Diagnosis Of Pituitary Apoplexy Research Articles

Pituitary Apoplexy: An Updated Review.

Pituitary apoplexy (PA) is an acute, life-threatening clinical syndrome caused by hemorrhage and/or infarction of the pituitary gland. It is clinically characterized by the sudden onset of headache. Depending on the severity, it may also be accompanied by nausea, vomiting, visual disturbances, varying degrees of adenohypophyseal hormone deficiency, and decreased level of consciousness. Corticotropic axis involvement may result in severe hypotension and contribute to impaired level of consciousness. Precipitating factors are present in up to 30% of cases. PA may occur at any age and sometimes develops during pregnancy or the immediate postpartum period. PA occurs more frequently in men aged 50-60, being rare in children and adolescents. It can develop in healthy pituitary glands or those affected by inflammation, infection, or tumor. The main cause of PA is usually spontaneous hemorrhage or infarction of a pituitary adenoma (pituitary neuroendocrine tumor, PitNET). It is a medical emergency requiring immediate attention and, in many cases, urgent surgical intervention and long-term follow-up. Although the majority of patients (70%) require surgery, about one-third can be treated conservatively, mainly by monitoring fluid and electrolyte levels and using intravenous glucocorticoids. There are scoring systems for PA with implications for management and therapeutic outcomes that can help guide therapeutic decisions. Management of PA requires proper evaluation and long-term follow-up by a multidisciplinary team with expertise in pituitary pathology. The aim of the review is to summarize and update the most relevant aspects of the epidemiology, etiopathogenesis, pathophysiology, clinical presentation and clinical forms, diagnosis, therapeutic strategies, and prognosis of PA.

The acute stage of pituitary apoplexy complicated with sinusitis

The timely diagnosis and optimal therapy of the pituitary apoplexy is challenging. We report a case about our treatment experience for the acute stage of pituitary apoplexy complicated with sinusitis. It is the strong predictor for the acute stage of pituitary apoplexy when magnetic resonance imaging(MRI) presented the both signs simultaneously, the pituitary ring sign and the sphnoid sinus mucosal thickening. Once the diagnosis of pituitary apoplexy is established, hypocortisolism and hyponatremia should be considered intensely. Surgical decompression via transsphnoid approach has favorable prognosis for the visual involvement of the pituitary apoplexy. Effective antibiotic for sphenoid sinusitis before surgery may could minimize the postoperative risk of intracranial infection. Otherwise, the sign of the sphenoid sinus mucosal thickening is not a contraindication for the transnasal transsphnoidal surgery.

Pituitary apoplexy – A single center retrospective study from the neurosurgical perspective and review of the literature

ObjectiveThunderclap headache and visual disturbances are typical clinical features of pituitary apoplexy (PA). Because of the acute symptomatology, many patients are referred to a neurosurgical department without prior endocrinological assessment. It is the aim of the present study to analyze initial presenting symptoms, outcome and associated endocrine disturbances in a cohort of patients with pituitary apoplexy primarily seen by neurosurgeons. Patients and methodsRetrospective single-center study in a neurosurgical department. Patients’ records were reviewed for clinical, neuropathological and endocrinological findings. The diagnosis of PA was based on clinical, imaging and histological findings. ResultsA total of 60 patients were studied. They were referred most often by neurologists (n=16), and family physicians (n=12). Only 2 patients received an endocrinological work-up prior to admission. The most frequently documented presenting symptoms were headache (n=54), visual field defects (n=13), reduction of visual acuity (n=17) and/or diplopia (n=19). An endocrinological history had rarely been taken and hormone blood tests were oftentimes incomplete or not ordered. At 3-month follow-up 18/44 patients had complete anterior hypopituitarism. At 12 months, 21/60 patients were lost to endocrinological follow-up. ConclusionsThe classic neurological symptoms of PA were well documented in our patient cohort, whereas endocrinological symptoms, especially those indicative of pituitary dysfunction were underreported. Neurologists and neurosurgeons need to be aware of the endocrinological sequelae of pituitary apoplexy in order to avoid potentially lethal complications. Patients should be counselled to adhere to long-term endocrinological and neurosurgical follow-up.

Pituitary apoplexy: a rare complication of leuprolide therapy in prostate cancer treatment

Gonadotropin-releasing hormone agonists, used widely in the treatment of metastatic prostate cancer and hormone receptor-positive breast cancer, are associated with a rare but potentially fatal outcome of pituitary apoplexy (PA)....

