MANAGEMENT OF LUNG ABSCESS WITH PERCUTANEOUS CATHETER DRAINAGE

Percutaneous catheter drainage was used to treat 12 among 34 cases of lung abscesses, who were refractory to medical therapy, severely ill and high risk cases for surgery. A complete clinical and radiological recovery was achieved in all the cases who underwent catheter drainage, thereby obviating the need for surgery. None of the cases had catheter or procedures related complications. From this study it is inferred that percutaneous transthoracic catheter drainage is a safe and an effective modality of therapy for patients with lung abscess in whom medical therapy has failed and those who are unsuitable for surgery.KEYWORDS: Lung abscess, Percutaneous catheter drainage     

PREVALENCE OF MICROALBUMINURIA IN NON-INSULIN-DEPENDENT DIABETES MELLITUS

The prevalence of microalbuminuria was assessed in 50 patients of non-insulin dependent diabetes mellitus. The mean age of patients was 52.1 ± 11.6 years and the duration of diabetes was 8.3 ± 6.8 years. Twenty (40%) patients had microalbuminuria. Microalbuminuria was more common in patients with a longer duration of diabetes (more than 5 years), a poor glycaemic control, and higher systolic blood pressure.KEY WORDS: Microalbuminuria, Diabetes mellitus, Diabetic nephropathy, Chronic renal failure     

Reconstruction of Complex Abdominal Wall Defects

Introduction

Reconstruction of large abdominal wall defects not amenable to primary closure remains a challenging problem. These defects result from trauma, previous surgery, infection and tumour resection. The primary objectives of abdominal wall reconstructions are to protect abdominal contents and provide functional support. The abdominal wall reconstruction aims at providing basic component parts, i.e. skin, soft tissue and fascia. For large soft tissue defects, pedicled or free flap closure can be used. In clean wounds, fascial replacement is accomplished with synthetic mesh provided there is adequate soft tissue coverage.

Methods

We treated a total of 20 consecutive patients with complex abdominal wall defects utilizing various reconstructive procedures. There were 15 males (75%) and 5 females (25%). The aetiology included dehiscence of laparotomy wounds in eight (40%), following ablative surgery for malignant tumours in seven (35%), trauma in three (15%) and congenital defects in two (10%) cases. The reconstructive procedures consisted of onlay prolene mesh in seven (35%), Gore-Tex (PTFE) dual mesh both as inlay and onlay in five (25%), facial partition release technique in three (15%), inlay prolene mesh covered with omentum and split skin graft in two (10%), inlay prolene mesh covered with expanded skin in two (10%), and Gore-Tex dual mesh covered with latissimus dorsi myocutaneous flap in one (5%) case. Postoperatively none developed mesh infection or extrusion. Three patients with malignant aetiology received postoperative radiotherapy. During follow up, one patient developed ventral hernia cephalad to the repair and one died due to recurrence of abdominal wall malignancy.

Conclusion

The reconstruction of an abdominal wall defect requires a comprehensive plan of preoperative and post operative care of the patient and aims toward restoration of abdominal structural integrity by a variety of procedures. The use of new biomaterials and tissue expanders provides reliable and durable abdominal wall closure along with good aesthetic results.Key Words: Abdominal wall defect, Mesh repair, Abdominal wall reconstruction     

恩替卡韦与拉米夫定治疗HBeAg阴性慢性乙型肝炎的对照研究

Ⅱ期临床试验已经证实恩替卡韦是一种治疗HBeAg阴性慢性乙型肝炎有效和可选择的抗病毒药物。采用双盲法将648例未曾接受过核苷类药物治疗的HBeAg阴性慢性乙型肝炎随机分配进入恩替卡韦（0．5mg／d）治疗组或拉米夫定（100mg／d）治疗组，疗程至少52wk。     

Rapid shrinkage of rat striatal extracellular space after local kainate application and ischemia as recorded by impedance

Early changes in tissue extracellular space following exposure to the excitotoxin kainate in the striatum were compared to those following cardiac arrest of rats anesthetized by chloral hydrate. Tissue extracellular space was monitored by impedance measurements. The possible role of voltage-sensitive Na channels and energy metabolism was studied by local and systemic application of tetrodotoxine (TTX) and glucose, respectively. After both kainate intoxication and cardiac arrest the extracellular space (normally about 20%) became less than one-half within 15 min. TTX caused a delay in the effect of cardiac arrest, and a slight attenuation of that of kainate. Glucose was ineffective in both preparations. Parallel to a decrease in the extracellular space whole tissue Na/K ratio increased. These experiments show that excitotoxins and cardiac arrest cause similar (and not additive) changes in the extracellular space and that these changes are not mediated by Na channels. In cardiac arrest the onset of the extracellular space alterations is triggered by Na+ influx, thus presumably by neurotransmitter release. It is suggested that most (if not all) currently described protective measures against ischemic, hypoxic, or hypoglycemic brain damage are based on a prolongation of the time of onset leading to cell depolarization, rather than suppressing damaging processes during depolarization.     

Cerebral cation shifts in hypoxic-ischemic brain damage are prevented by the sodium channel blocker tetrodotoxin

We investigated the effect of the sodium channel blocker, tetrodotoxin, in two animal models of brain pathology. In the first, an acute model, we recorded the interstitial brain potential in the striatum of rats after cardiac arrest. The time of deflection of this potential, an indication of changes in cerebral cation concentrations, was determined in control rats, and in rats pretreated with intrastriatal tetrodotoxin. In control rats a deflection of the brain potential was noted 2 min after cardiac arrest; tetrodotoxin pretreatment delayed this deflection to about 5 min. The second, a survival model, was based on the Levine preparation in rats. A combination of ischemia and hypoxia produced unilateral, cerebral infarcts, which were characterized by a decrease of brain [K+], and by increases of [Ca2+] and [Na+] and thus of the Na+:K+ ratio. Data on the cation shifts, determined by chemical assay methods, were complemented by those of more conventional methods of assessment of brain damage, such as the determination of survival, of Evans blue staining, and of brain water content. Cation shifts could be prevented locally by tetrodotoxin. In conclusion, the drug can, at least partially, prevent the detrimental effects of an ischemic insult. In addition, our results showed that protective effects observed in the acute model may sometimes offer an indication of the effects to be expected in the survival model. Furthermore, the effect of tetrodotoxin on the brain potentials in the acute model showed that its protective action in the survival model may be brought about by delaying cell depolarization and by shortening the actual duration of the depolarized state. We conclude that Na+ influx and, consequently, neurotransmission may play a crucial role in the development of cerebral damage.     

Role of phosphoinositide metabolism in functional antagonism of airway smooth muscle contraction by beta-adrenoceptor agonists

Histamine and the muscarinic agonists, methacholine, oxotremorine, and McN-A-343, were used to contract guinea-pig tracheal smooth muscle preparations. Cumulative dose-relaxation curves with isoprenaline were performed subsequently. In addition, the concentration-dependent induction of phosphoinositide metabolism by the contractile agonists was measured in bovine tracheal smooth muscle. All agonists were found to induce a decrease of the apparent affinity of isoprenaline and a loss of relaxation, depending on the concentration and type of contractile agonist used. The differential effects of the contractile agonists, especially at higher and supramaximal concentrations, on these beta-adrenergic parameters could be explained by differences in phosphoinositide metabolism.