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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sclerosing encapsulating peritonitis (SEP) was diagnosed in four dogs and one cat. Clinical signs included vomiting, abdominal pain, palpable abdominal mass, and ascites. The abdominal fluid was red-tinged and contained large numbers of red blood cells, macrophages, mixed inflammatory cells, reactive mesothelial cells, and fibroblasts. At surgery, the typical appearance was of multiple surfaces covered with granulation tissue or fibrous tissue or both. Multiple adhesions were often present. Causes of SEP included steatitis, fiberglass ingestion, and bacterial infection. Treatment included administration of antibiotic, corticosteroid, and diuretic medications. The major long-term management problems were chronic weight loss, ascites, and progression of concurrent disease.
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PMID:Sclerosing encapsulating peritonitis in four dogs and a cat. 819 69

We report a patient undergoing femoral callotasis lengthening using the dynamic axial fixator to correct a post-infective leg length discrepancy of 7.8 cm. Seventeen days after the operation, the patient developed a pin site infection, which was successfully treated by oral antibiotics. On the 34th post-operative day, the infection reoccurred, and was accompanied by generalized malaise, vomiting and pyrexia. Serology identified Staphylococcus aureus enterotoxin. Following removal of the fixator, the child recovered, but only four cm of lengthening was achieved. The pins probably acted as a persistent foreign body, with local inflammation creating favorable ground for bacterial infection. The role of the previous multifocal osteomyelitis unclear, but it could have acted as a continuous source of pathogens. The resulting toxemia was not immediately suspected, and could have resulted in the loss of the patient had the fixator not been removed promptly.
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PMID:Septicemia in a child undergoing callotasis limb lengthening. 882

Antimicrobial therapy for pyelonephritis in children must quickly eradicate the bacterial infection and prevent scars in renal parenchyma. Escherichia coli (E Coli) is found in about 90% of cases of acute pyelonephritis in outpatients, 40% of E coli being ampicillin-resistant. The present effective antibiotics are: 3rd-generation cephalosporines, amoxicillin-clavulanic acid association, and aminoglycosides. In the literature therapeutical guides are divergent concerning the route of administration (oral or i.v.), mono or bitherapy, the duration of the treatment (usually for 10 days), and the need for hospitalisation. The criteria for choice are risk factors such as: very young age (< 6 months), fever with toxic symptoms, vomiting, dehydration, uropathy, and poor compliance. There are few long term studies which compare two, therapeutic regimens and no evaluation of the frequency of consequent chronic pyelonephritis in adult age has taken place. Recent data suggest that an oral sequential treatment may permit a shorter hospital stage. The trend is chiefly to do bona fide recommendations more than elaboration of a true consensus.
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PMID:[Antibiotic treatment of acute pyelonephritis in the child]. 975 22

A 4-yr-old cheetah (Acinonyx jubatus) with a 2-yr history of chronic intermittent vomiting and spiral bacteria-associated gastritis presented with dramatically increased vomiting frequency and marked intermittent abdominal distention. Physical examination revealed loss of muscle mass and poor fur coat quality. Contrast radiography was consistent with delayed gastric emptying due to presumed gastric outlet obstruction. Both Y-U pyloroplasty and incisional gastropexy were performed, and no subsequent vomiting has been observed for 3 yr with the exception of three episodes during the immediate postoperative period. The cause of delayed gastric emptying was not determined, although a gastric motility disorder associated with gastric bacterial infection and elevated gastrin levels was suspected.
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PMID:Use of pyloroplasty (Y-U) to treat presumed delayed gastric emptying in a cheetah (Acinonyx jubatus). 1142 4

