Israel Medical Association Journal

Background: Community-acquired pneumonia requiring hospitalization is a severe illness with high mortality, especially if the appropriate treatment is delayed. Sometimes diagnosis is difficult due to an equivocal clinical picture or chest film, or to accompanying diseases that mask or simulate pneumonia.

Objectives: To assess the usefulness of certain inflammatory markers to differentiate pulmonary edema from pneumonia throughout the hospital stay in patients admitted for pneumonia or pulmonary edema of non-infectious origin and to monitor the response to treatment.

Methods: The study group comprised 50 patients admitted for pneumonia, 50 admitted for pulmonary edema and 30 healthy individuals. Blood samples for determination of leukocyte count, erythrocyte sedimentation rate (ESR), fibrinogen, C-reactive protein (CRP), albumin, sCD14 and oxidized fibrinogen were drawn upon admission, at 48 and 72 hours after admission, and at discharge from the intensive care unit.

Results: The levels of sCD14 were similar in both patient groups but higher than control levels during the first 48 hours (P < 0.03). They decreased gradually with hospital stay. The concentration of oxidized fibrinogen was similar in both patient groups and significantly lower than that of the healthy control group throughout the hospitalization period.

Conclusions: Oxidized fibrinogen and sCD14 are not reliable markers for the diagnosis of pneumonia, for its differential diagnosis from pulmonary edema, and for patient follow-up throughout hospitalization. The finding of elevated levels of oxidized fibrinogen in the group of healthy controls warrants further study to identify the factors responsible for altering fibrinogen oxidation. The other markers are more indicative.
 

Background: The causative role of diffuse macular edema in various etiologies is often undetermined.

Objectives: To describe an association between extrafoveal vitreous traction and non-diabetic diffuse macular edema secondary to various ocular entities.

Methods: In a retrospective study of eyes with non-diabetic diffuse macular edema, charts and optical coherence tomography scans demonstrating extrafoveal vitreous traction were analyzed. Excluded were diabetic patients and eyes that had vitreofoveal traction. A control group (n=12) allowed for mapping of normal macular thickness.

Results: Five eyes with macular edema were associated with extrafoveal traction, each secondary to and representing a different etiology. The causes were penetrating injury, cataract extraction, branch retinal vein occlusion, central retinal vein occlusion, and idiopathic. Vitreous traction was detected either at the papillomacular bundle (n=3), superonasally to the fovea (n=1), and at the optic nerve head (n=1). The associated retinal edema (all eyes) and serous retinal detachment (four eyes) at the traction sites were in continuum with the foveal edema in each eye, manifesting as diffuse macular edema. Of the two modalities, the OCT[1]-Line group program and the OCT-Automatic central program, only the former enabled detection of extrafoveal traction in each.

Conclusions: Diffuse macular edema secondary to various ocular diseases may be associated with extrafoveal vitreous traction. The OCT-Automatic central program may omit some of these extrafoveal traction sites. Further studies are required to validate these findings and to assess whether early vitrectomy may improve visual prognosis in these eyes.

Hereditary angioedema is a rare genetic disorder, manifested by recurrent edema leading to disfigurement, organ dysfunction and life-threatening respiratory impairment that may become fatal. The hallmark of HAE is a C1 esterase inhibitor deficiency, but recent evidence points at bradykinin as the main mediator that causes hyperpermeability of small vasculature, leading to accumulation of edema fluid. Current therapeutic options for HAE[1] are limited, and consist of drugs, replacement therapy, and supportive treatment. In view of many disadvantages of the current therapeutic modalities new approaches to the treatment of HAE are now being offered. This review summarizes our experience with a new line of medications developed for the treatment of acute exacerbations and prophylaxis of HAE – icatibant: bradykinin receptor antagonist, ecallantide: kallikrein inhibitor, and two C1 INH[2] preparations: Berinert-P, human plasma-derived concentrate, and Rhucin: novel recombinant C1-INH produced in transgenic rabbits. Preliminary results of these studies are encouraging and may bring new hope to the patients with this distressing condition. The exact number of HAE patients in Israel is unknown and because patients are treated individually and comprehensive laboratory assessment is partial, many cases might be missed or not treated according to accepted guidelines. We offer a new specialty center for HAE patients, addressing the medical and psychosocial needs of patients and their families.

Objectives: To evaluate the long-term efficacy and safety of an intravitreal injection of triamcinolone acetonide for clinically significant diabetic macular edema.

Methods: In a retrospective case series 31 diabetic patients with persistent, recurrent or diffuse clinically significant diabetic macular edema received a single 4 mg (0.1 ml) intravitreal triamcinolone acetonide injection and were followed for at least 6 months. The main outcome measures evaluated were classified as primary: visual acuity and central macular thickness, and secondary: intraocular pressure and cataract progression. Statistical analyses included Student’s t-test, chi-square test and the McNamar test.

Results: Best visual acuity results were observed 2.6 ± 2.4 months post-injection. At that time the mean foveal thickness had decreased by 37% from a baseline of 455 ± 100 to 288 ± 99 µ (P < 0.001) and the mean visual acuity improved from 6/42 to 6/23 (P < 0.001). Final mean visual acuity after an average of 10 ± 1.8 months follow-up (range 6–13 months) was identical to the baseline, although mean foveal thickness was still significantly lower than the initial thickness (368 ± 166 vs. 455 ± 100 µ, P < 0.01). Statistical analysis did not identify any pre-injection prognostic factors for improved visual acuity. The only complications that occurred were elevated intraocular pressure in 42% of patients and cataract progression in 21%. There was no endophthalmitis.

Conclusions: Intravitreal injection of triamcinolone acetonide for clinically significant diabetic macular edema is effective in reducing foveal thickness and improving visual acuity in the short term. Longer follow-up revealed that visual acuity returned to pre-injection values, even though a modest decrease in the foveal thickness persisted. Further studies are needed to evaluate the long-term efficacy in conjunction with laser photocoagulation treatment.

Background: Diabetic macular edema causes visual loss in almost one-third of diabetic patients. There is currently no treatment for the accompanying cystoid foveal changes.

Objectives: To assess the clinical outcome, i.e., change in visual acuity, in patients treated with steroids for long-standing diabetic macular edema with foveal cystoid changes.

Methods: In the ophthalmology department of a tertiary care university‑affiliated medical center and the ophthalmology service of a health management organization, 46 diabetic subjects (56 eyes) who had diabetic macular edema with cystoid foveal changes received one intravitreal injection of 4 mg triamcinolone acetonide.

Results: The mean baseline (pre‑injection) visual acuity of 0.21 increased to 0.31 and 0.48 at 1 and 3 months, respectively, after which it decreased to 0.33 at 6 months. The mean intraocular pressure was 15.07 mmHg at baseline, 15.83 at day 1, gradually rising to 17.16, 18.38 and 18.57 mmHg at 1, 3 and 6 months respectively. Three patients suffered immediate visual decline after the injection.

Conclusions: Intravitreal triamcinolone acetonide may be a therapeutic option for long‑standing diabetic macular edema with foveal cystoid changes.
 

Diabetic retinopathy is one of the leading causes of blindness worldwide.