Cerebral hemodynamic and metabolic profiles in fulminant hepatic failure: relationship to outcome.

The purpose of this retrospective study was to examine the potential role of cerebral hemodynamic and metabolic factors in the outcome of patients with fulminant hepatic failure (FHF). Based on the literature, a hypothetical model was proposed in which physiologic changes progress sequentially in five phases, as defined by intracranial pressure (ICP) and cerebral blood flow (CBF) measurements. Seventy-six cerebral physiologic profiles were obtained in 26 patients (2 to 5 studies each) within 6 days of FHF diagnosis. ICP was continuously measured by an extradural fiber optic monitor. Global CBF estimates were obtained by xenon clearance techniques. Jugular venous and peripheral artery catheters permitted calculation of cerebral arteriovenous oxygen differences (AVDO2), from which cerebral metabolic rate for oxygen (CMRO2) was derived. A depressed CMRO2 was found in all patients. There was no evidence of cerebral ischemia as indicated by elevated AVDO2s. Instead, over 65% of the patients revealed cerebral hyperemia. Eight of the 26 patients underwent orthotopic liver transplantation-all recovered neurologically, including 6 with elevated ICPs. Of the 18 patients receiving medical treatment only, all 7 with increased ICP died in contrast to 9 survivors whose ICP remained normal (P < 0.004). Hyperemia, per se, was not related to outcome, although it occurred more frequently at the time of ICP elevations. Six patients were studied during brain death. All 6 revealed malignant intracranial hypertension, preceded by hyperemia. In conclusion, the above findings are consistent with the hypothetical model proposed. Prospective longitudinal studies are recommended to determine the precise evolution of the pathophysiologic changes.     

The tuberous breast revisited.

BACKGROUND: The tuberous breast presents a problem for which many surgical solutions have been described. Current teaching describes how the tuberous breast deformity is the result of skin shortage as well as herniation of breast tissue through the nipple-areola complex. However, through careful clinical observation we now believe that the only abnormality present is herniation of breast tissue through the nipple-areola complex. METHODS: Using this principle, we have refined a one-stage surgical procedure that can be used to correct any type of tuberous breast deformity. Since 2001 we have performed our technique on a series of 13 tuberous breasts of widely varying appearances in eight patients (age 17-24 years) with a follow up varying between 3 and 56 months. Our new understanding of the tuberous breast deformity has also made it possible to develop an objective, reproducible method for defining the tuberous breast based on the degree of areola herniation. RESULTS: All patients reported high levels of satisfaction with the procedure. Assessment of the results by an independent panel of attending surgeons showed all results to be good/excellent. Moreover, the results have improved with time and no revisions have been needed. Our method of defining the tuberous breast (based on the ratio of areola herniation:areola diameter) enabled us to identify a cut-off to decide (objectively) when a breast was tuberous. This allowed us to anticipate when an areola reduction/tightening procedure would be necessary to avoid a 'double-bubble' deformity. CONCLUSION: We propose a one-stage surgical procedure which is applicable to all degrees of tuberous breast deformity. The results appear to confirm our theory that the only abnormality present in the tuberous breast is herniation of breast tissue through the nipple-areola complex. In patients with small breasts and a tuberous deformity, correction of the herniation changes the tuberous breast into a simple hypoplastic breast. The volume deficit can then be corrected by augmentation (if desired by the patient). In patients with sufficient breast volume, correction of the herniation alone will correct the deformity.     

Treatment of congenital cystic adenomatoid malformation-does resection in the early postnatal period increase surgical risk?

OBJECTIVE: The recent development of fetal ultrasonography has allowed for an increasing number of prenatal diagnoses for congenital cystic adenomatoid malformation (CCAM). However, the appropriate surgical timing of these patients has not been studied as of yet. The aim of this study is to suggest a safe strategy for the treatment of CCAM by identifying the relationship between the timing of surgery and postoperative outcome. METHODS: Between 1987 and 2003, 40 patients (28 males, 12 females) underwent surgical resection for CCAM. The mean age was 38.6+/-9.1 (2 days-13 years) months. CCAM was diagnosed by prenatal ultrasonography in eight patients. Early operations were performed in four out of the eight. Operation was deferred until 2-12 months of age for the remaining four patients. RESULTS: Type I CCAM was found in 20 patients, type II in 20 and no patient exhibited type III. Five patients had associated pectus excavatum anomaly. There were no cases of operative mortality. Seventeen minor postoperative complications developed in 16 patients (40.0%): prolonged chest tube drain in 10, wound infection in 4, and 1 case of pneumonia, empyema and pleural space, respectively. The average hospital stay was 11.8 (6-29) days. During the mean follow-up period of 67.5 months, one patient died of accidental aspiration 7 months after operation during the postoperative recovery course of Ravich operation for pectus excavatum. The remaining patients reported doing well with normal physical activity. All five patients who underwent surgery at the age of under 1 month did not exhibit increased postoperative morbidity. CONCLUSIONS: We concluded that surgery for CCAM could be safely performed in all age groups with satisfactory long-term outcomes. It is suggested that early elective surgical correction can be recommended for a patient whose diagnosis was made in utero.     

