scholarly journals Hyponatremia as the Initial Presentation of Evolving Pituitary Apoplexy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A586-A586
Author(s):  
Jovan Milosavljevic ◽  
Asha Mary Thomas
Keyword(s):  
Mental Status ◽  
Pituitary Apoplexy ◽  
Pituitary Tumors ◽  
Altered Mental Status ◽  
Clinical Syndrome ◽  
Medical Emergency ◽  
Fluid Restriction ◽  
Free T4 ◽  
Acute Hemorrhage ◽  
Initial Testing

Abstract Pituitary apoplexy (PA) is a known, often under-recognized medical emergency and is characterized by ischemic or hemorrhagic necrosis of the pituitary gland. It is a rare clinical syndrome that occurs in 2-12% of pituitary tumors. Hyponatremia can occur secondary to hypocortisolism (12-40%) or, rarely, to the syndrome inappropriate antidiuretic hormone (ADH) secretion. We present the case of a 69-year-old man who presented with altered mental status on post-operative day 3 from total knee replacement surgery. Initial testing revealed hyponatremia of 124 mmol/L, low serum osmolality of 266 mOsm/kg, and high urine osmolality of 664 mOsm/kg with urine sodium of 179 mmol/L. Head computerized tomography revealed a sellar mass of 1.8 x 2.4 cm. Initial testing revealed low prolactin (0.7 ng/mL), normal TSH (0.458 mcIU/mL) with borderline low free T4 of 0.72 ng/dL. Morning cortisol was 12.7 mcg/dL with ACTH of 8.5 pg/mL. Cosyntropin stimulation test was done revealing baseline cortisol of 5.8 mcg/dL (at midnight), increasing to 25.8 mcg/dL after 30 minutes and to 30.9 mcg/dL 60 minutes after cosyntropin administration. His sodium and mental status initially improved with fluid restriction and salt tablets, for the assumed syndrome of inappropriate ADH secretion. The patient remained hemodynamically stable. On the fourth day, however, his mental status deteriorated. Magnetic resonance imaging revealed expansion of sella with hyperintense mass 2.2 x 2.0 x 2.8 cm with compression of the optic chiasm. He was given stress dose hydrocortisone and levothyroxine and underwent emergency transsphenoidal resection. Biopsy revealed acute hemorrhage within infarcted adenoma. Postoperatively, both the patient’s sodium and mental status improved significantly and he was discharged to home on hydrocortisone and levothyroxine. The main clinical concern in the management of PA remains under-diagnosis at presentation. Prognosis is dependent on management during the acute phase. PA can present as hyponatremia even in the absence of overt hypocortisolism, presumably due to inappropriate ADH secretion. Therefore, PA should be considered as one of the differential diagnoses in hemodynamically stable patients with altered mental status and hyponatremia.

scholarly journals SAT-246 A Case of Cabergoline Induced Pituitary Apoplexy in a Patient with Prolactinoma

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Ashim Ahuja
Keyword(s):  
Pituitary Gland ◽  
Pituitary Apoplexy ◽  
Altered Mental Status ◽  
Young Female ◽  
Sudden Onset ◽  
Free T4 ◽  
Acute Hemorrhage ◽  
Healthy Female ◽  
Acute Change ◽  
Irregular Menses