Rare ocular involvement due to leukocidin “panton valentine” (pvl) positive staphylococcus aureus after bacterial endocarditis

AbstractPurpose To present an unusual case of a 38‐year‐old man with pituitary apoplexy, bacterial endocarditis, and chorioretinitis due to leukocidin “PVL” positive staphylococcus aureus, not reported in the current literature.Methods He presented with a history of sudden loss of vision, headache and high fever. Visual acuity (VA) was Hand Movements in both eyes with sluggish pupillary reflexes. Fundoscopy revealed bilateral yellowish focal retinal lesions and Roth’s spots in right eye, indicative of active chorioretinitis. Fluorescein angiography (FA) showed active chorioretinal lesions. Visual fields and OCT were normal. Brain MRI showed a pituitary adenoma. The diagnosis of pituitary apoplexy was made based on clinical history, systemic findings and MRI imaging. He was treated with high doses of IV steroids. Snellen Visual acuity (VA) was improved to 0.8 in the right eye and 0.9 in the left eye. Three days later he presented Osler΄s nodes and septic emboli on palms and soles, characteristics of bacterial endocarditis. Blood culture showed leukocidin “PVL” positive staphylococcus aureus. Transesophageal echocardiogram demonstrated prolapse and degenerative alterations of the mitral valve. A quadruple IV antibiotic treatment was initiated for eight weeks. An operation to remove the pituitary adenoma in two months was also scheduled.Results One year later his VA was 10/10 bilaterally. FA showed inactive chorioretinal scars. ISCEV standard full field ERG was affected bilaterally.Conclusion Ocular complications may follow pituitary apoplexy and bacterial endocarditis due to “PVL” (+) Staphylococcus aureus. Early diagnosis is important for an effective treatment.

Pituitary apoplexy in the emergency room: A prior history of pituitary adenoma may not be necessarily present!

Pituitary apoplexy is a rare but life-threatening medical emergency that results from either a sudden hemorrhage or infarction in a pituitary tumor. Unrecognized pituitary apoplexy can lead to serious hormonal and neuro-ophthalmic complications and even death. A major challenge in the diagnosis of pituitary apoplexy is that majority of such patients don't have a prior diagnosis of pituitary adenoma. Emergency magnetic resonance imaging of the pituitary gland is the diagnostic tool of choice for this condition. This may not be readily available in many emergency rooms. A previously healthy patient who presented with sudden severe headache and confusion and was found to have pituitary apoplexy is described and a focused review of the condition is given with emphasis on early recognition and complications of this condition

IMAGING DIAGNOSIS: PITUITARY APOPLEXY IN A CAT

A 7-year-old male neutered domestic short-haired cat had depression for 5 months and acute blindness. A lesion at the level of the rostral and middle cranial fossae was suspected. A large pituitary mass compressing the optic chiasm was detected in magnetic resonance images and there was also evidence of recent intratumoral hemorrhage, leading to a diagnosis of pituitary apoplexy; these findings were confirmed at postmortem examination. Pituitary apoplexy is a clinical syndrome characterized by acute neurologic signs related to hemorrhagic infarction within a pituitary tumor. Pituitary apoplexy should be considered in patients with acute onset of blindness and altered mental status.

Pituitary apoplexy can mimic acute meningoencephalitis or subarachnoid haemorrhage

