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Severe Headache and Vomiting

Try out this endocrine case and test your clinical knowledge. The answers are at the bottom.

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Questions

A 48-year-old man presents to his GP having vomited twice at home. As he sits down you note that he is very pale and is sweating profusely. He reports that he also has a severe headache which has been present for the last few hours and is worse in the parietal region.

Observations:

– SpO2: 97%
– Temperature: 37.2
– BP: 200/131
– HR: 110
– RR: 19

Examination:

Abdominal:
– NAD

Cranial nerves:
– NAD

Fundoscopy
– Flame hemorrhages present in upper R quadrant of both eyes

Q1: How should the GP manage this patient?

The GP manages the patient appropriately. Some point of care bloods are also taken:

Blood Results:

Q2: Interpret the blood results. What would be the most useful investigation to confirm the likely diagnosis?

The patient suddenly becomes drowsy and collapses. When a nurse tries to rouse him by applying supraorbital pressure he groans, flexes his left arm awkwardly but does not open his eyes.

Q3: Calculate his Glasgow Coma Scale (GCS) score. What is the clinical significance of this?

The patient regains consciousness but is still very drowsy and incoherent. On neurological examination it is noted that he has a left sided weakness and left sided hyperreflexia. Sensory examination is normal. An urgent CT Head is requested.

CT Head:

Image 1: Case courtesy of Dr Henry Knipe, Radiopaedia.org, rID: 46238 https://radiopaedia.org/cases/large-right-basal-ganglia-haemorrhage

Q4: Interpret the CT Head. (Bonus: What complication has occurred & why?)

Answers

The patient needs a same-day specialist assessment (i.e. admission to hospital to be seen by cardiology immediately) for two key reasons:

– The patient has a BP of >180/120 and is constitutional symptoms that may suggest a phaeochromocytoma (pallor, headache, diaphoresis)

– The patient has evidence of end-organ damage on fundoscopy (haemmorhages) likely caused by the extreme hypertension

Key points from the bloods:
– Borderline hypernatraemia
– Hypokalaemia
– Low renin
– Elevated aldosterone
– Normal cortisol and metanephrines

The bloods exclude a phaeochromocytoma and Cushing’s syndrome as causes of the hypertension (normal plasma metanephrines and cortisol). The raised aldosterone leads us to the diagnosis – elevated aldosterone leads to suppression of the RAAS axis by negative feedback (hence the low renin) and leads to increased K+ excretion coupled with Na+ absorption in the renal tubules (explaining the borderline hypernatremia and prominent hypokalemia). The gold standard blood test would be a corrected aldosterone:renin (ratio), which one would expect to be elevated.

The likely diagnosis here is Conn’s syndrome (primary hyperaldosteronism), likely caused by hyperplasia of the adrenal glands or a hyperfunctioning adenoma of the zona glomerulosa. The best investigation to assess for this would be a contrast-enhanced CT scan of the abdomen, coupled with bilateral adrenal vein sampling to assess whether any hyperplastic glands are actually functioning (i.e., a gland could be hyperplastic but be producing normal amounts of aldosterone)

E – 1 (no eye opening)
V – 2 (incomprehensible sounds)
M – 3 (abnormal flexion)

Total = 6

A GCS score of less than 8 is a concerning feature as it suggests a patient is unable to maintain their airway independently and is at high risk of airway compromise – in this scenario an anesthetist should be called urgently with a view to intubate the patient.

This is an axial non-contrast CT Head at the level of the basal ganglia. There is a large hyperdense region overlying the right basal ganglia and internal capsule – this is a large intracerebral bleed. In patients with chronic hypertension, microaneurysms can form in the neurovasculature which can then burst and cause intracerebral and subarachnoid haemmorhages – a phenomenon known as Charcot-Bouchard syndrome. In this case, the bleed in the basal ganglia suggests aneurysmal formation in the lenticulo-striate arteries that supply the basal ganglia and internal capsule. As the internal capsule is involved, the patient has experienced a pure motor ‘lacunar’ stroke, giving rise to his symptoms. The absence of sensory symptoms is confirmed by the lack of any thalamic or sensory cortical involvement.

To get more information about the conditions mentioned in this case including diagnosis and management, have a look at our free endocrine notes on In2Med. Written by medical students, we have pitched them just at the right level to help you ace your exams.

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