Myocardial microvascular permeability, interstitial oedema, and compromised cardiac function

**While this is an older article, it is just now available in full text.  Intersitial edema is what we deal with in our lymphedema and a number of us have had situations whereby we experiences interstitial edema in the cardiac cavity itself.  I was really shaken up when I experienced this a couple years ago.  This is very applicable even today.  Pat**

July 2010

Ranjeet M. Dongaonka,  Randolph H. Stewart,  Hans J. Geissler,  and Glen A. Laine

ABSTRACT

The heart, perhaps more than any other organ, is exquisitely sensitive to increases in microvascular permeability and the accumulation of myocardial interstitial oedema fluid. Whereas some organs can cope with profound increases in the interstitial fluid volume or oedema formation without a compromise in function, heart function is significantly compromised with only a few percent increase in the interstitial fluid volume. This would be of little consequence if myocardial oedema were an uncommon pathology. On the contrary, myocardial oedema forms in response to many disease states as well as clinical interventions such as cardiopulmonary bypass and cardioplegic arrest common to many cardiothoracic surgical procedures. The heart's inability to function effectively in the presence of myocardial oedema is further confounded by the perplexing fact that the resolution of myocardial oedema does not restore normal cardiac function. We will attempt to provide some insight as to how microvascular permeability and myocardial oedema formation compromise cardiac function and discuss the acute changes that might take place in the myocardium to perpetuate compromised cardiac function following oedema resolution. We will also discuss compensatory changes in the interstitial matrix of the heart in response to chronic myocardial oedema and the role they play to optimize myocardial function during chronic oedemagenic disease.

Full Text Article

Pub Med - Cardiovascular Rsearch

Volume-dependent effect of perihaematomal oedema on outcome for spontaneous intracerebral haemorrhages.

Jan 2013

Appelboom G, Bruce SS, Hickman ZL, Zacharia BE, Carpenter AM, Vaughan KA, Duren A, Hwang RY, Piazza M, Lee K,Claassen J, Mayer S, Badjatia N, Connolly ES Jr.

Source

Department of Neurological Surgery, The Neurological Institute, Columbia University College of Physicians and Surgeons, , New York, New York, USA.

Abstract

INTRODUCTION:

It is still unknown whether subsequent perihaematomal oedema (PHE) formation further increases the odds of an unfavourable outcome.

METHODS:

Demographic, clinical, radiographic and outcome data were prospectively collected in a single large academic centre. A multiple logistic regression model was then developed to determine the effect of admission oedema volume on outcome.

RESULTS:

133 patients were analysed in this study. While there was no significant association between relative PHE volume and discharge outcome (p=0.713), a strong relationship was observed between absolute PHE volume and discharge outcome (p=0.009). In a multivariate model incorporating known predictors of outcome, as well as other factors found to be significant in our univariate analysis, absolute PHE volume remained a significant predictor of poor outcome only in patients with intracerebral haemorrhage (ICH) volumes ≤30 cm(3) (OR 1.123, 95% CI 1.021 to 1.273, p=0.034). An increase in absolute PHE volume of 10 cm(3) in these patients was found to increase the odds of poor outcome on discharge by a factor of 3.19.

CONCLUSIONS:

Our findings suggest that the effect of absolute PHE volume on functional outcome following ICH is dependent on haematoma size, with only patients with smaller haemorrhages exhibiting poorer outcome with worse PHE. Further studies are needed to define the precise role of PHE in driving outcome following ICH.

PubMed

Angioneurotic edema associated with haloperidol.

2012

Kahlon S, Lee C, Chirurgi R, Worku Hassen G.

Source

Metropolitan Hospital Center, New York Medical College, New York, NY 10029, USA.

Abstract

Background. 

Angioneurotic edema is a life-threatening medical emergency that requires urgent diagnosis and treatment. Haloperidol is in the butyrophenone class of antipsychotic medications. Acute anaphylaxis to Haloperidol is very rare and no cases have been reported in literature. Objective. To report the association of life-threatening angioneurotic edema with intramuscular Haloperidol. Case Report. We present a case of an adult with no known allergies in whom angioneurotic edemawith tongue swelling and protrusion developed after the administration of a single IM dose of Haloperidol. Conclusion. We propose angioneurotic edema in a rare side effect of Haloperidol. The onset of the symptoms is abrupt, but it may take 12-36 hours to resolve completely. Therefore patient should be monitored for 12-36 hrs.

PubMed

Massive corneal edema treated with corneal cross-linking.

2012

Laborante A, Buzzonetti L, Longo C.