食管癌贲门癌术后胸胃排空障碍的临床分析

目的探讨食管癌贲门癌术后胸胃排空障碍的诱因、诊断和治疗。方法回顾性分析1990年1月-2003年12月我院施行1369例食管癌贲门癌切除术的病人临床资料。结果本组病例发生胸胃排空障碍17例,发生率1.24%,其中机械性胸胃排空障碍5例,功能性胸胃排空障碍12例,均发生于术后3～12d,再次手术治疗5例;治愈16例,死亡1例。结论上消化道造影、胃镜是鉴别机械性胃排空障碍和功能性胃排空障碍的重要方法,对食管癌术后机械性胃排空障碍应采取手术治疗,而功能性胃排空障碍采取保守治疗多能好转。     

对耳轮过度前突畸形的整复

对耳轮过度前突为对耳轮的角度过锐，致使耳轮的位置相应后移，表现为与招风耳完全相反的畸形。畸形虽不十分明显，但影响美观。自１９９２年４月开始应用患侧耳廓软骨和耳后皮瓣对５例患者８只外耳进行治疗得到满意效果。认为文中所述方法是矫正对耳轮过度前突畸形的良好方法。     

Effects of blood coagulation factor XIII on the development of experimental cerebral aneurysms in rats

Pathological and experimental studies have shown that cerebral aneurysms develop in part as a result of injury to the blood vessel wall. One of the peculiar aspects of aneurysm development is a defective proliferative or healing response to such injury. To examine this phenomenon, blood coagulation Factor XIII, which is known to enhance the healing process of wounds in general, was given to rats to induce experimental cerebral aneurysms. The rats were subjected to ligation of one common carotid artery and induction of hypertension, and were fed beta-aminoproprionitrile. Two weeks thereafter, Factor XIII was injected intravenously daily for 5 days (10 U/100 gm body weight/day). Twelve days after the start of Factor XIII injections, the rats were sacrificed and examined under light and electron microscopy. In seven of 12 bifurcations which developed small aneurysms, prominent intimal thickening was observed in the aneurysm lumen. In the most advanced cases, the aneurysm lumen was completely filled with proliferated smooth-muscle cells and collagen. In five of nine bifurcations that showed no aneurysm development, apparent intimal thickening was found at the site where aneurysms might be expected to grow. In the group of rats studied for induction of cerebral aneurysms but not given Factor XIII, none of 11 bifurcations with or without aneurysms showed such intimal thickening. The results indicated that the proliferative response at the sites of aneurysm development was modified by exogenous Factor XIII.     

High susceptibility of analbuminemic rats to neurogenic tumor induction by transplacental administration of N-ethyl-N-nitrosourea.

The susceptibilities of Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR) to N-ethyl-N-nitrosourea (ENU) were compared. In Experiment I, the rats were given daily subcutaneous injections of 10 mg/kg of ENU for a week from 4 weeks of age. In Experiment II, mother rats were given a single subcutaneous injection of 60 mg/kg of ENU on day 17 of pregnancy and tumor development in their offspring was examined. In Experiment I, the incidence of neurogenic tumors was slightly, but not significantly, higher in NAR than in control rats. In Experiment II, the incidence of total tumors including neurogenic tumors was significantly higher in NAR (40/43, 93.0%) than in SDR (13/61, 21.3%). NAR showed particularly high susceptibility to induction of neurogenic tumors (34/43, 79.1%) and renal tumors (15/43, 34.9%). In an attempt to elucidate the underlying mechanisms of the increased susceptibility of NAR to ENU, O6-ethylguanine, a major premutagenic ethylated DNA adduct, was quantitated in fetal brain DNA of NAR and SDR after a pulse exposure to 60 mg/kg ENU. No significant difference in the initial formation or subsequent repair of O6-ethylguanine was observed in the two strains, indicating that abnormality at some later stage(s) of chemical carcinogenesis may lead to the increased susceptibility of NAR to induction of neurogenic tumors.