted for weeks until the symptoms slowly declined. It was not accompanied by persistent general infection parameters. A biopsy taken from one patient demonstrated an aseptic inflammatory reaction and oedema of the subcutaneous tissue, with partial tissue necrosis. Neither surgical revision nor antibiotic therapy brought any improvement.

CONCLUSIONS: Retrospectively, one can consider these occurrences as a consequence of the use of Octenisept ((R)), since the changes are consistent with those described by Schülke & Mayr when Octenisept ((R)) was accidentally administered by subcutaneous injection or under pressure to flush deep hand stab wounds that were not drained. The underlying pathobiological mechanism remains unclear. Hence, we recommend not to apply Octenisept ((R)) in any wound cavity until further investigation has taken place. If aseptic fatty tissue necrosis and oedema develop after using Octenisept ((R)), further surgical intervention or antibiotic treatment will not give any benefit. Changes subside slowly. So far, adequate treatment is not available.

Thieme/eJournals

Sporadic In Utero Generalized Edema Caused by Mutations in the Lymphangiogenic Genes VEGFR3 and FOXC2.

2009-05-19T07:42:00.000-07:00

Sporadic In Utero Generalized Edema Caused by Mutations in the Lymphangiogenic Genes VEGFR3 and FOXC2.

J Pediatr. 2009 Apr 23

Ghalamkarpour A, Debauche C, Haan E, Van Regemorter N, Sznajer Y, Thomas D, Revencu N, Gillerot Y, Boon LM, Vikkula M.
Laboratory of Human Molecular Genetics (A.G., N.R., L.B., M.V.), de Duve Institute, Université Catholique de Louvain, Brussels, Belgium; Department of Neonatology (C.D.), Cliniques Universitaires Saint-Luc, Brussels, Belgium; Department of Genetic Medicine (E.H.), Women's and Children's Hospital, North Adelaide, Australia, and Department of Paediatrics, University of Adelaide, Adelaide, Australia; Centre de Génétique ULB (N.V., Y.S.), Hôpital Erasme, Brussels, Belgium; Unité de Génétique Clinique Pédiatrique (Y.S.), Université Libre de Bruxelles, Brussels, Belgium; Unité Diagnostic Anténatal, Hôpitaux Iris Sud (D.T.), Brussels, Belgium; Center for Human Genetics (Y.G.), Cliniques Universitaires Saint-Luc, Brussels, Belgium; and Centre for Vascular Anomalies (L.B.), Cliniques Universitaires Saint-Luc, Brussels, Belgium.

OBJECTIVES: To investigate the genetic causes of idiopathic sporadic prenatal generalized edema.

STUDY DESIGN: In a series of 12 patients, in whom in utero generalized skin edema or hydrops fetalis had been diagnosed, we screened 3 lymphangiogenic genes, VEGFR3, FOXC2, and SOX18.

RESULTS: In 3 of the patients, we identified a mutation: 2 in VEGFR3 and 1 in FOXC2. Two of the mutations were de novo and one was either de novo or nonpenetrant inherited. In these patients, the generalized edema resorbed spontaneously, either in utero or after birth. In the 2 individuals with a VEGFR3 mutation, edema remained limited to lower limbs.

CONCLUSIONS: Mutations in the VEGFR3 and FOXC2 genes account for a subset of patients with unexplained in utero generalized subcutaneous edema and hydrops fetalis without family history of lymphedema. Lymphangiogenic genes should be screened for mutations in sporadic patients diagnosed with fetal edema.

Elsevier/ScienceDirect

Treatment of hereditary angioedema: current perspectives

2008-12-30T08:27:00.000-08:00

Treatment of hereditary angioedema: current perspectives

Recent Pat Inflamm Allergy Drug Discov. 2008

Krassilnikova SI, Nikiforov YS, Craig TJ.
Section of Allergy, Asthma and Immunology, Penn State University, Milton S. Hershey Medical Center, Hershey, PA 17033, USA.

Hereditary angioedema (HAE) is a rare familial disease characterized by recurrent self-limiting episodes of soft tissue swelling affecting different parts of the body. Acute HAE attacks range from benign, but disfiguring skin edema, to painful abdominal, and even life-threatening laryngeal attacks. The disease is caused by an aberrant C1 esterase inhibitor (C1-INH), which regulates complement, fibrinolytic, and contact pathways. Elevated serum level of bradykinin as a result of contact pathway activation is thought to be the major mediator of pain and edema formation in HAE. Current therapy of acute HAE attacks is limited and mainly offers symptom control. In the United States only fresh frozen plasma provides some reconstitution of C1-INH, but the efficacy and safety of this treatment is controversial. In some European countries two human derived C1-INH concentrates have been used successfully. Prophylactic therapy for patients with frequent HAE attacks is confined to attenuated androgens and in some countries anti-fibrinolytics and C1-INH are also used. To satisfy the unmet needs, investigation of one recombinant C1-INH, two drugs working on bradykinin pathway and two human derived C1-INH concentrates are underway. This review article also discusses some recent patents related to the filed.

PubMed

Types of diabetic macular edema assessed by optical coherence tomography.

2008-11-22T03:52:00.000-08:00

Types of diabetic macular edema assessed by optical coherence tomography.

Koleva-Georgieva DN, Sivkova NP.
Department of Ophthalmology, Medical University, Plovdiv, Bulgaria.

AIM: To assess the types of diabetic macular edema (DME) in patients with type 2 diabetes mellitus by analyzing retinal thickness, morphology and presence of macular traction using optical coherence tomography (OCT).

PATIENTS AND METHODS: This prospective study included 74 diabetics with diabetic retinopathy (DR) (141 eyes), 29 diabetics without DR (57 eyes) and 25 healthy volunteers (39 eyes). The ophthalmic examination included best corrected visual acuity, stereo-ophthalmoscopy, fluorescein angiography and OCT. DME assessment was based on the analysis of several OCT features: macular thickness, retinal morphology and presence of macular traction--vitreomacular and/or from epiretinal membranes. Four OCT types of DME were suggested: type 1--early, type 2--simple, type 3--cystoid (3a--mild, 3b--intermediate, 3c--severe) and type 4--serous macular detachment. The distribution of the DME types and their correlation with retinal thickness and visual acuity were analyzed.

RESULTS: The distribution of eyes with DME was: type 1--14.1%, type 2--30.4%, type 3--45.7% (3a--14.1%, 3b--12%, 3c--19.6%) and type 4--9.8%. Macular traction with retinal distortion was detected in 31.5% of the eyes with DME. Retinal thickness at the fixation point was 176 +/- 16.8 microm (116 microm / 210 microm) in healthy eyes and 182.2 +/- 19.6 microm (138 microm / 212 microm) in eyes without DR. There was no statistically significant difference between the two groups (Independent samples test, P less then 0.05). The retina was significantly thicker in eyes with early DME (232.9 plus/minus 7.9 microm) than in healthy eyes and eyes without DR (Independent samples test, F = 16.274 and F = 13.100, P less then f equals 16.692.

CONCLUSION: OCT precisely differentiated 4 types of DME: early, simple, cystoid and serous macular detachment, as well as determined the presence of macular traction. The early diagnosis, high precision in retinal thickness measurement, assessment of the morphologic types and macular traction are of uppermost importance in determining the therapeutic approach, prognosis and the effect of treatment.

PMID: 19009748 [PubMed - in process]

Aplastic anemia induced disc edema and visual loss in pregnancy: a case report.

2008-11-22T03:47:00.000-08:00

Aplastic anemia induced disc edema and visual loss in pregnancy: a case report.

Published: 18 November 2008

Gupta SK, Brar VS, Murthy RK, Chalam KV.

Background

A case of aplastic anemia diagnosed during pregnancy, which developed bilateral disc edema and acute pre-retinal hemorrhage leading to vision loss. Case report: A 20 year old primagravid female developed acute vision loss in her right eye, during hospitalization for treatment of aplastic anemia diagnosed during her pregnancy. Her best-corrected visual acuity (BCVA) was hand motions and fundus evaluation revealed a large pre-macular hemorrhage in the right eye (OD) and bilateral disc edema. Neuro-imaging studies did not reveal any signs of intracranial mass lesion or edema.

Conclusion

There was resolution of the disc edema with improvement in the pre-macular hemorrhage resulting in 20/50 vision in the right eye, following supportive transfusions. Ophthalmic manifestations developing in a pregnant patient with aplastic anemia can be successfully managed with supportive care including red blood cell and platelet transfusions.

Cases Journal

Improved persistence and adherence to diuretic fixed-dose combination therapy compared to diuretic monotherapy - edema

2008-11-12T06:35:00.000-08:00

Improved persistence and adherence to diuretic fixed-dose combination therapy compared to diuretic monotherapy.

BMC Fam Pract. 2008 Nov

ABSTRACT: BACKGROUND: Diuretics are recommended as initial treatment for hypertension. Several studies have suggested suboptimal persistence and adherence to thiazide diuretic monotherapy; this study compared patient persistence and adherence with hydrochlorothiazide (HCTZ) monotherapy to fixed-dose combinations containing HCTZ.