Our article concentrates on two acute states, which develop less dramatically but their after-effects may be very serious: Spontaneous bacterial peritonitis and Ogilvie's syndrome. Spontaneous bacterial peritonitis is a bacterial infection of the ascitic fluid without any intraperitoneal source of infection. Ascites is a condition of the disease but need not be clinically manifested. Spontaneous bacterial peritonitis comes usually during heavy hepatic impairment. Diagnosis can be set according: 1. Positive cultivation of ascitic fluid, 2. PMN levels higher than 250/mm3, 3. No infection, which may require a surgical intervention is apparent. Liver disease, which brings about the spontaneous bacterial peritonitis can be: 1. Chronic (e.g. alcoholic cirrhosis), 2. Subacute (e.g. alcoholic hepatitis), 3. Acute (e.g. fulminant hepatic failure). Mortality of this form of peritonitis can reach up to 46%. The most frequent etiological factor is alcohol and viral hepatitis, the most frequent agents are E. coli and Klebsiella pneumoniae. The disease is most effectively cured by cefalosporins of the third generation. With inadequate treatment, prognosis may be poor. Intestinal pseudoobstruction syndrome has clinical symptomatology of a serious impairment with ileus without signs of any mechanical intestinal obstruction. Syndrome can be classified according to its development: 1. Acute form--acute intestinal pseudoobstruction syndrome--Ogilvie's syndrome, 2. Chronic form--chronic intestinal pseudoobstruction syndrome. Pathogenic mechanism of the syndrome is not known. The disease is related to immobility, administration of some drugs, electrolyte imbalance and concomitant diseases (most frequently malignant tumors). Clinical symptomatology dominates nausea, vomiting, diffuse abdominal pain, constipation or diarrhoea. For diagnostics the first step should be termination of all medication, which could have causing affects, then taking native abdominal X-ray picture where gaseous intestinal distension can be prominent (coecum distended up to 9-12 cm). Identification of fluid surfaces is not usual. Endoscopic examination can exclude obstruction in the distal part of gut minimally. The most frequent complication is perforation of coecum. Pharmacological treatment relays on prokinetics. The basic intervention remains decompression by a rectal catheter or an effective coloscopic decompression with subsequent introduction of a cannula. Mortality of the disease fluctuates between 43 and 46%.
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PMID:[Acute states in gastroenterology: spontaneous bacterial peritonitis and the acute intestinal pseudoobstruction syndrome]. 1150 91

Knowledge of the acute and late ionizing radiation exposure damage to the gastrointestinal tract, particularly injury of the small intestine, is of great significance in radiotherapy, as is management of accidental radiation exposure. Irradiation (X-ray, neutron, cobalt gamma) induces a series of events in this rapidly renewing tissue resulting in the well-known symptoms of the gastrointestinal (GI) radiation syndrome, such as GI haemorrhage, endotoxemia, bacterial infection, anorexia, nausea, vomiting, diarrhoea, and loss of electrolytes and fluid. In spite of the significant advances that have occurred in research on underlying mechanisms over the last two decades, the overall etiology and pathogenesis of the GI-syndrome still remains unclear. Currently, to our knowledge, these symptoms are probably due to a rapid modification of the intestinal motility and to the structural alteration of the intestinal mucosa (cell loss and altered crypt integrity). Several evidences suggest that radiation-induced dysfunctions and structural changes of this organ (either changes in subcellular, cellular, and histological structure) are mediated by concerted and interrelated changes of a plethora of various extracellular mediators and their intracellular messengers. The aim of this review is to summarize our current knowledge about the pathomorphology and cell biology of the ionizing radiation response of the GI tract with a focus on the small intestine.
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PMID:Morphological aspects of ionizing radiation response of small intestine. 1156 86

Group B beta-hemolytic streptococci and Escherichia coli strains account for approximately two thirds of all cases of neonatal meningitis, while bacteria that typically account for meningitis in older age groups (Haemophilus influenzae type B, Neisseria meningitidis, and Streptococcus pneumoniae) are infrequent causes of meningitis in the neonatal population. As with other medical problems in neonates, signs and symptoms of bacterial infection of the central nervous system are generally few in number and nonspecific in nature. Manifestations that can suggest meningitis, as well as other serious illnesses, include temperature instability, lethargy, respiratory distress, poor feeding, vomiting, and diarrhea. Signs suggestive of meningeal irritation, including stiff neck, bulging fontanelle, convulsions, and opisthotonus, occur only in a minority of neonates with bacterial meningitis and cannot be relied on solely to identify such patients. Ampicillin and either gentamicin or cefotaxime are recommended for initial empiric therapy of neonatal meningitis. When the results of the cerebrospinal fluid (CSF) culture and susceptibilities are known, therapy can be narrowed to cover the specific pathogen identified. In general, penicillin G or ampicillin is preferred for group B streptococcal meningitis, ampicillin for Listeria monocytogenes meningitis, and ampicillin plus either an aminoglycoside or cefotaxime for gram-negative meningitis. For the very low birth weight neonate who has been in the nursery for a prolonged period of time, organisms such as enterococci and gentamicin-resistant gram-negative enteric bacilli must also be considered. In patients with long-term vascular catheters, Staphylococcus aureus or coagulase-negative staphylococci must also be considered. Empiric combinations of antibiotics for such patients would include ampicillin or vancomycin, plus amikacin or cefotaxime. All neonates should undergo repeat CSF examination and culture at 48 to 72 hours after initiation of therapy. If organisms are observed on gram stain, modification of the therapeutic regimen should be considered, and neuroimaging should be performed. In general, therapy should be continued for 14 to 21 days for neonatal meningitis caused by group B streptococci or L. monocytogenes, and for at least 21 days for disease caused by gram-negative enteric bacilli. All patients with neonatal meningitis should have hearing and development monitored serially. The first audiologic evaluation should occur 4 to 6 weeks after resolution of the meningitis.
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PMID:Meningitis in the Neonate. 1193 31

