CASE STUDY
Aluminum toxicity in dialysis patient receiving TPN
The following case illustrates the encephalopathy, bone disease, and anemia that have been associated with aluminum toxicity in dialysis patients who are receiving aluminum-contaminated parenteral products and aluminum-containing phosphate binders. Regulations requiring aluminum content data on parenteral product labels were spurred by reports of aluminum toxicity in dialysis patients and neonates.
A 49-year-old male was diagnosed with chronic glomerulonephritis with uremia and was treated by peritoneal dialysis initially and later by hemodialysis. Twenty-eight months after dialysis was started, the patient's hemoglobin and hematocrit began to drop despite increasing doses of recombinant erythropoietin. Twelve months later, he began to exhibit slow, hesitant speech and stuttering. Periods of altered speech were variable in frequency and severity for the first few months. Difficulty finding words and dysgraphia became increasingly common. The patient developed progressive signs of dementia, with insidious onset of forgetfulness, irritability, and drowsiness. He became increasingly more apathetic toward his family and social contacts. Eight months after the onset of dialysis dementia, the patient was admitted to the hospital with confusion and disorientation to time and place. He exhibited groping, grasping, and sucking reflexes. An EEG showed frontal dominance with progressive slowing of waves with high-amplitude spikes. The patient continued to deteriorate and died of respiratory arrest 2 weeks after admission. Radiographs and scans conducted during the admission showed multiple sites of calcification consistent with fractures, including more than 20 rib fractures, the likely consequences of chronic accumulation of aluminum from parenteral sources.
 |
|
 |
| Aluminum concentrations were as follows: |
 |
l Serum aluminum = 99 µg/L ± 11 (based on 3 samples, normal = <10 µg/L) |
|
l Urinary aluminum = 121 µg/L ± 15 (based on 2 samples using 24 h urine collection, normal = 7 µg/L to 19 µg/L) |
|
|
Dialysis dementia and elevated serum and urinary aluminum levels in this patient were attributed to aluminum contamination of the dialysis fluids, as well as to the use of aluminum hydroxide to control hyperphosphatemia until approximately a year before his death. During the last year of his .life, the patient received calcium carbonate for phosphate binding instead of aluminum hydroxide.
[PRINTER FRIENDLY VERSION]
|
|
| |