METHODS: Patients with at least one prescription claim during 2001 to 2003 for either HCTZ or one of the following fixed-dose combinations: angiotensin-receptor blockers/HCTZ (ARB/HCTZ), angiotensin-converting enzyme inhibitor/HCTZ (ACEI/HCTZ), or beta blockers/HCTZ (BB/HCTZ) were identified. Patients were required to be continuously benefit-eligible six months pre- and one year post-index date, and to have no prescription claims for any antihypertensive therapy six months prior to the index date. Patients were followed for one year to assess persistence, medication possession ratio (MPR), adherence (MPR >80%), and proportion of days covered (PDC) with initial antihypertensive therapy. Logistic regression was used to calculate adjusted odds ratios for persistence, adherence and PDC, adjusted for age, gender, business segment, RxRisk disease categories, average co-pay and concurrent cardiovascular-related medication utilization. RESULTS: The study cohort consisted of 48,212 patients; 72.5% used HCTZ, 13.2% ACEI/HCTZ, 9.3% ARB/HCTZ, and 5.0% BB/HCTZ. Mean age was 53.7 years and 66.5% were female. A significantly lower proportion of patients using HCTZ (29.9%) remained persistent with therapy at 12 months compared with ARB/HCTZ (52.6%; OR=0.37, CI=0.36, 0.38), ACEI/HCTZ (51.4%; OR=0.38, CI=0.37, 0.39), and BB/HCTZ (51.9%; OR=0.38, 0.37, 0.40). Similarly, PDC was lower for HCTZ patients (32.5%) as compared to ARB/HCTZ (53.7%; OR=0.39, CI=0.37, 0.40), ACEI/HCTZ (50.9%; OR=0.42, CI=0.40, 0.43), and BB/HCTZ (51.3%; OR=0.44, CI 0.42, 0.45). MPR was also significantly lower for HCTZ patients as compared to those using fixed-dose combination therapies.

CONCLUSIONS: Initiating HCTZ fixed-dose combination therapy with an ACEI, ARB, or BB was associated with greater persistence and adherence as compared to HCTZ monotherapy. Further research is needed to determine the relationship between improved persistence and adherence with blood pressure control.

BioMed Central

[Pre-eclampsia (edema) screening in first and second trimester

2008-11-04T04:43:00.000-08:00

[Pre-eclampsia screening in first and second trimester
Ther Umsch. 2008 Nov

Kang A, Struben H.
Frauenklinik, Universitätsspital Basel.

Pre-eclampsia is a pregnancy-associated disease of the second part of the pregnancy, occuring mainly after 20 weeks gestation. The prevalence of hypertension in pregnancy is between 5 to 11% and affects mainly women under 20 years of age. An inadequate invasion of trophoblasts with consequential placental ischemia as a result of insufficiently dilatated uterine spiral arteries is thought to be an initial cause in the pathogenesis of pre-eclampsia. The clinical symptoms of pre-eclamsia, such as loss of intravascular volume and edema, are caused by generalized endothelial dysfunction. These symptoms are potentiated by hypertension and reduced colloid osmotic pressure in the plama. The organs being affected by pre-eclamsia are those of the vascular-, hepatic-, renal-, cerebral- and coagulatory systems. The prognosis is much more severe when pre-eclampsia develops very early in the pregnancy. The symptoms include elevated blood pressure (over 140 mmHg systolic, 90 mmHg diastolic) combined with proteinuria. Frequent symptoms are hyperreflexia and edema. The etiology of pre-eclampsia has not been clearly defined. Risk factors/triggers for the development of pre-eclampsia can include chronic hypertension, advanced maternal age at first pregnancy (over 35 y), nephropathy, thrombophilia (heterozygous factor V Leiden mutation, antiphospholipid syndrome, heterozygous prothrombin mutation and homozygous MTHFR), multiple gestation and prior pregnancy with preeclampsia. The incidence of preeclampsia is higher in nulliparous than multiparous women. In many countries pre-eclampsia is still most frequent cause of maternal perinatal mortality. HELLP-Syndrom (haemolysis-elevated liver enzyme- low platelets) is a severe progressive course of this disease. Eclampsia, caracterized by generalized tonic-clonic convulsion, is the most dangerous complication of pre-eclampsia, and may develop before or after delivery. This form of pre-eclampsia is associated with higher maternal and fetal mortality. Constant maternal hypertension potentially alter vascular integrity of the placenta with further consequences in fetal blood supply leading to growth restriction or zero growth and subsequently resulting in low birth weight or fetal death. The sooner the disease is detected and confirmed, the better the maternal and fetal prognoses are. This is the reason why it is major importance, together with the employment of preventive measures, to identify patients with risk factors with pre-eclampsia though an adequate screening method, thereby detecting the disease earlier and ensuring better pregnancy outcomes for both mother and child.

PMID: 18979429 [PubMed - in process]

Cardiac toxicity and edema

2008-10-26T10:04:00.000-07:00

Cardiac toxicity and edema
Gan To Kagaku Ryoho. 2008 Oct

Takeuchi S, Sakai H.
Department of Respiratory Disease, Saitama Cancer Center, Saitama, Japan.

Anticancerdrug-induced cardiac toxicity has been recognized since the introduction and widespread use of the anthracycline derivative doxorubicin in the 1970's. Risk factors for cardiac toxicity have increased along with the development of multidisciplinary therapy, high-dose combination chemotherapy, and molecular-targeted therapy. Cardiac toxicity is now recognized as a common adverse effect. Cardiac toxicity as an adverse event caused by molecular targeted agents such as trastuzumab may lead to irreversible cardiac dysfunction. The developmental mechanism of cardiac toxicity has not been fully defined for any agent. At present, practical strategies include the evaluation of cardiac function before treatment and the monitoring of cardiac function during treatment to determine whether chemotherapy should be administered or withdrawn. Edema caused by molecular-targeted agents such as imatinib is considered a relatively new adverse event. Prompt and accurate differential diagnosis of edema is essential, followed by appropriate action. Currently, however, only symptomatic treatment is available. Future studies should attempt to elucidate the mechanisms of cardiac toxicity and edema associated with molecular-targeted agents, as well as develop new treatment strategies.

PierOnline

Digital edema, adhesion formation and resistance to digital motion after primary flexor tendon repair.

2008-10-26T09:59:00.000-07:00

Digital oedema, adhesion formation and resistance to digital motion after primary flexor tendon repair.

J Hand Surg Eur Vol. 2008 Oct 20

Cao Y, Chen CH, Wu YF, Xu XF, Xie RG, Tang JB.

Department of Hand Surgery, Hand Surgery Research Center, Affiliated Hospital of Nantong University and Jiangsu Hand Surgery Center, Nantong, China.

The development of digital oedema, adhesion formation, and resistance to digital motion at days 0, 3, 5, 7, 9 and 14 after primary flexor tendon repairs using 102 long toes of 51 Leghorn chickens was studied. Oedema presented as tissue swelling from days 3 to 7, which peaked at day 3. After day 7, oedema was manifest as hardening of subcutaneous tissue. The degree of digital swelling correlated with the resistance to tendon motion between days 3 and 7. At day 9, granulation tissues were observed around the tendon and loose adhesions were observed at day 14. Resistance to digital motion increased significantly from day 0 to day 3, but did not increase between days 3 and 9. The early postoperative changes appear to have three stages: initial (days 0-3, increasing resistance with development of oedema), delayed (days 4-7, higher resistance with continuing oedema) and late (after day 7-9, hardening of subcutaneous tissue with development of adhesions).

Elsevier

Encephalopathy and Cerebral Edema in the Setting of Acute Liver Failure: Pathogenesis and Management.

2008-08-12T08:13:00.000-07:00

Encephalopathy and Cerebral Edema in the Setting of Acute Liver Failure: Pathogenesis and Management.

Neurocrit Care. 2008 Aug 8

Wendon J, Lee W.
Liver Intensive Therapy Unit, Institute of Liver Studies, Kings College Hospital, Denmark Hill, London, SE5 9RS, UK, Julia.wendon@kcl.ac.uk.

Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. The pathogenesis of cerebral edema in this setting remains controversial, although recent work suggests a pivotal role for arterial ammonia, whose effects appear to be potentiated by the presence of systemic inflammation. Recent work has also suggested the import of free radical formation occurring at a mitochondrial level as being the potential mediator of cellular dysfunction as opposed to ammonia per se. Treatment of such patients requires a multi-disciplinary approach incorporating both hepatology and critical care. In a significant proportion of such cases, consideration of liver transplantation may be required. Treatment should be focused at optimizing liver function and regenerative capacity and minimizing the inflammatory milieu. Controlled studies are lacking and much of the management has been extrapolated from neurocritical care. Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited.

SpringerLink

Severe peripheral edema during an outpatient continuous epidural morphine infusion trial in a patient with failed back surgery syndrome.

2008-08-04T01:26:00.000-07:00

Severe peripheral edema during an outpatient continuous epidural morphine infusion trial in a patient with failed back surgery syndrome.