Pituitary apoplexy is an uncommon but life-threatening condition that is often overlooked and underdiagnosed. We report a 45-year-old man who presented to our emergency department with a sudden onset headache, acute confusion, signs of meningeal irritation and ophthalmoplegia. An initial diagnosis of acute meningoencephalitis was made, which was amended to pituitary apoplexy following thorough investigation within the emergency department.A 45-year-old man was brought to our emergency department by ambulance with a history of sudden onset of frontal headache and acute confusion. His wife provided the history. There was no significant past medical history of diabetes, hypertension, recent travel abroad, exposure to sick contacts, involvement in outdoor pursuits such as hiking/cave diving, or trauma. He worked in a bank and had been well until 24 h prior to the onset of sudden headache, which was gradually worsening in nature and associated with increasing confusion. The patient's wife reported that he had neither experienced any fevers, night sweats, or coryzal symptoms nor received any recent vaccinations. He was not on any regular medications. He was a non-smoker and occasionally consumed alcohol. There was no significant family history. On examination in the ED, his temperature was 37.6°C, his pulse was 110/min, and he was normotensive and normoglycaemic. A macular blanching rash was noted over the patient's trunk. The patient was disoriented to time and place. Neurological examination revealed reduced GCS (11/15-E3, M6, V2), marked neck stiffness, a positive Kernig's sign and a right sixth nerve palsy.A provisional diagnosis of acute meningoencephalitis was made and the patient was started on a course of intravenous antibiotics with benzyl penicillin 1.2 g, cefotaxime 2 g and acyclovir 750 mg. Baseline blood investigations revealed hyponatraemia (122 mmol/l), a white-cell count of 11 × 109/l and a C-reactive protein > 250. Due to the sudden onset of the symptoms and lack of prodrome, an urgent CT head scan was performed to rule out a cerebrovascular event. The scan demonstrated an enlarged pituitary gland (3 cm in diameter) with impingement of the optic chiasm. The centre of the enlarged pituitary gland was noted to be hypodense in comparison to its periphery, which was consistent with a diagnosis of pituitary apoplexy. A subsequent MRI confirmed the diagnosis (Figure 1) of an enlarged sella containing abnormal soft tissue with increased signal intensity suggestive of haemorrhage (Figure 1A).Post-MRI a lumbar puncture was performed revealing glucose 3.4 mmol/l, protein 1.0 g/l, red cells of 53/mm3 and white cells of 174/mm3 with predominant neutrophilia. No organisms were seen, and CSF cultures and HSV DNA tests were found to be negative. Endocrinological investigations demonstrated low concentrations of thyroid hormones [TSH: 0.14 mIu/l (0.35-5.5 mlU/l), FT3: 1.1 nmol/l (1.2-3.0 nmol/l), FT4: 9.6 pmol/l (8-22 pmol/l)], gonadal hormones (LH: < 1 u/l) and prolactin: 16 u/l (<450 u/l). Serum FSH was 2.9 u/l (0.8-11.5 u/L) and cortisol 575 nmol/l (450-700 nmol/l). The patient was treated for hypopituitarism based on clinical and radiological findings with intravenous fluids, hydrocortisone (100 mg) and thyroxine (50 μg) as loading doses in the ED.Within 24 h of commencement of therapy the patient's GCS rose to 15, and within 48 h there was marked improvement in the right sixth cranial nerve palsy. Formal visual field assessment demonstrated temporal visual field loss in the left eye. The patient was discharged to his usual residence a week later and follow-up was organised with both the endocrinologists and ophthalmologists. Follow-up MRI demonstrated that there was no significant change in either size or signal characteristics of the pituitary fossa mass (Figure 1B).

Pituitary tumor apoplexy presenting as infective meningoencephalitis

We report on a case of a 80-year-old man who developed progressive drowsiness with headache, fever and signs of meningeal irritation 2 days after a head trauma. Suspecting an infective meningoencephalitis, the patient was treated with wide spectrum antibiotic and antiviral therapy. Brain CT scan revealed a previously unknown pituitary expansive lesion. A brain MRI study confirmed the presence of an intrasellar lesion, which presented remarkable contrast ring enhancement, and showed non-specific inflammatory tissue on the clivus, possibly responsible of the clinical features of sterile meningitis. A biopsy proven diagnosis of pituitary apoplexy was made. This case highlights MRI as an important investigation for earlier recognition of pituitary apoplexy that can present with a clinical picture resembling an infective meningoencephalitis.

An Intrasellar Meningioma Masquerading as Pituitary Apoplexy

Intrasellar meningiomas are uncommon tumours, and rarely present with acute symptoms. We describe a 63-year-old woman with an intrasellar mass that presented with sudden headache and severe loss of vision. Magnetic resonance imaging (MRI) was consistent with the clinical diagnosis of pituitary apoplexy, but trans-sphenoidal surgery and biopsy unexpectedly revealed an intrasellar meningioma, and excision could not be completed. A subsequent craniotomy was performed in order to remove the remainder of the tumour. Pre-operative differentiation of an intrasellar meningioma from a pituitary macroadenoma is important as it determines the method of surgical excision, but the two lesions may be indistinguishable even with modern neuro-imaging techniques.

Difficulté du diagnostic différentiel entre l’apoplexie hypophysaire et le craniopharyngiome

Pituitary apoplexy is characterized by an abrupt neurological deteriorating condition associated with rapid expansion of the pituitary gland, caused by ischemic necrosis and hemorrhage. Craniopharyngioma may be difficult to distinguish from pituitary apoplexy. In this study, we discuss a case of pituitary apoplexy in a 19-year-old male patient. In our patient, the tumor was confused with a craniopharyngioma because of the suprasellar extension of the tumor on magnetic resonance (MR) images and the hyperintensity in T1-weighted images, the young age of the patient, and the gradually progressive onset of the symptoms. In conclusion, even without a known history of pituitary adenoma or an abrupt onset of the clinical symptoms, the diagnosis of pituitary apoplexy should be considered in a patient with a suprasellar mass hyperintensity in T1-weighted MR images, which may mimic craniopharyngioma.

