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

  1. Describe the acid-base disturbance. (10% marks)
  2. List three likely causes. (15%marks)

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College answer

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
 

Discussion

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:

Causes of Metabolic Alkalosis; Organised by Inorganic Ion

Anions

Cations

Chloride depletion

  • Gastric losses by vomiting or drainage
  • Diuretics: loop or thiazides
  • Diarrhoea
  • Posthypercapneic state
  • Dietary chloride deprivation
  • Gastrocystoplasty
  • Cystic fibrosis (loss due to high sweat chloride content)

Bicarbonate excess (real or apparent)

  • Iatrogenic alkalinisation
  • Recovery from starvation
  • Hypoalbuminemia

Potassium depletion

  • Primary hyperaldosteronism
  • Mineralocorticoid oversupplementation
  • Licorice (glycyrrhizic acid)
  • β-lactam antibiotics
  • Liddle syndrome
  • Severe hypertension
  • Bartter and Gitelman syndromes
  • Laxative abuse
  • Clay ingestion

Calcium excess

  • Hypercalcemia of malignancy
  • Milk-alkali syndrome

References

References

Cogan, Martin G. "Chronic hypercapnia stimulates proximal bicarbonate reabsorption in the rat." Journal of Clinical Investigation 74.6 (1984): 1942.

Khanna, Apurv, and Neil A. Kurtzman. "Metabolic alkalosis." studies 28 (2006): 29.

Tripathy, Swagata. "Extreme metabolic alkalosis in intensive care." Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine 13.4 (2009): 217.

Galla, John H. "Metabolic alkalosis." Journal of the American Society of Nephrology 11.2 (2000): 369-375.

Pahari, D. K., et al. "Diagnosis and management of metabolic alkalosis."JOURNAL-INDIAN MEDICAL ASSOCIATION 104.11 (2006): 630.

Palmer, Biff F., and Robert J. Alpern. "Metabolic alkalosis." Journal of the American Society of Nephrology 8.9 (1997): 1462-1469.

Gennari, F. John. "Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport." American Journal of Kidney Diseases 58.4 (2011): 626-636.