Acute epidural hematoma: an analysis of factors influencing the outcome of patients undergoing surgery in coma

Mortality due to epidural hematoma is virtually restricted to patients who undergo surgery for that condition while in coma. The authors have analyzed the factors influencing the outcome of 64 patients who underwent epidural hematoma evacuation while in coma. These patients represented 41% of the 156 patients operated on for epidural hematoma at their centers after the introduction of computerized tomography (CT). Eighteen patients (28.1%) died, two (3.1%) became severely disabled, and 44 (68.8%) made a functional recovery. The mortality rate for the entire series was 12%, significantly lower than the 30% rate observed when only angiographic studies were available. A significant correlation was found between the final result and the mechanism of injury, the interval between trauma and surgery, the motor score at operation, the hematoma CT density (homogeneous vs. heterogeneous), and the hematoma volume. The patient's age, the course of consciousness before operation (whether there was a lucid interval), and the clot location did not correlate with the final outcome. The mortality rate was significantly higher in patients operated on within 6 hours or between 6 and 12 hours after injury than in those undergoing surgery 12 to 48 hours after injury. Compared with the patients operated on later, the patients undergoing surgery in the early period were, on the average, older and had more rapidly developing symptoms, more pupillary changes, lower motor scores at surgery, larger hematomas, a higher incidence of mixed CT density clots, more severe associated intracranial lesions, and higher postoperative intracranial pressure (ICP). The mechanism of trauma seems to influence the course of consciousness before and after surgery. Passengers injured in traffic accidents had a lower incidence of a lucid interval and longer postoperative coma than patients with low-speed trauma, suggesting more frequent association of diffuse white matter-shearing injury. The duration of postoperative coma correlated with the morbidity rate in survivors. Forty-eight patients (75%) had one or more associated intracranial lesions, and 70% of these required treatment for elevation of ICP after hematoma evacuation. An ICP of over 35 mm Hg strongly correlated with poor outcome; administration of high-dose barbiturates was the only effective means for lowering ICP in nine of 15 patients who developed severe intracranial hypertension after surgery. This study attempts to identify patients at greater risk for presenting postoperative complications and to define a strategy for control CT scanning and ICP monitoring.     

Carcinoma of the hepaticopancreatic ampullar region: role of US

Hepaticopancreatic ampullar tumors are so called because they are located at the confluence of the bile duct, pancreatic duct, and duodenum. Jaundice is an early sign of the disease and often leads to early diagnosis and favorable prognosis compared with other tumors that occur in this area. Of eight patients who underwent ultrasound (US) in the past 5 years, six (75%) were found to have tumor. The sizes of the tumors ranged from 1.6 to 2 cm. An intraluminal, polypoid mass in the distal part of the common bile duct was seen in four patients. In the other two patients, a sharply delineated mass gave rise to abrupt termination of the distal duct. Improved US resolution, more experience with this modality, and accurate diagnosis of these tumors with US will contribute to improved detection and prompt treatment.     

Paget's disease primarily involving the scrotum

Three cases of Paget's disease primarily involving the scrotum are reported. One case exhibited positive staining for prostate specific antigen (PSA) and was associated with an underlying, invasive poorly differentiated adenocarcinoma of unknown primary. The other cases were not associated with any underlying or visceral malignancy. The literature on Paget's disease primarily involving the scrotum including clinical presentation, differential diagnosis, treatment, prognosis, and possible histogenetic mechanisms of this disease is discussed.     

Determinants of dietary intake during childhood diarrhea and implications for appropriate nutritional therapy

Diarrheal diseases have a well recognized negative effect on children's growth, probably due in part to reduced dietary intake during illness. Previous studies have shown that the effects of diarrhea on dietary intake are greater among hospitalized children than among those observed in their homes. Breast milk intake does not change during diarrhea, however, so breast-fed children are less likely to reduce their total energy and nutrient intakes. Recent analyses of clinical studies found that acidosis and dehydration were most closely associated with reduced dietary intake of hospitalized patients. The implications of these and other studies for the dietary management of patients during and after diarrhea are discussed.     

Murine CD9 is the receptor for pregnancy-specific glycoprotein 17.

Pregnancy-specific glycoproteins (PSGs) are a family of highly similar secreted proteins produced by the placenta. PSG homologs have been identified in primates and rodents. Members of the human and murine PSG family induce secretion of antiinflammatory cytokines in mononuclear phagocytes. For the purpose of cloning the receptor, we screened a RAW 264.7 cell cDNA expression library. The PSG17 receptor was identified as the tetraspanin, CD9. We confirmed binding of PSG17 to CD9 by ELISA, flow cytometry, alkaline phosphatase binding assays, and in situ rosetting. Anti-CD9 monoclonal antibody inhibited binding of PSG17 to CD9-transfected cells and RAW 264.7 cells. Moreover, PSG17 binding to macrophages from CD9-deficient mice was significantly reduced. We then tested whether PSG17 binds to other members of the murine tetraspanin family. PSG17 did not bind to cells transfected with CD53, CD63, CD81, CD82, or CD151, suggesting that PSG17-CD9 binding is a specific interaction. We have identified the first receptor for a murine PSG as well as the first natural ligand for a member of the tetraspanin superfamily.     

Reversibility of calcitriol-induced medial artery calcification in rats with intact renal function.

