Infantile acute hemorrhagic edema

Infantile acute hemorrhagic edema and rotavirus infection.

Operative Unit of Dermatology, 1st Medical Department, Arcispedale Santa Maria Nuova, Reggio Emilia, Italy.

vito.dilernia@asmn.re.it

Infantile acute hemorrhagic edema (AHE) is a benign condition characterized by a dramatic onset of inflammatory edema and ecchymotic purpura in a target or cockade pattern. It is considered an uncommon form of cutaneous vasculitis occurring in children younger than 2 years of age. The outbreak is frequently preceded by an immunization or various infections. We describe an 11-month-old girl with rosette-shaped purpuric plaques on the face and limbs, clinically consistent with a diagnosis of AHE of the skin, associated with fever and diarrhea. Laboratory investigations showed a rotavirus infection, which has not previously been reported in association with AHE of the skin. The disease had a benign course without relapses. Appropriate microbiologic investigations are advisable to confirm the possible etiologic role of rotavirus.

Publication Types:
Case Reports

PMID: 15461759 [PubMed - indexed for MEDLINE]

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Report of eight infants with acute infantile hemorrhagic edema and review of the literature

Caksen H, Odabas D, Kosem M, Arslan S, Oner AF, Atas B, Akcay G, Ceylan N.

Department of Pediatrics, Yuzuncu Yil University, Faculty of Medicine, Van, Turkey.

Acute infantile hemorrhagic edema (AIHE) is a cutaneous leukocytoclastic vasculitis, clinically characterized by the symptom triad of fever, large purpuric skin lesions, and edema. The clinical picture has a violent onset, a short benign course, and spontaneous complete recovery. In this article, we present eight patients who were admitted with rashes on the skin and edema on the eyelids and extremities, and were diagnosed with AIHE according to their clinical and histopathological features (immunohistological study was also performed in three of them). Our purpose was to emphasize that, aside from Henoch-Schonlein purpura, meningococcemia, septicemia, and purpura fulminans, AIHE benign disorder should also be considered in the differential diagnosis to determine the clinical course and treatment protocol in patients with purpuric rashes.

Publication Types:
Case Reports
Review

PMID: 12081160

[PubMed - indexed for MEDLINE]

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Infantile acute hemorrhagic edema of the skin.

Paradisi M, Annessi G, Corrado A.

Istituto Dermopatico dell'Immacolata, Rome, Italy.

Infantile acute hemorrhagic edema (AHE) of the skin is an uncommon form of cutaneous leukocytoclastic vasculitis that occurs in children younger than 3 years. We describe a 10-month-old boy with AHE, in whom the disease appeared after antibiotic treatment for an acute respiratory illness. AHE presented with fever, acral edema, and rosette-shaped purpuric plaques on the face and limbs. The causes of AHE are unclear, as is its nosologic position. Some authors consider the disease as a purely cutaneous form of Henoch-Schonlein purpura, and others believe that AHE should be regarded as a distinct clinicobiologic entity within the spectrum of leukocytoclastic vasculitis.

Publication Types:
Case Reports

PMID: 11534914 [PubMed - indexed for MEDLINE]

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Infantile Acute Hemorrhagic Edema Diagnostic Images

Acute Hemorrhagic Edema of Infancy - eMedicine

Acute Hemorrhagic Edema of Infancy - Isreal Medical Assoc. Journal

Urticarial vasculitis of infancy (Acute hemorrhagic edema)

Approach to Leg Edema of Unclear Etiology

The Journal of the American Board of Family Medicine 19:148-160 (2006)
Evidence-Based Clinical Medicine
Approach to Leg Edema of Unclear Etiology John W. Ely, MD, MSPH, Jerome A. Osheroff, MD, M. Lee Chambliss, MD, MSPH and Mark H. Ebell, MD, MS

Department of Family Medicine, University of Iowa Carver College of Medicine, Iowa City, IA (JWE)Thomson MICROMEDEX, Greenwood Village, CO (JAO)Moses Cone Hospital Family Medicine Residency, Greensboro, NC (MLC)Department of Family Practice, Michigan State University, East Lansing, MI (MHE)

Correspondence: Corresponding author: John W. Ely, MD, MSPH, University of Iowa College of Medicine, Department of Family Medicine, 200 Hawkins Drive, 01291-D PFP, Iowa City, IA 52242
(E-mail: john-ely@uiowa.edu)

