Case Study 2: Primary Adrenal
Insufficiency - Addison’s Disease
Harjoeth Singh Bassra
18688528
Word count: 2,197
, Clinical presentation
A 30-year-old female patient was admitted to the surgical ward with abdominal pain and
emesis over two days. She later disclosed her history of weight loss, anorexia, fatigue and
skin pigmentation; she has not been administered any long-term medication. The physical
examination revealed her blood pressure was below the optimal range (120/90 mmHg)
measuring at 109/64mmHg and her pulse rate was 89bpm. Although her pulse rate is within
the normal range (60-100bpm), it’s in the upper limit indicating her heart rate is
compensating for the reduced blood pressure (Staessen, et al, 2017; Avram, et al, 2019).
Based on these symptoms, intestinal obstruction was the provisional diagnosis, further
investigation was required following the initial tests.
Laboratory investigations
An electrolyte panel was performed to ensure the patient was healthy enough to potentially
undergo surgery for suspected intestinal obstruction without complications.
Table 1: Electrolyte panel & Urea and Creatinine results of the patient
Serum analyte Results Reference
ranges
Sodium ions (Na+) 127mmol/L 135 -
145mmol/L
Potassium ions (K+) 6.0mmol/L 3.4 – 4.9mmol/L
Chloride ions (Cl-) 91mmol/L 95 – 105mmol/L
Bicarbonate ions 18mmol/L 21 – 28mmol/L
-
(HCO3 )
Urea 10.9mmol/L 2.5 – 8.0mmol/L
Creatinine 181µmol/L 40-130µmol/L
Electrolyte panels are a standard routine procedure for screening a patient’s blood to
ascertain whether an electrolyte imbalance is causing the patient’s symptoms (fatigue,
emesis, abdominal pain). Electrolyte imbalances can cause intestinal obstruction therefore
electrolyte panels can aid with correct diagnosis (Choudhury, et al, 2015; Shrimanker and
Bhattarai, 2019). The electrolyte panel results (table 1), shows the patient exhibiting multiple
electrolyte abnormalities.
The patient’s sodium levels are <135mmol/L which is observed with hyponatraemia.
Hyponatraemia is clinically defined as serum sodium concentrations of <135mmol/L and
, imbalanced sodium to water ratios in the body. Hyponatraemia is observed in 15-30% of
hospitalised patients and has varied aetiologies making it complex to determine the
underlying cause (Sahay and Sahay, 2014) (Rondon and Badireddy, 2017). A prospective
analysis by Anderson et al (1985) revealed that non-osmotic secretion of vasopressin was
identified in 97% of hyponatraemic patients, amplifying the importance of vasopressin in the
pathogenesis of hyponatraemia. Vasopressin is an antidiuretic hormone responsible for
regulating water excretion thus affecting the ratio of total body water to serum sodium
concentrations (Cuzzo, et al, 2020; Abdalla, et al, 2021).
Clinical manifestations of hyponatraemia reflect disturbances in water movement in the brain
inducing cerebral oedema which gives rise to neurological symptoms ranging from
headaches, confusion, to seizures, coma, and even death (Sahay and Sahay, 2014).
The patient is exhibiting ~2-fold elevation in serum potassium levels, which falls within the
mild hyperkaliaemic range (>5.5mmol/L). ~1-10% of hospitalised patients exhibit
hyperkalaemia caused by kidney degradation, with symptoms arising once the glomerular
filtration rate (GFR) is <30ml/min. The accumulation of potassium in the bloodstream can
induce muscular dysfunction, cardiac arrythmias and paralysis (Hollander-Rodriguez and
Calvert, 2006; Simon, et al, 2020). Hyperkalaemia may also occur due to an aldosterone
deficiency (hypoaldosteronism), resulting in reduced potassium excretion via urine due to
potassium retention (Abdalla, et al, 2021). Although hypoaldosteronism is characterised by
hyponatraemia, hyperkalaemia and metabolic acidosis (MA), quantification
of aldosterone in the blood is required to confirm this
suspicion (Eleftheriadis, et al, 2012). Adrenal
insufficiency should be suspected in patients
with hyperkalaemia when coupled with hyponatraemia
(Hollander-Rodriguez and Calvert, 2006).
