International Journal of Human Capital Management (IJHCM)
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Spontaneous Bacterial Peritonitis
No full textInfected ascites is one of the complication happened in liver cirrhotic patient in ascites. There are 5 infected ascites classifications i.e. Spontaneous Ascites Infection Consist of Spontaneous Bacterial Peritonitis, Monomicrobial Non Neurocytic Bacteriascites, Culture Negative Neurocytic Ascites, Secondary Bacterial Peritonitis and Iantrogenic Polimicrobial Bacterascites. Spontaneous Bacterial Peritonitis (SBP) is the infection in ascites without unrecognized intra abdominal infection source.The normal floras in the gastrointestinal, respiratory or urinal tract are the important infection source in SBP. As we know that normal ascites has ability to kill micro organism through phagocitosis function, opsonization, but when infected occurs ; phagocitosis function, opsonization, and MPS could be worst so that the possibility of being SBP increased. The common frequently sign and symptom of SBP are fever, abdominal pain, consciousness assault, tenderness, diarrhea, paralytic ileus, hypotension and hypothermia. Some of the invasive actions like endoscopy, variceal sclerotherapy and ligation may cause intestine flora translocation to mesenteric gland, bacterimia and infected ascites also made transmural passage intestine micro organism to ascites may cause infected ascites. Cefotaxime is the antibiotic that more frequently studied to SBP patient. The dose of cefotaxime to SBP patient show that 2 gram/6 hours and 2 gram/12 hours injected produce SBP resolution and the same survival, besides that 2 gram/8 hours injected for 5 and 10 days also show the same effectively. The antibiotic prophylaxis such as quinolon group show the effective result in liver cirrhotic with the gastroentestinal tract bleeding and low total protein (<1 gram/dl ) or has the SBP experience patients
The Role of Gastrointestinal Bacterial Ecology in Inflammatory Bowel Disease (IBD)
No full textThe pathogenesis of inflammatory bowel disease (IBD) is not yet fully understood. A genetic predisposition, some environmental factors and microbial flora of the gut are the key factors. The presence of bacteria in the intestinal lumen is a prerequisite for the development of IBD. In animal models, mice incapable of expressing IL2 or IL10 invariably develop a colitis- or Crohn-like inflammation. No inflammation occurs if they grow up in a pathogen-free environment or if they are fed with Lactobacillus sp when exposed to environmental bacteria. Thus, the absence of luminal bacteria or a different make-up there of prevents the development of inflammatory bowel disease in this model. Patients with IBD have been found to have a decreased stool excretion of Lactobacillus and/or Bifidobacteria. Furthermore, an increased number of bacteria adherents to the mucosa and within the epithelium has been demonstrated in quantitative studies. It appears that these bacteria trigger a strong abnormal mucosal immunological response, leading to intestinal epithelial cell injury mediated by activated T-cells, mononuclear cells and macrophages. If this response can not be down regulated by regulatory T-cells, numerous inflammatory cytokines are activated by stimulation of the intracellular transcription factor NF-kB. Recently it was shown that bacterial lipopolysaccharides can activate NF-kB by binding to two specific receptors on the cell membrane (Toll-like receptors [TLR’s]) or intracellular receptors (NOD’s). New insights of the role of bacteria in IBD became available by identifying susceptibility genes for IBD. Several IBD susceptibility loci were recently identified. The IBD-1 locus on chromosome 16 shows positive evidence for linkage in Crohn’s disease and IBD-2 locus on chromosome 12 for ulcerative colitis. The evidence for an association with Crohn’s disease at the IBD-1 locus have been shown to be attributed to mutations in the CARD15/NOD2 gene. This gene is expressed in peripheral blood monocytes and in intestinal epithelial cells and serves as a key factor of innate mucosal response to luminal bacteria as an antibacterial factor. The intact intercellular NOD2 protein binds LPS and activates NF-kB. This activation of the NF-kB signalling pathway in response to bacterial components plays a protective role in the mucosal epithelial cells for the host against inviting pathogens and an increased apoptosis of infected cells. There is evidence, that the defective NOD2 protein variants increase the susceptibility to pathogen invasion and a decrease in cellular apoptosis. NF-kB plays a dual role in IBD. On the mucosal epithelial cells, bacterial components bind on NOD2 proteins and protect bacterial invasion. If this barrier mechanism is not intact, the bacterial invasion stimulates via TLR- and NOD2 receptors in immune-active cells (macrophages, T-cells and monocytes) NF-kB and triggers an aberrant inflammatory response leading to tissue damage. These new insights in the pathogenesis in IBD have led to new treatment possibilities including pre- and probiotics. These therapies are aimed at directly modulating the host immune system to suppress intestinal inflammation. This has prompted considerable interest in manipulating the enteric microenvironment as a novel therapeutic strategy. Several clinical studies showed promising results using pre- and probiotics in patients with ulcerative colitis, pouchitis and Crohn’s disease. The introduction of genetically engineered probiotic organism to produce and deliver anti- inflammatory cytokines or other biological relevant molecules to the mucosa offers further new potential for the treatment of IBD. Keywords : Inflammatory Bowel Disease, inflammatory cytokine