Abstract

A common challenge for primary care physicians is to determine the cause and find an effective treatment for leg edema of unclear etiology. We were unable to find existing practice guidelines that address this problem in a comprehensive manner. This article provides clinically oriented recommendations for the management of leg edema in adults. We searched on-line resources, textbooks, and MEDLINE (using the MeSH term, "edema") to find clinically relevant articles on leg edema. We then expanded the search by reviewing articles cited in the initial sources. Our goal was to write a brief, focused review that would answer questions about the management of leg edema. We organized the information to make it rapidly accessible to busy clinicians. The most common cause of leg edema in older adults is venous insufficiency. The most common cause in women between menarche and menopause is idiopathic edema, formerly known as "cyclic" edema. A common but under-recognized cause of edema is pulmonary hypertension, which is often associated with sleep apnea. Venous insufficiency is treated with leg elevation, compressive stockings, and sometimes diuretics. The initial treatment of idiopathic edema is spironolactone. Patients who have findings consistent with sleep apnea, such as daytime somnolence, load snoring, or neck circumference >17 inches, should be evaluated for pulmonary hypertension with an echocardiogram. If time is limited, the physician must decide whether the evaluation can be delayed until a later appointment (eg, an asymptomatic patient with chronic bilateral edema) or must be completed at the current visit (eg, a patient with dyspnea or a patient with acute edema [<72>Figure 1 could be used as a guide. If the full evaluation could wait for a subsequent visit, the patient should be examined briefly to rule out an obvious systemic cause and basic laboratory tests should be ordered for later review (complete blood count, urinalysis, electrolytes, creatinine, blood sugar, thyroid stimulating hormone, and albumin).

Edema is defined as a palpable swelling caused by an increase in interstitial fluid volume. The most likely cause of leg edema in patients over age 50 is venous insufficiency. Venous insufficiency affects up to 30% of the population,1,2 whereas heart failure affects only approximately 1%.34 The most likely cause of leg edema in women under age 50 is idiopathic edema, formerly known as cyclic edema.5 Most patients can be assumed to have one of these diseases unless another cause is suspected after a history and physical examination. However, there are at least 2 exceptions to this rule: pulmonary hypertension and early heart failure can both cause leg edema before they become clinically obvious in other ways.

Complete Article with Graphs and References

Retisert and Macular Edema

Retisert - fluocinolone ophthalmic (flu nis O lone Opt hal mick)

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

Contact your doctor if your symptoms begin to get worse or if you do not see any improvement in your condition after a few days.

What is Retisert?

Fluocinolone is in a class of drugs called corticosteroids. It inhibits processes in the body that cause inflammation. Therefore, the swelling and pain of inflammatory conditions is decreased.

Retisert is used to treat eye inflammation caused by infections, injury, surgery, or other conditions.

Retisert may also be used for purposes other than those listed in this medication guide.
What should I discuss with my healthcare provider before using Retisert?

It is not known whether Retisert will harm an unborn baby Do not use Retisert without first talking to your doctor if you are pregnant.

It is also not known whether Retisert passes into breast milk. Do not use Retisert without first talking to your doctor if you are breast-feeding a baby.

How should I use Retisert?

Use Retisert eyedrops exactly as directed by your doctor. If you do not understand these directions, ask your pharmacist, nurse, or doctor to explain them to you.

What happens if I miss a dose?

Talk to your doctor if a dose has been missed.

What happens if I overdose?

An overdose of this medication is unlikely to occur. If you do suspect an overdose, call an emergency room or poison control center near you. If the drops have been ingested, call an emergency center for advice.

What should I avoid while using Retisert?

Use caution when driving, operating machinery, or performing other hazardous activities. Retisert may cause blurred vision. If you experience blurred vision, avoid these activities.

If you wear contact lenses, ask your doctor if you should wear them during treatment with Retisert.

What are the possible side effects of Retisert?

Serious side effects are not expected with this medication. Rarely, an increase in the pressure inside of the eye, formation of cataracts, or perforation of the cornea have been reported. Talk to your doctor about any possible side effects.

More commonly, some burning, stinging, irritation, itching, redness, blurred vision or sensitivity to light may occur. Continue to use Retisert and talk to your doctor about any side effects that you experience.

What other drugs will affect Retisert?

Do not use other eyedrops or eye medications during treatment with Retisert without first talking to your doctor.

Before using this medication, tell your doctor if you are taking an oral steroid medication such as prednisone (Deltasone, Orasone, others), methylfluocinolone (Medrol), hydrocortisone (Cortef, Hydrocortone), and others.

Drugs other than those listed here may also interact with Retisert. Talk to your doctor or pharmacist before taking any prescription or over-the-counter medicines.

Where can I get more information?

Your pharmacist has additional information about Retisert written for health professionals that you may read.

