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

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

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]

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).

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.

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

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.

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.

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

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

[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]