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At least 991 records · Page 55Linked to original sources
PubMed2001

[Clinical and pathologic analysis of Sjögren's syndrome with renal impairment: a report of 84 cases].

OBJECTIVE: To further study the renal damage of Sjögren's syndrome (SS) and its clinical and pathologic characteristics with biopsy and recent technology. METHODS: 84 patients of SS with renal impairment from 1993 to 1999 were analyzed by routine, immunoassay, tubular function and biopsy examination. RESULTS: 55 of the 84 cases presented with renal tubular acidosis (RTA), 5 with diabetes insipidus and 3 with hypokalemic paralysis. Glomerulopathy occurred in 22 cases (nephrotic syndrome 12, glomerulonephritis 10) and mild renal failure (RF) was found in 14. 69.1% of the patients had hypergamma-globulinemia. 64.3% and 44.1% of the patients showed positive anti SS-A and anti SS-B. In 37 renal biopsy specimens 21 showed chronic interstitial nephritis (CIN) with extensive lymphoplasmic cell infiltration and tubular atrophy. 10 of the 37 specimens revealed lupus nephritis (LN, type III and IV) and 5 mesangial proliferative glomerulonephritis (MsPGN). With immunofluorescence tests, no positive findings were seen in most of the specimens, but deposition of IgA, IgM or C(3) was seen in some patients. IgG deposits in the interstitial lymphoplasmic cells were found in 1 patient. 25 patients were treated with prednisone combined with cytoxan (CTX). In 14 patients with renal failure, serum creatinine level returned to normal after treatment. CONCLUSION: Renal impairment may be the presenting or predominant feature in SS. The major clinical manifestations are RTA and GN. Treatment with prednisone may decrease the infiltration of lymphoplasmic cells in the interstitium, improve the renal function and correct RTA.

Adolescent↗
PubMedDate not supplied

Ketamine anaesthesia for caesarean section in poor-rick patients.

Caesarean section in a poor-risk patient treated intensively before and after operation is described. The operation was carried out when the patient was in diabetic coma with metabolic acidosis, electrolyte disturbances and low arterial blood pressure. Anaesthesia was conducted using ketamine with nitrous oxide and oxygen. Controlled respiration was performed administering fractionated doses of suxzmethonium.

Adult↗
PubMed1989

Metabolic acidosis.

This article reviews acid-base homeostasis and discusses the approach to the acidotic patient, with special reference to problems commonly encountered in emergency practice. General principles of therapy are presented, and their application to specific types of life-threatening metabolic acidosis addressed. By extension, recommendations are made concerning the treatment of the acidosis associated with cardiac arrest. Finally, preliminary information is presented on promising new approaches to the treatment of metabolic acidosis that are currently under investigation.

Acid-Base Equilibrium↗
PubMed1989

Pediatric organ donor maintenance: pathophysiologic derangements and nursing requirements.

A retrospective chart review was conducted of 26 organ donors to determine hemodynamic and metabolic derangements encountered and nursing requirements for donor organ maintenance. There were 15 boys and 11 girls with a mean age 6.57 +/- 5.46 years. Mean donor maintenance time was 10.5 +/- 6.7 hours. Cardiorespiratory derangements included hypotension in 16, hypertension in 6, arrhythmias in 17 (premature ventricular contraction in 4, bradycardia in 8, paroxysmal atrial tachycardia in 3, and ventricular tachycardia in 2), asystolic events in 5, pulmonary insufficiency in 6, anemia in 8, and thrombocytopenia in 8. Metabolic and hormonal derangements included hyperglycemia in 18, hypokalemia in 20, hyperkalemia in 4, hyponatremia in 3, hypernatremia in 17, metabolic acidosis in 10, and diabetes insipidus in 15. Hypothermia (temperature 33.3 degrees +/- 0.4 degrees C, mean +/- SD) occurred in 14 donors. The mean physiologic Stability Index score was 22.2 +/- 4.7 and mean Therapeutic Intervention Score was 46.7 +/- 5.8. Total number of nursing hours spent in donor maintenance was 424.5 hours. Therapies offered included diuretics in 10, sodium bicarbonate in 8, antibiotics in 6, insulin in 12, pitressin in 13, verapamil in 3, isoproterenol in 3, dopamine in 17, and intravenous potassium boluses in 14. Of the potential 26 donors, 46 kidneys, 8 hearts, 14 livers, 3 pancreas, and 9 corneas were retrieved in transplantable condition. With appropriate donor maintenance, organs suitable for transplantation can be retrieved despite significant pathophysiologic derangements. Physicians intending to provide donor support should be comfortable with invasive monitoring and cardiorespiratory support and be prepared to provide a nurse to patient ratio of 2:1 at the bedside.

Adolescent↗
PubMed1985

Can marked hyperglycemia occur without ketosis?

The significance of ketosis in this syndrome has been evaluated from several viewpoints. With respect to acid-base considerations (pH, anion gap), ketosis was not very significant. However, with respect to sustained hyperglycemia, the combustion of less glucose than normal by the brain is critical and it is likely that ketone body metabolism plays an important role in this regard. This point can be underscored by a quantitative example. First, assume that the maximum rate of new glucose production in a fasted subject is less than 100 g of glucose per day. Second, since the brain will burn 100 g of glucose per day in a non-ketotic subject, it follows that, even in the absence of glucosuria, there will be a net daily consumption of glucose. Since the hyperglycemic individual has only an extra 100 or so g of glucose, it follows that the blood glucose concentration would approach the renal threshold in several days in the absence of ketosis. Recall that this is a minimum estimate because glucose oxidation in other organs and glucosuria will remove an additional quantity of glucose. Hyperglycemia can only be maintained in the absence of glucose intake if there is a reduced rate of glucose metabolism in the brain. The brain can diminish its rate of glucose catabolism by several mechanisms, including a diminished metabolic rate in the brain and/or the consumption of non-glucose fuels (free fatty acids or beta-hydroxybutyrate) by this organ.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