Abstract: TH-PO1095

Unique Case Renal Failure with Severe Metabolic Alkalosis and Hypermagnesaemia Requiring Hemodialysis

Session Information

Category: Fluid, Electrolytes, and Acid-Base

  • 704 Fluid, Electrolyte, Acid-Base Disorders

Authors

  • Thimmisetty, Ravi K., Wayne State University, Detroit, Michigan, United States
  • Alrawi, Omer, Wayne State University, Detroit, Michigan, United States
  • Osman Malik, Yahya M., Wayne State University Medical School, Detroit, Michigan, United States
  • Bhat, Zeenat Yousuf, Wayne State University, Detroit, Michigan, United States
Background

We are presenting an interesting case of renal failure, severe metabolic alkalosis and symptomatic hypermagnesemia that required dialysis for correction.

Methods

60-year-old African American male with history of metastatic sigmoid colon cancer s/p resection with end-colostomy and Hartmann’s stump admitted with abdominal pain, vomiting and dyspnea. Other medical problems were hypertension and left ureteral obstruction from colonic mass s/p left percutaneous nephrostomy tube. Home medications include flomax, protonix, over the counter Alka-seltzer. Admission vitals were -temperature 97.5 fahreinheit, blood pressure of 95/77, heart rate 98 beats per minute, respiratory rate 16 per minute and saturating 97% on 40% fiO2. On exam, he was cachectic, mild somnolent and dry. There was no edema. Laboratory values on admission revealed sodium 135, K is 4.7, chloride 80, bicarbonate >45, creatinine is 5.5 mg/dl (baseline Cr is of 1.5), calcium 9, magnesium 5.6 and phosphorus 9.9. ABG results showed pH is 7.59, pCO2 is 71, pO2 183, bicarb is 59.9. After volume resuscitation, patient became bradypnea, more somnolent and further worsening of respiratory status requiring intubation. Immediately hemodialysis was started for treating symptomatic hypermagnesemia and severe metabolic alkalosis in the setting of acute renal failure. Urine output started increasing. With 2 sessions of renal replacement therapy, patient improved significantly interims of mental status and biochemically. Creatinine down to 2.4 and pH is 7.37. All other electrolytes were normalized and patient was extubation. Severe alkalosis could have been multifactorial oral alkali intake and vomiting in setting of renal failure and week ago, had gastrograffin for small bowel obstruction which can sometime result in metabolic alkalosis.

Conclusion

Gastrograffin sometimes prepared with solutions containing alkali. Caution should be taken while giving these solutions containing alkali especially in the setting of renal failure. Concomitant severe metabolic alkalosis and hypermagnesemia can contribute to high mortality and poses a therapeutic challenge especially in the setting of renal failure. Renal replacement therapy is required in these cases.