Abstract Objective To report a case in which Cabergoline led to pituitary apoplexy (PA) in a young female patient with a macroprolactinoma. Methods A 28 y/o F presented with 10 months of irregular menses followed by 6 months of amenorrhea. She reported a dull supranasal headache, and nipple crusting without obvious galactorrhea. She denied visual changes, dizziness nausea or vomiting. Her Prolactin (PRL) was elevated at 194ng/mL, and she was started on Cabergoline 0.25mg twice per week and sent for a pituitary MRI. Four weeks later, the patient presented to the emergency department with an acute worsening of headache after being found to have a pituitary hemorrhage on MRI. On PE there were no obvious neurologic deficits. Neurosurgery recommended no acute intervention and she was managed conservatively. Results Labs prior to Cabergoline: bHCG (-), PRL 194 ng/mL; LH 3.1 µIU/mL; FSH 4.9 µIU/mL; Estradiol <11 pg/mL; Cortisol 11.44 ug/dL; TSH 1.080 µIU/mL; Free T4 0.76 ng/dL. Labs after 1 month of Cabergoline treatment: PRL 84.3 ng/mL; FSH 2.2 µIU/mL; LH 2.8 µIU/mL; TSH 1.23 µIU/mL; FT4 0.82 ng/dL; Cortisol 15.43 ug/dL. MRI 1 month after Cabergoline was performed and showed a 1.4 x 1.4 x 1.5cm hemorrhagic mass of pituitary gland. Discussion PA is the acute hemorrhage or infarction of the pituitary gland, commonly presenting with sudden onset of severe headache, visual field impairment, vomiting or altered mental status. However, like our patient, 25% of patients may present with subclinical apoplexy. Bromocriptine and Cabergoline are the two main treatments for prolactinoma. Both have been linked to PA, though the number of reports on Cabergoline is much less. There are now 10 cases of apoplexy reported with Cabergoline. PA can be spontaneous or precipitated by angiography, surgery, head trauma, hypertension, thrombocytopenia, diabetes, radiotherapy, coagulopathies, and Dopamine Agonists (DA). Most cases occur in older patients (50–60’s) with comorbidities, and incidence in patients <35 is rare. Moreover, PA is more common in males. Therefore, PA presenting in a young, healthy female suggests that Cabergoline may have been the precipitating factor. Conclusion It is important to be aware that Cabergoline can precipitate PA in patients being treated for a Prolactinoma. We recommend a thorough history, physical exam and baseline imaging before starting Cabergoline therapy. We also recommend emergent imaging if there is an acute change in symptoms.

scholarly journals Postpartum pituitary apoplexy with isolated oculomotor nerve palsy: A rare medical emergency

2015 ◽  
Vol 06 (04) ◽  
pp. 598-600
Author(s):  
Sujeet Raina ◽  
Vaneet Jearth ◽  
Ashish Sharma ◽  
Rajesh Sharma ◽  
Kewal Mistry
Keyword(s):  
Nerve Palsy ◽  
Pituitary Apoplexy ◽  
Sella Turcica ◽  
Altered Mental Status ◽  
Sudden Onset ◽  
Clinical Syndrome ◽  
Medical Emergency ◽  
Oculomotor Nerve Palsy ◽  
Hormonal Dysfunction ◽  
Third Cranial Nerve Palsy

ABSTRACTPituitary apoplexy is a clinical syndrome characterized by sudden onset headache, visual deficits, ophthalmoplegia, altered mental status, and hormonal dysfunction due to an expanding mass within the sella turcica resulting from hemorrhage or infarction of pituitary gland. We report a case of pituitary apoplexy that developed in postpartum period following postpartum hemorrhage and presented with isolated third cranial nerve palsy.

Hemorrhagic and nonhemorrhagic Rathke cleft cysts mimicking pituitary apoplexy

2008 ◽  
Vol 108 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Mandy J. Binning ◽  
James K. Liu ◽  
John Gannon ◽  
Anne G. Osborn ◽  
William T. Couldwell
Keyword(s):  
Mr Imaging ◽  
Pituitary Tumor ◽  
Pituitary Apoplexy ◽  
Pituitary Tumors ◽  
Imaging Features ◽  
Mr Images ◽  
Acute Hemorrhage ◽  
Consistent Finding ◽  
Imaging Characteristics ◽  
Intracystic Hemorrhage

