Smoke inhalation injury: diagnosis and respiratory management

Smoke inhalation is a significant comorbid factor following major thermal injury. Smoke exposure is only a trigger for the sequence of events responsible for the development of inhalation injury. Noxious chemicals generated by incomplete combustion injure the exposed bronchoepithelium and stimulate the release of chemical mediators that cause a progressive inflammatory process. Airway inflammation and pulmonary edema impair gas exchange and increase the susceptibility to pulmonary infection. Earlier diagnosis and treatment of inhalation injury is an important element to improve the clinical course of severe burn patients. The American Burn Association, however, recently concluded that there are insufficient data to support a treatment standard for the diagnosis of inhalation injury. At present, the diagnosis of inhalation injury is supported by the combination of history, physical examination, bronchoscopy, and laboratory findings For accurate diagnosis of inhalation injury, helical CT scanning and examination to detect activated leukocytes in bronchoalveolar lavage fluid may be warranted. In the respiratory management of inhalation injury, repeated removal of pseudomembrane by fiberoptic bronchoscopy and the use of adequate PEEP to avoid airway obstruction are essential. High-frequency percussive ventilation can be a suitable mode of ventilation for inhalation injury.     

Bladder outlet obstruction accelerates bladder carcinogenesis

OBJECTIVE

To examine the correlation between partial bladder outlet obstruction (PBOO) and bladder carcinogenesis.

MATERIALS AND METHODS

Female Wistar rats (6 weeks old) were divided into three groups of 10 each: group 1 was exposed to n‐butyl‐n‐butanol nitrosamine (BBN, a carcinogen) in drinking water for 8 weeks; group 2 had PBOO induced surgically after exposure to BBN for 8 weeks; group 3 had a sham operation and the rats drank normal water (control group). After 20 weeks, all of the rats were killed humanely and their bladders analysed.

RESULTS

There were no significant differences in body weight among the groups. The bladder weight of group 2 was significantly greater than either group 1 or group 3. Histopathologically, bladder smooth muscle hypertrophy was the major cause of the increased bladder weight for group 2. In group 2 there were increases in bladder wall thickness and many nipple‐shaped urothelial tumours. Basic fibroblast growth factor and hypoxia‐inducible factor‐1α expression were significantly greater in group 2 than in groups 1 and 3.

CONCLUSIONS

Exposure of the bladder to carcinogens during bladder hyperplasia and hypertrophy induced by PBOO results in a greater incidence of superficial bladder carcinoma.     

Cerebral aneurysms: evaluation with three-dimensional CT angiography.

PURPOSETo evaluate the usefulness of three-dimensional CT angiography (CTA), in which contrast material is used to create reformations of dynamic scans, in the diagnosis and the preoperative evaluation of cerebral aneurysms.METHODSWe used 3-D CTA to examine 65 patients with suspected or angiographically verified cerebral aneurysms. A blind study was performed to evaluate the diagnostic accuracy of 3-D CTA for cerebral aneurysms with the use of conventional angiography as the reference standard.RESULTSIn 50 patients, conventional angiography revealed 73 cerebral aneurysms ranging from 2 to 32 mm in maximum diameter. Three of the 73 cerebral aneurysms were located outside the imaging volume of 3-D CTA. The sensitivities of the two neuroradiologists for the remaining 70 aneurysms were 67% and 70%, respectively. Although 3-D CTA depicted cerebral aneurysms 5 mm or larger with good accuracy, it was less useful for the detection of smaller aneurysms. For the evaluation of giant aneurysms, this technique elucidated the relationships among the aneurysm, surrounding arteries, and neighboring bone structure.CONCLUSIONThree-dimensional CTA is useful for the diagnosis of cerebral aneurysms with diameters of 5 mm or more. This technique is especially useful in the preoperative evaluation of giant aneurysms.     

Targeted biopsy based on ADC map in the detection and localization of prostate cancer: A feasibility study

Purpose:

To investigate the feasibility of targeted biopsy based on an apparent diffusion coefficient (ADC) map in the detection and localization of prostate cancer.

Materials and Methods:

This study included 288 consecutive patients with high or increasing serum prostate‐specific antigen (PSA) levels who underwent prostatic magnetic resonance imaging (MRI) examination with an ADC map. Four core‐targeted biopsies of low ADC lesions were performed under transrectal‐ultrasound guidance with reference to ADC map. The positive predictive values (PPVs) of low ADC lesions were calculated and compared for the peripheral zone (PZ), transition zone (TZ), and anterior portion, respectively. Comparisons of ADC values and sizes between malignant and nonmalignant lesions were also performed.

Results:

A total of 313 low ADC lesions were detected in 195 patients and sampled by targeted biopsies. The PPVs were 55.3% (95% confidence interval [CI]: 50–61) in total, 61.0% (95% CI: 53–69) for PZ, 50.6% (95% CI: 43–58) for TZ, and 90.9% (95% CI: 81–100) for the anterior portion. The most common nonmalignant pathology of low ADC lesions was hyperplasia, followed by chronic prostatitis. There were significant differences in ADC values and sizes between malignant and nonmalignant low ADC lesions.

Conclusion:

Targeted biopsies could be capable of detecting cancers well wherever they may be in the prostate, although the PPVs varied depending on the location of low ADC lesions. J. Magn. Reson. Imaging 2013;37:1168–1177. © 2012 Wiley Periodicals, Inc.     

