Comparison of anatomical and visual outcomes following different anti-vascular endothelial growth factor treatments in subretinal neovascular membrane secondary to type 2 proliferative macular telangiectasia

Graefe's Archive for Clinical and Experimental Ophthalmology - To evaluate central macular thickness (CMT), subfoveal choroidal thickness (SFCT), and visual outcomes following different...     

The effect of metoclopramide on gastric emptying in traumatic brain injury.

OBJECTIVE: Gastric paresis in traumatic brain injury (TBI) hinders the effectiveness of enteral support in this patient group. In this study we have investigated the effect of metoclopramide on gastric emptying in TBI patients. METHOD: In this prospective, randomized, controlled, double-blind study, 19 TBI patients with Glasgow Coma Scale scores of 3-11 were included. In all patients, enteral nutrition was commenced with a nasogastric feeding tube within 48 hours of trauma. Patients were randomized into two groups. In the metoclopramide (M) group, 10 mg metoclopramide was delivered intravenously three times daily for 5 days. In the control (C) group, an equal volume of saline was administered. Besides demographics, gastric emptying according to a paracetamol absorption test at days 0 and 5, time to reach target nutritional requirements, gastric residues, intolerance to feeding, nutritional complications, and clinical outcomes were recorded for each patient. RESULTS: The gastric residue rates were 2.7+/-7.4 mL and 8.1+/-17.7 mL per 100 patient days for groups C and M respectively (p=0.408). Similarly, feeding intolerance and complication rates did not significantly differ between groups C and M, (respectively p=0.543 and 0.930). Gastric emptying parameters also were similar between the study groups. CONCLUSION: We were unable to document any advantage to using metoclopramide in TBI patients. Simple intragastric enteral feeding with close monitoring of the possible complications seems to be sufficient with acceptable morbidity rates.     

Cerebellar abscess and syringomyelia due to isoniazid-resistant Mycobacterium tuberculosis.

A 19-year-old immunocompetent man was admitted to hospital with diplopia, nausea, vomiting and change in mental status. The patient had a history of tuberculous meningitis that was diagnosed at another hospital 6 months before the present admission, and at that time anti-tuberculosis treatment was initiated using a first-line drug combination. A computed tomography (CT) scan of the brain revealed non-communicating hydrocephalus. A ventriculo-peritoneal shunt was inserted surgically. Two months later, the patient was hospitalized again for fever, dysphagia and left hemiparesis. At that time, his cranial CT findings were within normal limits; however, magnetic resonance imaging (MRI) revealed an irregular multilocular peripheral contrast-enhancing lesion in the posterior fossa. The abscess was surgically drained. The presence of acid-fast bacilli in the abscess material was demonstrated by Ziehl-Neelsen staining. Mycobacterium tuberculosis grew on Lowenstein-Jensen culture medium, and the strain was found to be resistant to isoniazid. One month after the operation, the patient became quadriparetic. Cervical MRI revealed a cervico-thoracic syringomyelitic cavity, after which a syringoperitoneal shunt was placed. Treatment with four drugs was continued for 10 months, and then treatment with three drugs for a total period of 18 months. The patient recovered, with residual quadriparesis. Even though very rare, isoniazid-resistant M. tuberculosis may be the causative agent of progressive tuberculosis.     

Glomerular changes in BK virus nephropathy

This study seeks to define the glomerular changes that are associated with human BK virus nephropathy (BKVN). It is based on histopathologic review of 124 biopsies showing light-microscopic changes of viral nephropathy. The diagnosis of BKVN was confirmed by immunohistochemistry or by in situ hybridization. Histological lesions were scored by the Banff 97 criteria for renal allograft pathology and were correlated with clinical parameters. Viral cytopathic effect in the parietal Bowman's capsular epithelium was seen in 21/124 (17%) biopsies. Immunohistochemistry showed infection of Bowman's capsular epithelium in an additional 15/124 (12%) biopsies. Crescents were found in 15/124 (12%) samples. Glomerulitis exceeding grade Banff g1 was only occasionally shown (4/124=3% biopsies). Other pathologic lesions documented include mild increase in mesangial matrix in 23% biopsies, aneurysmal dilatation of glomerular capillaries in 28%, ischemic glomerulopathy in 62%, and chronic transplant glomerulopathy graded as mild (cg1) in 62% of biopsies and as moderate (cg2) in 2/124 (1.9%) biopsies. These findings show that infection of the glomerular epithelium cells can occur in a subset of patients with BKVN, most often in biopsies with high viral load in the tubular epithelium. Isolated crescents can occur in BKVN biopsies, but rapidly progressive glomerulonephritis is not observed. Two biopsies showed electron-dense deposits on ultrastructural examination, but a cause and effect relationship to BK virus infection could not be established.     

Clinical and immunological studies in a case of selective complete C1q deficiency

A 10-year-old male with recurrent skin lesions and chronic infections was found to have a selective deficiency of C1q after functional analysis of all complement components. The addition of highly purified human C1q to the patient's serum restored C1 activity, indicating the presence of C1r and C1s and the absence of C1q. Titration of highly purified C1q with patient serum as a source of C1r and C1s resulted in a linear dose-response curve. The undetectable CH50 activity temporarily returned to normal within a few hours of plasma infusion, but the C1 titres were still only 1–3% of normal. Following plasma administration, the peak of C1q activity was reached after 30 min and returned to undetectable levels within 24 hr. The patient serum was not anti-complementary when incubated with normal serum. Nine members of the family, including the parents and two healthy siblings, were subjected to complement studies and HLA typing. The C1 titres and CH50 activity were found to be normal in all except the paternal grandmother who showed reduced levels of all the complement components. There was no linkage for the gene of C1q deficiency and HLA antigens. Among the various laboratory studies performed, anti-smooth muscle antibodies, immune complexes and anti-HBsAg antibody were found to be positive. The child died of a disease compatible with septicaemia. Post mortem tissue studies by light, fluorescent and electron microscopy have shown the presence of a mesangioproliferative glomerulonephritis.     

Isolated coarctation of the aorta in the fetus: A diagnostic challenge

Isolated coarctation of the aorta (CoA) is estimated by the Centers for Disease Control and Prevention to account for 4%–6% of all congenital heart disease (CHD) in the United States, with a reported prevalence of ~4 per 10 000 live births. Prenatal recognition of coarctation is important as it may improve neonatal survival and reduce morbidity. However, despite advances in imaging and the trend toward detailed aortic arch assessment as part of a comprehensive fetal echocardiogram, isolated CoA may still elude prenatal detection, with potentially lethal consequences if the diagnosis is not suspected and the patent ductus arteriosus (PDA) closes spontaneously in postnatal life. The purpose of this review is to outline the methods of antenatal aortic arch evaluation in the current era, discuss “red flags” that raise the suspicion for CoA, including associated anomalies and serve as a repository of the most up to date information regarding its diagnosis in utero and its perinatal management. Other aortic arch abnormalities, such as interrupted aortic arch, or CoA associated with complex single ventricles, are not included in this review.