Object Rathke cleft cysts (RCCs) are infrequently symptomatic, and apoplexy is one of the most unusual presentations. Only a few cases of apoplexy associated with RCCs have been reported, and their clinical, imaging, surgical, and pathological features are poorly understood. In the cases that have been reported, intracystic hemorrhage has been a consistent finding. The authors report 6 cases of RCCs in which the presenting clinical and imaging features indicated pituitary apoplexy, both with and without intracystic hemorrhage. Methods The authors retrospectively reviewed charts and magnetic resonance (MR) imaging studies obtained in patients who underwent transsphenoidal surgery for RCC. Six patients were identified who presented with symptoms and MR imaging characteristics consistent with pituitary apoplexy but were found intraoperatively to have an RCC. All 6 patients presented with a sudden headache, 2 with visual loss, and 1 with diplopia. Review of the preoperative MR images demonstrated mixed signal intensities in the sellar masses suggestive of a hemorrhagic pituitary tumor. In all patients there was a presumed clinical diagnosis of pituitary tumor apoplexy and an imaging-documented diagnosis of hemorrhagic pituitary tumor. Results All 6 patients underwent transsphenoidal resection to treat the suspected pituitary apoplexy. Intraoperative and histopathological findings were consistent with the diagnosis of an RCC in all cases. Only 2 cases showed evidence of hemorrhage intraoperatively. In all cases, an intracystic nodule was found within the RCC at surgery, and this intracystic nodule was present on the initial MR imaging when retrospectively reviewed. The imaging characteristics of the intracystic nodules were similar to those of acute hemorrhage seen in cases of pituitary apoplexy. Conclusions The clinical and imaging features of RCCs appear similar to those of hemorrhagic pituitary tumors, making them often indistinguishable from pituitary apoplexy.

scholarly journals Multidisciplinary Management of Pituitary Apoplexy

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Adriana Albani ◽  
Francesco Ferraù ◽  
Filippo Flavio Angileri ◽  
Felice Esposito ◽  
Francesca Granata ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Pituitary Gland ◽  
Multidisciplinary Approach ◽  
Pituitary Apoplexy ◽  
Clinical Syndrome ◽  
Surgical Decompression ◽  
Medical Emergency ◽  
Multidisciplinary Management ◽  
Pituitary Tumours ◽  
Haemorrhagic Necrosis

Pituitary apoplexy is a rare clinical syndrome due to ischemic or haemorrhagic necrosis of the pituitary gland which complicates 2–12% of pituitary tumours, especially nonfunctioning adenomas. In many cases, it results in severe neurological, ophthalmological, and endocrinological consequences and may require prompt surgical decompression. Pituitary apoplexy represents a rare medical emergency that necessitates a multidisciplinary approach. Modalities of treatment and times of intervention are still largely debated. Therefore, the management of patients with pituitary apoplexy is often empirically individualized and clinical outcome is inevitably related to the multidisciplinary team’s skills and experience. This review aims to highlight the importance of a multidisciplinary approach in the management of pituitary apoplexy and to discuss modalities of presentation, treatment, and times of intervention.

scholarly journals Conditions associated with giant pituitary tumors at the time of surgery effecting outcome morbidity and mortality

2019 ◽  
Vol 10 ◽  
pp. 92
Author(s):  
Marc Billings ◽  
Robert Dahlin ◽  
Bailey Zampella ◽  
Raed Sweiss ◽  
Shokry Lawandy ◽  
...  
Keyword(s):  
Mental Status ◽  
Expectant Management ◽  
Pituitary Tumors ◽  
Mass Effect ◽  
Brain Structures ◽  
Altered Mental Status ◽  
Time Of Surgery ◽  
Presenting Symptoms ◽  
Imaging Characteristics ◽  
Brainstem Compression

Background: Surgical outcome prediction has assisted physicians in discussing surgical intervention or expectant management. While increasing pituitary tumor size would seem to be associated with increasing challenge of removal and associated complications, that relationship has not been borne in the literature. Methods: We performed a retrospective review of a consecutive cohort of pituitary surgeries completed at our institution. Data included age at the time of surgery, presenting symptoms and Glasgow Coma scale (GCS), GCS at discharge or 7 days postoperatively, GCS at 6 months, adenoma size, imaging characteristics of the tumor and brain before resection, postoperative complications, the presence of preoperative hydrocephalus, brainstem compression, and patient mortality. Results: Patients with giant adenomas were more likely to present with a cranial nerve palsy (P = 0.019), altered mental status (P = 0.0001), hydrocephalus (P = 0.002), and mass effect on the brainstem (P = 0.020). Patients who experienced a postoperative decline in mental status were more likely to present with altered mental (P = 0.006), had an increased prevalence of mass effect on the brainstem (P = 0.005), and were more likely to have either an ischemic stroke (P = 0.0001) and vasospasms or new intraparenchymal hemorrhage (P = 0.013). Conclusion: The results of this study demonstrate that postoperative mental status declines after pituitary adenoma resection can be directly related to brainstem compression and further surgical irritation of the surrounding vasculature. The intraoperative irritation can be multifactorial and may result as the decompressed brain structures assume their anatomical position.

