A woman in her 50s with chronic fatigue syndrome, sepsis and hyponatraemia

A woman in her 50s was found at home by her husband, who was unable to communicate with her. She had been coughing and feeling lethargic and unwell for the previous few days. The woman used no drugs on a regular basis. When the ambulance crew arrived, she was disorientated, with a Glasgow Coma Scale (GCS) score of 13. Her temperature was 40.5 °C. She was given 500 ml Ringer’s acetate intravenously on her way to Acute Admissions.

In Acute Admissions, she could move her extremities, was free of pain and her neck was not stiff. Her GCS score was unchanged. Her skin was dry, warm and without petechiae. Her blood pressure was low (88/61 mm Hg – 105/51 mm Hg – 91/60 mm Hg – despite infusion of 2 000 ml Ringer’s acetate. Her pulse was regular, between 113 and 126 beats/minute, her temperature was 39.7 °C, SpO₂ was 97 % with 3 l O₂ and her respiratory rate 20 – 25 per minute. On auscultation, reduced respiratory sound over the right lung, most pronounced basally.

Blood tests on admission are shown in Table 1. Blood gases were taken arterially in room air. The urine strip test showed traces of albumin and blood, otherwise normal findings. The rapid urine antigen test for pneumococcus was negative. Chest x-ray showed an opacity in hilar position on the right side, consistent with pneumonia infiltrate.

Treatment commenced with penicillin, 5 mill. IU × 4 and gentamicin 360 mg × 1 intravenously. She was moved to the Intensive Care Department, where because of her persistently low blood pressure despite rehydration treatment, she received vasopressor therapy in the form of noradrenaline. She did not require ventilatory support.

Some nine years earlier, the patient had been put on 100 % invalidity following an upper respiratory tract infection, because of nautical vertigo, fatigue, lethargy and occasional numbness of the arms and legs. She had also developed problems with loose stools and reduced appetite, and had lost 13 kg. She had low blood pressure of around 100/70 mm Hg (compared with 140/90 mm Hg previously), headache and joint pain.

She was assessed by her GP, a neurologist, an ear, nose and throat specialist, an ophthalmologist and a gastroenterologist, without any definite diagnosis being made. Gastroscopy with biopsy showed non-specific changes, colonoscopy with biopsy was normal, CT abdomen revealed hepatic steatosis (at the time the patient drank about 10 units of alcohol per month), while an MRI of the small intestine revealed no definite pathology. MRI of the head was normal, and the conclusion after a neurological assessment was balance disorder, probably as a sequela of an influenza-like illness. Values for TSH and free T₄ were normal. After two years of extensive workup, she finally received the diagnosis myalgic encephalomyelitis (ME). She was put on a disability pension and stated up to the time of the current hospitalisation that she had permanently reduced quality of life.

The day after her admission the patient was awake, in reduced general condition. She had difficulty finding words and was slightly disorientated. She still did not have a stiff neck, rash or headache, so no lumbar puncture was performed. A clinical examination revealed normal conditions apart from abundant crepitations over the whole surface of her right lung. She still had a tendency to hypotension, with systolic pressure of 90 – 100 mg Hg, but normal diuresis and normalised renal function. Noradrenaline was tapered and discontinued, and she was moved to a ward, where her antibiotics treatment continued.

Four days after her admission, her penicillin dose was reduced to 2 mill. IU × 4 intravenously because of clinical improvement and falling infection markers. Cultures of blood samples taken on admission showed no microbial growth. A deep nasal swab showed abundant growth of Staphylococcus aureus, regarded as normal flora. However, the patient had falling serum sodium to 121 mmol/l (137 – 145 mmol/l) despite infusion of a total of 2 l NaCl 9 mg/ml. A number of laboratory tests, shown in Table 2, were performed as part of hyponatraemia assessment, but the results were only available after her discharge.

Six days after admission, the woman was discharged in relatively good general condition. She was treated further with phenoxymethylpenicillin 660 mg × 4 and potassium chloride 750 mg × 3. Blood tests now showed CRP 69 mg/l (0 – 4 mg/l), leukocytes 4.4 · 10⁹/l (3.5 – 10 · 10⁹/l), sodium 131 mmol/l (137 – 145 mmol/l), potassium 3.2 mmol/l (3.6 – 5.0 mmol/l), creatinine 47 μmol/l (45 – 90 μmol/l).