Transarterial internal radiation therapy with I-131 lipiodol for multifoca hepatocellular carcinoma: Immediate and long-term results

Transarterial internal radiation with I-131 Lipiodol (TAIR) was performed in 21 patients with multifocal hepatic carcinoma. Eight patients were treated by TAIR alone and 13 by combination of TAIR and intraarterial infusion ofcis-diamminedichloroplatinum (CDDP) and/or adriamycin mitomycin C oil suspension (ADMOS). TAIR was found effective immediately and long-term. Serum α-fetoprotein (AFP) levels dropped to 50% or less in 7 of 14 patients. Eleven of 21 patients (52%) showed 50% or greater decrease in tumor size. The overall 1-year survival rate was 43% and 67% in patients who received 50 Gy or greater tumor dose. Lipiodol distribution pattern of the tumor indicated some difference in the prognosis between the scattered pattern and solid pattern. The solid pattern showed a statistically significant better survival rate. Patients treated with TAIR alone versus those treated with TAIR and chemotherapy showed no difference in their survival rate.     

NPHS2 mutations in sporadic steroid-resistant nephrotic syndrome in Japanese children

Podocin is an integral membrane protein encoded by NPHS2, which is mapped to 1q25-31 and is exclusively expressed in glomerular podocytes. NPHS2 mutations are responsible for autosomal recessive familial steroid-resistant nephrotic syndrome (SRNS) with minor glomerular abnormalities or focal segmental glomerulosclerosis (FSGS), which is characterized by early childhood onset (age less than 6 years) and rapid progression to chronic renal insufficiency. This gene mutation is also responsible for an adolescent/adult onset form of autosomal recessive familial FSGS with heavy proteinuria. It has been demonstrated that sporadic SRNS and heavy proteinuria are also due to NPHS2 gene mutations. We isolated genomic DNA from 36 Japanese children with chronic renal insufficiency caused by SRNS or heavy proteinuria, and analyzed all eight exons and exon-intron boundaries of NPHS2 using the polymerase chain reaction and direct sequencing. The age at onset of disease was 3.9+/-0.5 years. There were 29 patients with SRNS and 7 with heavy proteinuria without nephrotic syndrome at the onset, but all patients developed chronic renal insufficiency 4.6+/-0.8 years after the onset. A new homozygous missense variant of NPHS2, G34E (G101A) in exon 1, was detected in 1 of 36 patients. However, this homozygous variant was also found in 1 of 44 normal controls, suggesting that the mutation is a polymorphism. Two silent variants (T954C and A1038G) in exon 8 of this gene were also identified in some of the patients and normal controls, indicating that the silent variants are also polymorphisms. There was no significant difference in the genotypic and allelic frequencies of T954C and A1038G polymorphisms between the patients and normal controls. In conclusion, NPHS2 gene mutations are not a major cause of chronic renal insufficiency caused by sporadic SRNS or heavy proteinuria in Japanese children.     

Comparison of grey matter and metabolic reductions in frontotemporal dementia using FDG-PET and voxel-based morphometric MR studies

Purpose  The aim of this study was to investigate the regional differences between the morphologic and functional changes in the same patients with frontotemporal dementia (FTD) using statistical parametric mapping and voxel-based morphometry (VBM). Methods  Thirteen FTD patients (mean age, 64.9 years old; mean MMSE score, 17.7), 20 sex-matched Alzheimer’s disease (AD) patients (mean age, 65.0 years old; mean MMSE score, 17.5), and 20 normal volunteers (mean age, 65.2 years old; mean MMSE score, 29.0) underwent both [¹⁸F]FDG positron emission tomography and three-dimensional spoiled gradient echo MRI. Statistical parametric mapping was used to conduct a VBM analysis of the morphologic data, which were compared voxel by voxel with the results of a similar analysis of glucose metabolic data. Results  FTD patients showed decreased grey matter volume and decreased glucose metabolism in the frontal lobe and anterior temporal lobe. In addition, there was a clear asymmetry in grey matter volume in FTD patients by the VBM analysis while the glucose metabolic data showed little asymmetry. In AD patients, glucose metabolic reduction occurred in the bilateral posterior cingulate gyri and parietal lobules while grey matter density decreased the least in the same patients. Conclusion  In FTD, metabolic and morphologic changes occur in the bilateral frontal lobe and temporal lobe with a limited asymmetry whereas there was considerable discordance in the AD group.     

Clinical impact of the callosal angle in the diagnosis of idiopathic normal pressure hydrocephalus

The utility of measuring the corpus callosal angle (CA) for the diagnosis of idiopathic normal pressure hydrocephalus (INPH) was investigated. Three-dimensional magnetic resonance imaging (MRI) was performed in 34 INPH patients, 34 Alzheimer’s disease (AD) patients, and 34 normal control (NC) subjects. Measurement of the CA on the coronal MR images of the posterior commissure perpendicular to the anteroposterior commissure plane was performed for all subjects. The CA of the INPH group (mean ± SD, 66 ± 14°) was significantly smaller than those of the AD (104 ± 15°) and NC (112 ± 11°) groups. When using the threshold of the mean − 2SD value of the NC group (= 90°), an accuracy of 93%, sensitivity of 97%, and specificity of 88% were observed for discrimination of INPH from AD patients. Measuring the CA helps in differentiating INPH patients from AD and normally aged subjects.     

Mild hypercapnia induces vasodilation via adenosine triphosphate-sensitive K+ channels in parenchymal microvessels of the rat cerebral cortex

BACKGROUND: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex. METHODS: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 microm) was monitored using computerized videomicroscopy. RESULTS: During contraction to prostaglandin F2alpha (5 x 10(-7) m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10(-6) m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10(-7) m) as well as the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (10(-4) m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10(-8) to 3 x 10(-7) m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide. CONCLUSION: These results suggest that in parenchymal microvessels of the rat cerebral cortex, decreased pH corresponding with hypercapnia, but not hypercapnia itself, contributes to cerebral vasodilation produced by carbon dioxide and that ATP-sensitive K+ channels play a major role in vasodilator responses produced by mild hypercapnia.