Source

Ophthalmic Complex Operating Unit, IRCCS-Hospital Casa Sollievo Della Sofferenza, San Giovanni Rotondo (Foggia), Italy. antoniolaborante@virgilio.it

Abstract

INTRODUCTION:

Massive corneal edema disrupts the fine architecture of corneal stroma that guarantees its transparency, causing opacities that seriously impair clear vision and are usually solved by corneal transplant. Corneal cross-linking, a treatment developed to halt keratoconus progression, results in a loss of water and a compaction of corneal stroma. It might therefore be useful to improve the pathologic edematous condition of some corneas, ameliorating visual acuity and allowing more time for a surgical procedure of keratoplasty.

PATIENTS AND METHODS: 

Six patients with visual impairing corneal edemas further to lens phacoemulsification, penetrating keratoplasty, or post-infective neovascularization were treated with corneal cross-linking alone, or in combination with amniotic membrane apposition with or without anti-angiogenic therapy.

RESULTS:

 All patients partly resolved the edematous condition, improving both corneal transparency and visual acuity.

CONCLUSIONS:

 Corneal cross-linking appears to be a useful method to treat massive corneal edemas, so that keratoplasty can be at least delayed, and need not to be an emergency treatment in these cases.

La Clinica Terapeutica

Ranibizumab for the treatment of diabetic macular oedema

Ranibizumab for the treatment of diabetic macular edema

National Institute for Health and Clinical Excellence

Nice

Additional information published in 2012

Diabetic Macular Edema Responds Best to Frequent Ranibizumab

Medscape Medical News

Angioedema.

Kaplan AP.

Source

From the National Allergy, Asthma, and Urticaria Centers of Charleston, Charleston, SC.

Abstract

Angioedema can be caused by either mast cell degranulation or activation of the kallikrein-kinin cascade. In the former case, angioedema can be caused by allergic reactions caused by immunoglobulin E (IgE)-mediated hypersensitivity to foods or drugs that can also result in acute urticaria or a more generalized anaphylactic reaction. Nonsteroidal anti-inflammatory drugs (cyclooxygenase 1 inhibitors, in particular) may cause angioedema with or without urticaria, and leukotrienes may have a particular role as a mediator of the swelling. Reactions to contrast agents resemble allergy with basophil and mast cell degranulation in the absence of specific IgE antibody and can be generalized, that is, anaphylactoid. Angioedema accompanies chronic urticaria in 40% of patients, and approximately half have an autoimmune mechanism in which there is IgG antibody directed to the subunit of the IgE receptor (40%) or to IgE itself (5%-10%). Bradykinin is the mediator of angioedema in hereditary angioedema types I and II (C1 inhibitor [INH] deficiency) and the newly described type III disorder some of which are caused bya mutation involving factor XII. Acquired C1 INH deficiency presents in a similar fashion to the hereditary disorder and is due either toC1 INH depletion by circulating immune complexes or to an IgG antibody directed to C1 INH. Although each of these causes excessive bradykinin formation because of activation of the plasma bradykinin-forming pathway, the angioedema due to angiotensin-converting enzyme inhibitors is caused by excessive bradykinin levels due to inhibition of bradykinin degradation. Idiopathic angioedema (ie, pathogenesis unknown) may be histaminergic, that is, caused by mast cell degranulation with histamine release, or nonhistaminergic. The mediator pathways in the latter case are yet to be defined. A minority may be associated with the same autoantibodies associated with chronic urticaria. Angioedema that is likely to be life threatening (laryngeal edema or tongue/pharyngeal edema that obstructs the airway) is seen in anaphylactic/anaphylactoid reactions and the disorders mediated by bradykinin.

PubMed

Morbihan disease.

Dec 2012

Hu SW, Robinson M, Meehan SA, Cohen DE.

Source

The Ronald O. Perelman Department of Dermatology, New York University School of Medicine.

Abstract

Morbihan disease, which consists of solid facial edema, is a rare complication of rosacea, a common cutaneous disorder in middle-aged individuals. The characteristic features of Morbihan disease are its chronic course, typical clinical picture, lack of specific laboratory and histopathologic findings, and refractoriness to therapeutic measures. Since its initial description in 1957, only a small number of cases have been reported in the dermatologic literature. We report a 54-year-old man who developed a two-year duration of erythema and edema that affects the upper and mid face, with accentuation in the periorbital region. Patch tests excluded an allergic contact dermatitis and histopathologic investigation showed small, nodular clusters of epithelioid cells in the dermis that were consistent with sarcoidal granulomata. A diagnosis of Morbihan disease was made owing to the combination of clinical and histopathologic findings. Therapeutic options for the disease remain unsatisfactory and treatments reported in the literature include systemic glucocorticoids, oral tetracyclines, thalidomide, isotretinoin, ketotifen, and clofazimine. Our patient failed a six-to-seven months course of minocycline prior to presentation and has since experienced improvement on gradually-increasing doses of isotretinoin.

PubMed