A paraneoplastic potassium and acid-base disturbance

Samuel P. Wiles; Matthew Kiczek; Gregory W. Rutecki

doi:10.3949/ccjm.86a.18014

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Figure 1
Algorithms for determining causes of metabolic acid-base disturbances.
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Figure 2
The hypothalamic-pituitary-adrenal axis.
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Figure 3
Computed tomography of the chest depicting biopsy-proven small-cell carcinoma (arrows).

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TABLE 1

Laboratory results on presentation and 1 year earlier

Test	Current level^a	1 year earlier	Reference range
Sodium (mmol/L)	144	135	136–144
Potassium (mmol/L)	2.8	4.0	3.7–5.1
Chloride (mmol/L)	96	100	97–105
Bicarbonate (mmol/L)	40	28	22–30^b
Serum creatinine (mg/dL)	1.2	1.2	0.58–0.96
Blood urea nitrogen (mg/dL)	28	19	7–21
Glucose (mg/dL)	197		74–99
Calcium and magnesium	Normal
Arterial blood gases
pH	7.50	7.34	7.35–7.45
PCo₂ (mm Hg)	51	40	34–46^c
PaO₂ (mm Hg)	75	76	85–95
Bicarbonate (mmol/L)	40		22–26

↵a Abnormal results are shown in bold.
↵b For acid-base problem-solving, a value of 25 mmol/L is considered normal.
↵c For acid-base problem-solving, a value of 40 mm Hg is considered normal.

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TABLE 2

‘Rules of 5’ for acid-base problem-solving

1 Determine the arterial pH	pH < 7.38 is acidemic, pH > 7.42 is alkalemic^a Normal pH does not rule out an acid-base disorder

2 If the arterial pH is abnormal, determine whether the primary process is respiratory, metabolic, or both		pH	PCO₂	HCO₃
	Respiratory acidosis^a	Low	High	—
	Metabolic acidosis	Low	—	Low
	Mixed respiratory and metabolic acidosis	Low	High	Low
	Respiratory alkalosis	High	Low	—
	Metabolic alkalosis	High	Varies^b	High
	Mixed respiratory and metabolic alkalosis	High	Low	High

3 Calculate the anion gap	Anion gap = sodium – (chloride + bicarbonate) If serum albumin is low, add 2.5 mmol/L to the anion gap for every 1 g the serum albumin is below normal

4 Check the degree of compensation (respiratory or metabolic)	Pco₂ and bicarbonate should increase or decrease together
	Normal levels: bicarbonate 25 mmol/L, PCO₂ 40 mm Hg
	Acute respiratory acidosis: For every 10-mm Hg increase in Pco₂, bicarbonate should increase by 1 mmol/L
	Chronic respiratory acidosis (> 48 hours): For every 10-mm Hg increase in Pco₂, bicarbonate should increase by 4 mmol/L
	Metabolic acidosis: For every 1-mmol/L decrease in bicarbonate, Pco₂ should decrease by 1.3 mm Hg
	Acute respiratory alkalosis: For every 10-mm Hg decrease in Pco₂, bicarbonate should decrease by 2 mmol/L
	Chronic respiratory alkalosis (> 48 hours): For every 10-mm Hg decrease in Pco₂, bicarbonate should decrease by 5 mmol/L
	Metabolic alkalosis: For every 1-mmol/L increase in bicarbonate, Pco₂ may increase by 0.6 mm Hg

5 If the patient has metabolic acidosis with an elevated anion gap, assess for ‘delta gap’ (whether the decrease in bicarbonate = the increase in anion gap)	Delta gap = change in anion gap / change in bicarbonate ([anion gap – 10] / [24 – bicarbonate])
	> 1: Additional metabolic alkalosis
	1: No additional disturbance present
	< 1: Additional non-anion gap metabolic acidosis present

↵a Acidosis and alkalosis refer to acid-base disturbances with determined metabolic or respiratory etiologies. Alkalemia and acidemia refer to disturbances in blood pH prior to determination of the underlying metabolic/respiratory cause.
↵b Pco₂ in metabolic alkalosis may vary depending on the clinical context, as compensation for metabolic alkalosis requires decreased respiratory drive, which may be influenced by other factors (ie, hypoxia).
Pco₂ = partial pressure of carbon dioxide
Adapted from Mani S, Rutecki GW. A patient with altered mental status and an acid-base disturbance. Cleve Clin J Med 2017; 84(1):27–34. Copyright © 2017 The Cleveland ClinicFoundation. All rights reserved.

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TABLE 3

Renin and aldosterone values in hypokalemic metabolic alkalosis with high urine chloride

Renin and aldosterone	Elevated blood pressure	Normotensive
High renin, high aldosterone, normal ratio of plasma aldosterone concentration(PAC) to plasma renin activity(PRA)	Renal artery stenosis Renin-secreting tumor Diuretics	Bartter syndrome Gitelman syndrome Severe potassium depletion (villous adenoma) Diuretics
Low renin, high aldosterone, high PAC–PRA ratio	Primary hyperaldosteronism
Low renin, low aldosterone, normal PAC–PRA ratio	Licorice Cushing disease or syndrome Hydroxylase deficiencies Liddle syndrome

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TABLE 4

Effects of hypercortisolism

Organ system	Manifestation
Cardiovascular	Hypertension, thromboembolism, cardiomyopathy
Metabolic	Glucose intolerance/diabetes, hyperlipidemia, obesity
Reproductive	Menstrual irregularities, hirsutism, changes in libido, virilization
Dermatologic	Easy bruisability, striae, skin atrophy, hyperpigmentation, oily skin
Musculoskeletal	Proximal muscle wasting, osteopenia/ osteoporosis
Neuropsychiatric	Psychosis, emotional lability, depression, anxiety, sleep apnea
Immunologic function	Increased susceptibility to fungal and bacterial infection, opportunistic infections
Ophthalmologic	Glaucoma, cataracts, central serous chorioretinopathy, hypertensive retinopathy