Drugs.com

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See also: Retisert

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Diabetic Macular Edema trial with Retisert(TM); Positive Results for pSivida

2/21/2006 8:00:00 AM EST

Global bio-nanotech company pSivida Limited (NASDAQ:PSDV)(ASX:PSD)(Xetra:PSI) today announced the publication of preliminary three year follow-up data from Bausch and Lomb's multi-center, randomized, controlled clinical trial of Retisert(TM) for the treatment of diabetic macular edema (DME). Global eye health company, Bausch and Lomb (NYSE:BOL), exclusive licensee of Retisert(TM) from pSivida, conducted the study in hospitals in the United States in which 197 patients were randomized to receive either standard of care (repeat laser or observation) or a Retisert(TM) implant. The study concluded that significantly more patients receiving a Retisert(TM) implant had improved visual acuity (of three or more lines on an eye chart) than those receiving standard of care.

DME, a common complication of Diabetic Retinopathy (DR), is the leading cause of vision loss in people under the age of 65 in the United States with an estimated 500,000 treatable cases. DME is characterized by swelling of the retina and loss of vision. Currently the only FDA approved treatment is laser therapy in which holes are burned into the macula with a laser. This treatment is often ineffective or generally provides only temporary benefit. There are no approved drug therapies for the treatment of either DME or DR. Retisert(TM) for DME is surgically implanted into the eye and releases a constant amount of the drug, fluocinolone acetonide. Retisert(TM) is FDA approved for the treatment of posterior uveitis with a duration of 30 months and is licensed to Bausch & Lomb and co-promoted by Novartis.

Medidur(TM) is pSivida's next generation product. It is a tiny, injectable device that can release the same drug as Retisert(TM). Unlike Retisert(TM), which is surgically implanted, Medidur(TM) is injected into the eye during an office visit. Medidur(TM) is in Phase III clinical trials in DME in collaboration with Alimera Sciences Inc., a specialty pharmaceutical company focused on the ophthalmic industry.

"As Retisert(TM) and Medidur(TM) can deliver the same drug, at a similar rate, to the back of the eye, we hope the Medidur(TM) trials in DME show a very similar improvement in visual acuity to that shown in the Retisert(TM) DME trial. Medidur(TM) differs from Retisert(TM) in that it is a smaller device that can be inserted without the need for surgery," said Mr Gavin Rezos, CEO of pSivida Limited.

Results of the Bausch & Lomb study has shown that a statistically significant number of eyes treated with Retisert(TM) had an improvement of visual acuity of three or more lines on an eye chart compared to eyes receiving standard of care (28% versus 15%, p less than 0.05). Additionally, a statistically significant number of eyes treated with Retisert(TM) showed an improvement in their diabetic retinopathy severity score, a measure of the severity of their disease (13% versus 4% p less than 0.001). More eyes receiving Retisert(TM) also showed a reduction in their edema and there was also no evidence of edema in 58% of eyes receiving the implant versus 30% of eyes receiving standard of care (p less than 0.001).

Side-effects of Retisert(TM) in patients with DME were similar to those reported in patients with uveitis for which Retisert(TM) is approved. Of the patients with DME receiving Retisert(TM), at three years 33% required an operation to relieve elevated intraocular pressure (IOP) and 95% required cataract surgery. Cataract surgery is a relatively uncomplicated and established procedure with a high success rate. The abstract (#5442) detailing the DME data is available on the website of the Association for Research in Vision and Ophthalmology www.arvo.org. The three year uveitis data is available at the same website (abstract #1523). Fuller data will be presented at the ARVO conference in May 2006.

pSivida receives royalties from sales of Retisert(TM) for chronic non-infectious posterior segment uveitis, a sight threatening condition that affects an estimated 175,000 people in the United States and an estimated 800,000 people worldwide. The product is presently priced at US$18,250 and is approved as a 30 month treatment. Covered in the United States by Medicare and Medicaid, Retisert(TM) is co-marketed in the United States by Bausch & Lomb and Novartis. In the event that Retisert(TM) is approved for DME and Bausch & Lomb decide to market Retisert(TM) for DME, then pSivida will receive royalty payments from Bausch & Lomb for Retisert(TM) sales for DME.

GenUpdates

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Additional Product Information

Lev Pharmaceuticals to Present at Hereditary Angioedema Conference

March 17, 2006, 12:10PM

PRNewswire-FirstCall

NEW YORK, March 17 /PRNewswire-FirstCall/ --

Lev Pharmaceuticals, Inc. ("LevPharma") (OTC Bulletin Board: LEVP), a developer of therapeutics for inflammatory diseases, announced today that the Company will be presenting information on its ongoing Phase III study for hereditary angioedema ("HAE") at the 2006 Dallas Regional Meeting of the Hereditary Angioedema Association, March 17-19, at the Harvey Hotel in Irving, Texas. The presentation, to be given by Jason Bablak, the Company's Vice President, Regulatory Affairs, is scheduled for Saturday, March 18 at 11:15 am (CT).

