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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty infants and young children with hereditary fructose intolerance (HFI) were admitted to hospital. None was diagnosed at admission. Referals were for vomiting of unknown aetiology (16X), pyloric stenosis or hiatus hernia (5X), toxic condition (3X), and hepatomegaly of unknown origin (5X). Feeding difficulties (20X), vomiting (18X), and failure to thrive (16X) were leading symptoms. The most frequent clinical findings were hepatomegaly (18X), pallor (14X), haemorrhages (13X). Ascites, oliguria, tachypnoea, fever, splenomegaly and rickets were less frequent. Laboratory findings were indicative of disturbed hepatic and renal tubular function and also of disturbed intermediary metabolism (hypokaliaemia, hypophosphataemia). However, hypoglycaemia was found in only 4 out of 15 patients tested. Differential diagnosis after hospital admission centered on metabolic disorders such as glycogenoses, galactosaemia, tyrosinosis, or Wilson's disease. Hepatitis, toxic hepatosis, liver tumour, intrauterine infection and sepsis were also considered. Eleven children had first ingested fructose within the first 6 weeks of life. The diagnosis was usually established only many weeks or months after first fructose intake and appearance of symptoms. This documents how difficult the diagnosis of this disease can be both in practice and in hospital. The course was severe in 11 children and lethal in 4. In only 5 patients was the course mild. The 16 survivors are doing well under fructose-exclusion diet. Irreversible visual impairment after intraocular haemorrhage occurred once. In each case HFI could have been suspected immediately, had a detailed nutritional history been taken. Practising paediatricians should know the composition of commonly used infant formulae. They should never prescribe sugared condensed milk for intractable vomiting prior to excluding HFI. Solution for intravenous infusion containing fructose and sorbitol are life-threatening for undiagnosed HFI patients.
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PMID:Hereditary fructose intolerance in early childhood: a major diagnostic challenge. Survey of 20 symptomatic cases. 73

Shock continues to be associated with a high mortality rate primarily because of delays in diagnosis and therapy. To diagnose shock early, and thereby increase the chances of reversal before there is extensive deterioration of vital organs, one should look for any decrease in pulse pressure, urine output, urine sodium concentration, alertness or any increase in urine osmolarity, tachypnea or tachycardia. Systolic hypotension, oliguria, metabolic acidosis and a cold clammy skin are late signs of shock. The pathophysiology of early hypovolemic shock includes hyperventilation, vasoconstriction, cardiac stimulation, fluid shifts into the vascular system and platelet aggregation. Late shock is characterized by lysosomal breakdown, subsequent release of kinins (especially bradykinin), impaired cell metabolism and organ function, fluid shifts out of the vascular system because of capillary endothelial damage and intravascular coagulation. The primary cause of shock should not be neglected in favor of treating signs, symptoms, and laboratory data. The resuscitation from the shock process itself involves correction of pathophysiologic changes, based on objective trends and responses rather than isolated measurements. A suggested outline of therapies in order of their use includes: 1) correction of the primary problem; 2) ventilation and oxygen; 3) fluid-loading: 4) inotropic agents; 5) correction of acid-based and electrolyte abnormalities; 6) steroids ("physiologic" or "pharmacologic" doses); 7) vasopressors (especially in elderly, severely hypotensive patients); 8) vasodilators (if excess vasoconstriction); 9) diuretics (if oliguric in spite of the above), and 10) heparin (if DIC). The most common errors are 1) late diagnosis; 2) inadequate control of the primary problems; 3) inadequate fluid loading; 4) delayed ventilator assistance, and 5) excessive reliance on and use if vasopressors and diuretics.
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PMID:Shock in the emergency department. 79 60

In a retrospective analysis of 2110 admissions to the pediatric intensive care unit, 564 cases of septic shock were identified (26.7% of the total admissions). Septic shock was defined in patients with: (1) clinical evidence of sepsis; (2) fever (greater than 38.3 degrees C) or hypothermia (less than 35.6 degrees C); (3) tachycardia; (4) tachypnea; and (5) inadequate organ perfusion. Inadequate perfusion was defined as hypotension or evidence of peripheral hypoperfusion (poor capillary refill or cyanosis with hypoxemia, oliguria, acidosis or altered mentation). Inotropic support was required to maintain an adequate blood pressure and perfusion in 268 of 564 patients (47.5%). Septic shock with confirmed bacterial infection occurred in 143 patients (143 of 564, 25.2%); these cases were caused by Haemophilus influenzae, type b (59 of 143, 41.3%), Neisseria meningitidis (26 of 143, 18.2%) and Streptococcus pneumoniae (16 of 143, 11.2%). Eight of 564 (1.4%) cases of septic shock were not clinically apparent on initial evaluation and were diagnosed within 24 hours after admission to the hospital. We conclude that septic shock occurs more frequently in children than previously appreciated and may develop after admission to the hospital.
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PMID:Septic shock in children: bacterial etiologies and temporal relationships. 233