scholarly journals Myxedema Coma Disguised as Alcohol Withdrawal

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A942-A943
Author(s):  
Dhivya Pahwa ◽  
Alexander Belkin ◽  
Neeraj Katriyar
Keyword(s):  
Mental Status ◽  
Alcohol Withdrawal ◽  
Clinical Symptoms ◽  
Female Gender ◽  
Laboratory Diagnosis ◽  
Medical Emergency ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Myxedema Coma ◽  
Multiple Organs

Abstract Introduction: Myxedema coma is a medical emergency whose symptoms may sometimes mimic other diseases such as alcohol withdrawal. Case: A 64-year-old male with a history of alcohol abuse and bipolar disorder (on no medications) presented to the emergency department after being found on the floor surrounded by multiple open alcohol bottles. He was a poor historian but reported a previous fall. Vitals on presentation were BP 109/70, HR 110, RR 22, SpO2 of 90% on room air, and rectal temperature of 97.6 F. The remainder of the exam revealed he was alert and oriented to self and place but not time; his neck was supple and no thyroid masses were palpated; he had tremors, head swelling and abdominal tenderness. Labs demonstrated CPK 1300 U/L, Creatinine 1.0 mg/dl, glucose 120 mg/dl, and sodium 142 mmol; urine toxicology was negative and alcohol level was not elevated. He was admitted and treated for suspected alcohol withdrawal and rhabdomyolysis with intravenous fluids and benzodiazepines. However, his mental status continued to decline; he became obtunded and was hypothermic and bradycardic. Thyroid function tests (TFT) revealed TSH 98.9 uIU/mL with free T4 0.27 ng/dl. He was subsequently managed for myxedema coma and given IV levothyroxine and hydrocortisone. He improved clinically after initiation of therapy and was transitioned to oral thyroid replacement. The patient was pending discharge to sub-acute rehab however his hospital course was later complicated by aspiration pneumonia. Discussion: Myxedema coma is a medical emergency as severe hypothyroidism leads to slowed functioning of multiple organs. Risk factors include female gender and age above 60 years; it is seen more commonly in colder months. Symptoms include decreased mental status, feelings of cold and tongue swelling while physical exam may reveal hypothermia, hypoventilation, bradycardia, an enlarged goiter, thinning hair and non-pitting edema. Lab studies usually reveal an elevated TSH with low T4; there may also be hyponatremia and hypoglycemia. Myxedema coma is a clinical and laboratory diagnosis; if there is clinical suspicion for myxedema coma, IV thyroid replacement should be administered promptly without waiting for lab results. Stress-dose steroids should also be administered and TFTs should be monitored every 48 hours. Clinical symptoms usually improve over one week of treatment. Mortality of myxedema coma is reported to be up to 40% in hospitalized patients. Our patient’s presentation of suspected alcohol withdrawal masked his diagnosis of myxedema coma. Conclusion: Physicians should keep myxedema coma in the differential for patients who present with suspected alcohol withdrawal and develop worsening mental status and hypothermia. Reference: DynaMed. (2020, October 22). Myxedema Coma. Retrieved October 23, 2020, from https://www-dynamed-com.arktos.nyit.edu/topics/dmp~AN~T1584563697784.

scholarly journals Evaluation of thyroid status in patients with thyrotoxicosis

1996 ◽  
Vol 42 (1) ◽  
pp. 174-178 ◽  
Author(s):  
L E Braverman
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Pituitary Tumors ◽  
Clinical Syndrome ◽  
Thyroid Peroxidase ◽  
Free T4 ◽  
Serum Thyroglobulin ◽  
Autoimmune Thyroid ◽  
Resistance To Thyroid Hormones ◽  
Autonomously Functioning Thyroid Nodules

