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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to use data from an electronic medical record system (EMR) to look for factors that would help us diagnose acute myocardial infarction (AMI) with the ultimate aim of using these factors in a decision support system for chest pain. We extracted 887 records from the electronic medical record system (EMR) in Selayang Hospital, Malaysia. We cleaned the data, extracted 69 possible variables and performed univariate and multivariate analysis. From the univariate analysis we find that 22 variables are significantly associated with a diagnosis of AMI. However, multiple logistic regression reveals that only 9 of these 22 variables are significantly related to a diagnosis of AMI. Race (Indian), male sex, sudden onset of persistent crushing pain, associated sweating and a history of diabetes mellitus are significant predictors of AMI. Pain that is relieved by other means and history of heart disease on treatment are important predictors of a diagnosis other than AMI. The degree of accuracy is high at 80.5%. There are 13 factors that are significant in the univariate analysis but are not among the nine significant factors in the multivariate analysis. These are location of pain, associated palpitations, nausea and vomiting; pain relieved by rest, pain aggravated by posture, cough, inspiration and exertion; age more than 40, being a smoker and abnormal chest wall and face examination. We believe that these findings can have important applications in the design of an intelligent decision support system for use in medical care as the predictive capability can be further refined with the use of intelligent computational techniques.
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PMID:How well can signs and symptoms predict AMI in the Malaysian population? 1593 3

Postsurgical gastroparesis syndrome (PGS) is a complex disorder characterized by post-prandial nausea and vomiting, and gastric atony in the absence of mechanical gastric outlet obstruction, and is often caused by operation at the upper abdomen, especially by gastric or pancreatic resection, and sometimes also by operation at the lower abdomen, such as gynecological or obstetrical procedures. PGS occurs easily with oral intake of food or change in the form of food after operation. These symptoms can be disabling and often fail to be alleviated by drug therapy, and gastric reoperations usually prove unsuccessful. The cause of PGS has not been identified, nor has its mechanism quite been clarified. PGS after gastrectomy has been reported in many previous studies, with an incidence of approximately 0.4-5.0%. PGS is also a frequent complication of pylorus-preserving pancreatoduodenectomy (PPPD), and the complication occurs in the early postoperative period in 20-50% of patients. PGS caused by pancreatic cancer cryoablation (PCC) has been reported about in 50-70% of patients. Therefore, PGS has a complex etiology and might be caused by multiple factors and mechanisms. The frequency of this complication varies directly with the type and number of gastric operations performed. The loss of gastric parasympathetic control resulting from vagotomy contributes to PGS via several mechanisms. It has been reported that the interstitial cells of Cajal (ICC) may play a role in the pathogenesis of PGS. Recent studies in animal models of diabetes suggest specific molecular changes in the enteric nervous system may result in delayed gastric emptying. The absence of the duodenum, and hence gastric phase III, may be a cause of gastric stasis. It was thought that PGS after PPPD might be attributable, at least in part, to delayed recovery of gastric phase III, due to lowered concentrations of plasma motilin after resection of the duodenum. The damage to ICC might play a role in the pathogenesis of PGS after PCC, for which multiple factors are possibly responsible, including ischemic and neural injury to the antropyloric muscle and the duodenum after freezing of the pancreatoduodenal regions or reduction of circulating levels of motilin. As the treatment of gastroparesis is far from ideal, non-conventional approaches and non-standard medications might be of use. Multiple treatments are better than single treatment. This article reviews almost all the papers related to PGS from various journals published in English and Chinese in recent years in order to facilitate a better understanding of PGS.
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PMID:Advances in mechanisms of postsurgical gastroparesis syndrome and its diagnosis and treatment. 1664 34

Splenic abscess is an uncommon but potentially life-threatening disease. Recent advances in radiology have affected the diagnosis and management of this disease entity. The purpose of this study was to review our experience in managing these patients. We retrospectively reviewed the medical records of 51 patients with splenic abscess as seen in a tertiary medical center between 1998 and 2003. We analyzed the demographics, clinical manifestations, etiology, predisposing factors, diagnostic modalities, bacteriologic profile, treatment, and outcome of these patients. The mean age was 59.9 +/- 14.2 years (ranging from 21-89 years). The male:female ratio was 29:22. Common symptoms included fever (82%), abdominal pain (71%), and nausea and vomiting (46%). The majority of these patients (83%) had leukocytosis. Thirty-six patients had associated parenchymal liver diseases and 26 patients had diabetes mellitus. Abdominal sonogram or computed tomography was performed to establish the diagnosis. Most cultures from the abscess cavities grew gram-negative enteric bacilli. Patients were treated with antimicrobial therapy only (n = 33), additional percutaneous drainage with a pigtail catheter (n = 11), or splenectomy (n = 7), and the survival rates were 48 per cent, 45 per cent, and 100 per cent, respectively. Splenic abscess should be considered in a patient with fever, left upper abdominal pain, and leukocytosis. Splenectomy appears to have better treatment outcome than percutaneous drainage or intravenous antibiotics alone.
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PMID:Splenic abscess: an easily overlooked disease? 1667 56