LevPharma's Phase III trial, designated CHANGE (C1-Inhibitor in Hereditary Angioedema Nanofiltration Generation evaluating Efficacy), is a multi-center, placebo-controlled, double-blind study designed to examine the efficacy of the Company's lead product candidate, nano-filtered C1-esterase inhibitor ("C1- INH"). The first part of the Phase III study, which began in March 2005 and is ongoing, is designed to examine the efficacy and safety of C1-INH in the treatment of acute inflammatory attacks in HAE. The second part of the study, which began in October 2005, is examining the efficacy of C1-INH in preventing the onset of such inflammatory attacks in severely affected patients. In 2004 LevPharma received orphan drug designation from the United States Food and Drug Administration for C1-esterase inhibitor (human) in treating hereditary angioedema. Upon product licensure, orphan drug designation could provide the Company with seven years of marketing exclusivity for its C1-INH product as a treatment for HAE in the United States.

Patients and physicians interested in obtaining more information about the Phase III trial should contact LevPharma directly at 212-682-3096, or visit the Company's website at http://www.levpharma.com.

LevPharma is developing its C1-INH product through an agreement with Sanquin Blood Supply Foundation ("Sanquin"), an Amsterdam-based not-for-profit organization that provides blood and plasma products and related services, carries out research and provides education, primarily in the Netherlands. Sanquin has been producing and selling successive generations of C1-INH, prepared from human plasma, in the Netherlands for over 30 years for the treatment of HAE.

Continuous product development efforts at Sanquin have resulted in the product under investigation, a highly purified C1-INH that is the next generation of the product that has been available in the Netherlands since 1997. Despite its long record of use in Europe, however, C1-INH, has never been introduced in the United States. Through a supply and distribution agreement with Sanquin, LevPharma has the exclusive right to market and sell C1-INH prepared by Sanquin for the treatment of HAE in North America and certain other geographic regions.

About Hereditary Angioedema

HAE is a genetic disorder characterized by episodes of edema (swelling) in the extremities (the hands and feet), the face, the abdomen, and the larynx. There are thought to be 6,000 or more people with HAE in the United States. The majority of patients experience episodes of severe abdominal pain, nausea, and vomiting that is caused by swelling in the intestinal wall. Attacks that involve the face and throat can result in closure of the airway passages, and the mortality rate from untreated airway obstruction has been reported to be over 30% with death most frequently caused by asphyxiation due to airway closure. HAE is caused by a deficiency of C1-INH, and there are currently no approved treatments for acute attacks available in the United States.

About Lev Pharmaceuticals, Inc.

LevPharma is a biopharmaceutical company focused on developing and commercializing therapeutic products for the treatment of inflammatory diseases. LevPharma's product candidates are based on C1-esterase inhibitor ("C1-INH"), a human plasma protein that mediates inflammation and is potentially applicable as a treatment for a range of medical indications. The Company initiated a Phase III clinical trial of its lead product candidate, C1-INH for the treatment of hereditary angioedema, in March 2005. LevPharma is also developing C1-INH for the treatment of acute myocardial infarction, or heart attack, and selective other diseases and disorders in which inflammation is known or believed to play an underlying role.

Legal notice to investors: Certain matters discussed in this news release are "forward-looking statements." These forward-looking statements, which apply only on the date of this release, generally can be identified by the use of forward-looking terminology such as "may," "will," "expects," "intends," "estimates," "anticipates," "believes," "continues" or words of similar import. Similarly, statements that describe LevPharma's future plans, objectives or goals are also forward-looking statements, which generally involve known and unknown risks, uncertainties and other facts that may cause the actual results, performance or achievements of LevPharma to be materially different from those expressed or implied by such forward-looking statements. Such factors may include the following: uncertainties associated with product development, the risk that LevPharma will not obtain approval to market its products, the risk that LevPharma's products will not gain market acceptance, the risks associated with dependence upon key personnel and the need for additional financing.

