Pituitary apoplexy case reports

A 40-year-old male patient presents with an abrupt onset headache associated with left partial oculomotor nerve palsy. The MRI shows a sellar lesion involving the left cavernous sinus with a heterogenous anterior aspect of the lesion with hemorrhagic zones in favor of pituitary apoplexy. Endocrine work-up shows a high testosterone level in a patient who was using exogenous testosterone without a medical prescription for a month.

The association between PA and AAS should be considered a potential risk ¹⁾.

A 20-year-old woman was brought to the emergency room with headache, breathlessness, and altered sensorium. The clinical and biochemical evaluation revealed SVT, diabetic ketoacidosis, and right lower limb ALI. On inquiry, the patient was found to be diagnosed with pituitary adenoma 2 years ago and lost to follow-up. PA was detected on neuroimaging and confirmed histopathologically. The possibility of PA presenting as diabetic ketoacidosis (DKA) and its sequelae exists ²⁾.

A case of a man in his late 50s who developed pituitary apoplexy following treatment of PCa with leuprolide. His symptoms developed insidiously and he presented 6 months after symptom onset. Anterior pituitary hormone workup along with pituitary MRI confirmed the diagnosis of PA and the patient was subsequently treated with adequate replacement of pituitary hormone with significant improvement in his symptoms. It is very important to keep a high index of suspicion for PA, especially among elderly patients receiving gonadotropin-releasing hormone agonist treatment for prostate cancer ³⁾.

A 38-year-old female presented with acute onset of severe headache decreased level of consciousness, decreased visual acuity bilaterally, aphasia, and right hemiparesis. Computed tomography angiography showed a hyperdense sellar mass with left internal carotid artery stenosis. The patient underwent emergent endoscopic transsphenoidal surgery for sellar decompression.

The epidemiology, presentation and diagnosis, and strategy of treatments as well as their outcomes were discussed.

Pituitary apoplexy should be taken into consideration in a patient with increasing headache and neuro-ophthalmic symptoms. Pituitary apoplexy presenting as a cerebral infarction is rare. The aim of surgery in an emergency setting was sellar decompression. Endoscopic transsphenoidal surgery was an effective treatment ⁴⁾.

An 84-year-old man presented with a frontal headache and easy bruising. He had a background history of pituitary macroadenoma, diagnosed incidentally a year earlier. Investigations showed hemorrhage into the pituitary macroadenoma leading to a diagnosis of pituitary apoplexy in the context of low platelet count secondary to immune thrombocytopenia. He was treated with intravenous hydrocortisone, platelet transfusion, intravenous immunoglobulin, and high-dose steroid. Neurosurgical intervention was not indicated initially. Five days into his admission, he developed bilateral ptosis and ophthalmoplegia. MRI confirmed further hemorrhage associated with compression of the optic chiasm. He was transferred to a tertiary neurosurgical center where he underwent urgent surgical decompression. To date, there has been a minor improvement in his neurological symptoms. Management of this patient required considerable multidisciplinary teamwork between the clinics of endocrinology, hematology, neurosurgery, ophthalmology, and geriatrics ⁵⁾.

A Cushing's disease patient experienced corticotroph releasing hormone (CRH)-induced pituitary apoplexy during inferior petrosal sinus sampling (IPSS). The IPSS blood samples from Cushing's disease patient were retrospectively analyzed for cytokine markers. For comparison, we also analyzed cytokine markers in blood samples from two pituitary ACTH-secreting microadenoma patients and one patient with an ectopic ACTH-secreting tumor.

Acute elevation of interleukin 6 (IL-6) and matrix metalloproteinase 9 (MMP9) was observed in the IPSS blood sample on the apoplectic hemorrhagic site of the tumor. In contrast, such a change was not observed in the blood samples from the contralateral side of the apoplexy patient and in other IPSS samples from two non-apoplexy Cushing's disease patient and a patient with ectopic Cushing's syndrome.

IL-6 and MMP9 may be involved in the acute process of pituitary apoplexy in Cushing's disease ⁶⁾.

A 14-year-old girl was admitted for evaluation of a possible Cushing's syndrome (CS). Her symptoms and initial laboratory tests were suggestive of Cushing's disease. Magnetic resonance imaging (MRI) revealed a microadenoma of the pituitary gland. As part of her evaluation, she was submitted to a corticotropin-releasing hormone stimulation test. Two and a half months later the patient was re-evaluated and presented with both clinical improvement of CS, biochemical resolution of hypercortisolism, and tumor size reduction in the MRI, also evidencing a hemorrhagic component favoring the diagnosis of pituitary apoplexy after CRH stimulation test. The patient denied any episodes of severe headache, nausea, vomiting, or visual changes.

This is the first case of a pituitary apoplexy after a corticotropin-releasing hormone stimulation test in the pediatric age ⁷⁾.

Sanz-Sapera et al. reported the case of a 50-year-old man who attended the emergency department for a sudden onset of headache. A computed tomography (CT) scan at admission revealed pituitary hemorrhage and the blood test confirmed the clinical suspicion of acromegaly and associated hypopituitarism. The T1-weighted magnetic resonance imaging (MRI) showed the classic pituitary ring sign on the right side of the pituitary. Following admission, he developed acute-onset hyponatremia that required hypertonic saline administration, improving progressively. Surprisingly, during the follow-up, IGF1 levels became normal and he progressively recovered pituitary function.