Thyroid tests – TSH 0.78 mIU/l (0.5 – 3.6 mIU/l) and free T₄: 4.5 pmol/l (6 – 20 pmol/l) – led to the condition being perceived as hypothyroidism. She was started on levothyroxine 25 μg × 1, a dose that her GP doubled after a week. Follow-up at the hospital «electrolyte clinic» was agreed.

As soon as the results of the hormone analyses were available, the patient was contacted by telephone. She came for a further consultation and was then lethargic, tired and dizzy. She explained that for the past five months, she had had problems with varying sight in her left eye. She had seen a general ophthalmologist, but so far without any conclusion. She did not report headache, nausea or a craving for salt, but felt very tired and was unable to eat; her fluid intake was adequate.

At the clinical examination she was orientated with respect to time, place and situation, but tired. She had no signs of hyperpigmentation of the skin or the mouth cavity. Her weight was 56.8 kg, body mass index (BMI) 19.2 kg/m². The blood pressure measurements were: sitting 98/50 mm Hg, pulse 80 regular, standing immediately 88/62 mm Hg, pulse 102 regular and standing after three minutes 70/43 mm Hg, pulse 110 regular. She then became dizzy. Donders’ test revealed a normal field of vision for the right eye and a reduced field temporally for the left eye.

Blood tests showed sodium 136 mmol/l (137 – 145 mmol/l), potassium 4.8 mmol/l (3.6 – 5.0 mmol/l). Further hormone analyses were performed on suspicion of hypopituitarism; see Table 3.

Clinical and laboratory findings were consistent with secondary adrenal insufficiency. Treatment with cortisone acetate tablets began – 50 mg in the morning and 25 mg in the evening for three days, then 25 mg in the morning and 12.5 mg in the evening. An MRI scan of the pituitary gland was ordered. Potassium chloride was discontinued as normokalaemia had been attained.

At follow-up two weeks later, the patient related that she felt considerably better. «I’m like a new person.» The dizziness was gone, she had a good appetite, was sleeping well and for the first time in many years felt that she had energy. She did not experience an orthostatic fall in blood pressure any longer. New blood tests showed sodium 141 mmol/l (137 – 145 mmol/l), potassium 4.5 mmol/l (3.6 – 5.0 mmol/l), creatinine 52 μmol/l (45 – 90 μmol/l), carbamide 5.6 mmol/l (3.1 – 7.9 mmol/l), glucose 4.9 mmol/l (4 – 6 mmol/l), TSH 0.21 mIU/l (0.5 – 3.6 mIU/l) and free T₄ 15.3 pmol/l (8 – 21 pmol/l).

An MRI scan of the pituitary gland (Fig. 1a) revealed a large (31 mm × 29 mm × 26 mm) cystic intracellular tumour, with a large supracellular component that raised the optic nerve decussation. The finding was assumed to represent either a craniopharyngioma or a cystic pituitary macroadenoma.

An endocrinologist was consulted. Because the patient did not have elevated prolactin and had insulin-like growth factor 1 (IGF-1) in the lower normal range, she was referred for neurosurgery.

In a neuro-ophthalmological assessment prior to the operation, best corrected visual acuity was 1.6 for the right eye and 0.25 for the left eye. The patient read Ishihara’s colour plates a little hesitantly with the right eye and did not manage any plates with the left eye. Field of vision tested with threshold perimetry (Fig. 2A) showed a bitemporal reduction in sensitivity, but more so for the left eye. The left pupil had a slightly impaired direct light reflex. A fundoscopic examination revealed the left optic nerve to be a little pale compared with the right, compatible with slight optic atrophy. Neurological status was otherwise normal.

The patient underwent surgery with transsphenoidal resection of the tumour in the hypophyseal recess, with uncomplicated post-operative course.

An MRI scan of the pituitary gland immediately postoperatively (Fig. 1B) showed no sign of residual tumour, and the optic paths were free. The histology results revealed that the tumour was a non-hormone-producing pituitary adenoma with a low level of the proliferation marker ki67.

A synacthen test was performed at follow-up three months postoperatively, and was normal. The treatment with cortisone acetate could be discontinued. She continued with levothyroxine 50 μg × 1. The function of the growth hormone axis was not tested, but the possibility of growth hormone deficiency cannot be excluded, even though IGF-1 lay in the normal range.

The patient experienced rapid postoperative normalisation of her vision. At a check-up with the ophthalmologist five months after the operation, best corrected visual acuity was 1.25 for both eyes. She now read Ishihara’s colour plates for both eyes, but still more easily with the right than with the left. Threshold perimetry (Fig. 2B) revealed considerable improvement in the earlier bitemporal reduction in sensitivity.