The septic syndrome can be defined using clinical criteria in patients with clinical evidence of an infectious process. The other criteria include fever or hypothermia, tachypnea, tachycardia, and evidence of impaired organ perfusion or function as manifested by either altered mentation, hypoxemia, elevated plasma lactate, or oliguria. A multicenter trial using these criteria found positive blood cultures in 45 per cent of 382 patients. The mortality rate was approximately 30 per cent and 25 per cent of the patients developed ARDS. With respect to these characteristics, this septic syndrome population was very similar to the more traditionally defined populations with sepsis. Using the septic syndrome definition may allow for earlier detection of septic patients and possibly allow for earlier therapeutic intervention. The septic syndrome may help identify a population of patients at risk for the various complications of sepsis (that is, ARDS), aid in the search for pathophysiologic mechanisms, and allow for pharmacological trials earlier in the disease process.
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PMID:The septic syndrome. Definition and clinical implications. 264 21

The sepsis syndrome represents a systemic response to infection and is defined as hypothermia (temperature less than 96 degrees F) or hyperthermia (greater than 101 degrees F), tachycardia (greater than 90 beat/min), tachypnea (greater than 20 breath/min), clinical evidence of an infection site and with at least one end-organ demonstrating inadequate perfusion or dysfunction expressed as poor or altered cerebral function, hypoxemia (PaO2 less than 75 torr), elevated plasma lactate, or oliguria (urine output less than 30 ml/h or 0.5 ml/kg body weight.h without corrective therapy). One hundred ninety-one patients with the sepsis syndrome were evaluated prospectively and comprised the placebo group of a multicenter trial of methylprednisolone in sepsis syndrome and septic shock. Forty-five percent of the patients were found to be bacteremic. Thirty-six percent of the patients were in septic shock (sepsis syndrome plus a systolic BP less than 90 mm Hg or a decrease from baseline in systolic BP greater than 40 mm Hg) on study entry. An additional 23% of the patients developed shock after admission with 70% doing so within 24 h of study entry. Shock reversal occurred with a 73% frequency. Twenty-five percent of the patients developed the adult respiratory distress syndrome (ARDS). Mortality for the patients with sepsis syndrome who did not develop shock was 13%. Mortality for the groups of patients with shock on admission and shock postadmission was 27.5% and 43.2%, respectively. Forty-seven percent of the bacteremic patients developed shock after study admission compared to 29.6% of the nonbacteremic patients (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sepsis syndrome: a valid clinical entity. Methylprednisolone Severe Sepsis Study Group. 239 10

The use of high-dose corticosteroids in the treatment of severe sepsis and septic shock remains controversial. Our study was designed as a prospective, randomized, double-blind, placebo-controlled trial of high-dose methylprednisolone sodium succinate for severe sepsis and septic shock. Diagnosis was based on the clinical suspicion of infection plus the presence of fever or hypothermia (rectal temperature greater than 38.3 degrees C [101 degrees F] or less than 35.6 degrees C [96 degrees F]), tachypnea (greater than 20 breaths per minute), tachycardia (greater than 90 beats per minute), and the presence of one of the following indications of organ dysfunction: a change in mental status, hypoxemia, elevated lactate levels, or oliguria. Three hundred eighty-two patients were enrolled. Treatment--either methylprednisolone sodium succinate (30 mg per kilogram of body weight) or placebo--was given in four infusions, starting within two hours of diagnosis. No significant differences were found in the prevention of shock, the reversal of shock, or overall mortality. In the subgroup of patients with elevated serum creatinine levels (greater than 2 mg per deciliter) at enrollment, mortality at 14 days was significantly increased among those receiving methylprednisolone (46 of 78 [59 percent] vs. 17 of 58 [29 percent] among those receiving placebo; P less than 0.01). Among patients treated with methylprednisolone, significantly more deaths were related to secondary infection. We conclude that the use of high-dose corticosteroids provides no benefit in the treatment of severe sepsis and septic shock.
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PMID:A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. 330 74