Pain Physician. 2008 May-Jun

Ruan X, Tadia R, Couch JP, Ruan J, Chiravuri S.
Physicians Pain Specialists of Alabama, Mobile, AL, USA. xiuluruan@yahoo.com

BACKGROUND: Intraspinal drug delivery therapy has been increasingly used in patients with intractable, nonmalignant pain who fail to respond to conventional treatment or cannot tolerate systemic opioid therapy due to side effects. By infusing small amount of analgesics directly into the cerebrospinal fluid in close proximity to the receptor sites in the spinal cord, one is able to achieve the spinally mediated analgesia, sparing side effects due to systemic opioids. Prior to permanent intraspinal pump implantation, an intraspinal opioid screening trial is required to document the efficacy of intraspinal opioid for analgesia. Although there are a few approaches in conducting such screening trials, a patient controlled continuous epidural morphine infusion trial, performed in an outpatient setting, is widely accepted by many interventional pain specialists. The major advantage of conducting an outpatient trial is that it mimics what patients do in their daily living, therefore minimizing the false positive rate.

OBJECTIVE: To report a case of severe peripheral edema observed during an outpatient continuous epidural morphine infusion trial.

CASE REPORT: A 64-year-old female, with a 7-year history of severe low back pain and bilateral leg pain due to failed back surgery syndrome, was referred to our clinic for intraspinal drug delivery therapy after failing to respond to conservative treatment, including a previous history of 3 lumbosacral surgeries. Following a pre-implantation psychological evaluation confirming her candidacy, she underwent an outpatient patient-controlled continuous epidural morphine trial. A tunneled lumbar epidural catheter was placed at L2-L3 with catheter tip advanced to T12 under fluoroscopic guidance. Satisfactory catheter placement was confirmed by epidurogram. The proximal tip of the catheter was then tunneled, subcutaneously and connected to a Microject PCEA pump (Codman, Raynham, MA, USA) and reservoir bag containing preservative-free morphine 0.5 mg/mL. The pump was programmed to deliver a basal rate of 0.5 mL/hr. The bolus dose was 0.2 mL with 60 minute lock-out interval. The patient was instructed how to operate the infusion pump before discharging home. During the following 2 weeks, she reported more than 90% reduction of her low back and leg pain. She only had to use the on-demand bolus doses averaging 2 - 3 times a day. She was able to wean off her oral opioids completely. However, she developed bilateral leg edema and gained over 12 pounds during the 2-week infusion trial, despite wearing elastic stockings and keeping her legs elevated whenever possible. She did not experience any other significant side effects. Her edema finally resolved 2 days after termination of the epidural infusion.

CONCLUSION: Peripheral edema may occur and persist during epidural morphine infusion. This report represents the first case report, to the best of our knowledge, describing severe peripheral edema in an otherwise healthy patient while on epidural morphine administration during an outpatient epidural morphine infusion trial. This case report shows that continuous epidural morphine infusion, even in small dose, may cause peripheral edema in some patients.

Pain Physician

Anti-inflammatory effects of leaf and twig of Tripterygium ilfordii on paw edema in mice.

2008-08-04T01:21:00.000-07:00

Anti-inflammatory effects of leaf and twig of Tripterygium ilfordii on paw edema in mice.

Yu L, Ao M, Wan J, Zhang Y.
School of Life Science and Technology, Huazhong University of Science and Technology, 430074 Wuhan, PR China.

The root of Tripterygium wilfordii (TWH) is a traditional Chinese herb used to treat the immune-related diseases such as rheumatoid arthritis, whereas the leaf and twig of TWH was considered useless and discarded. We performed a study on the anti-inflammatory effects on the leaf and twig portion agent using carrageenan- and adjuvant-induced paw edema in rats. They showed a marked inhibitory effect on edema in both models of inflammation in rats, at the dose of 50, 100 and 200 mg/kg, especially on secondary immunological arthritis. Based on this study, we confirmed that the leaf and twig of TWH is a potentially useful drug suitable for further evaluation for rheumatoid arthritis and can replace root of TWH.

Elsevier

Pulmonary Edema After Electroconvulsive Therapy.

2008-07-13T03:08:00.000-07:00

Pulmonary Edema After Electroconvulsive Therapy.
J ECT. 2008 Jul 2
Sargent P, Reeves J.
From the Naval Medical Center San Diego, San Diego, CA.

A 42-year-old right-handed man with major depression, posttraumatic stress disorder, gastroesophageal reflux disease, and hypertension received 7 treatments of right unilateral electroconvulsive therapy, with the only complications being elevated blood pressure up to 180/120 mm Hg and agitation upon awakening. During eighth treatment, he experienced blood pressures as high as 210/130 mm Hg with severe agitation upon awakening from anesthesia followed by pulmonary edema. Pulmonary edema is rarely seen as a complication in electroconvulsive therapy, but if the airway becomes obstructed or there is excessive sympathetic discharge during the procedure, pulmonary edema may be more likely to occur.

PubMed

Do we have a "best practice" for treating high altitude pulmonary edema?

2008-06-29T05:17:00.000-07:00

Do we have a "best practice" for treating high altitude pulmonary edema?
High Alt Med Biol. 2008 Summer

Luks AM.
Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington, USA.

Abstract Luks, Andrew M. Do we have a "best practice" for treating high altitude pulmonary edema? High Alt. Med. & Biol. 9:111-114, 2008.-

High-altitude pulmonary edema (HAPE) is a rare, but potentially fatal, non-cardiogenic pulmonary edema that affects unacclimatized lowlanders ascending to altitudes above 2500 m. A review of the literature on the disease suggests that a wide range of strategies is employed for treatment purposes. This situation raises questions as to whether a "best practice" exists for treating HAPE and whether clinicians are using greater measures than necessary to ensure good outcomes. This review considers these issues in greater detail, examining the current state of research and clinical practice in HAPE treatment, addressing important questions raised by documented treatment practices, such as the utility of beta agonists, acetazolamide and diuretics and, finally, proposing reasonable, parsimonious treatment approaches that reflect the setting in which the patient is being treated.

Mary Ann Liebert

Acute pulmonary edema as a first manifestation of hyperthyroidism in a pregnant woman. Report of one case

2008-06-27T02:58:00.000-07:00

Acute pulmonary edema as a first manifestation of hyperthyroidism in a pregnant woman. Report of one case

Rev Med Chil. 2008 Mar

Díaz N R, Silva G D.
Unidad de Cuidados Intensivos de Adultos, Departamento de Cardiología, Clínica Reñaca, Vina Del Mar, Chile. cardio@entelchile.net

We report a 36 year-old pregnant woman who presented with acute pulmonary edema in the absence of preexisting cardiac disease. On admission she was on sinus rhythm and her blood pressure was mildly elevated. No cardiac abnormalities were detected by color Doppler echocardiography and no ischemic changes were seen on the electrocardiogram. Cardiac enzymes were normal. Thyroid function tests were diagnostic for hyperthyroidism. She was treated with propylthiouracil and propranolol and discharged in good conditions seven days after admission. This case emphasizes the need to consider hyperthyroidism as the cause of unexplained pulmonary edema in young patients with no history of heart disease who present with heart failure.

SciELO

Corneal edema after cataract surgery: predisposing factors and corneal graft outcome.

2008-06-10T07:33:00.000-07:00

Corneal edema after cataract surgery: predisposing factors and corneal graft outcome.

Acta Ophthalmol. 2008 Jun 5

Claesson M, Armitage WJ, Stenevi U.
Department of Ophthalmology, Sahlgrenska University Hospital, Mölndal, Sweden.

Purpose: Pseudophakic bullous keratopathy (PBK) is one of the main indications for corneal transplantation. Graft survival and visual outcome in this group are often poorer than for other indications. The aim of this study was to find risk factors for developing corneal edema after cataract surgery and factors that influence the subsequent survival of the graft and the visual outcome.

Methods: We carried out an observational, retrospective cohort study using data from the Swedish Cornea Transplant Register and patient medical records. A total of 273 patients whose indication for corneal transplantation was corneal oedema after cataract surgery were included in the study. Multiple logistic regression analysis and, where appropriate, univariate analyses were applied.

Results: A total of 43% of the patients developed persistent corneal oedema immediately after cataract surgery, the main risk factors for which were phacoemulsification and pre-existing endothelial disease. Almost a third (32%) of the transplants for PBK failed within 2 years, for which rejection and other postoperative complications increased the risk. Half (50%) the patients had visual acuity less then 0.1 at 2 years after keratoplasty. Comorbidity, increasing duration of the bullous keratopathy and increasing age affected the visual outcome negatively.

Conclusions: Phacoemulsification was a risk factor for immediate persistent corneal oedema after cataract surgery, although it did not increase the overall risk of developing PBK. However, transplants for immediate PBK had a better survival rate than those for later onset PBK. Shorter duration of PBK and intraocular lens exchange at the time of penetrating keratoplasty increased the likelihood of good visual acuity.