Abstract The generic term thyrotoxicosis defines the clinical syndrome of hypermetabolism associated with excess amounts of circulating free thyroxine (T4) and (or) triiodothyronine (T3) concentrations, irrespective of the source of the excess hormones. The term hyperthyroidism is reserved for those patients with thyrotoxicosis caused by increased synthesis and secretion of thyroid hormones from the gland due either to thyroid stimulators in the blood or to autonomously functioning thyroid nodules and is almost always associated with an increased radioactive iodine uptake (RAIU) by the thyroid. Another major cause of thyrotoxicosis is increased release of thyroid hormone from the gland, not associated with increased synthesis, caused by inflammatory changes, and always associated with a low thyroid RAIU. The most common miscellaneous cause of thyrotoxicosis is the exogenous ingestion of excess thyroid hormone, associated with a low thyroid RAIU. The serum concentration of thyrotropin (TSH) is low in all causes of thyrotoxicosis, except for TSH-secreting pituitary tumors and selective pituitary resistance to thyroid hormones. Anti-thyroglobulin and anti-thyroid peroxidase antibodies are present in patients with autoimmune thyroid disease, and serum thyroglobulin is increased in all patients with thyrotoxicosis except those with thyrotoxicosis facticia. A decreased serum TSH and normal concentrations of serum free T4 and T3 define the syndrome of subclinical thyrotoxicosis.

scholarly journals Myxedema Coma: Improving Outcomes With Prompt Recognition and Therapy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A943-A943
Author(s):  
Aisha Parihar
Keyword(s):  
Mental Status ◽  
Vital Signs ◽  
Altered Mental Status ◽  
Morbidity And Mortality ◽  
Free T4 ◽  
Early Improvement ◽  
Delay In Diagnosis ◽  
Myxedema Coma ◽  
Artery Disease ◽  
Work Up

Abstract Background: Myxedema coma, a misnomer for severe hypothyroidism, is a rare endocrine emergency with an incidence of 1.08 cases per million people per year and a high mortality rate ranging from 30-50%. A delay in diagnosis and treatment worsens the prognosis and increases morbidity and mortality. Delayed management often leads to decompensation, presenting as uncontrolled persistent hypothermia, severe electrolyte derangements, and a potential for ventilator requirement needing ICU care. We present a patient in hypothyroid crisis who was promptly managed in a non-ICU setting who demonstrated a relatively early improvement in vital signs, thyroid lab values, and return to baseline mental status. Clinical Case: A 75 year old female with past medical history of hypothyroidism, atrial fibrillation, hypertension, coronary artery disease, depression, tardive dyskinesia, and dementia presented to the hospital in the month of December due to confusion after a mechanical fall that resulted in a head laceration requiring multiple stitches. Trauma work up included a CT scan of the head that was negative. On presentation, patient was also hypothermic, bradycardic, hypotensive, and lethargic with an altered mental status. Sepsis work up was negative. TSH was checked on day of admission and found to be significantly elevated to > 100 mcIU/mL, consistent with severe hypothyroidism. Free T4 and total T3 levels were low. Patient was immediately given intravenous levothyroxine 300 mcg followed by oral levothyroxine 125 mcg daily. In addition, intravenous hydrocortisone 100 mg every 8 hours was started until adrenal insufficiency was ruled out with a normal cortisol level. Upon discussion with family, it was learned that patient had not been taking her home medications indicating non-compliance to thyroid replacement therapy as the etiology for her hypothyroid crisis. Within a day of initiating therapy, TSH levels drastically improved with a reduction by 50%. Bradycardia, hypotension, and hypothermia resolved as well. In three days, patient’s mentation improved back to baseline and TSH, free T4, and total T3 continued to normalize. Conclusion: This case demonstrates how prompt recognition of hypothyroid crisis and immediate therapy can lead to early improvement in outcomes such as reversibility of mental status, normalization of vital signs and lab values, prevention of escalation of care to an ICU setting, and overall morbidity and mortality.

