Chapter 6 Metabolic alkalosis (& chloride homeostasis)
6.1 Causes of a metabolic alkalosis
The causes of a metabolic alkalosis can be classified as being either due to chloride depletion (and therefore chloride responsive) or due to other causes (chloride resistant) (Luke & Galla, 2012).
| LOW ECF VOLUME = CHLORIDE-DEPLETION / CHLORIDE-RESPONSIVE | GI chloride loss | vomiting / NG losses |
| GI chloride loss | colonic villous adenoma / congenital chloride diarrhoea / high-volume ileostomy (rare) | |
| loop / thiazide diuretics * | ||
| Bartter / Gitelman * | ||
| NORMAL ECF VOLUME = CHLORIDE-RESISTANT | renal H + loss | true mineralocorticoid XS (low-renin / high-renin) |
| apparent mineralocorticoid XS (and Liddle’s) | ||
| Cushings | ||
| post-hypercapnic alkalosis (UCl < 10 mM) | ||
| milk-alkali syndrome | ||
| hypokalaemia |
* in chloride-responsive states UCl < 10 mM except where chloride is being lost in the urine (i.e. diuretics / Gitelman / Barrter syndrome).
As a general rule, extreme alkalosis (HCO3 > 45 mM) can only be due to vomiting (and consider pyloric stenosis / Zollinger Ellison syndrome).
Post-hypercapnic alkalosis occurs if chronic hypercapnia suddenly corrected (e.g. by mechanical ventilation).
The milk-alkali syndrome is the triad of hypercalcaemia, metabolic alkalosis and ingestion of large quantities of calcium with alkali; hypercalcaemia increases renal bicarbonate reabsorption (exacerbating alkalosis).
6.2 Chloride
UCl NR = 100 – 250 mmol / 24 hrs
In chloride-responsive alkalosis, UCl < 10 mM:
- vomiting
- villous adenoma
- congenital chloride diarrhoea
- recent diuretics (pause on clinic day in surruptitious use)
In chloride-resistant alkalosis UCl > 10 – 30 mM (and also if chloride loss is due to diuretics / tubulopathies).
UCl is persistently low after vomiting and is therefore a useful test for surreptitious vomiting.
6.2.1 Chloride-depletion alkalosis
In chloride depletion, reduced ECF volume leads to reduced GFR (less filtered NaHCO3) and increased Na reabsorption. Thus NaHCO3 reabsorption is increased. Increased distal Na reabsorption leads to increased acid excretion. Therefore, after vomiting, an acid urine is produced (paradoxically) in the face of a metabolic alkalosis. Treatment is volume expansion with NaCl and correction of hypoK.