PMID: 18537927 [PubMed - as supplied by publisher]

In vivo pharmacological evaluation of compound 48/80-induced airways edema by MRI

2008-05-14T05:25:00.000-07:00

In vivo pharmacological evaluation of compound 48/80-induced airways edema by MRI

Br J Pharmacol. 2008 May 12

Karmouty-Quintana H, Blé FX, Cannet C, Zurbruegg S, Fozard JR, Page CP, Beckmann N.

[1] 1Global Imaging Group, Novartis Institutes for BioMedical Research, Basel, Switzerland [2] 2King's College, Division of Pharmaceutical Sciences, Sackler Institute of Pulmonary Pharmacology, London, UK [3] 3Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.

Correspondence: Dr N Beckmann, Global Imaging Group, Novartis Institutes for BioMedical Research, Forum 1, Novartis Campus, WSJ-386.2.09, Basel CH-4056, Switzerland. E-mail: nicolau.beckmann@novartis.com

Background and purpose: Allergen-induced airways edema in actively sensitized rats has been studied earlier by magnetic resonance imaging (MRI). We used MRI to follow the consequences of non-immunological mast cell activation induced by compound 48/80 in the rat lungs in vivo.

Experimental approach: Male naïve rats were scanned by MRI prior to and at several time points following intratracheal administration of the mast cell secretagogue, compound 48/80. The effects of a range of drugs on the response induced by compound 48/80 were studied.

Key results: Strong fluid signals were detected by MRI in the lungs at 24 h after compound 48/80, correlating with increased protein concentration and inflammatory cell infiltration in bronchoalveolar lavage, and with perivascular oedema observed histologically. Pharmacological intervention demonstrated that the increase in MRI signal volume induced by compound 48/80 24 h after challenge was blocked by disodium cromoglycate and the glucocorticoid, budesonide.

Pretreatment with wortmannin, capsazepine, DNK333 (a dual neurokinin (NK) 1 and NK2 antagonist) or the anti-allergy drug CGS8515, but not indomethacin, resulted in partial inhibition.

Conclusions and implications: Compound 48/80 induced a complex inflammatory reaction which did not solely involve mast cell degranulation but also activation of sensory nerves and was qualitatively similar to allergen challenge. Changes observed by MRI correlated with decreases in protein concentration in BAL fluid. However, the magnitude of the changes detected was greater using MRI.

Our results demonstrate that MRI is a sensitive and efficient tool to assess the effects of drugs on lung inflammation.

British Journal of Pharmacology advance online publication, 12 May 2008; doi:10.1038/bjp.2008.174.

Keywords:
prostaglandin, leukotriene, cromoglycate, wortmannin, PI3-kinase, capsazepine, imaging, magnetic resonance imaging (MRI), lung, rat

Abbreviations:
AA, arachidonic acid; BAL, bronchoalveolar lavage; DSCG, disodium cromoglycate; EPO, eosinophil peroxidase; LO, lipoxygenase; 5-LO, 5-lipoxygenase; MRI, magnetic resonance imaging; NK, neurokinin; PG, prostaglandin; PI-3K, PI-3-kinase; TRPV, transient receptor potential vanilloid

Nature

Intravitreal pegaptanib sodium for refractory pseudophakic macular oedema.

2008-04-22T06:32:00.000-07:00

Intravitreal pegaptanib sodium for refractory pseudophakic macular oedema.

Eye. 2008 Apr 18

Cervera E, Diaz-Llopis M, Udaondo P, Garcia-Delpech S.
1Department of Ophthalmology, Hospital General de Valencia, Valencia, Spain.

Purpose

Evaluate the efficacy of intravitreal pegaptanib sodium (Macugen((R))) in refractory pseudophakic cystoid macular oedema (CME).

Design and methods

Prospective, nonrandomized, interventional case series. Four eyes of four patients with refractory pseudophakic CME to pars plana vitrectomy and intravitreal bevacizumab and triamcinolone, were treated with pegaptanib sodium, with a mean follow up of 4 months. Pre- and postinfection examinations included assessment of best-corrected visual acuity (BCVA) using the Early Treatment Diabetic Retinopathy Study chart (ETDRS), fluorescein angiography (FA), and optical coherence tomography (OCT).

Results

Visual acuity increased in all patients after intravitreal pegaptanib sodium. OCT showed improvement of the retinal thickness in the macular area.

Conclusion

Intravitreal pegaptanib sodium (Macugen((R))) is a promising treatment for pseudophakic cystoid macular oedema resistant to other medical treatment strategies. However, further study is needed to assess the treatment's long term efficacy and the need for retreatment.Eye advance online publication, 18 April 2008; doi:10.1038/eye.2008.2.

PubMed

Ranibizumab for macular edema due to retinal vein occlusions: implication of VEGF as a critical stimulator

2008-03-27T10:26:00.000-07:00

Ranibizumab for macular edema due to retinal vein occlusions: implication of VEGF as a critical stimulator

Mol Ther. 2008 Apr

Campochiaro PA, Hafiz G, Shah SM, Nguyen QD, Ying H, Do DV, Quinlan E, Zimmer-Galler I, Haller JA, Solomon SD, Sung JU, Hadi Y, Janjua KA, Jawed N, Choy DF, Arron JR.
Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-9277, USA. pcampo@jhmi.edu

Macular edema is a major cause of vision loss in patients with central retinal vein occlusion (CRVO) or branch retinal vein occlusion (BRVO). It is not clear how much of the edema is due to hydrodynamic changes from the obstruction and how much is due to chemical mediators. Patients with macular edema due to CRVO (n = 20) or BRVO (n = 20) were randomized to receive three monthly injections of 0.3 or 0.5 mg of ranibizumab. At the primary endpoint, month 3, the median improvement in letters read at 4 m was 17 in the 0.3-mg group and 14 in the 0.5-mg group for CRVO, and 10 and 18, respectively for the BRVO group. Optical coherence tomography (OCT) showed that compared to injections of 0.3 mg, injections of 0.5 mg of ranibizumab tended to cause more rapid reductions of central retinal thickening that lasted longer between injections, but in 3 months, excess central retinal thickening which is a quantitative assessment of the macular edema, was reduced by approximately 90% in all four treatment groups. There was no correlation between the amount of improvement and duration of disease or patient age at baseline, but there was some correlation between the aqueous vascular endothelial growth factor (VEGF) level at baseline and amount of improvement. These data indicate that excess production of VEGF in the retinas of patients with CRVO or BRVO is a major contributor to macular edema and suggest that additional studies investigating the efficacy of intraocular injections of ranibizumab are needed.

Nature

Intravitreal steroids for macular edema: the past, the present, and the future

2008-03-20T17:35:00.000-07:00

Intravitreal steroids for macular edema: the past, the present, and the future

Surv Ophthalmol. 2008 Mar-Apr

Cunningham MA, Edelman JL, Kaushal S.
Department of Ophthalmology, University of Florida College of Medicine, Gainesville, Florida.

Macular edema, a condition usually associated with an underlying disease process, is a common cause of severe visual loss. There have been a variety of approaches to the treatment of macular edema; within the past few years, however, intravitreal corticosteroid treatments have emerged as an increasingly used treatment option for patients with macular edema. Intravitreal delivery allows the steroid to bypass the blood-retinal barrier, leading to a more concentrated dose of steroid for a prolonged period of time. Corticosteroids have likely been successful in the treatment of various forms of macular edema, due to their known anti-angiogenic, anti-edematous, anti-inflammatory, anti-apoptotic, and anti-proliferative effects. Intravitreal triamcinolone acetonide has been repeatedly successful in reducing macular edema and improving visual acuity, although the duration of action is typically short-term. Due to the recurrent and chronic nature of macular edema, biodegradable implants may be the future of intravitreal steroids. Intravitreal corticosteroids are not without risks. Steroid-related side effects include cataract formation and elevated intraocular pressure. Injection-related side effects include retinal detachment, vitreous hemorrhage, bacterial endophthalmitis, and sterile endophthalmitis. This article reviews the evolving role of intravitreal corticosteroids in the treatment of macular edema secondary to uveitis, diabetes, and retinal vascular disorders.

Elsevier

Histopathological perspective on bone marrow edema, reactive bone change and haemorrhage.

2008-03-14T05:46:00.000-07:00

Histopathological perspective on bone marrow oedema, reactive bone change and haemorrhage.

Eur J Radiol. 2008 Mar 11

Thiryayi WA, Thiryayi SA, Freemont AJ.
Department of Histopathology, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, United Kingdom.

This article presents a systematic review of the current biomedical literature surrounding the aetiopathogenesis and histopathological features of bone marrow oedema, reactive bone change and haemorrhage. Bone marrow oedema is generally demonstrated as a non-specific finding on magnetic resonance imaging in association with infections, tumours and avascular necrosis. When it occurs in isolation as a primary event not triggered by any obvious bony pathology in the clinical setting of debilitating joint pain, it constitutes the "bone marrow oedema syndrome". Although the latter diagnosis is based on magnetic resonance (MR) imaging, showing the lesion as areas of signal hyperintensity within the marrow, recent radiology-histology correlational studies have shown variably interstitial marrow oedema, necrosis, fibrosis and trabecular bone abnormalities. In light of these facts, the use of the term bone marrow oedema syndrome in a radiological context might be considered questionable, but histopathological techniques are not sensitive in detecting increased extracellular fluid. Reactive bone changes may be focal or diffuse and usually amount to increased bone formation. Bone marrow haemorrhage, due to trauma, results in bone bruising, a condition in which the size of the bruise and associated osteochondral injury determines the outcome, although the natural history of these lesions is still being researched.