Patients with pituitary apoplexy may have a spontaneous remission of hormonal hypersecretion. If it is not an emergency, we should delay a decision to undertake surgery following apoplexy and re-evaluate hormone secretion. Hyponatremia is an acute sign of hypocortisolism in pituitary apoplexy. However, SIADH although uncommon, could appear later as a consequence of direct hypothalamic insult and requires active and individualized treatment. For this reason, closely monitoring sodium at the beginning of the episode and throughout the first week is advisable to guard against SIADH. Despite being less frequent, if pituitary apoplexy is limited to the tumor, the patient can recover pituitary function previously damaged by the undiagnosed macroadenoma ⁸⁾.

Pituitary Apoplexy Presenting as Status Migrainosus ⁹⁾.

A 45-year-old man who suffered an attack of pituitary apoplexy while being treated for dengue hemorrhagic fever (DHF). The issues pertaining to the management of hydrocephalus, timing of surgical intervention, and treatment of electrolyte imbalances encountered in the dual setting of DHF and pituitary apoplexy are discussed with reference to the outcome in this case.

Although patients suffering from DHF harbor multiple factors, which may be precipitants of pituitary apoplexy, the association between these two conditions is rare and only few case reports document their coexistence ¹⁰⁾.

A case of a 40-year-old male patient who presented with headache and sudden visual loss for 3 days. He was diagnosed with pituitary apoplexy and had transnasal-transsphenoidal resection. Three days later, he achieved a complete recovery of his vision.

This report is an addition to several studies that favor early surgical decompression of pituitary fossa for apoplexy cases with severe neuro-ophthalmologic involvement. There is an increasing trend for early surgical intervention for pituitary apoplexy in the literature, especially for severe visual deterioration.

The visual outcome appears to be better in early intervention as compared to late. Nevertheless, good visual recovery is also seen in late surgical intervention ¹¹⁾.

A patient in his late 30s presented with sudden and severe frontal headache, fever, blurred vision, nausea, confusion, as well as oculomotor palsy (CN III) with partial ptosis of the left eyelid, dilated left pupil and left eye globe deviation inferiorly and laterally. The final diagnosis was acute pituitary apoplexy complicating a pituitary macroadenoma. In this setting, headache is usually present due to stretching and irritation of the dura mater, and fever due to meningeal irritation or upward expansion leading to hypothalamic dysfunction. Decreased visual acuity and defects in visual fields are caused by upward expansion, which compresses the optic chiasm. Ophthalmoplegia can also be observed due to lateral expansion with invasion of the cavernous sinus ¹²⁾.

Rais et al., report the case of an older lady who was admitted to a tertiary teaching hospital with sub-acute functional decline of two months' duration, which was initially attributed to a concomitant urinary tract infection. Further investigations, however, revealed the diagnosis of pituitary apoplexy with central hypocortisolism. Subsequent treatment with physiological doses of steroids improved patient's function and overall well-being. This report adds to the sparse literature on pituitary apoplexy in the older adults and emphasizes the non-specific presentation of this clinical syndrome ¹³⁾.

Pituitary apoplexy causing clival and spinal haematoma ¹⁴⁾.

A case of pituitary apoplexy associated with cerebral infarction ¹⁵⁾.

Akakın et al. describe the first case of PA following posterior lumbar fusion surgery performed while the patient was prone. In patients with a preexisting pituitary adenoma, thorough clinical and laboratory investigations should be conducted using an interdisciplinary approach before any planned surgery. In unknown cases of pituitary adenoma, PA should be kept in mind for the differential diagnosis in a case with headache, nausea, vomiting, ophthalmoplegia, visual loss, and electrolyte imbalance concurrent with an ongoing disease state ¹⁶⁾.

One case of rare pituitary adenoma apoplexy caused by the rupture of an anterior communicating artery aneurysm. The patient was a 49-year-old male who had an untreated pituitary adenoma for 3 years. The patient experienced a sudden headache; computed tomography (CT) and magnetic resonance imaging (MRI) revealed pituitary adenoma apoplexy and significant subarachnoid hemorrhage. Cranial CT angiography (CTA) showed a communicating artery aneurysm. Supratentorial intracranial aneurysm clipping and pituitary adenoma resection were performed. The aneurysm was a ruptured aneurysm located inside the pituitary adenoma. During the surgery, the aneurysm was clipped, and the majority of the tumor was resected. The patient recovered well after the surgery and received radiotherapy.

This rare case demonstrates that when pituitary adenoma apoplexy is combined with subarachnoid hemorrhage, the possibility of a combined intrasellar aneurysm should be considered. During transsphenoidal tumor resection, aneurysm rupture should be avoided to prevent disastrous consequences ¹⁷⁾.

A 42-year-old man who had been diagnosed of pituitary adenoma presented with a sudden onset of unconsciousness, left hemiplegia and right ptosis. Investigations revealed the development of pituitary apoplexy. The extension of tumor mass compressed the supraclinoid portion of the right internal carotid artery, resulting in the cerebral infarction in the right anterior and middle cerebral artery territory. Left anterior cerebral artery territory infarction was also found, which could be caused by vasospasm provoked by pituitary apoplexy. The patient underwent decompression surgery via transsphenoidal approach after four weeks' conservative treatment, and pathological examination revealed hemorrhage and necrosis of the pituitary adenoma. His symptoms improved within five months' follow-up. Since pituitary apoplexy producing cerebral infarction is rare, clinicians should be alert to that possibility, and delayed transsphenoidal surgery following conservative management with steroids is the appropriate management of such an occurrence ¹⁸⁾.