Acute stroke in pituitary adenomas complicated by pituitary apoplexy

2016 ◽  
Vol 21 (3) ◽  
pp. 136-139
Author(s):  
Miralim M. Azizov
Keyword(s):  
Pituitary Adenoma ◽  
Pituitary Apoplexy ◽  
Clinical Signs ◽  
Pituitary Tumors ◽  
Clinical Syndrome ◽  
Left Internal Carotid Artery ◽  
Left Middle Cerebral Artery ◽  
Ischemic Brain ◽  
Left Middle ◽  
Visual Disturbances

Pituitary apoplexy is a clinical syndrome that is manifested by headache, visual disturbances, ophthalmoplegia or impaired consciousness. It can develop as a result of necrosis or hemorrhage in the pituitary gland or in cases of pituitary tumors. A favorable prognosis is possible if early diagnosis and timely surgical treatment. Pituitary apoplexy complicated by the disorder of the cerebral circulation occurs relatively rare. We observed the female patient aged of 51 year with pituitary adenoma, clinical signs of which were sudden depression of consciousness, right hemiparesis and left-sided ptosis. Signs of pituitary apoplexy were revealed after performed examinations. The sharp increase in the size of the tumor resulted in a compression of supraclinoid portion of the left internal carotid artery, which was the cause of ischemic brain damage in the pool left middle cerebral artery. After 2 weeks of conservative treatment, the patient was undergone to the surgery via transsphenoidal access. Histological examination confirmed the hemorrhage and necrosis of the pituitary adenoma. Complication developed 3 months after surgery partially regressed. Taking into account the relatively rare occurrence of pituitary apoplexy complicated with cerebrovascular ischemic type, clinicians should be alert to this complication. The method of choice is transsphenoidal delayed adenomectomy with conservative therapy.

Presenting Symptoms of Pituitary Apoplexy

2017 ◽  
Vol 79 (01) ◽  
pp. 052-059 ◽  
Author(s):  
Ioannis Mavridis ◽  
Maria Meliou ◽  
Efstratios-Stylianos Pyrgelis
Keyword(s):  
Pituitary Apoplexy ◽  
Sella Turcica ◽  
Abrupt Onset ◽  
Sudden Onset ◽  
Clinical Syndrome ◽  
Medical Emergency ◽  
Sudden Expansion ◽  
Visual Field Defects ◽  
Imaging Method ◽  
Presenting Symptoms

AbstractThe classical term “pituitary apoplexy” (PA) describes a clinical syndrome usually characterized by abrupt onset of headache accompanied by neurologic and/or endocrinologic deterioration due to sudden expansion of a mass within the sella turcica as a result of hemorrhage or infarction within a pituitary tumor and adjacent pituitary gland. PA is a medical emergency and a difficult diagnosis to establish. Thus this article reviews the presenting symptoms of PA patients to help clinicians recognize or at least suspect this critical condition early on. PA commonly occurs in the setting of a preexisting adenoma, and several patients are unaware of its existence prior to the onset of apoplexy symptoms, which are mainly of a neurologic, ophthalmologic, and endocrinologic nature. Neurologic symptoms include sudden-onset severe headache and other symptoms of subarachnoid hemorrhage, symptoms from compression of the cavernous sinus contents, nausea/vomiting, impaired consciousness, and symptoms of meningeal irritation. Ophthalmologic symptoms include visual field defects, visual loss, diplopia, and ophthalmoplegia. Endocrinologic disturbances include pituitary adenoma symptoms, cortisol deficiency, panhypopituitarism, diabetes insipidus, and syndrome of inappropriate secretion of antidiuretic hormone. Magnetic resonance imaging is the imaging method of choice to aid the PA diagnosis. Its differential diagnoses include cerebrovascular accidents, infectious diseases, and other causes of endocrinologic imbalance. Transsphenoidal surgery is the treatment of choice, especially if there are associated visual abnormalities and ophthalmoplegia. Clinicians should be aware of the presenting symptoms because early diagnosis may reduce the morbidity and mortality of this neurosurgical emergency.

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