PMID: 18337044 [PubMed - as supplied by publisher]

Bone Marrow Edema in the Cervical Spine of Symptomatic Rheumatoid Arthritis Patients

2008-03-14T05:39:00.000-07:00

Bone Marrow Edema in the Cervical Spine of Symptomatic Rheumatoid Arthritis Patients

Semin Arthritis Rheum. 2008 Mar 11

Narváez JA, Narváez J, Albert MD, De Lama E, Serrallonga M, Nolla JM.
Department of Radiology, Hospital Universitario de Bellvitge-IDIBELL, Barcelona, Spain.

OBJECTIVE: To investigate the frequency and clinical significance of bone marrow edema (BME) in a series of patients with rheumatoid arthritis (RA) and symptomatic involvement of the cervical spine.

METHODS: We studied 19 consecutive RA patients with cervical spine magnetic resonance imaging (MRI) according to a specifically designed protocol that included short inversion time inversion recovery sequences. All cases had neck pain unresponsive to conventional treatment, neurological symptoms, or signs suggestive of cervical myelopathy, or cervical pain with evidence of atlantoaxial subluxation on radiographs.

RESULTS: The mean age of the 19 patients (15 women and 4 men) at time of the study was 59 +/- 12 years (range, 23-82) and the median disease duration was 14 +/- 7.4 years (range, 4-30). BME was observed in 74% (14/19) of the patients: at the atlantoaxial level alone in 16% of the patients; subaxially alone in 16%; and at both levels in 42% of the patients. At the atlantoaxial level, BME was usually observed involving the odontoid process, whereas subaxially BME was limited to the vertebral plates and the interapophyseal joints. Patients with BME had higher erythrocyte sedimentation rate (ESR) values at the time of MRI examination (P = 0.014) and more severe atlantoaxial joint MRI synovitis scores (P = 0.05) compared with the remaining patients; the frequency of odontoid erosions was also greater in this group, but the difference did not reach statistical significance. Altogether, these data suggest a more severe inflammatory response in these patients. In this group a significant correlation was found between BME scores at atlantoaxial level and (1) ESR values (r = 0.854; P = 0.001) and (2) atlantoaxial joint MRI synovitis scores (r = 0.691; P = 0.001).

CONCLUSION: BME is frequently observed in patients with established RA and symptomatic cervical spine involvement. Both atlantoaxial and subaxial levels are equally affected. Presence of BME seems related to the intensity of the inflammatory response and to the severity of the atlantoaxial joint synovitis.

PubMed

Burn Plasma Transfer Induces Burn Edema in Healthy Rats

2008-03-08T18:32:00.000-08:00

Burn Plasma Transfer Induces Burn Edema in Healthy Rats
Shock. 2008 Feb 21
Kremer T, Abé D, Weihrauch M, Peters C, Gebhardt MM, Germann G, Heitmann C, Walther A.
*Department of Hand, Plastic and Reconstructive Surgery, Burn Center-BG Trauma Center Ludwigshafen, Plastic and Hand Surgery, University of Heidelberg, Ludwigshafen; †Departments of Anesthesiology and ‡Experimental Surgery, University of Heidelberg, Heidelberg, Germany.

Thermal injuries greater than 20% body surface area (BSA) result in systemic shock with generalized edema in addition to local tissue destruction. Burn shock is induced by a variety of mediators, mainly immunomodulative cytokines. This experimental study evaluates if burn shock can be induced in healthy rats by transfer of burn plasma (BP) with mediators. Thermal injury was induced by hot water (100 degrees C water, 12 s, 30% BSA) in male syngenic Wistar rats. Donor rats were killed 4 h posttrauma, and BP was harvested. Burn plasma was transferred to healthy animals by continuous intravenous infusion in three types of dilution (100%, 10%, and 1%). Positive controls were directly examined 4 h after thermal injury, and negative control rats had a continuous infusion done with sham burn (SB) plasma (37 degrees C water, 12 s, 30% BSA). Afterwards, intravital fluorescence microscopy was performed in postcapillary mesenteric venules at 0, 60, and 120 min. Edema formation was assessed by relative changes over time in fluorescence intensity of fluorescein isothiocyanate-albumin in the intravascular versus the extravascular space. The interactions of leucocytes and endothelium were evaluated by quantification of leukocyte sticking. Additionally, microhemodynamic (volumetric blood flow, erythrocyte velocity, venular wall shear rate, venular diameters) and macrohemodynamic parameters (blood pressure, heart frequency, temperature) were assessed online (arterial catheter). For statistics, an ANOVA was performed with Bonferroni adjustment procedure. Differences were considered significant when P less 0.05. There are no statistically significant differences in microhemodynamics or macrohemodynamics between study groups. Burn plasma infusion and thermal injury lead to significant increases in fluorescein isothiocyanate-albumin extravasation, whereas SB plasma shows no significant changes. Even BP diluted in 0.9% saline (10% and 1%) results in a similar transvascular flux of plasma proteins as direct thermal injury. Differences between positive controls and BP infusion are not significant, whereas all groups are statistically different from the SB group (P less than 0.05). Leukocyte sticking is significantly increased in all groups except the SB group, and the number of adherent leukocytes is dose dependent. The present study demonstrates that as early as 4 h after thermal injury, there are sufficient factors (e.g., cytokines) in BP to induce systemic burn shock in healthy rats even in diluted plasma (1%). However, the "key" cytokines are not identified at this point. The burned tissue is no longer required for burn shock induction, and the pathophysiologic process seems to be self-perpetuating as early as 4 h posttrauma. Leukocytes are activated by thermal injury and BP infusion. The role of leukocyte-endothelium interactions for edema formation remains uncertain and requires further investigation.

PubMed

The Role of Aquaporin-4 Polymorphisms in the Development of Brain Edema After Middle Cerebral Artery Occlusion.

2008-03-02T19:29:00.000-08:00

The Role of Aquaporin-4 Polymorphisms in the Development of Brain Edema After Middle Cerebral Artery Occlusion.

Stroke. 2008 Feb 28

Ilka Kleffner MD*; May Bungeroth; Hagen Schiffbauer MD; Wolf-Ruediger Schäbitz MD; E. Bernd Ringelstein MD; and Gregor Kuhlenbäumer MD
From the Departments of Neurology (I.K., W.R.S., E.B.R., G.K.), and Clinical Radiology (H.S.), and the Leibniz-Institute of Atherosclerosis Research (M.B., E.B.R., G.K.), University of Münster, Münster, Germany.

* To whom correspondence should be addressed. E-mail: kleffnil@uni-muenster.de

BACKGROUND AND PURPOSE: Some patients develop severe brain edema after complete middle cerebral artery occlusion, whereas others do not. Aquaporin-4 (AQP4) is the main water channel in the brain and has been shown to be critical for the development of brain edema after ischemia. We asked whether genetic variation in the AQP4 gene is related to the severity of brain edema after middle cerebral artery occlusion.

METHODS: We genotyped 10 single nucleotide polymorphisms distributed across the AQP4 gene in 41 patients with middle cerebral artery occlusion with and without severe brain edema and assessed single marker association as well as the linkage dysequilibrium structure across AQP4.

RESULTS: One single nucleotide polymorphism (rs9951307) at the 3' end of AQP4 was associated with severe brain edema (dominant model, P=0.01; OR, 0.10; 95% CI, 0.02 to 0.49 for the protective G-allele). Linkage dysequilibrium across AQP4 was low; no clear haplotype blocks could be identified for the assessment of haplotype association.

CONCLUSIONS: This explorative study shows that genetic variation in AQP4 might contribute to brain edema formation after middle cerebral artery occlusion and warrants further investigation.

ahajournals

Hereditary angioedema

2008-03-01T19:25:00.000-08:00

Hereditary angioedema

J Allergy Clin Immunol. 2008 Feb

Frank MM.
Department of Pediatrics, Duke University Medical Center, Durham, NC 27710-0001, USA. frank007@mc.duke.edu

Hereditary angioedema is an episodic swelling disorder with autosomal dominant inheritance. Attacks are characterized by brawny, self-limited, nonpruritic edema of the deep dermal layers of the skin that most often involve the hands and feet. They usually begin in childhood and become more severe after puberty. Patients also have episodic attacks of severe abdominal pain caused by edema of the gastrointestinal mucosa. Swelling attacks are life threatening when they involve the airway. Estrogens exacerbate attacks, and in some patients attacks are precipitated by trauma or psychologic stress. The disease is caused by a mutation in one of the 2 copies of the gene for the plasma protein C1 inhibitor, with the product of 1 gene unable to control generation of bradykinin. Eighty-five percent of patients have low antigenic levels of C1 inhibitor, and 15% have normal levels of poorly functioning protein. Most patients have decreased plasma complement protein C4 levels. Impeded androgens and, less frequently, epsilon-aminocaproic acid are currently the mainstays of chronic treatment. These agents or fresh frozen plasma are also used for prophylaxis. At this time, acute therapy is mostly supportive. There are currently ongoing multiple trials of new therapeutic agents. In half a century, a life-threatening disease has become one that is manageable and rarely causes death.