From November 1, 1982 through December 31, 1985, there were 19 centers and 382 patients that evaluated the effect of methylprednisolone sodium succinate (MPSS) on the septic syndrome. Seventeen of these centers enrolled 304 patients in a prospective, randomized, double-blind, placebo-controlled study to determine if early treatment with MPSS would decrease the incidence of severity of the adult respiratory distress syndrome (ARDS) in patients at risk of ARDS from sepsis. To ensure early institution of the MPSS or placebo therapy (PLA), patients with the presumptive diagnosis of sepsis were identified. That diagnosis was based on the presence of fever or hypothermia (temperature greater than 38.3 degrees C or less than 35.5 degrees C, rectal), tachypnea (greater than 20 bpm), tachycardia (greater than 90 bpm) and the presence of one of the following indices of organ dysfunction: a change in mental status, hypoxemia, elevated lactate levels or oliguria. The treatment, either MPSS 30 mg/kg or PLA, was given in four 20-minute infusions six hours apart and was initiated within two hours of the presumptive diagnosis of sepsis. The development and reversal of the adult respiratory distress syndrome (ARDS) was followed and resulted in data on 304 of the 382 randomized patients. A trend toward increased incidence of ARDS was seen in the MPSS group 50/152 (32 percent) compared to the placebo group 38/152(25 percent) p = 0.10. Significantly fewer MPSS patients reversed their ARDS 15/50 (31 percent) compared to placebo 23/38 (61 percent) p = 0.005. The 14-day mortality in patients with ARDS treated with MPSS was 26/50 (52 percent) compared to placebo 8/22 (22 percent) p = 0.004. We conclude that early treatment of septic syndrome with MPSS does not prevent the development of ARDS. Additionally, MPSS treatment impedes the reversal of ARDS and increases the mortality rate in patients with ARDS.
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PMID:Early methylprednisolone treatment for septic syndrome and the adult respiratory distress syndrome. 331 78

The process of adaptation for extrauterine life can be easily disturbed by respiratory insufficiency. The surfactant deficiency as well as anatomical and physiological immaturity of a newborn can be considered as etiological factors in some diseases, such as respiratory distress syndrome (RDS), transient tachypnoea (TT) syndrome, segmental atelectasis or pneumonia complicated by atelectasis. The widespread used method of treatment is based on mechanical increase of difference between alveolar and atmospheric pressure. So-called constant distending pressure (CDP) increases functional residual capacity (FRC), keeps alveoli open and finally increases oxygenation of arterial blood. During 3 years period continuous positive airway pressure by nasal route (n-CPAP) was used as only one method in 26 newborns. The newborns were treated because of RDS (15 cases) and pneumonia with atelectasis (11 cases). n-CPAP was starting with pressure 8 cm H2O (0.8 kPa) and FIO2 0.5, if atelectasis with severe dyspnea, hypoxia and forced hyperventilation were found. This method was very well tolerated. 22 newborns treated for 2-7 days--survived, 4 small-for-date babies--died. The most common cause of death was septicaemia complicated by disseminated intravascular coagulation. The moderate hyperbilirubinemia, oliguria with tissue oedema was observed in many cases. The light nostril decubitus were only complications. No pneumothorax was detected. We found n-CPAP as a simple, safe method in treatment of atelectasis in newborns.
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PMID:[Continuous positive pressure respiration by nasal route (n-CPAP) as a preferred treatment method in various types of acute respiratory insufficiency in newborn infants]. 637 92

Acute intrinsic renal failure was diagnosed in a two-year-old, male, German shepherd dog following a Vipera aspis bite. Clinical signs included depression, hypersalivation, vomiting, tachypnoea, abdominal pain, splenomegaly, oliguria with haematuria and haemolysed serum. Leucocytosis with a shift to the left, thrombocytopenia, prolonged coagulation times (activated partial thromboplastin time, prothrombin time and thrombin time), hypofibrinogenaemia, azotaemia and hyposthenuria were the most prominent laboratory abnormalities. Histopathological evaluation of the kidneys showed a discrete glomerular hypercellularity, mesangial lysis and renal tubules filled with many hyaline casts and some necrotic cells.
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PMID:Acute intrinsic renal failure and blood coagulation disorders after a snakebite in a dog. 747 66

A 23-year-old man with relapsing pneumothorax underwent surgical removal of left apical lung bullae and pleural rubbing down. Forty-eight hours later, he suddenly developed a state of shock together with tachypnoea, oliguria, and a scarlet-like erythema of the face and trunk. Haemodynamic and other investigations led to the diagnosis of septic shock, although no portal of entry could be found. Despite antibiotics (vancomycin, gentamycin and pefloxacine) and symptomatic treatment, the patient's condition continued to worsen. He had a fever (40 degrees C) with abdominal tenderness. Exploratory laparotomy failed to disclose a septic foyer. On aspiration of the left thoracic cavity, a large pyothorax was found and 600 mls of pus were drained. Gram-positive cocci were found on staining and pefloxacine was replaced by mezlocillin. Nevertheless, the patient died within 24 h. Blood and pus cultures confirmed that the infection was due to a pyrogenic penicillin-sensitive group A Streptococcus. Similar cases have been described recently. Group A Streptococcus is suspected to cause severe infections with multiple organ failure, termed "toxic shock-like syndrome". The clinical similarity between the streptococcal and staphylococcal shocks calls for a precise bacteriological diagnosis, and treatment with antibiotics active on both germs.
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PMID:[Fatal streptococcus A shock after thoracic surgery]. 833 69


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