The study suggests that midodrine may be as effective as albumin in preventing PICD in cirrhotics, but at a fraction of the cost, and can be administered orally. Midodrine also resulted in an increase in 24-h urine volume and sodium excretion.
Background:Acute onset fever with altered mentation is a common problem encountered by the physician practicing in tropical countries. Central nervous system (CNS) infections are the most common cause resulting in fever with altered mentation in children.Aim:In this study, we have tried to analyze the cause of encephalopathy following short febrile illness in adults presenting to a tertiary care center in Northwestern part of India.Setting and Design:A prospective observational study carried out in a tertiary care center in the Northwestern India over a period of 1 year.Material and MethodsA total of 127 patients with fever of less than 2 weeks duration along with alteration in mentation were studied prospectively over a period of 12 months. The demographic variables were recorded in detail. In addition to routine investigations, cerebrospinal fluid analysis, noncontrast- and contrast-enhanced computed tomography, along with magnetic resonance imaging were performed in all the subjects.Statistical AnalysisThe results were analyzed using SPSS statistical software. The values were expressed as mean with standard deviation for contiguous variable as percentage for the others.Results and ConclusionOut of these, 70% had primary CNS infection as the etiology. A total of 33% patients had meningitis, 29.9% had evidence of meningoencephalitis, and 12.7% were diagnosed as sepsis-associated encephalopathy. These were followed by cerebral malaria, leptospirosis, and brain abscess as the cause of febrile encephalopathy in adults. Among the noninfectious causes, acute disseminated encephalomyelitis, cortical venous thrombosis, and neuroleptic malignant syndrome were documented in 2.36% each. In 11% of the patients, the final diagnosis could not be made in spite of the extensive investigations. Our study demonstrates that acute febrile encephalopathy in adults is a heterogeneous syndrome with primary CNS infections being the commonest etiology.
Cure rates for adult acute lymphoblastic leukemia (ALL) in developing countries are significantly lower because of problems unique to these countries. We assessed some of the problems in adult ALL patients (>12 years of age) in a tertiary care hospital of northwest India with modified BFM regimen. The diagnosis of ALL was made according to FAB criteria. The protocol consisted of Phase I & II induction, consolidation, reinduction and maintenance phases. CNS prophylaxis was administered with 24 Gy radiation and intrathecal methotrexate. One hundred and eighteen patients (72.9% males), aged 12-68 years (median 23 years) were treated from January 1997 till December 2003. Follow-up of patients was done till December 2005. Complete remission (CR) was achieved in 85.6% patients after induction therapy and 40% patient relapsed. Most patients (23.7%) relapsed during the maintenance phase or after completion of chemotherapy. At least 15% of patients (15/101) after successful induction abandoned the treatment because of financial constraints, prolonged travel time to treatment facility and switching over to alternative medicines. Fatal infectious complications occurred in 19.5% of patients. The 3-year and 5-year event free survival rates were 29.8% and 21.6% respectively. In conclusion, modified BFM regimen resulted in high induction rates but relatively poor 5-year event free survival. Infections related death and post induction abandonment of treatment were the main reasons for poor overall results.
Acalculous cholecystitis should be strongly suspected in patients with dengue fever presenting with abdominal pain. Our study has shown that acalculous cholecystitis occurred in 14 out of 27 patients with dengue fever.
Jaundice in patients with amoebic liver abscess is a frequent occurrence. However, the pathophysiology of jaundice in these patients is not fully understood. Hepatic necrosis leads to damage to bile ducts as well as various vascular structures, which in turn leads to biliovascular fistula and jaundice. We studied the mechanism of jaundice in patients with amoebic liver abscess. We prospectively evaluated 12 patients with amoebic liver abscess and jaundice from February 2002 to August 2007. All patients underwent various investigations, including imaging studies. There were 11 males and 1 female patient with a mean age of 41.3 years. Mean duration of illness before presentation was 13.8 days. All patients had fever and jaundice. We detected damaged hepatic veins and bile ducts in all patients with amoebic liver abscess causing biliovascular fistula and hyperbilirubinemia, which reverted to normal after biliary diversion with nasobiliary drainage. Jaundice in patients with amoebic liver abscess is caused by biliovascular fistula resulting from hepatic necrosis leading to damage to bile ducts and hepatic veins.
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