Elsevier

Ten-year study of causes of moderate to severe angioedema seen by an inpatient allergy/immunology consult service

2008-03-01T19:18:00.000-08:00

Ten-year study of causes of moderate to severe angioedema seen by an inpatient allergy/immunology consult service

Allergy Asthma Proc. 2008 Jan-Feb

Banerji A, Oren E, Hesterberg P, Hsu Y, Camargo CA Jr, Wong JT.
Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.

The causes of angioedema are not well described, especially in the inpatient setting. The purpose of this study was to examine the causes of moderate to severe angioedema in patients requiring inpatient treatment. We performed a retrospective review in patients requiring inpatient consultation by the Division of Allergy and Immunology at our institution between 1995 and 2004. We focused on potential interactions among medications that elicited life-threatening angioedema requiring intubation. The allergy/immunology service was consulted on 69 patients with moderate to severe angioedema. Medications were the most common cause of angioedema (n = 64, 93%). In most cases (n = 46, 67%), the angioedema was attributed to two or more medications. Patients previously stable on ACE inhibitors (ACEI), aspirin (ASA), or non-steroidal anti-inflammatory drugs (NSAIDs) appeared more likely to develop angioedema soon after the addition of another drug (i.e., ACEI, ASA/NSAIDs, direct mast cell degranulators, and antibiotics). ACEI, ASA/NSAID, and direct mast cell degranulators were contributing causes in 36 patients (56%), 45 patients (70%), and 23 patients (36%), respectively. Twenty patients required intubation, 14 (70%) patients were on ACEI, 12 (60%) patients were on ASA/NSAID, and 7 (35%) patients were on direct mast cell degranulators. ACEI, ASA/NSAID, or direct mast cell degranulators were a cause in 95% (n = 19) of patients requiring intubation. The combination of ACEI and ASA/NSAID was the most frequent cause of angioedema among all patients (n = 17, 25%) and those requiring intubation (n = 8, 40%). Moderate to severe angioedema often is a result of interactions between two or more medications involved in different pathways causing angioedema. In particular, combinations of ACEI, ASA/NSAID, or direct mast cell degranulators may lead to life-threatening angioedema requiring intubation.

PMID: 18302843 [PubMed - in process]

Treatment of Lung Edema (Pleural Effusions) with Pleur(x) Catheter

2008-02-26T17:59:00.000-08:00

Management of malignant pleural effusions using the Pleur(x) catheter.

Ann Thorac Surg. 2008 Mar

Warren WH, Kalimi R, Khodadadian LM, Kim AW.
Department of Cardiovascular-Thoracic Surgery, Rush University Medical Center, Chicago, Illinois, USA. wwarren@rush.edu

BACKGROUND: A malignant pleural effusion can cause significant morbidity to terminal patients. Drainage and control of the fluid can provide great palliation. Improving the quality of life for these patients on an outpatient basis is a worthy goal.

METHODS: We have inserted 231 Pleur(x) (Cardinal Health Systems, McGaw Park, IL) catheters into 202 patients with symptomatic malignant pleural effusions with the goal of treating the fluid on an outpatient basis. The catheters were drained at home, using vacuum bottles, every other day after an initial week of draining daily. No sclerosing agents were instilled. The catheters were removed when drainage was less than 50 mL/day. Primary tumor sites, irradiation to the hemithorax, and incomplete re-expansion of the lung were studied for their ability to predict prolonged drainage (over 100 days).

RESULTS: In all cases, evacuation of the fluid with a Pleur(x) catheter palliated the patient's symptoms. Overall, 134 of 231 (58.0%) catheters were removed after the drainage tapered off. Reaccumulation of the pleural effusion occurred in 5 of 132 (3.8%) patients. The incidence of infection was 5 of 231 (2.2%) and was usually limited to cellulitis at the insertion site. The incidence of blockage was 11 of 231 (4.8%) and was most common in patients with an underlying cancer at sites other than breast and gynecologic primaries. Drainage for more than 100 days was seen most often in patients who had incomplete reexpansion of the underlying lung. Primary tumor site and irradiation did not have significant predictive value.

CONCLUSIONS: Insertion of Pleur(x) catheters is an effective way to treat patients with a malignant pleural effusion on an outpatient basis with a high degree of patient compliance and few complications. Overall, almost 60% of the catheters can be removed with a very low chance of reaccumulation, and without the need to instill a sclerosing agent. Even patients with a trapped lung can be palliated and released from hospital, although the likelihood of removing the catheter is small.

PMID: 18291195 [PubMed - in process]

Identification of clinical factors predicting Pleur(x)((R)) catheter removal in patients treated for malignant pleural effusion.

Eur J Cardiothorac Surg. 2008 Jan

Warren WH, Kim AW, Liptay MJ.
Department of Cardiovascular-Thoracic Surgery, Rush University Medical Center, Chicago, IL 60612, USA.

Objective: The objective of the study was to review the clinical records of patients undergoing insertion of a Pleur(x)((R)) catheter in the management of malignant pleural effusions. In particular, clinical parameters were analyzed for their influence on catheter removeability.

Methods: Between January 1998 and July 2006, 263 patients underwent insertion of 295 Pleur(x)((R)) catheters for malignant pleural effusion(s). Patients were allocated to one of four groups based upon the site of the primary tumor: group 1 (breast), group 2 (lung), group 3 (gynecologic), and group 4 (all others). A history of prior chest irradiation, cytologic analysis (positive or negative for malignant cells), and incidence of trapped lung were also studied to determine if, in addition to the primary site, these influenced the incidence of pleurodesis.

Results: Overall, 58.6% of Pleur(x)((R)) catheters were removed prior to death. The incidence of spontaneous symphysis and catheter removal in groups 1 (69.6%) and 3 (72.5%) was significantly higher than in groups 2 and 4 (p<0.001).>

Conclusions: Pleur(x)((R)) catheters effectively relieve patients of dyspnea by evacuating the pleural space. Spontaneous pleural symphysis and catheter removal is more likely in patients with breast or gynecologic primary tumors, absence of chest wall irradiation, cytologic positivity, and complete re-expansion of the underlying lung.

PubMed

Surgical and other invasive approaches to recurrent pleural effusion with malignant etiology.

Support Care Cancer. 2008 Feb 8

Neragi-Miandoab S.
Department of Surgery, School of Medicine, Case Western Reserve University, 11100 Euclid Ave. LKS 7109, Cleveland, OH, USA, Sneragi@yahoo.com.

With an increasing number of cancer survivors, the annual incidence of malignant pleural effusions has been rising in recent decades worldwide. Many patients with various forms of cancer develop malignant pleural effusions at some point in their life. Patients most commonly present with progressive dyspnea. These effusions are refractory and are associated with impaired quality of life for these patients. The main goals of management are evacuation of the pleural fluid and prevention of its re-accumulation. The therapy plan should consider the general health of the patients, their performance status, the presence of trapped lung, and the primary malignancy. However, there is no universally established, standard approach. Surgical options include thoracentesis, chest tube drainage, thoracoscopy followed by chemical and mechanical pleurodesis, Pleur-X catheter drainage, and pleurectomy. Chemical pleurodesis is the most common modality of therapy for patients with recurrent pleural effusion. For example, Talc is the most successful pleurodesis agent with similar equal to that of poudrage or slurry. Pleur-X catheter can reduce hospital stay and adds value to the treatment of patients with trapped lung, who are not appropriate candidates for pleurodesis. Furthermore, a mechanical pleurodesis has been shown to be effective particularly in pleural effusions with lower pH. This article reviews the surgical and other invasive options as well as their technical aspects in the management of recurrent malignant pleural effusions.

SpringerLink

Neuroprotective effect of erythropoietin after experimental cold injury-induced vasogenic brain edema in rats.

2008-02-23T04:06:00.000-08:00

Neuroprotective effect of erythropoietin after experimental cold injury-induced vasogenic brain edema in rats.

February 2008

Okutan O, Turkoglu OF, Gok HB, Beskonakli E.
Department of Neurosurgery, Ankara Ataturk Research and Education Hospital, Ankara, Turkey.

BACKGROUND: The aims of this study were to evaluate the efficiency of EPO in the treatment of cold injury-induced brain edema, apoptosis, and inflammation and to compare its effectiveness with DSP.

METHODS: One hundred fifteen adult male Sprague-Dawley rats weighing between 280 and 300 g were used for the study. Rats were divided into 5 groups. Controls received craniotomy only. The injury group underwent cold injury and had no medication. In the EPO group, a single dose of 1000 IU/kg body weight of EPO was administered. The DSP group received 0.2 mg/kg body weight of DSP. The vehicle group received a vehicle solution containing human serum albumin, which is the solvent for EPO. Brain edema was formed by cold injury using metal sterile rods with a diameter of 4 mm that were previously cooled at -80 degrees C. Twenty-four hours after the injury, animals were decapitated and brain tissues were investigated for brain edema, tissue MPO and caspase-3 levels, and ultrastructure.