VC is an important clinical entity; however, very little information is available on its resolution. Induction and regression of calcitriol-induced VC was studied in 47 rats. After calcitriol withdrawal, there was a relatively rapid regression of VC mediated by an active cellular process. INTRODUCTION: Vascular calcifications (VCs) represent an important risk factor for cardiovascular death. Although VCs are prevalent in relevant diseases (e.g., chronic kidney disease, osteoporosis, diabetes), the reversibility of extraskeletal calcifications is an unresolved issue. This study was conducted to investigate (1) the in vivo effect of calcitriol on VC and (2) whether calcitriol-induced VC would regress after suppression of calcitriol treatment. MATERIALS AND METHODS: The calcifying effect of calcitriol was studied in four groups of rats (n = 8) that received calcitriol (1 mug/kg, IP) for 2, 4, 6, and 8 days. The reversibility of VC was studied in three additional groups (n = 5) treated with 1 mug/kg of calcitriol for 8 days that were subsequently killed 1, 2, and 9 weeks after the last calcitriol dose. Aortic VC was assessed by histology and by quantification of aortic calcium and phosphorus content. The aortic wall was studied by histology and immunohistochemistry. Statistical analysis was performed by ANOVA and t-tests. RESULTS: Calcitriol administration resulted in a time-dependent induction of VC, with aortic calcium and phosphorus being significantly increased at 6 and 8 days. Treatment with calcitriol for 8 days resulted in massive medial calcification of the aorta with a 10- to 30-fold increase in the aortic Ca and P content. After suppressing calcitriol administration, a progressive decrease in von Kossa staining and aortic Ca (from 32.8 +/- 2.5 to 9.3 +/- 1.8 mg/g of tissue, p < 0.001) and P (from 11.9 +/- 1.2 to 2.7 +/- 1.8 mg/g of tissue, p = 0.001) content was evidenced. Histology of the aortic wall showed monocytes adhered to the aortic endothelium and macrophages involved in the reabsorption of calcium deposits. CONCLUSIONS: Our results show that calcitriol treatment induces time-dependent VC. After calcitriol withdrawal, VC regress rapidly with aortic calcium and phosphorus decreasing by 75% in the course of 9 weeks. An active cellular process seems to be involved in regression of VC.     

Severe cerebral edema in a patient with anasarca and hypernatremia.

We describe a woman whose fatal post-liver transplantation cerebral edema was unexpected and of unusual pathogenesis. Her severe cerebral edema is of considerable pathophysiologic interest: 1) it developed in the setting of marked anasarca and persistent hypernatremia, and 2) although hepatic function was poor, it was not considered sufficiently deranged to induce cerebral edema. Furthermore, there was no histologic evidence of hepatic rejection or antemortem hepatic necrosis. We postulate that an impairment of the blood brain barrier in association with a degree of hepatic dysfunction insufficient by itself to cause cerebral edema permitted the brain interstitial fluid volume to increase pari passu with ECF expansion. Cytotoxic cerebral edema and vascular engorgement may also have contributed to a life-threatening increase in intracranial pressure.     

Prophylactic laparoscopic-assisted total gastrectomy for hereditary diffuse gastric cancer.

BACKGROUND: Ten percent of gastric cancer (GC) cases are familial, with one third resulting from a mutation in the tumor suppressor gene CDH1. Loss of this important structure can result in hereditary diffuse gastric cancer (HDGC), which carries a high mortality if early diagnosis is not made. Despite its clear genetic origin, optimal management of HDGC family members is controversial, as the utility and efficacy of current cancer screening programs for mutation carriers are unproven. METHODS: A 53-year-old Caucasian woman was initially seen for genetic screening because multiple family members had mutations of the CDH1 gene. Her pedigree analysis demonstrated 4 generations of gastric cancer, and 2 of the generations carried the CDH1 germline mutation, consistent with HDGC. At endoscopy, the patient's gastric mucosa was normal and random biopsies were also normal. The patient underwent a laparoscopic total gastrectomy. RESULTS: The gross examination of her stomach appeared normal. On histologic examination, however, the stomach was found to have diffuse (signet ring cell) adenocarcinoma in-situ with 11 microscopic foci of invasive adenocarcinoma limited to the lamina propria. CONCLUSION: Our case is the first reported prophylactic total gastrectomy utilizing a laparoscopic approach, and it highlights the importance of taking a thorough family history and obtaining a pedigree analysis. Endoscopic screening in HDGC cannot rule out diffuse GC, because the stomach and biopsies can be normal despite the presence of adenocarcinoma. Therefore, our case supports the recommendation for prophylactic gastrectomy in HDGC.     

Defining the Role of Surgery for Primary Gastrointestinal Tract Melanoma

Objective The objective of the study was to determine the outcomes for primary gastrointestinal melanomas (PGIM). Material and methods The Surveillance, Epidemiology, and End Results database (1973–2004) was queried. Results Overall, 659 cases of PGIM were identified. The annual incidence of PGIM was approximately 0.47 cases per million in 2000. Overall median survival time was 17 months. Tumors were identified in the oral–nasopharynx (32.8%), anal canal (31.4%), rectum (22.2%), esophagus (5.9%), stomach (2.7%), small bowel (2.3%), gallbladder (1.4%), and large bowel (0.9%). Univariate analysis demonstrated age, tumor location, stage, surgery, and lymph node status were significant predictors of improved survival. MST has not been reached for tumors located in the large bowel, while tumors located in the stomach demonstrated the shortest median survival (5 months). Improvement in MST was observed for those patients undergoing surgical resection. The presence of lymph node involvement conferred a poorer prognosis. Multivariate analysis of the cohort identified that location, advanced tumor stage, failure to undertake surgical resection, positive lymph node status, and age were all independent predictors of poorer outcome. Conclusion PGIM occurs most often in the oral–nasopharynx and anal canal. Surgical extirpation is the only identifiable treatment modality that significantly improves survival.