Edema and Related Medical Conditions

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Friday, March 30, 2007

Leg edema due to urinary obstruction

Leg swelling due to urinary obstruction

Vasc Med. 2006 Nov

Lokhandwala J,
Gornik H.
Section of Vascular Medicine, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA.

An 85-year-old man presented with bilateral leg edema and urinary incontinence. Abdominal examination revealed a severely distended bladder. Venous duplex of the legs demonstrated monophasic waveforms bilaterally, suggesting obstruction of proximal lower extremity veins. Relief of urinary obstruction was associated with the prompt return of normal respiratory variation of flow in the veins and improvement of leg swelling. Non-thrombotic obstruction of the proximal veins of the lower extremities by a severely enlarged urinary bladder is an infrequent yet potentially reversible cause of lower extremity edema. Subtle clues in the Doppler waveforms of an otherwise normal lower extremity venous duplex examination are crucial in establishing this diagnosis.

PMID: 17390552 [PubMed - in process]

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Thursday, March 22, 2007

Effect of AVP on brain edema following traumatic brain injury.

Effect of AVP on brain edema following traumatic brain injury.

Chin J Traumatol. 2007 Apr
Xu M,
Su W,
Huang WD,
Lu YQ,
Xu QP,
Chen ZJ.
Department of Critical Care Medicine, Sir Run Run Shaw Hospital, Medical College of Zhejiang University, Hangzhou 310016, China.

Objective:To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema.

Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS less than or equal to 8) and moderate traumatic brain injury group (MTBI, GCS larger than 8).Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group)and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan.

Results: plasma AVP levels (ng/L) were (mean+/-SD): control, 3.06+/-1.49; MTBI, 38.12+/-7.25; and STBI, 66.61+/-17.10.The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P less than 0.01). And the AVP level was correlated with the severity (STBI r equal to 0.919, P less than 0.01; MTBI r equal to 0.724, P less than 0.01) and the duration of brain edema (STBI r equal to 0.790, P less than 0.01; MTBI r equal to 0.712, P less than 0.01).

Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.

PMID: 17371619 [PubMed - in process]

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Inhaled nitric oxide does not prevent postpneumonectomy pulmonary edema in pigs

Inhaled nitric oxide does not prevent postpneumonectomy pulmonary edema in pigs
2007 The American Association for Thoracic Surgery

Marc Filaire, MDa, Elie Fadel, MDb, Benoît Decanteb, Frédéric Seccatoreb, Guy-Michel Mazmanian, MDb, Philippe Hervé, MDb,*
a CHU Clermont-Ferrand, Service de Chirurgie Générale et Thoracique, Hôpital Gabriel Montpied, and Université d’Auvergne, Laboratoire d’Anatomie, Clermont-Ferrand, Franceb Experimental Surgery Laboratory and Department of Thoracic and Vascular Surgery and Heart-Lung transplantation, Centre Chirurgical Marie Lannelongue, Paris-Sud University, Le Plessis-Robinson, France.

Received for publication May 11, 2006; revisions received July 22, 2006; accepted for publication September 5, 2006.

* Address for reprints: Philippe Hervé, MD, Centre Chirurgical Marie Lannelongue, Paris-Sud University, Le Plessis-Robinson, France. (Email: pherve@ccml.com)

Objective: Increase in lung permeability is an inevitable consequence of pneumonectomy in relation to inflammatory injury and increased perfusion flow. We tested whether inhaled nitric oxide, a potent vasodilatator and anti-inflammatory agent, prevents postpneumonectomy edema in the first 24 hours after pneumonectomy in pigs.

Methods: We assessed hemodynamics, gas exchange, extravascular lung water estimated with the double-indicator dilution method, and lung neutrophil sequestration measured on the basis of lung myeloperoxidase activity at 1 and 24 hours after left pneumonectomy in 14 pigs randomly assigned to inhaled nitric oxide (10 ppm) or control groups.

Results: Extravascular lung water content markedly increased at 1 and 24 hours after pneumonectomy, with no difference between the 2 groups. Hemodynamics did not differ between the 2 groups. Myeloperoxidase activity was higher and PaO 2 values were lower in the nitric oxide group compared with in the control group.

Conclusions: Over the 24 hours after pneumonectomy, intraoperative inhaled nitric oxide levels neither improved gas exchange nor attenuated accumulation of lung water. On the contrary, they were associated with an increase in lung neutrophil sequestration and deterioration of arterial oxygenation, suggesting the occurrence of an early and toxic effect of nitric oxide.