Contacts:
Joshua D. Schein, Ph.D. Chief Executive Officer

Sharon Weinstein Director of Investor Relations
Lev Pharmaceuticals, Inc. Noonan Russo
212-682-3096 212-845-4271

jschein@levpharma.com sharon.weinstein@eurorscg.com

chron.com

Edema of cardiac origin

Edema of cardiac origin. Studies of body water and sodium, renal function, hemodynamic indexes, and plasma hormones in untreated congestive cardiac failure

Abstract

IS Anand, R Ferrari, GS Kalra, PL Wahi, PA Poole-Wilson and PC Harris Department of Cardiology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

This study provides data on plasma hormone levels in patients with severe clinical congestive cardiac failure who had never received therapy and in whom the presence of an accumulation of excess water and sodium had been established. Eight patients were studied; two had ischemic cardiac disease, and six had dilated cardiomyopathy. Mean hemodynamic measurements at rest were as follows: cardiac index, 1.8 l/min/m2; pulmonary wedge pressure, 30 mm Hg; right atrial pressure, 15 mm Hg. Total body water content was 16% above control, extracellular liquid was 33% above control, plasma volume was 34% above control, total exchangeable sodium was 37% above control, renal plasma flow was 29% of control, and glomerular filtration rate was 65% of control. Plasma norepinephrine was consistently increased (on average 6.3 times control), whereas adrenaline was unaffected. Although plasma renin activity and aldosterone varied widely, they were on average above normal (renin 9.5 times control, aldosterone 6.4 times control). Plasma atrial natriuretic peptide (14.3 times control) and growth hormone (11.5 times control) were consistently increased. Cortisol was also increased on average (1.7 times control). Vasopressin was increased only in one patient.

Article

Quantification of rebound edema after steroid treatment

Abstract

Odland R, Wigley T, Kim T, Kizziar R, Davamony D.

Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, Loma Linda University, Loma Linda, CA, USA.

OBJECTIVE:

Return of edema after abrupt discontinuation of steroid treatment has never been studied or quantified. The purpose of this study was to measure the effect of abrupt cessation and tapering doses of steroids on tissue water content (TWC) in a rat skin flap model.

DESIGN:

A randomized controlled animal trial was designed to study the effects of discontinuation of steroid on skin flap edema. The animals were assigned to a control group (C), a steroid group (S), an abrupt steroid cessation (SC) group, or a tapering steroid (ST) group.Main Outcome Measures: In each group the skin flaps were biopsied at 30 and 36 hours. TWC was determined by a biopsy-drying technique.

RESULTS:

A significant difference (P = 0.05) was found between the C and S groups and between the SC and S groups at both 30 and 36 hours, with the C group having the highest TWC. No significant difference was noted between the SC and C groups. The ST group had significantly less edema than the C group and similar TWC to that of the S group.

CONCLUSION:

Edema rebounded in the skin flaps after abrupt cessation of steroids (SC was not different from C), presumably because of destabilization of inflammatory mediators. The rebound effect was not observed in the ST group. The control of rebound edema by a tapering steroid protocol may be important in skin flap survival and may have implications for the management of airway edema.

PMID: 10889480

[PubMed - indexed for MEDLINE]

Ischemic brain edema

Cellular Injury During Ischemia

Edema Formation

Ischemic brain edema is a combination of two major types of edema: cytotoxic (cellular) and vasogenic [Fishman RA. Cerebrospinal Fluid in Diseases in the Nervous System. 2nd Ed. Philadelphia, PA: W.B. Saunders Co; 1992:103-155]. Cytotoxic edema evolves over minutes to hours and may be reversible, while the vasogenic phase occurs over hours to days, and is considered an irreversibly damaging process.

Cytotoxic edema is characterized by swelling of all the cellular elements of the brain (shown). In the presence of acute cerebral ischemia, neurons, glia (indicated by astrocytes), and endothelial cells swell within minutes of hypoxia due to failure of ATP-dependent ion (sodium and calcium) transport. With the rapid accumulation of sodium within cells, water follows to maintain osmotic equilibrium. Increased intracellular calcium activates phospholipases and the release of arachidonic acid, leading to the release of oxygen-derived free radicals and infarction.

Vasogenic edema (not shown) is characterized by an increase in extracellular fluid volume due to increased permeability of brain capillary endothelial cells to macromolecular serum proteins (e.g., albumin). Normally, the entry of plasma protein-containing fluid into the extracellular space is limited by tight endothelial cell junctions, but in the presence of massive injury there is increased permeability of brain capillary endothelial cells to large molecules. Vasogenic edema can displace the brain hemisphere and, when severe, lead to cerebral herniation.

Acute hypoxia initially causes cytotoxic edema, followed within the next hours to days by the development of vasogenic edema as infarction develops (Fishman, 1992). The delayed onset of vasogenic edema suggests that time is needed for the defects in endothelial cell function and permeability to develop.

Internet Stroke Center

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