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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infectious tenosynovitis was diagnosed in three separate outbreaks in a commercial White Leghorn hens, though not previously reported in adult White Leghorns (3). Clinically affected flocks had decreased production and increased daily mortality, with many hens showing signs of the so called "cage-fatigue bluecomb" syndrome. Most sick birds had lesions typical of infectious tenosynovitis, with pronounced cyanosis and dehydration. Dead birds had signs of acute septicemia. The course of the disease (about 8 weeks) was not altered by the medicinal regimens tried. Young laying-age flocks were most seriously affected. Production losses averaged 15 to 20%, and mortality reached 5% per month during the recovery phase.
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PMID:Infectious tenosynovitis in commercial White Leghorn chickens. 18 15

A retrospective study of 35 newborn with acute renal failure is presented. The main causes of renal failure were neonatal hypoxia by asfixia or hemorrhagic shock (eight), congenital malformations (two) and hypertonic dehydration (25). Mortality rate was 22% including two neonates with severe congenital malformations. Sepsis was considered as the main complicating factor and often as inducer of renal failure. It was present on 55% of cases and on 75% of the deceased newborn. Cerebral injury was frequent but a follow-up study is necessary to establish the rate of neurologic sequelae. Early diagnosis and treatment of renal failure will decrease complications with improvement in prognosis. Etiological analysis of neonatal renal failure shows the need of a better health education of people and also medical control of pregnancy and perinatal period.
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PMID:[Morbidity and mortality of acute renal failure in neonatal period (author's transl)]. 46 2

Two cases of infants with shock are presented. Cardiac output was determined in both with dilution dye using an auricular oxymeter, with three determinations: at 0, 30 and 60 minutes while receiving intranvenous fluids. At the same time, blood gases and blood lactatewere determined. The first case showed hypodynamic shock secondary to hypovolemia due to severe dehydration, associated to low central venous pressure, low arterial tension, increased peripheral resistance and increased arteriovenous difference of oxygen. The second case was a newborn with sepsis and disseminated intravascular coagulation with hyperdynamic shock with very high cardiac output, low peripheral resistance and low arteriovenous difference of oxygen. Both cases had an initial increase of lactate and a mild decrease at the end of the period of clinical observation.
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PMID:[Hemodynamometabolic changes in shock in infants. Report of 2 cases]. 62 52

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

A 6 month-old mulatto boy was admitted on account of acute gastroenteritis, malnutrition and dehydration. In the hospital, the child developed septicemia, and temperature reached up to 38.6 degrees C. Despite intensive antibiotic treatment the patient died 12 days after admission. Necropsy disclosed bilateral bronchopneumonia, bilateral fronto-parietal subarachnoid hemorrhage, and extensive necrosis of the inferior half of both cerebellar hemispheres. On histopathological examination of the necrotic cerebellar cortex, numerous sickled erythrocytes were observed in petechial hemorrhages, and, in lesser quantities, inside capillaries. Lesions of the central nervous system in sickle cell anemia most often involve the cerebral cortex, and a single extensive cerebellar infarction as present in this case seems extremely rare. The pathogenetic mechanism of the necrosis is unclear, since thrombosis was not observed either in large blood vessels or in capillaries. Possible contributory factors were the infectious condition (septicemia), fever, and anoxia caused by the extensive bronchopneumonia.
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PMID:[Extensive cerebellar necrosis in sickle cell anemia. Report of a case]. 75 14

The general features and problems of renal vein thrombosis in children are first discussed. The records of 11 children with this condition, 7 ill neonates and 4 older children with burns, are then reviewed, indicating the clinical course of the disease, how they were treated, the results, and pathological findings. From this study, the natural history is assembled and a protocol for treatment is proposed. Supportive therapy is necessary in all cases to correct dehydration and sepsis. Many children will develop a consumptive coagulopathy. Others will develop pulmonary emboli associated with thrombosis of the inferior vena cava. Anticoagulation should be achieved for these two conditions. Nonvisualization of affected renal units upon initial urographic examination virtually assures an atrophic, functionless kidney later. Nephrectomy will be required because of hypertension, persistent infection, and scarring. Thrombectomy may be attempted when bilateral nonvisualization on urography is associated with a positive venacavogram.
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PMID:Natural history and treatment of renal vein thrombosis in children. 91 51