Abbreviations and Acronyms: CI = cardiac index; EVLW = extravascular lung water; FIO 2 = inspired oxygen fraction; MPAP = mean pulmonary artery pressure; MPO = myeloperoxidase; MSAP = mean systemic artery resistance; NO = nitric oxide; PBV = pulmonary blood volume; SVRI = indexed value of systemic vascular resistance

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Wednesday, March 21, 2007

Bevacizumab and the treatment of macular edema

Bevacizumab for the treatment of macular edema secondary to retinal vein occlusion

Ophthalmologe. 2007 Mar 20
Schaal KB,
Hoh AE,
Scheuerle A,
Schutt F,
Dithmar S.
Schwerpunkt Retinologie, Universitatsaugenklinik Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Deutschland,

BACKGROUND: Retinal vein occlusion often leads to macular edema as a result of an elevated level of intravitreal VEGF. We report on the anatomic and functional results after intravitreal bevacizumab injections in patients with retinal vein occlusion.

METHODS: In a prospective study, 18 patients with central, and 22 patients with branch retinal vein occlusion, all of whom had persistent macular edema (>300 mum) received 2.5 mg intravitreal bevacizumab. ETDRS visual acuity, ophthalmic examination and stratus OCT were performed at baseline, 1 week after injection and then monthly. Further injections were given every 6 weeks in patients with persistent or recurring macular edema.

RESULTS: The findings did not deteriorate in any of the 40 patients. The injections (mean of 2.6+/-1.4 injections/patient) were very well tolerated in all cases during a mean follow-up of 23+/-13 weeks. On the last visit, 73.3% of patients with central retinal vein occlusion and 76.5% of those with branch retinal vein occlusion were found to have significantly improved visual acuity (by at least 3 lines). Mean central retinal thickness had decreased from 921+/-264 to 239+/-66.2 mum in patients with central retinal vein occlusion, and from 678+/-221 to 236+/-78 mum in patients with branch retinal vein occlusion.

CONCLUSIONS: Neither intraocular nor systemic side-effects were observed in this study after repeated intravitreal injections of 2.5 mg bevacizumab. Current results suggest that intravitreal anti-VEGF therapy is a promising option in macular edema secondary to retinal vein occlusion.

PMID: 17372737 [PubMed - as supplied by publisher]

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Tuesday, March 13, 2007

Aquaporin-4 and brain edema.

Aquaporin-4 and brain edema.

Pediatr Nephrol. 2007 Mar 9

Departments of Medicine and Physiology, University of California, San Francisco, CA, 94143-0521, USA.

Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid (CSF) and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. Experiments using AQP4-null mice provide strong evidence for AQP4 involvement in cerebral water balance. AQP4-null mice are protected from cellular (cytotoxic) brain edema produced by water intoxication, brain ischemia, or meningitis. However, AQP4 deletion aggravates vasogenic (fluid leak) brain edema produced by tumor, cortical freeze, intraparenchymal fluid infusion, or brain abscess.

In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 deletion also worsens obstructive hydrocephalus. Recently, AQP4 was also found to play a major role in processes unrelated to brain edema, including astrocyte migration and neuronal excitability.

These findings suggest that modulation of AQP4 expression or function may be beneficial in several cerebral disorders, including hyponatremic brain edema, hydrocephalus, stroke, tumor, infection, epilepsy, and traumatic brain injury.

Keywords: AQP4 - Brain swelling - Water channel - Hydrocephalus - Hyponatremia

Springer link

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Tuesday, March 06, 2007

Recurrent abdominal pain due to hereditary angioedema

Recurrent abdominal pain due to hereditary angioedema

Indian J Pediatr. 2007 Jan

Janardhanan D,
Nair S,
Subramanian TS.
Department of Pediatrics, Amrita Institute of Medical Sciences, Elamakkara (P.O.), Kochi, Kerala, India.

Recurrent abdominal pain is a common problem in children that may need invasive procedures for diagnosis. Hereditary angioedema (HAE) is rarely considered in the differential diagnosis. Here it is reported a girl with HAE, who presented initially as recurrent abdominal pain without cutaneous manifestations. Each episode was managed elsewhere as an acute surgical emergency and an exploratory laparotomy was planned. Diagnosis was confirmed by quantitative assay of C1 inhibitor. On detailed evaluation, many members of her family were affected.

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