Specimen Name Result Units Range

Plasma Sodium 148 mmol/L (135-145)
Potassium 1.9 mmol/L (3.5-5.5)
Chloride 89 mmol/L (100-109)
Bicarbonate 58 mmol/L (22-32)
Anion Gap 3 mmol/L (7-17)
Glucose 6.6 mmol/L (3.8-5.5)
Urea 4.3 mmol/L (2.7-7.2)
Creatinine 81 μmol/L (60-110)
Magnesium 1.11 mmol/L (0.70-0.95)

ABG pH 7.52 (7.36-7.44)
PaO2 128 mmHg (70-100)
PaCO2 59 mmHg (35-45)
HCO3- 47 mmol/L (21-26)
BE 21 mmol/L (±3)

35yo male admitted for elective knee arthroscopy

Asymptomatic except for knee pain

Hypertensive, BP ≈ 180/110mmHg

Pigmented palmar creases


Cushing's Syndrome

 

Causes of hypertension and hypokalaemic alkalosis

  • Cushing's syndrome
  • primary hyperaldosteronism
  • essential hypertension & diuretic use
  • essential hypertension & 2° hyperaldosteronism
    • malignant hypertension
    • renovascular hypertension
    • drugs - steroids, oestrogen
    • renin-secreting tumour
  • congenital adrenal enzyme deficiencies
  • carbenoxolone
  • Liddle's syndrome - 'pseudohyperaldosteronism'

Cushing's Syndrome

  • iatrogenic steroid administration → most common
  • pituitary adenoma (≈70%) - of remainder
  • ectopic ACTH (≈15%) → biochemical effects, not clinically Cushingoid
  • adrenal adenoma / carcinoma (≈15%)
  1. Clinical Features:
    • truncal obesity ≈ 90%
    • hypertension ≈ 80%
      ↑renin, ↑vascular reactivity, ↑blood volume 2° fluid retention
    • plethoric face ≈ 75%
    • hirsutism ≈ 70%
    • proximal myopathy ≈ 60%
    • osteoporosis ≈ 60%
    • bruising, striae ≈ 50%
    • poor wound healing ≈ 40%
    • NB: usual "ACTH" picture ∝ rate of tumour growth →
      • rapidly growing tumours - eg. oat cell
        → hypokalaemia, muscle weakness & wasting, and hyperpigmentation
      • slowly growing tumours - e.g. ovary, thyroid medullary, thymic, pancreatic, bronchial adenoma
        → classical Cushingoid features
  2. Electrolyte Abnormalities
    • high Na+, HCO3- & glucose
    • low K+ & Ca++
    • metabolic alkalosis
  3. Secondary Endocrine Effects
    • insulin resistance / glucose intolerance
    • 2° hyperparathyroidism ∝ ↑ urinary Ca++ excretion / ↓ GIT absorption
    • antagonism of GH effects
    • ↑ACTH → ↑pigmentation
    • androgen excess

 

Hypokalaemic Metabolic Alkalosis
Diuretics (esp. loop agents) - low Na+, Cl- / high urea
Mineralocorticoid excess - normal-high Na+, Cl- / normal urea
Vomiting / Gastric outlet obs. - very low Cl- / low-normal Na+ / high urea
Diarrhoea / laxatives - low Cl- / normal Na+ / high urea
Post massive transfusion - citrate metabolism & acidosis correction