As the incidence of diabetes mellitus continues to increase in the United Kingdom, more diabetic patients will present for both elective and emergency surgery. Whilst the underlying pathophysiology of type 1 and type 2 diabetes differs, there is much good evidence that controlling the blood glucose to < or = [corrected] 10 mmol.l(-1) in the peri-operative period for both types of diabetic patients improves outcome. This should be achieved with a glucose-insulin-potassium regimen in all type 1 diabetics and in type 2 diabetics undergoing moderate or major surgical procedures. After surgery, a decrease in the catabolic hormone response resulting from good analgesia and the avoidance of nausea and vomiting should allow early re-establishment of normal glycaemic control.
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PMID:Diabetes mellitus: anaesthetic management. 1750 48

Patients with diabetes are prone to metabolic derangements because of their lack of effective insulin. Comorbid conditions, such as coronary artery disease, nephropathy, and autonomic neuropathy warrant preoperative assessment to ensure safety in the perioperative period. Preoperative evaluation must include assessment of chronic complications of diabetes. A thorough history and physical should guide preoperative testing which should be aimed at detecting correctable abnormalities and assessing the extent of end-organ disease. Surgery poses special challenges to patients with diabetes because the stress response, interruption of food intake, altered consciousness, and circulatory alterations all lead to unpredictable glucose and electrolyte levels. The management of insulin perioperatively depends on the preparation normally taken by the patient, and the glucose level on the morning of surgery. The goal is to avoid hypoglycemia and extreme hyperglycemia. Oral hypoglycemic agents should be held on the morning of surgery. Metformin should be discontinued 48 hours prior to and subsequent to surgery in order to reduce the risk of lactic acidosis. The avoidance of hypoglycemia and excessive hyperglycemia intraoperatively is best achieved with frequent monitoring of blood glucose and treating abnormalities according to patients' preoperative regimen and current condition. Maintaining blood glucose levels below 110 mg/dL reduces morbidity and mortality in critically ill patients. Measure blood glucose immediately following surgery because progression of the stress response postoperatively, in addition to possible nausea and vomiting, can complicate the patient's management. Precautions should be taken to prevent damage to peripheral nerves while diabetics are on the operating table because their nerves and limbs are already vulnerable to pressure and stretch injuries secondary to neurologic and vascular disease. With thorough and careful management, metabolic control in the perioperative period is a goal that is attainable for most patients.
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PMID:Optimizing the medical management of diabetic patients undergoing surgery. 1719 Mar 91

Exenatide (synthetic exendin-4) is the analog of glucagon-like peptide 1 (GLP-1), the major physiologic incretin. The latter is an intestinal hormone that enhances glucose-induced insulin secretion after meals. In addition, GLP-1 stimulates insulin synthesis, inhibits glucagon secretion, delays gastric emptying, and may promote satiety. These glucoregulatory actions help control plasma glucose in the postprandial period. However, in diabetes, the GLP-1 response to nutrient intake is impaired, leading to exacerbation of postprandial hyperglycemia. Exenatide was recently approved as adjunctive therapy in diabetic patients failing sulfonylureas and/or metformin. In clinical trials lasting 30 weeks, exenatide therapy was associated with moderate reduction in mean hemoglobin A1c (HbA1c) levels of approximately 0.8%, and an average weight loss of approximately 2 kg compared with baseline. Hypoglycemia was generally mild and occurred more commonly when exenatide was used in conjunction with sulfonylureas. The requirement of subcutaneous injections twice a day, and the frequent occurrence of nausea and vomiting, represent the main limitations of exenatide. Nevertheless, this agent may be a useful add-on therapy in obese diabetic patients with suboptimal control as a result of continuing weight gain and/or severe postprandial hyperglycemia. The introduction of GLP-1-based antidiabetic drugs is a novel and promising strategy to treat diabetes.
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PMID:Exenatide: a novel approach for treatment of type 2 diabetes. 1719 23

Chronic vomiting in diabetic patients often is unresponsive to prokinetic agents and poorly explained by delayed gastric emptying or neuropathy. This retrospective study examines clinical response to tricyclic antidepressants, a treatment of reported benefit in nondiabetic patients with unexplained vomiting syndromes. Outcomes were studied in 24 diabetic outpatients who had been treated with tricyclic antidepressants specifically for nausea and vomiting after an unsatisfactory response to prokinetic therapy. Symptom patterns and treatment response were determined from chart review and telephone interview. Ten patients (42%) had recurrent, stereotypical vomiting episodes with symptom-free intervals suggesting cyclic vomiting syndrome; 14 (58%) had persistent symptoms. By chart review, at least moderate symptom response to tricyclic antidepressant treatment (median dosage, 50 mg/day) occurred in 88% of subjects, with complete or nearly complete resolution of symptoms in one-third. At follow-up interview, 77% self-reported at least moderate symptom improvement during therapy and 68% rated tricyclic antidepressants the most effective treatment received. Duration of diabetes, presence of neuropathy, and psychiatric status were not predictive of treatment outcome in multivariate analysis, but a cyclical symptom pattern attenuated antidepressant response (P< 0.05). In this retrospective review, the majority of diabetic patients with chronic vomiting and incomplete response to prokinetic therapy benefited from tricyclic antidepressants in low-dose, open-label regimens and rated them the most effective treatment received. This therapeutic option should be further studied in diabetic patients considering the morbidity of chronic vomiting in this population.
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PMID:Tricyclic antidepressants for chronic vomiting in diabetic patients. 1719 23