RESULTS: A significant increase in brain water content was revealed in injury group of rats at 24 hours after cold injury. Injury significantly increased tissue MPO and caspase-3 levels and resulted in ultrastructural damage. Both EPO and DSP markedly decreased tissue MPO and caspase-3 levels and preserved ultrastructure of the injured brain cortex.

CONCLUSIONS: Erythropoietin and DSP were found to be neuroprotective in cold injury-induced brain edema model in rats via anti-apoptotic and anti-inflammatory actions.

PMID: 18291472 [PubMed - as supplied by publisher]

Comparison of obstructive sleep apnea patients with and without leg edema

2008-02-22T15:26:00.000-08:00

Comparison of obstructive sleep apnea patients with and without leg edema.

Sleep Med. 2008 Feb 11

Iftikhar I, Ahmed M, Tarr S, Zyzanski SJ, Blankfield RP.
Department of Internal Medicine, Fairview Hospital, Cleveland Clinic System, Cleveland, OH, United States.

BACKGROUND: To determine the proportion of patients with obstructive sleep apnea (OSA) who have leg edema, and to identify differences between edematous and non-edematous OSA patients.

METHODS: Retrospective, cross-sectional study of 378 patients with OSA (apnea/hypopnea index [AHI] 15) who had neither heart failure nor chronic lung disease.

RESULTS: Thirty-five percent (133/378) of the subjects with OSA had bilateral leg edema. Eighty-one percent (108/133) of the edematous subjects had mild pitting that was 1+. Compared to the non-edematous OSA subjects, the edematous subjects were older (age=51+/-13 versus 45+/-13 years, p=0.001), more obese (body mass index=39+/-9 versus 33+/-8kg/m(2), p=0.001), had more severe OSA (AHI=46+/-71 versus 27+/-29, p=0.004), spent a greater proportion of sleep time with an oxygen saturation <90% p="0.001)," p="0.001)" p="0.001)." p="0.04).

CONCLUSIONS: Approximately one-third of OSA patients have edema. Edematous OSA patients are older, more obese, more likely to have diabetes mellitus and hypertension, and have more severe OSA than OSA patients who lack edema.

Elsevier

Short-term Safety and Efficacy of Intravitreal Triamcinolone Acetonide for Uveitic Macular Edema in Children.

2008-02-18T17:13:00.000-08:00
Short-term Safety and Efficacy of Intravitreal Triamcinolone Acetonide for Uveitic Macular Edema in Children.
Arch Ophthalmol. 2008 Feb

Sallam A, Comer RM, Chang JH, Grigg JR, Andrews R, McCluskey PJ, Lightman S.
Department of Clinical Ophthalmology, Institute of Ophthalmology, Moorfields Eye Hospital, City Road, London EC1V 2PD, England. s.lightman@ucl.ac.uk.

OBJECTIVES: To evaluate the short-term safety and efficacy of intravitreal (IV) triamcinolone acetonide (TA) for treating pediatric cystoid macular edema (CME) secondary to noninfectious uveitis.

METHODS: A retrospective noncomparative interventional case series. The medical records of 15 consecutive children (16 eyes) with uveitic CME treated with IVTA (2 or 4 mg) were reviewed. Data collected included details of uveitis, CME, visual acuity, intraocular pressure, and cataract development. The median follow-up time was 16 months (range, 9-36 months).

RESULTS: Resolution of CME was achieved in all of the treated eyes. The median time taken for CME to resolve was 3 weeks (range, 1-24 weeks). The mean improvement of visual acuity after IVTA was 0.6 logarithm of the minimum angle of resolution. Following initial response to IVTA, CME relapsed in 5 eyes (31%) after a median time of 7 months (range, 3-13 months). The most common adverse effect was increased intraocular pressure, with an increase of more than 15 mm Hg in 5 eyes (31%). Steroid-induced cataract was observed in 6 of 11 phakic eyes (55%).

CONCLUSIONS: We found that IVTA is efficacious in the treatment of uveitic CME in children and results in CME resolution and visual acuity improvement. As in adults, treatment in children may be associated with elevated intraocular pressure and cataract.

Journal of Ophthalmology

Bone marrow edema pattern in advanced hip osteoarthritis

2008-02-16T05:22:00.000-08:00
Bone marrow edema pattern in advanced hip osteoarthritis: quantitative assessment with magnetic resonance imaging and correlation with clinical examination, radiographic findings, and histopathology.

Skeletal Radiol. 2008 Feb 15
Taljanovic MS, Graham AR, Benjamin JB, Gmitro AF, Krupinski EA, Schwartz SA, Hunter TB, Resnick DL.

Department of Radiology, The University of Arizona HSC, 1501 N. Campbell Ave, Tucson, AZ, 85724, USA, mihrat@radiology.arizona.edu.

OBJECTIVE: To correlate the amount of bone marrow edema (BME) calculated by magnetic resonance imaging(MRI) with clinical findings, histopathology, and radiographic findings, in patients with advanced hip osteoarthritis(OA).

MATERIALS AND METHODS: The study was approved by The Institutional Human Subject Protection Committee. Coronal MRI of hips was acquired in 19 patients who underwent hip replacement. A spin echo (SE) sequence with four echoes and separate fast spin echo (FSE) proton density (PD)-weighted SE sequences of fat (F) and water (W) were acquired with water and fat suppression, respectively. T2 and water:fat ratio calculations were made for the outlined regions of interest. The calculated MRI values were correlated with the clinical, radiographic, and histopathologic findings.

RESULTS: Analyses of variance were done on the MRI data for W/(W + F) and for T2 values (total and focal values) for the symptomatic and contralateral hips. The values were significantly higher in the study group. Statistically significant correlations were found between pain and total W/(W + F), pain and focal T2 values, and the number of microfractures and calculated BME for the focal W/(W + F) in the proximal femora. Statistically significant correlations were found between the radiographic findings and MRI values for total W/(W + F), focal W/(W + F) and focal T2 and among the radiographic findings, pain, and hip movement. On histopathology, only a small amount of BME was seen in eight proximal femora.

CONCLUSION: The amount of BME in the OA hip, as measured by MRI, correlates with the severity of pain, radiographic findings, and number of microfractures.
PMID: 18274742 [PubMed - as supplied by publisher]

Effects of medroxyprogesterone acetate on cerebral edema

2008-02-03T05:49:00.000-08:00
Effects of medroxyprogesterone acetate on cerebral oedema and spatial learning performance after traumatic brain injury in rats.

Brain Inj. 2008 Feb

Wright DW, Hoffman SW, Virmani S, Stein DG.
Department of Emergency Medicine, Emory University School of Medicine, Atlanta, GA, USA.

Background: Given after brain injury (TBI), progesterone reduces cerebral oedema and facilitates functional recovery. Progesterone analogues have been synthesized for use in many medical conditions and exhibit different chemical and biological properties.

Medroxyprogesterone acetate (MPA) is widely used in clinical practice, but oestrogen/MPA combinations may increase the risk of stroke and cardiovascular disease rather than preventing them. In some conditions, MPA can exhibit pharmacological actions that are different from those of natural progesterone.

Primary objective and hypothesis: Using laboratory rats, this study assessed the efficacy of MPA to determine whether this progestin and natural progesterone exert similar effects as a treatment after bilateral injury to the frontal cortex.

Main outcomes and results: MPA produced a dose-related reduction of cerebral oedema at 48 hours post-TBI but neither 4 nor 16 mg/kg doses of MPA enhanced behavioural recovery.

Conclusion: These findings help to clarify the divergent results from prior positive progesterone studies and the negative MPA clinical trials for hormone replacement therapy. The results can be taken to suggest that the control of cerebral oedema, while clearly desirable, is not the only contributor to progesterone-induced behavioural recovery.

Informa Healthcare

Acute dermatomyositis associated with generalized subcutaneous edema.

2008-01-19T06:44:00.000-08:00

Acute dermatomyositis associated with generalized subcutaneous edema.
Rheumatol Int. 2008 Jan 12
Lee KH, Lim SR, Kim YJ, Lee KJ, Myung DS, Jeong HC, Yoon W, Lee SS, Park YW.
Department of Rheumatology, Chonnam National University Medical School and Hospital, 8 Hak-dong, Dong-ku, Gwangju, 501-757, Republic of Korea, parkyw@chonnam.ac.kr.

Generalized subcutaneous edema is an uncommon manifestation of inflammatory myopathy. We report a 48-year-old female patient who presented with severe generalized edema, an erythematous skin rash, dysphagia and proximal muscle weakness. She was diagnosed with dermatomyositis from the clinical signs, increased muscle enzymes, electromyographic findings and a muscle biopsy. Magnetic resonance imaging revealed increased signal intensity in the muscular and subcutaneous layers. The conditions causing generalized edema were excluded. It was concluded that the generalized edema was secondary to dermatomyositis. Aggressive treatments with high-dose glucocorticoids and immunosuppressive agents were used to control the severe subcutaneous edema.