Diagnostic Findings and ERCP Treatment in Patients with Obstructive Jaundice during two years at H. Adam Malik Hospital, Medan
No full textBackground: The methods of ERCP have been used for diagnostic and therapeutic purposes to pass bile fluid and extract stones from the bile duct in patients with obstructive extrahepatic jaundice. Method: A retrospective study was performed on patients with obstructive extrahepatic jaundice patients who underwent ERCP during a two-years time period from January 1999 to December 2000. ERCP was performed with a premedication of 10 mg midazolam, followed by a chollangiography contrast containing 1 mg/dl of Garamicin and 25 mg of Pethidine if sphincterotomy was performed. Results: From 126 patients with obstructive extrahepatic jaundice treated with ERCP, the male to female ratio was 1.86:1. The majority of the (group) of patients were between 51-60 years of age (33.3 % ). The youngest patient (group) was 24 years and the oldest 97 years. The diagnostic study found the following cases: normal 3 cases (2.8%), bile duct stone 46 cases (43.4%), carcinoma of ampula vater 20 cases (18.9%), CBD tumor 7 cases (6.6%), carcinoma of head of pancreas 2 cases (1.9%), diverticle 4 cases (3.8%), duodenal tumor 1 case (0.9%), carcinoma of ampula vater and bile duct stone 1 case (0.9%), SOD 5 cases (4.7%), CBD stricture 1 case (0.9%) and failure 16 cases (15.1%). The patients receivied the following treatment: sphyncterotomy 36 cases (51.4%), stent application 11 cases ( 15.7%), sphincterotomy with stent 18 cases (25.7%) and basket method 5 cases (7.1%). Keywords: ERCP, obstructive jaundic
The Role of Ascitic Paracentesis in Liver Cirrhosis in Improving the Function and Structure of the Heart
No full textBackground: Heart abnormalities in cirrhotic patients have been known for five decades, with atria and ventricular dilatation. Pozzi et al reported that in cirrhotic patients with or without ascites, the diastolic function was lower than control. Ascitic paracentesis improved diastolic function. The diameter of both atria was larger in cirrhotic patients with or without ascites. The diastolic diameter of left ventricle did not differ significantly in cirrhotic patients with or without ascites compared to control, but there was an increase after paracentesis. Ejection fraction was lower in cirrhotic and increased after ascitic parancentesis although the increase was not significant. The aim of the Study: To compare the function and structure of the heart before and after ascitic paracentesis in cirrhotic patients. Methods: This study took place from February 2000 to April 2001 in dr. Pringadi Hospital/H.Adam Malik Hospital. There were 18 samples (12 men and 6 women), 15 of which were cirrhotic patients with tense ascites and 3 cirrhotic patients with refractory ascites. The mean age was 51,8 + 8,28 years, the youngest being 29 years and the oldest 65 years. The mean ascitic fluid removed by paracentesis was 7,20 liters with a range of 5 to 9 liters. Immediately following paracentesis, Dextran 40 % was administered at a dose of 8g/ 1L ascitic fluid aspirated. Results: The diameter of the four heart chambers decreased after paracentesis, but the decrease was not statistically significant. There was increase in E/A ratio after ascitic paracentesis, from 0,93 + 0,370 to 1,06 + 0,383 (significant, p0,05). Conclusion: After paracentesis, there was a significant improvement in diastolic function while the diameter of the four heart chambers decreased and the ejection fraction increased insignificantly. Keywords: Ascitic paracentesis - liver cirrhosis - heart function and structure
Management of Duodenal Ulcer with Gastroesophageal Reflux Disease (GERD) with Intravenous Pantoprazole
No full textProton pump inhibitors (PPIs) are the most effective anti secretory drugs available for controlling gastric acid acidity and volume. They are the drug of choice in the treatment for gastro esophageal reflux disease (GERD), Helicobacter pylori eradication, peptic ulcer and non steroidal anti-inflammatory drug (NSAID) gastropathy: For acute cases, an intravenous PPI is needed, especially for hospitalized patient. Recently, intravenous pantoprazole represents an alternative to intravenous histamine-2 receptor antagonists. We observed 2 patients who were treated with pantoprazole for duodenal ulcer, where one case had a complication of bleeding with a history of long term use of NSAID. After two weeks of treatment with pantoprazole, significant lesion healing from endoscopy findings was achieved in both cases. Keywords: peptic ulcer, upper gastrointestinal bleeding, proton pump inhibitors, pantoprazol
Advanced Gastric Cancer in a Young Patient
