- Headache is usually frontal, although may take any form. It is primarily caused by pressure effects in the pituitary fossa and often induces nausea and vomiting.
- If blood escapes into the subarachnoid space, this may be accompanied by meningism. Cranial nerve III, IV and VI palsies result from compression of the adjacent cavernous sinuses, and visual field/acuity deficits from compression of the optic chasm lying superior to the fossa. Haemorrhage and the resultant pressure effects may not be maximal at presentation and repeated examination is essential to detect progressive neurological deficit, the presence of which may trigger escalation to emergency neurosurgical intervention.
- Some degree of pituitary hormone insufficiency is a feature of most cases of apoplexy, with ACTH and consequently cortisol insufficiency being both common, and the most important of these. If severe enough this may manifest as haemodynamic instability, since the lack of glucocorticoid obtunds the pressor effect of catecholamine signals. Delay in glucocorticoid replacement in these patients may be fatal.
- Apoplexy may be precipitated by many factors; hypertension is the commonest. Conditions causing wide variations of blood pressure, including major surgery, are frequently implicated. Other known risk factors include head trauma, anticoagulant therapy or clotting disorders and pregnancy (especially in the peripartum phase, when pituitary apoplexy is known as Sheehan syndrome).
In the first hour of treatment the following goals should be achieved:
- Rapid assessment of airway, breathing, circulation and conscious level.
- Airway management by competent staff if the airway is compromised or the Glasgow Coma Scale score is less than 8.
- Supplemental oxygen, if needed to achieve arterial saturation 94–96%.
- Fluid resuscitation in the shocked or otherwise haemodynamically compromised patient, with the addition of immediate administration of a sufficient dose of glucocorticoid on the presumption of ACTH insufficiency, for example 100–200 mg intravenous hydrocortisone to be followed by 50–100 mg every 6h (preferably by intramuscular injection as this provides a predictable pharmacokinetic profile and therefore more consistent glucocorticoid activity when compared to intravenous boluses).
- Visual field examination by confrontation (with a red pin if available), Snellen chart visual acuity and cranial nerve III, IV, Va and VI examination. Document these clearly in the notes for later comparison.
- Request urgent dedicated pituitary imaging, preferably MRI as this is the most sensitive modality. General cerebral imaging not dedicated to the pituitary fossa cannot be relied upon to reveal the diagnosis, with CT demonstrating a pituitary mass in less than 80% of cases and pituitary haemorrhage in only 20%.
- Other investigation needed urgently is given in Table 93.1.