The acute onset of oliguria and azotemia in the postoperative setting may be caused by pre-renal causes or intrinsic renal damage. The first step in arriving at a diagnosis is to review the history as noted above for clues regarding fluid balance, treatment with nephrotoxins, etc. The typical patient with prerenal azotemia will present with evidence of the recent onset of worsening of pre-existing cardiac disease, renal or gastrointestinal fluid loss, or the accumulation of acites, edema, or retroperitoneal fluid. In the absence of very recent diuretic therapy, he will be excreting a scant amount of concentrated (greater than 400 mOsm per L) sodium free (less than 10 to 20 mEq per L) urine. The serumBUN/Cr ratio is often greater than 15 to 20:1, and their urinary sediment will be bland. In an occasional patient in whom these studies give equivocal results, additional help may be obtained with measurements of central venous pressure (CVP) or pulmonary wedge pressure (PWP) and by noting their response to intravenous fluid loading. A rising CVP or PWP in the face of salt loading is, of course, evidence against prerenal azotemia. Patients with obstructive uropathies may be oligoanuric or polyuric-occasionally a characteristic alternating polyuria and oliguria is found (due to displacement of a stone or relief of edema). When oliguric their urine typically contains substantial amounts of sodium (greater than 20 mEq per L), is isotonic, and their OsmU:OsmP is les s than or equal to 1.2. Their urinary sediment will reflect the cause of their obstruction as noted above. A renal scan, ultrasound study, or infusion IVP are mandatory to rule out the possibility of obstructive uropathy. If these nonivasive studies are equivocal, one must consider doing a unilateral retrograde. The development of ATN usually occurs in the setting of hypotension, sepsis, dehydration, and with exposure to nephrotoxins. Most patients with be excreting scant amounts of isotonic urine containing more than 20 to 30 mEq per L of sodium. Their CrU:CrP is less than or equal to 20:1 and their urinary sediment reveals many epithelial cells and casts. Those patients with nonoliguric ATN have urine outputs which may exceed 2 liters per day. Despite this output they demonstrate a stepwise increase in serum urea and creatinine. Urine sodium and osmolality are not very helpful in this setting. Many such patients do have low (less than 20 mEg per L) urine sodium concentration and excrete isotonic urine.
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PMID:Pre- and postoperative renal failure. 96 Mar 14

Early diagnosis is mandatory in the adult respiratory distress syndromes, particularly in sepsis, and therapy should begin as soon as there is a reasonable suspicion that this problem is developing. Blood-gas changes cannot usually be appreciated clinically until the respiratory problem is quite severe. Accordingly, serial blood-gas analyses should be performed in any septic patient who has an increased chance of developing ARDS. Any deterioration in the patient's condition, blood gases, or ventilatory effort should be considered as an indication for early ventilatory assistance. Control of the primary process, high tidal volumes, PEEP, and careful dehydration are the mainstays of therapy. Serial blood gases and careful observation of the patient's effective compliance are essential to determine the optimal ventilator settings and the optimal PEEP. Early administration of massive steroids should be considered if the patient fails to respond to correction of the underlying etiologic problem (particularly sepsis), careful progressive dehydration, and optimal expansion of the alveoli (using high tidal volumes and/or PEEP).
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PMID:The diagnosis and treatment of acute respiratory failure in sepsis. 104 56

The pathogenic effects produced in mice by intraperitoneal (i.p.) injection of a Bacillus species (OSU 372) are presented. This organism belongs to group 3 of the genus, and members of this group have not heretofore been shown to be pathogenic for mice even under experimental conditions. However, this organism is capable of producing a fatal involvement in doses which are not considered to be overwhelming. The mean lethal dose (LD50) of the organism for 20-25 g mice by the i.p. route is about 1 times 10-8 bacteria/mouse. A rapid drop in body temperature along with severe dehydration were noted in infected animals, and hematologic studies indicated that leukopenia and hemoconcentration also occurred. Although a transient septicemia developed, the bacteria could not be recovered from the tissues of fatally infected mice after a certain point in time. Results prevented indicate that the animals died of hypovolemic shock. A possible parallel with human bacillary infection is drawn.
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PMID:An experimentally pathogenic Bacillus species. II. The pathogenicity of the organism for mice. 112 25

Gangrene of the newborn is an uncommon condition usually resulting from decreased perfusion of a part, usually an extremity. There are a variety of situations which can result in this condition. Knowledge of the exact sequence of events which lead to the insult and the conditions surrounding it is helpful in determining the etiology and as a consequence the treatment of the lesion. In the patient described, direct pressure from the maternal pelvis was probably the contributing factor which led to venous occlusion of the extremity. Arterial thrombosis, emboli, trauma, congenital heart disease, sepsis, dehydration, coagulopathies, and venipuncture are other possible causes which should be considered. The treatment is in general supportive, allowing the ischemic area to demarcate and slough. Range-of-motion exercises and splinting to avoid contracture are helpful in the rehabilitative phase.
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PMID:Gangrene of the newborn. A case report. 112 62


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