ABSTRACT
BACKGROUND: Hyponatremia has a number of different causes; some may have serious untoward implications for patients undergoing chronic ambulatory peritoneal dialysis (CAPD). OBJECTIVE: To determine the pathophysiology of hyponatremia in patients on CAPD. METHODS: A retrospective analysis was carried out on 210 patients on CAPD. We selected patients with 2-4 consecutive periods when the plasma sodium concentration was < or =130 mmol/L and again when it was > 133 mmol/L. Exclusion criteria included hyperglycemia, orthostatic hypotension, edema, and inadequate records. RESULTS: An electrolyte-free water gain appeared to be the main cause of hyponatremia in only 1 of 5 patients because this was the only patient with a significant increase in body weight. In 1 patient, there was weight loss in the hyponatremic period, suggesting tissue catabolism was present. In 3 patients, there was neither weight gain nor evidence for a contracted extracellular fluid volume in the hyponatremic period, suggesting that intracellular potassium and phosphate loss could be the major mechanism for their hyponatremia. CONCLUSION: When hyponatremia is due to a catabolic state, its management should aim to restore intracellular fluid composition (i.e., to correct malnutrition).
Subject(s)
Hyponatremia/physiopathology , Nutrition Disorders/complications , Peritoneal Dialysis, Continuous Ambulatory , Water-Electrolyte Balance/physiology , Female , Humans , Hyponatremia/etiology , Male , Middle Aged , Retrospective Studies , Weight GainABSTRACT
The basis for hyponatremia is a negative balance for sodium (Na+) plus potassium (K+) and/or a positive balance for water. In patients with normal renal function, vasopressin is needed to prevent the excretion of electrolyte-free water. Vasopressin is not important when there is little residual renal function. If hyponatremia is accompanied by a quantitatively appropriate gain in weight, this implies that a gain of electrolyte-free water was the basis for hyponatremia. In the absence of this weight gain, a loss of salts is to be suspected. If the extracellular fluid (ECF) volume is obviously low, hyponatremia is due to a deficit of NaCl, unless there is a deficit of K+. With a KCl deficit and a contracted ECF volume, there should also be a large shift of Na+ into cells, so metabolic alkalosis would not be an expected finding. In contrast, those patients with no change in weight who have a normal or expanded ECF volume are subdivided into those with a gain of solutes restricted to the ECF compartment (glucose, mannitol), or those with a deficit of solutes of intracellular fluid origin, which implies that a catabolic state (malnutrition) may be present.
Subject(s)
Hyponatremia/physiopathology , Peritoneal Dialysis , Extracellular Space/metabolism , Humans , Hyponatremia/etiology , Hyponatremia/metabolism , Peritoneal Dialysis, Continuous Ambulatory , Potassium/metabolism , Sodium/metabolism , Weight GainABSTRACT
PURPOSE: To evaluate the technical success, complication rates, and survival time of the Uldall double-lumen catheter placed by interventional radiologists in patients presenting to a hemodialysis clinic. MATERIALS AND METHODS: Patients eligible for this study included those with end-stage renal disease (ESRD) who had failed peripheral vascular access or who were awaiting access at a hemodialysis unit between June 1993 and March 1996. All catheters were placed under fluoroscopic and ultrasound guidance in the angiography suite. RESULTS: Attempts were made to insert 130 catheters into jugular veins in a consecutive series of 61 patients with ESRD. The accumulated catheter experience in this cohort was 15,380 days and the median survival time was 141 days (95% confidence interval [CI]; 116 days-166 days). One hundred twenty-one catheters (93%) were successfully inserted, mainly (94%) into the internal jugular vein. Excellent dialysis blood flow rate was obtained-on average 365 mL/min (95% CI; 350-379 mL/min). The overall infection rate, including exit site (n = 13), sepsis (n = 19), and clavicular osteomyelitis (n = 1), was 2.1 episodes per 1,000 catheter days. CONCLUSIONS: This catheter is recommended for acute and longer term hemodialysis for patients without peripheral vascular access. It can be inserted percutaneously, the same internal jugular vein can be used repeatedly with few complications and good blood flow, and the technique can be easily learned by any experienced angiographer.
Subject(s)
Catheters, Indwelling , Radiology, Interventional/methods , Renal Dialysis/methods , Adult , Aged , Aged, 80 and over , Angiography/methods , Blood Flow Velocity , Catheters, Indwelling/adverse effects , Equipment Failure , Female , Follow-Up Studies , Humans , Jugular Veins/diagnostic imaging , Jugular Veins/physiopathology , Kidney Failure, Chronic/therapy , Male , Middle Aged , Renal Dialysis/adverse effects , Renal Dialysis/instrumentation , Retrospective Studies , Treatment Outcome , Ultrasonography, Interventional/methodsABSTRACT
To find out whether internal jugular vein cannulation with a soft silastic hemodialysis access catheter causes jugular vein thrombosis, the authors carried out Doppler ultrasound examinations on 96 patients receiving hemodialysis who had undergone 144 separate catheter insertion episodes in 116 veins. Two internal jugular vein thromboses were found in 101 veins that had been the site of percutaneous insertions only. In addition, 5 internal jugular vein thromboses were identified in 15 veins that had been cannulated surgically with the Quinton PermCath. The authors conclude that percutaneous internal jugular vein cannulation for hemodialysis access causes an acceptably low incidence of jugular vein damage. This strengthens the case for preferential use of the internal jugular vein for vascular access in patients with end-stage renal failure, and suggests that percutaneous cannulation is less damaging than surgical insertion.