No full textGastric cancer remains the second most common cancer in the world, and is usually found in men, especially those over 50 years of age. The diagnosis is made by endoscopic biopsy. The high frequency of late diagnosis or advanced stages accounts for the overall poor prognosis for this tumor. Surgery is the most frequently employed modality for both cure and palliation. However, most patients present with advanced disease that is incurable. We reported a rare case of young female patient aged 23 years old with advanced gastric carcinoma. The main clinical features were epigastric discomfort, vomiting, and weight loss. An abdominal mass was palpable on physical examination. Endoscopy showed a giant tumor mass causing gastric outlet obstruction, nodular lesion, ulcerative and hemorrhagic. The histopathologic examination revealed mucinous gastric carcinoma. Palliative resection could not be performed because the tumor tightly adhered to adjacent structures. Jejunostomy was performed to allow enteral nutrition. Best supportive care is very important to improve the quality of life. Keywords: Gastric cancer, young patien
Management of Upper Gastrointestinal Bleeding due to NSAID Gastropathy that is Unresponsive to Ranitidine
No full textNon steroidal anti-inflammatory drugs (NSAIDS) are now commonly used in clinical practice. On the other hands, this drug could result severe complication such as bleeding and perforation. In such condition, proton pump inhibitor can be used to stop bleeding than H2 antagonists. We reported one cases of upper gastrointestinal bleeding due to NSAID gastropathy that was unresponsive to Ranitidine. The treatment was suitable to proton pump inhibitor that could overcome upper gastrointestinal bleeding
Early Acute Liver Failure In Severe Acute Hepatitis B
No full textEarly acute liver failure is defined by the presence of a drop below 50% of the normal prothrombine ratio, jaundice, and clotting factors of less than 50% in any patient with acute liver disease. Clinical features and laboratory manifestations of viral hepatitis range from unapparent disease, asymptomatic infection, to culminant disease, which has the highest mortality rate of up to over 80 %. We report a case of a 22-year old man who was treated in a private hospital with early acute liver failure caused by hepatitis B infection. The diagnosis was based on clinical symptoms and laboratory test Results such as jaundice, hepatomegaly, ascites, 34% prothrombine ratio, elongated prothrombine time (37,1 seconds), hypoalbuminemia (1,9 g/dL), hyperbillirubinemia (total billirubin 26,35 mg/dL, direct billirubin 16,66 mg/dL, HbsAg (+), IgM anti- HBc (+), IgM anti HAV (-), and anti HCV (-). The patient suffered from jaundice for 6 weeks and on the third week, he suffered from ascites. He had improved clinical condition and laboratory test results with conservative therapy after the seventh week. At the end of the tenth week, the patient’s clinical condition and laboratory test results had reached normal, with HBsAg (-) and HBsAb (+). Whether or not interferon should have been given to this patient is still arguable. Key words: Early acute liver failure, Severe acute hepatitis
Clinical Manifestation and Management of Extra-Esophageal Gastroesophageal Reflux Disease
No full textGERD is a condition that gastric content go back into the esophagus. This condition could came disturbances in the respiratory tract, heart and otolaryng. Those extra-esophageal clinical manifestation are common but often miss our attention. So it is important to explorate it further. The management of extra-esophageal GERD is similar with management of GERD. It is included life style modification and reducing refluxate with controlling pH with aggressiveness. Keywords: extra gerd, non cardiac chest pain, respiratory disturbance, omeprazol
The Relationship between Gastric Mucosa Mucous Thickness and Gastroscopic Findings in Patients Receiving Non-Steroidal Anti-Inflammatory Drugs
No full textNon-steroid anti-inflammatory drugs (NSAID) can cause gastropathy and gastric mucosa, especially the mucous may play an important prevention role. This cross-sectional, single group study was conducted to know the difference in mucous thickness in antrum or corpus mucosa and the correlation of gastric mucous thickness to gastropathy. Patients who received NSAID from the rheumatology clinic were studied. Healthy subjects of 14 – 65 years old who never received NSAID were included as normal controls. Piroxicam 20 mg daily was given to the patients for 7 days, then gastroscopy and gastric mucosa biopsy with frozen section were performed. Specimens were stained with haematoxyline eosin and thickness of the mucous layer was measured using ocular micrometer. Thirty-two out of 70 patients participated in the study. All cases had hyperemia on gastroscopy with erosions and ulcer in 32 and 9 cases, respectively. The mean thickness of mucosa in distal antrum, proximal antrum and corpus was 28.5 ± 9, 37.4 ± 13.1 and 43.3 ± 13.1 microns, respectively. There was significant relationship between gastric mucosa mucous thickness with gastroscopic findings. In conclusion, this study confirmed that thickness of gastric mucosa mucous has an important role in preventing NSAID gastropathy and dyspeptic complaints in this kind of patients does not suggest abnormalities of gastric mucosa. Key Words: Gastric mucosa mucous thickness, NSAID, gastroscop