A Case of Pituitary Apoplexy Induced by a Bromocriptine Test With a TSH- and GH-Producing Pituitary Adenoma

We report a 54-year-old Japanese woman with enlargement of her hands and feet, and tachycardia over the previous 3 years. She had a TSH- and GH-producing pituitary adenoma 3.5 × 3.0 × 2.0 cm. A bromocriptine test was performed. Bromocriptine was slightly effective for GH inhibition, but, she complained of headaches, nausea, and impaired vision 24 hours after bromocriptine administration. MRI examination showed heterogeneous mixed intensity lesions in the pituitary adenoma, compatible with pituitary apoplexy. The tumor was removed by the transsphenoidal approach 24 hours later, and histologic examination confirmed the diagnosis of pituitary apoplexy. Although pituitary apoplexy associated with bromocriptine is very rare, this case suggests a casual relationship is possible in some instances.

Frequent occurrence of pituitary apoplexy in patients with non‐functioning pituitary adenoma

There is agreement in the literature that pituitary apoplexy is a rare disorder. As our experience differs from this view, we analysed the incidence in patients operated on for a nonfunctioning pituitary adenoma. One hundred ninety-two consecutive patients with a suprasellar, clinically inactive adenoma operated on during the period 1985-1996 were retrospectively reviewed. A diagnosis of pituitary apoplexy was made from relevant neurological symptoms together with pertinent findings at operation. Pituitary apoplexy occurred in 41 patients (21%), in 23 patients within 12 days prior to the operation. The male/female ratio was 1.9. Median follow-up time was 13.7 years (range 8.9-19.9). During this period, 12 patients had died, yielding a standard mortality ratio of 1.09 (95% CI 0.62-1.92), similar to that in the patients who had not sustained pituitary apoplexy. Postoperatively, 24% of the patients had normal pituitary function, 38% were panhypopituitary and partial pituitary insufficiency was present in 38%. Subnormal GH secretion was present in virtually all patients tested. Two patients died within 60 days of surgery and in two no or incomplete data were available, although they most likely were panhypopituitary. Most of our findings add little to what is known about pituitary apoplexy. On one point, however, they are contrary to previously presented data. We found a much higher incidence of pituitary apoplexy despite rather rigorous criteria for the diagnosis. The outcome as regards survival and endocrine function was not different from that in patients with a nonfunctioning adenoma who did not suffer pituitary apoplexy.

Clinical versus Subclinical Pituitary Apoplexy: Presentation, Surgical Management, and Outcome in 21 Patients

A retrospective review of 16 consecutive patients with pituitary apoplexy treated over a 10-year period is reported. Eight men and 8 women (mean age, 48 years) underwent transsphenoidal decompression after an average duration of symptoms of 19 days. The diagnosis of pituitary apoplexy was made by the sudden onset of headache (88%), nausea (56%), or meningismus (13%), with or without visual disturbances (75%), in the setting of a sellar tumor on computed tomographic or magnetic resonance imaging scans. Thirteen of 16 patients showed significant improvement of symptoms after surgery (average follow-up, 2.5 years). In addition, 5 patients with clinically silent yet extensive pituitary hemorrhage were treated. Although extensive pituitary hemorrhage often produced fulminant apoplexy, it also presented insidiously over many days with few, if any, clinical signs. Rapid diagnosis, endocrine replacement, and transsphenoidal decompression constituted effective therapy. Magnetic resonance imaging (after at least 12 hours of symptoms) was superior to computed tomography in detecting hemorrhage.

Pituitary apoplexy: A cause for painful third nerve palsy

A series of cases of painful third nerve palsy due to pituitary apoplexy is reported to highlight this less recognized cause. Four cases presented with sudden onset of headache associated with an oculomotor nerve palsy. CT scan showed assymmetrical expansion of a pituitary adenoma into the corresponding cavernous sinus in each patient. All palsies recovered spontaneously post transsphenoidal resection of the tumour. The problems associated with the diagnosis of pituitary apoplexy are discussed and the vital role of positive radiological findings is emphasized.

The Unusual Association of Transient Resolving Thyrotoxicosis due to Painless Thyroiditis, Hypopituitarism and Central Diabetes Insipidus Associated with Spontaneous Pituitary Apoplexy

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.