SpringerLink

Massive arm edema following arteriovenous dialysis shunt creation in a patient with ipsilateral permanent pacemaker.

2007-12-24T04:03:00.000-08:00
Massive arm edema following arteriovenous dialysis shunt creation in a patient with ipsilateral permanent pacemaker.

J Clin Ultrasound. 2007

Maher J, Rivero A, Zaim S, Pappas PJ, Labropoulos N, Klapholz M, Saric M.
Department of Medicine, New Jersey Medical School, University of Medicine and Dentistry (UMDNJ), 185 South Orange Avenue, Newark, NJ 07103.

Asymptomatic subclavian vein occlusion following insertion of a permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD) is not uncommon. We report a case of a dual-chamber PPM in a patient with an unrecognized left subclavian vein occlusion who developed massive left arm edema following ipsilateral implantation of an arteriovenous (AV) hemodialysis graft. We recommend that patients with pre-existing PPM or ICD leads who are in need of vascular access for hemodialysis should have the AV shunts placed in the contralateral arm. If this is unavoidable, then preoperative subclavian vein screening for patency should be mandatory, even in asymptomatic patients. Sonography is an appropriate initial test in such a situation.

(2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2007.

A Case of Negative-Pressure Pulmonary Edema After Electroconvulsive Therapy.

2007-12-21T01:47:00.000-08:00

A Case of Negative-Pressure Pulmonary Edema After Electroconvulsive Therapy.
J ECT. 2007 Dec
Myers CL, Gopalka A, Glick D, Goldman MB, Dinwiddie SH.
From the *Departments of Psychiatry and †Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, IL.

Pulmonary edema after electroconvulsive therapy (ECT) is a rarely reported condition that can result in serious morbidity and even death if not promptly recognized and treated. We report the case of 21-year-old man with FG syndrome and schizophrenia who developed negative-pressure pulmonary edema after his 28th ECT. The patient developed acute hypoxemia requiring positive-pressure ventilation and was observed overnight in the intensive care unit. He recovered fully and received 43 subsequent ECT treatments without complication. This case illustrates the importance of taking steps to prevent airway obstruction as well as recognizing this rare but serious complication.

PMID: 18090704 [PubMed - as supplied by publisher]

Pulmonary edema after electroconvulsive therapy in a patient treated for long-standing asthma with a beta2 stimulant.

2007

Case Reports Journal of ECT. 23(1):26-27, March 2007.Hatta, Kotaro MD, PhD; Kitajima, Akiyoshi MD, PhD; Ito, Masanobu MD; Usui, Chie MD, PhD; Arai, Heii MD, PhD

Abstract: A 68-year-old man was scheduled to receive 8 treatments of electroconvulsive therapy (ECT) for severe depression. He was being treated for long-standing asthma with a [beta]2 stimulant, clenbuterol hydrochloride, and had experienced no asthma attack for 9 years. Although he experienced no adverse consequence in his 7 treatments, pulmonary edema ensued from his eighth treatment despite no change in anesthesia and in the technical parameters of ECT. He was treated with oxygen and intravenous hydrocortisone, after which he quickly recovered. Transient eosinophilia was observed, but clinical symptoms of asthma did not appear. Although the association between pulmonary edema and well-controlled asthma was unclear, thiopental as induction of anesthesia or esmolol as poststimulus delivery might have played a role in the event. There may be a possibility of pulmonary edema even after several uneventful ECT treatments in a patient with asthma.

Lippincott Williams & Wilkins, Inc.

An investigation of cerebral edema and injury volume assessments for controlled cortical impact injury.

2007-12-15T03:27:00.000-08:00

An investigation of cerebral edema and injury volume assessments for controlled cortical impact injury.
J Neurosci Methods. 2007 Nov
Elliott MB, Jallo JJ, Tuma RF.
Department of Physical Therapy, Temple University, 3307 North Broad Street, Philadelphia, PA 19140, United States.

Using the controlled cortical impact (CCI) model, our laboratory compared edema in contralateral and ipsilateral regions to help clarify conflicting reports of contralateral edema and for enhanced assessment and interpretation of CCI injury pathophysiology. This investigation examined regional edema in response to graded injury severities over time with regards to tissue damage. Prior to injury rats were anesthetized with ketamine and xylazine (1:1). CCI injury parameters were set at 4.0m/s and 120 to 130ms. Rats were randomized to receive moderate or severe injuries set at 2.0 and 3.0mm depths, respectively. Cerebral edema and injury volume were examined separately following euthanasia with pentobarbital. Cerebral edema was measured using the wet-dry weight technique at 24 or 48h after injury. Sham animals underwent all surgical procedures except the impact injury. Injury volume was quantified using 2,3,5-triphenyltetrazolium chloride staining at 24h or 7 days after injury. The results of this investigation confirm that cerebral edema is absent in the uninjured, contralateral hemisphere after moderate and severe CCI injury. There were regional differences in cerebral edema formation in the hemisphere ipsilateral to injury that were dependent on injury severity and the length of time after injury. Tissue damage was reduced over 7 days following moderate CCI injury. Conclusions: (1) the absence of edema in the contralateral hemisphere allows it to serve as a valid control for edema formation, (2) misrepresenting injury volume because of edema continues to be a problem for evaluating CCI injury and treatment efficacy, and (3) reduced injury volume over 7 days following CCI injury suggests tissue recovery after initial dysfunction.

PMID: 18076998 [PubMed - as supplied by publisher]

Leg edema from intrathecal opiate infusions.

2007-11-30T02:52:00.000-08:00
Leg edema from intrathecal opiate infusions.
Eur J Pain. 2000

Aldrete JA, Couto da Silva JM .
Department of Anesthesiology, University of South Florida School of Medicine, Tampa, Florida, USA. taldrete@arachnoiditis.com

Despite the increasing popularity of intrathecal infusions to treat patients with long-term non-cancer-related pain, this therapy is not without serious side-effects. Five out of 23 patients who had intrathecal infusions of opiates for longer than 24 months developed leg and feet edema. As predisposing factors, cardiovascular disease, deep venous thrombosis, peripheral vascular disease, and venous stasis of the lower extremities were considered. Every patient who developed pedal and leg edema after the implantation of an infusion pump was also found to have leg edema and venous stasis prior to the time when the pump was inserted. This complication was severe enough to limit their physical activity, and to produce lymphedema, ulcerations and hyperpigmentation of the skin. Reduction of the edema occurred when the dose of the opiate was decreased, and in two cases in which the infusion was discontinued, there was almost complete resolution of the syndrome. It appears that the pre-existence of pedal edema and of venous stasis is a relative contraindication to the long-term intrathecal infusion of opiates in patients with chronic non-cancer pain. Copyright 2000 European Federation of Chapters of the International Association for the Study of Pain.
PMID: 11124008 [PubMed - indexed for MEDLINE]

The Incidence of Arm Edema in Women with Breast Cancer

2007-11-22T04:40:00.000-08:00

The Incidence of Arm Edema in Women with Breast Cancer
Int J Radiat Oncol Biol Phys. 2007 Oct 27
Deutsch M, Land S, Begovic M, Sharif S.
National Surgical Adjuvant Breast and Bowel Project (NSABP) Operations and Biostatistical Centers, Pittsburgh, PA; University of Pittsburgh Medical Center, Department of Radiation Oncology, Pittsburgh, PA.

PURPOSE: To determine the incidence and factors associated with the development of arm edema in women who participated in the National Surgical Adjuvant Breast and Bowel Project (NSABP) study B-04.

METHODS AND MATERIALS: Between 1971 and 1974, the NSABP protocol B-04 randomized 1,665 eligible patients with resectable breast cancer to either (1) the Halstead-type radical mastectomy; (2) total mastectomy and radiotherapy to the chest wall, axilla, supraclavicular region, and internal mammary nodes if by clinical examination axillary nodes were involved by tumor; and (3) for patients with a clinically uninvolved axilla, a third arm, total mastectomy alone. Measurements of the ipsilateral and contralateral arm circumferences were to be performed every 3 months.

RESULTS: There was at least one recorded measurement of arm circumferences for 1,457 patients (87.5% of eligible patients). There were 674 women (46.3%) who experienced arm edema at some point during the period of follow-up until February 1976. For radical mastectomy patients, total mastectomy and radiotherapy patients, and total mastectomy patients alone, arm edema was recorded at least once in 58.1%, 38.2%, and 39.1% of patients, respectively (p < .001) and at last recorded measurement in 30.7%, 14.8%, and 15.5%, respectively (p = <.001). Increasing body mass index (BMI) also showed a statistically significant correlation with arm edema at any time (p = .001) and at last assessment (p = .005).

CONCLUSIONS: Patients who undergo mastectomy, including those whose treatment plans do not include axillary dissection or postoperative radiotherapy, suffer an appreciable incidence of arm edema.
PMID: 18029105 [PubMed - as supplied by publisher]
See also:
Arm or Leg Swelling After Cancer
Complications of Breast Cancer Radiotherapy
Lymphedema After Cancer - How Serious Is It?