Under development - incomplete
A 16 year boy was admitted with
several days history of increasing malaise, generalised weakness and
vomiting. He had a past history of bladder exstrophy & epispadias.
He had had surgical bladder reconstruction & augmentation with
sigmoid colon combined with ureteric re-implantation. Voiding was
managed with an artificial sphincter prosthesis (inflatable urethral
cuff with scrotal pump control). Urine on admission was clear.
examination: He was alert & afebrile. BP 120/70. Pulse
80/min. Chest was clear. A generalised muscle weakness (3/5) was present
and hypotonia & hyporeflexia was noted..
on admission: Na 134, K 1.5, Cl 116, HCO3
6, glucose 5.5, urea 17.1, creatinine 0.234 (all in mmol/l). [Hb] 128
g/l. White cell count 12 x 109/l
Firstly, initial clinical assessment:
A severe acidosis with a
severe hypokalaemia is present. The
muscle weakness due to the hypokalaemia and may be
life-threatening at this low level.
In the first 12 hours he received 4
litres of N/saline and received 140 mmol of KCl. His condition
deteriorated with lethargy & increasing muscle weakness. He was not
able to pass any urine. An ultrasound scan revealed gross bladder
distension & bilateral hydronephrosis. Respiratory difficulty (with
increasing arterial pCO2)
was noted by 20 hours after admission. He was intubated, ventilated and
managed in the Intensive Care Unit. Urine was drained supra-pubically:
1500 mls immediately then 500mls/hr! He was extubated at 42 hours from
admission. He received a total of 1,860 mmol of potassium in this 42
Ileal or colonic bladders do not lead to significant acidosis unless
there is inadequate drainage resulting in prolonged contact time with
the mucosa. Chloride exchanges for bicarbonate leading to a
hyperchloraemic acidosis. An additional factor in this patient is the
use of Normal saline as a resuscitation fluid: this in itself leads to a
hyperchloraemic acidosis (eg see abstract below).
This case was reported:
Dunn SR, Farnsworth TA & Karunaratne WU. Hypokalaemic,
hyperchloraemic metabolic acidosis requiring ventilation.
Anaesthesia, 1999, 54: 566-568
Scheingraber S, Rehm M, Sehmisch C, Finsterer U. Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic
surgery. Anesthesiology 1999 May;90(5):1265-70
BACKGROUND: Changes in acid-base balance caused by infusion of a 0.9% saline solution during anesthesia and surgery are poorly characterized. Therefore, the authors evaluated these phenomena in a dose-response study.
METHODS: Two groups of 12 patients each who were undergoing major intraabdominal gynecologic surgery were assigned randomly to receive 0.9% saline or lactated Ringer's solution in a dosage of 30 ml x kg(-1) x h(-1). The pH, arterial carbon dioxide tension, and serum concentrations of sodium, potassium, chloride, lactate, and total protein were measured in 30-min intervals. The serum bicarbonate concentration was calculated using the
Henderson-Hasselbalch equation and also using the Stewart approach from the strong ion difference and the amount of weak plasma acid. The strong ion difference was calculated as serum sodium +
serum potassium - serum chloride - serum lactate. The amount of weak plasma acid was calculated as the serum total protein concentration in g/dl x 2.43.
RESULTS: Infusion of 0.9% saline, but not lactated Ringer's solution, caused a metabolic acidosis with hyperchloremia and a concomitant decrease in the strong ion difference. Calculating the serum bicarbonate concentration using the Henderson-Hasselbalch equation or the Stewart approach produced equivalent results.
CONCLUSIONS: Infusion of approximately 30 ml x
kg(-1) x h(-1) saline during anesthesia and surgery inevitably leads to metabolic acidosis, which is not observed after administration of lactated Ringer's solution. The acidosis is
associated with hyperchloremia.
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