scholarly journals Acute Renal Failure with Metabolic Alkalosis Due to Gastric Scirrhous Carcinoma

2014 ◽  
Vol 15 (2) ◽  
pp. 136-139 ◽  
Author(s):  
Kiyoshi Shikino ◽  
Masatomi Ikusaka ◽  
Haruyuki Hayashi ◽  
Yoshio Ohtake ◽  
Yasubumi Irie
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Alkalosis ◽  
Scirrhous Carcinoma

scholarly journals Metabolic Alkalosis, Acute Renal Failure and Epileptic Seizures as Unusual Manifestations of an Upside-Down Stomach

2012 ◽  
Vol 6 (2) ◽  
pp. 452-458 ◽  
Author(s):  
Johannes Stephani ◽  
Martin Wagner ◽  
Thomas Breining ◽  
Jochen Klaus ◽  
Jan-Hendrik Niess
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Alkalosis ◽  
Epileptic Seizures

Acute renal failure and metabolic alkalosis in a patient with colorectal villous adenoma (McKittrick–Wheelock syndrome)

Surgery ◽  
2013 ◽  
Vol 154 (3) ◽  
pp. 643-644 ◽  
Author(s):  
Giacomo Pucci ◽  
Fabio Rondelli ◽  
Nicola Avenia ◽  
Giuseppe Schillaci
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Villous Adenoma ◽  
Metabolic Alkalosis

Impact of Continuous Veno-venous Hemofiltration on Acid-base Balance

2003 ◽  
Vol 26 (1) ◽  
pp. 19-25 ◽  
Author(s):  
J. Rocktäschel ◽  
H. Morimatsu ◽  
S. Uchino ◽  
C. Ronco ◽  
R. Bellomo
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Alkalosis ◽  
Base Excess ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Strong Ion Gap ◽  
Acid Base ◽  
Biophysical Analysis ◽  
Base Balance

Background Continuous veno-venous hemofiltration (CVVH) appears to have a significant and variable impact on acid-base balance. However, the pathogenesis of these acid-base effects remains poorly understood. The aim of this study was to understand the nature of acid-base changes in critically ill patients with acute renal failure during continuous veno-venous hemofiltration by applying quantitative methods of biophysical analysis (Stewart-Figge methodology). Methods We studied forty patients with ARF receiving CVVH in the intensive care unit. We retrieved the biochemical data from computerized records and conducted quantitative biophysical analysis. We measured serum Na+, K+, Mg2+, Cl-, HCO3-, phosphate, ionized Ca2+, albumin, lactate and arterial blood gases and calculated the following Stewart-Figge variables: Strong Ion Difference apparent (SIDa), Strong Ion Difference Effective (SIDe) and Strong Ion Gap (SIG). Results Before treatment, patients had mild acidemia (pH: 7.31) secondary to metabolic acidosis (bicarbonate: 19.8 mmol/L and base excess: −5.9 mEq/L). This acidosis was due to increased unmeasured anions (SIG: 12.3 mEq/L), hyperphosphatemia (1.86 mmol/L) and hyperlactatemia (2.08 mmol/L). It was attenuated by the alkalinizing effect of hypoalbuminemia (22.5 g/L). After commencing CVVH, the acidemia was corrected within 24 hours (pH 7.31 vs 7.41, p <0.0001). This correction was associated with a decreased strong ion gap (SIG) (12.3 vs. 8.8 mEq/L, p <0.0001), phosphate concentration (1.86 vs. 1.49 mmol/L, p <0.0001) and serum chloride concentration (102 vs. 98.5 mmol/L, p <0.0001). After 3 days of CVVH, however, patients developed alkalemia (pH: 7.46) secondary to metabolic alkalosis (bicarbonate: 29.8 mmol/L, base excess: 6.7 mEq/L). This alkalemia appeared secondary to a further decrease in SIG to 6.7 mEq/L (p <0.0001) and a further decrease in serum phosphate to 0.77 mmol/L (p <0.0001) in the setting of persistent hypoalbuminemia (21.0 g/L; p=0.56). Conclusions CVVH corrects metabolic acidosis in acute renal failure patients through its effect on unmeasured anions, phosphate and chloride. Such correction coupled with the effect of hypoalbuminemia, results in the development of a metabolic alkalosis after 72 hours of treatment.

scholarly journals Antacids, Altered Mental Status, and Milk-Alkali Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-3
Author(s):  
Simon C. Watson ◽  
Bonnie B. Dellinger ◽  
Katie Jennings ◽  
Lancer A. Scott
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Peptic Ulcer ◽  
Mental Status ◽  
Proton Pump ◽  
Metabolic Alkalosis ◽  
Altered Mental Status ◽  
Ulcer Disease ◽  
Calcium Supplements ◽  
Patients At Risk

The frequency of milk-alkali syndrome decreased rapidly after the development of histamine-2 antagonists and proton pump inhibitors for the treatment of peptic ulcer disease; however, the availability and overconsumption of antacids and calcium supplements can still place patients at risk (D. P. Beall et al., 2006). Here we describe a patient who presented with altered mental status, hypercalcemia, metabolic alkalosis, and acute renal failure in the context of ingesting large amounts of antacids to control dyspepsia.

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