A 76-year-old male with a background of emphysema is now Day 7 after an elective colectomy. His ICU stay was complicated by intra-abdominal sepsis and ongoing high-volume nasogastric aspirates. There is difficulty in weaning him from the ventilator. The following arterial blood gases are obtained:
Parameter |
Patient Value |
Adult Normal Range |
FiO2 |
0.35 |
|
pH |
7.58* |
7.35 – 7.45 |
pO2 |
82.0 mmHg (10.9 kPa) |
|
pCO2 |
52.0 mmHg (6.9 kPa)* |
35.0 – 45.0 (4.6 – 6.0) |
SpO2 |
94% |
|
Bicarbonate |
47.0 mmol/L* |
22.0 – 26.0 |
Base Excess |
23.7 mmol/L* |
-2.0 – +2.0 |
a) There is a primary metabolic alkalosis which is appropriately compensated.
b) Likely causes
1. Volume depletion due to high naso-gastric losses causing contraction alkalosis
2. Any cause of hyperaldosteronism (e.g., Glucocorticoids for emphysema, Barrter’s syndrome, Cushing’s disease etc)
3. Chloride loss in urine from diuretics; e.g. frusemide
Let us dissect these results systematically:
1)
The A-a gradient is significantly increased:
(0.35 x 713) - (52 x 1.25) - 82 = 102.55 mmHg
2) There is an alkalaemia
3) The CO2 is appropriately elevated
4) There is a metabolic alkalosis (the SBE is 23.7)
5) The respiratory compensation is appropriate: (0.7 × 47) + 20 = 52.9 mmHg, or (0.6 × 23.7) + 40 = 54.22 mmHg, depending on which formula you use.
Causes of metabolic alkalosis in this case could include a broad range of differentials, but the question text clearly describes a man who is losing chloride constantly from the NG tube and whose COPD history predisposes him to a compensatory post-hypercapnia alkalosis. One could also safely wager that steroids and frusemide have at some stage been used in their care. For completeness, here is the full list:
Anions |
Cations |
Chloride depletion
Bicarbonate excess (real or apparent)
|
Potassium depletion
Calcium excess
|
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