Disseminated mycobacteriosis was diagnosed in a 4-year-old, castrated male Domestic Shorthair cat following the observation of one to three retractile, non-staining bacilli in neutrophils and monocytes on a Wright-Leishman-stained blood smear Organisms were bright red following acid-fast staining by Kinyoun's technique. The cat had a history of progressive weight loss, anemia, fever, and sporadic vomiting after eating. In addition to blood smears, mycobacteria also were observed in bone marrow aspirates. During necropsy, multiple small white nodules were observed in the spleen and liver. An enlarged sternal lymph node and ascites also were present. In histologic sections, mycobacteria were observed in granulomas within the lungs, liver, spleen, colon, mesenteric and sternal lymph nodes, omentum, and kidney. Mycobacterium avium complex was isolated from cultures of liver, spleen, lung, and kidney. Occult feline leukemia virus infection, detected by immunofluorescent testing of bone marrow aspirates, may have predisposed this cat to bacterial infection. The serum ELISA test for group-specific feline leukemia virus antigen was negative.
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PMID:Disseminated Mycobacterium avium complex infection in a cat: presumptive diagnosis by blood smear examination. 1265 1

The present study, conducted from March 1998 to July 2000, determined the etiology of acute diarrhea in 253 young children and infants from Cartagena and Sincelejo, Colombia. In 253 stool samples, the following enteric pathogens were recovered: rotavirus type A (36.6%) as the major agent, Salmonella spp (9.0%), Shigella spp (8.0%), enteric pathogenic Escherichia coli (6.0%), enteric hemorragic Esc. coli (2.8%), Providencia alcalifaciens (2.8%), Aeromonas hydrophila (2.0%), Yersinia enterocolitica (0.8%), Entamoeba hystolitica (10%), Giardia lamblia (4%), Endolimax nana (3.2%), Ascaris lumbricoides (2.8%), Ent. coli (1.2%), Balantidium coli (0.8%), Blastocystis hominis (0.8%), Dypilidium caninum (0.4%) and hook worm sp. (0.4%). Infection with more than one pathogen occurred in 96 (37.9%) patients. Rotavirus and enteric pathogenic Esc. coli were frequent. Concurrent infection by more than one parasite occurred in 18.6% of the infants. Most rotavirus infections (76.7%) occurred in infants under 12 months. Vomiting, severe dehydration and fever were frequent in children with rotavirus infection. At least one fecal marker of inflammatory diarrhea was registered in patients with bacterial infection. To our knowledge, this is first report of P. alcalifaciens associated with infantile diarrhea in Colombia and the first description of Esc. coli O157:H7 and Y. enterocolitica in our region.
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PMID:Rotavirus type A and other enteric pathogens in stool samples from children with acute diarrhea on the Colombian northern coast. 1268 10

SCH351591, a novel phosphodiesterase-4 inhibitor under investigation as a potential therapeutic for asthma and chronic obstructive pulmonary disease (COPD), was evaluated in a 3-month rising-dose study in Cynomolgus monkeys. Four groups, containing four monkeys/sex, received vehicle control or rising doses up to 12, 24, or 48 mg/kg of SCH351591 daily. Although initial exposure produced clinical signs of emesis, reduced food intake, and reduced body weight, tachyphylaxis to the emesis allowed dose escalation up to 48 mg/kg/day. Two monkeys died and 3 were sacrificed in moribund condition over the course of the study. Early mortality, involving monkeys dosed with 12 or 24 mg/kg, was attributed to sepsis (2 monkeys) or colon inflammation (3 monkeys). Leukocyte function assays on low- and mid-dose group survivors revealed an inhibition of T lymphocyte proliferation for 12 mg/kg group males and 24 mg/kg group monkeys of both sexes. Necropsy findings, unassociated with early mortality, included reduced size and weight of the thymus, depletion of body fat, red discoloration of the gastric mucosa, and perivascular hemorrhage of the stomach and heart. Stomach and heart gross findings were present in the high-dose group only. Histopathologic lesions, in addition to those attributed to concurrent bacterial infection, included thymic atrophy, serous atrophy of fat, myocardial degeneration and acute to chronic inflammation of small to medium-sized arteries in various organs and tissues including the heart, kidneys, stomach, salivary glands, pancreas, esophagus, gallbladder, and mesentery. The findings of this study demonstrate the potential of a PDE4 inhibitor to alter immunologic response as well as to produce arteriopathy in nonhuman primates.
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PMID:The toxicity of SCH 351591, a novel phosphodiesterase-4 inhibitor, in Cynomolgus monkeys. 1520 71


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