Hereditary chronic pancreatitis (HCP) is a very rare form of early onset chronic pancreatitis. With the exception of the young age at diagnosis and a slower progression, the clinical course, morphological features and laboratory findings of HCP do not differ from those of patients with alcoholic chronic pancreatitis. As well, diagnostic criteria and treatment of HCP resemble that of chronic pancreatitis of other causes. The clinical presentation is highly variable and includes chronic abdominal pain, impairment of endocrine and exocrine pancreatic function, nausea and vomiting, maldigestion, diabetes, pseudocysts, bile duct and duodenal obstruction, and rarely pancreatic cancer. Fortunately, most patients have a mild disease. Mutations in the PRSS1 gene, encoding cationic trypsinogen, play a causative role in chronic pancreatitis. It has been shown that the PRSS1 mutations increase autocatalytic conversion of trypsinogen to active trypsin, and thus probably cause premature, intrapancreatic trypsinogen activation disturbing the intrapancreatic balance of proteases and their inhibitors. Other genes, such as the anionic trypsinogen (PRSS2), the serine protease inhibitor, Kazal type 1 (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR) have been found to be associated with chronic pancreatitis (idiopathic and hereditary) as well. Genetic testing should only be performed in carefully selected patients by direct DNA sequencing and antenatal diagnosis should not be encouraged. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications, such as pseudocysts, bile duct or duodenal obstruction. The disease course and prognosis of patients with HCP is unpredictable. Pancreatic cancer risk is elevated. Therefore, HCP patients should strongly avoid environmental risk factors for pancreatic cancer.
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PMID:Hereditary chronic pancreatitis. 1720 47

Niacin has beneficial effects on plasma lipoproteins and has demonstrated clinical benefits in reducing cardiovascular events and atherosclerosis progression. The side effects of niacin, however, have limited its use in general clinical practice. An understanding of cutaneous flushing based on the best available evidence should enhance patient education efforts and improve adherence. Although serious hepatic toxicity from niacin administration has been reported, it is largely confined to the use of slow-release formulations given as unregulated nutritional supplements. Niacin has been shown to induce insulin resistance in short-term trials, but the glycemic response in subjects with and without diabetes is usually minor. Niacin can be used safely in patients with diabetes. Despite a few case reports of myopathy associated with niacin-statin (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor) combination therapy, 2 decades of clinical evidence since the introduction of statins do not support a general myopathic effect of niacin either alone or in combination with statins. Rare, less well-defined side effects of niacin include blurred vision due to cystoid macular edema, nausea and vomiting, and the exacerbation of peptic ulcers. Laboratory abnormalities that are usually small (< or =10%) and clinically unimportant include increased prothrombin time, increased uric acid, and decreases in platelet count and serum phosphorus. Overall, the perception of niacin side effects is often greater than the reality. As a result, a valuable medication for cardiovascular risk is underused.
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PMID:Safety considerations with niacin therapy. 1736 76

Hereditary chronic pancreatitis (HCP) is a very rare form of early-onset chronic pancreatitis. Apart from young age at diagnosis and a slower progression, the clinical course, morphological features and laboratory findings of HCP do not differ from those of patients with alcoholic chronic pancreatitis. Diagnostic criteria and treatment of HCP also resemble those of chronic pancreatitis of other causes. The clinical presentation is highly variable and includes chronic abdominal pain, impairment of endocrine and exocrine pancreatic function, nausea and vomiting, maldigestion, diabetes, pseudocysts, bile-duct and duodenal obstruction, and rarely pancreatic cancer. Fortunately, the disease is mild in most patients. Mutations in the PRSS1 gene, encoding cationic trypsinogen, play a causative role in chronic pancreatitis. It has been shown that the PRSS1 mutations increase autocatalytic conversion of trypsinogen to active trypsin, and thus probably cause premature, intrapancreatic trypsinogen activation, disturbing the intrapancreatic balance of proteases and their inhibitors. Other genes--such as the anionic trypsinogen (PRSS2), the serine protease inhibitor Kazal type 1 (SPINK1), and the cystic fibrosis transmembrane conductance regulator (CFTR)--have also been found to be associated with chronic pancreatitis (idiopathic and hereditary). Genetic testing should only be performed in carefully selected patients by direct DNA sequencing, and antenatal diagnosis should not be encouraged. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications such as pseudocysts and bile-duct or duodenal obstruction. The disease course and prognosis of patients with HCP is unpredictable. The risk of pancreatic cancer is elevated. Therefore, HCP patients should strongly avoid environmental risk factors for pancreatic cancer.
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PMID:Hereditary chronic pancreatitis. 1820 17


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