A Case of Pituitary Apoplexy and Cavernous Sinus Syndrome during Hemodialysis.

Background: Pituitary apoplexy (PA) is a clinical syndrome of pituitary hemorrhage or infarction and can result in hypopituitarism as well as compression of adjacent brain structures. Visual loss occurs frequently, as a result of tumor expansion and compression of the optic chiasm and optic nerves. Additionally, with pituitary tumor invasion into the fixed space of the cavernous sinus, compression of multiple cranial nerves can result in cavernous sinus syndrome (CSS). We describe a case of an undiagnosed pituitary tumor manifesting as abrupt PA with CSS during hemodialysis (HD). Clinical Case. A 77-year-old male with end-stage renal disease (ESRD) presented with acute onset of severe headache, decreased vision, ophthalmoplegia of the left eye, and hypotension during HD. MRI of the brain revealed a 2.5 cm pituitary adenoma with acute hemorrhage, compression of the left prechiasmatic optic nerve, and invasion into the left cavernous sinus (CS). The hormonal profile was consistent with multiple pituitary hormone deficiencies. The patient was treated with glucocorticoids and underwent transsphenoidal resection of the tumor. He had an uneventful postoperative hospital course, and his left visual acuity stabilized, although there was no immediate improvement in his other ocular symptoms. Conclusion: Our case highlights a rare constellation of a pituitary adenoma with CS invasion complicated by PA and CSS during HD. The pathophysiology of PA is not well understood, and there are very limited data regarding PA in patients with end-stage renal disease (ESRD) on HD. Prompt recognition of PA in a patient presenting with CSS, particularly in the HD setting, is essential to ensure appropriate care is provided for this medical emergency.

Review of the Metabolic Risk Factors for Increased Severity of Coronavirus Disease-2019.

The coronavirus 2019 (COVID-19) pandemic has presented many new challenges to the healthcare community with the sheer number of individuals affected and the range of symptoms at presentation. Early findings have shown that increased age is an independent risk factor for COVID-19 severity. Diabetes and hypertension were also found to be strong independent risk factors for severe COVID-19. It was later discovered that obesity is a strong risk factor for severe disease as well. Possible mechanisms for the increased risk associated with metabolic disease include the increased prevalence of acute respiratory syndrome, immune cell dysfunction, and chronic inflammatory states associated with obesity and diabetes. Acknowledging these risk factors has consequences for addressing vaccination strategies as well as healthcare disparities.

Hyperglycemia in Medically Critically Ill Patients: Risk Factors and Clinical Outcomes.

BACKGROUND: We aimed to robustly categorize glycemic control in our medical intensive care unit (ICU) as either acceptable or suboptimal based on time-weighted daily blood glucose averages of <180 mg/dL or >180 mg/dL; identify clinical risk factors for suboptimal control; and compare clinical outcomes between the 2 glycemic control categories. METHODS: This was a retrospective cohort study in an academic tertiary and quaternary medical ICU. RESULTS: Out of total of 974 unit stays over a 2-year period, 920 had complete data sets available for analysis. Of unit stays 63% (575) were classified as having acceptable glycemic control and the remaining 37% were classified (345) as having suboptimal glycemic control. Adjusting for covariables, the odds of suboptimal glycemic control were highest for patients with diabetes mellitus (odds ratio [OR] 5.08, 95% confidence interval [CI] 3.72-6.93), corticosteroid use during the ICU stay (OR 4.50, 95% CI 3.21-6.32), and catecholamine infusions (OR 1.42, 95% CI 1.04-1.93). Adjusting for acuity, acceptable glycemic control was associated with decreased odds of hospital mortality but not ICU mortality (OR 0.65, 95% CI 0.48-0.88 and OR 0.81, 95% CI 0.55-1.17, respectively). Suboptimal glycemic control was associated with increased odds of longer-than-predicted ICU and hospital stays (OR 1.76, 95% CI 1.30-2.38 and OR 1.50, 95% CI 1.12-2.01, respectively). CONCLUSIONS: In our high-acuity medically critically ill patient population, achieving time-weighted average daily blood glucose levels <180 mg/dL reliably while in the ICU significantly decreased the odds of subsequent hospital mortality. Suboptimal glycemic control during the ICU stay, on the other hand, significantly increased the odds of longer-than-predicted ICU and hospital stay.

Acromegalic Cardiomyopathy: An Overview of Risk Factors, Clinical Manifestations, and Therapeutic Options.

Acromegaly is a rare endocrine disorder that carries a significant burden of cardiovascular morbidity and mortality. Abnormalities of the growth hormone/insulin-like growth factor-1 axis in acromegaly lead to the characteristic cardiovascular manifestations of this disease. One hallmark feature of the disease is acromegalic cardiomyopathy, a syndrome of progressive cardiac dysfunction characterized by left ventricular hypertrophy, diastolic dysfunction, and combined systolic and diastolic dysfunction in the very advanced stage. In this article, we review the current concepts regarding the pathophysiology of acromegalic cardiomyopathy and discuss the various risk factors for its development. We also explore the question of whether the alterations in cardiac function are reversible with successful biochemical control of growth hormone excess either medically or surgically.

Recurrent lactic acidosis and hypoglycemia with inadvertent metformin use: a case of look-alike pills.

Metformin is recommended as the first-line agent for the treatment of type 2 diabetes. Although this drug has a generally good safety profile, rare but potentially serious adverse effects may occur. Metformin-associated lactic acidosis, although very uncommon, carries a significant risk of mortality. The relationship between metformin accumulation and lactic acidosis is complex and is affected by the presence of comorbid conditions such as renal and hepatic disease. Plasma metformin levels do not reliably correlate with the severity of lactic acidosis. We present a case of inadvertent metformin overdose in a patient with both renal failure and hepatic cirrhosis, leading to two episodes of lactic acidosis and hypoglycemia. The patient was successfully treated with hemodialysis both times and did not develop any further lactic acidosis or hypoglycemia, after the identification of metformin tablets accidentally mixed in with his supply of sevelamer tablets. Early initiation of renal replacement therapy is key in decreasing lactic acidosis-associated mortality. LEARNING POINTS: When a toxic ingestion is suspected, direct visualization of the patient's pills is advised in order to rule out the possibility of patient- or pharmacist-related medication errors.Though sending a specimen for determination of the plasma metformin concentration is important when a metformin-treated patient with diabetes presents with lactic acidosis, complex relationships exist between metformin accumulation, hyperlactatemia and acidosis, and the drug may not always be the precipitating factor.Intermittent hemodialysis is recommended as the first-line treatment for metformin-associated lactic acidosis (MALA).An investigational delayed-release form of metformin with reduced systemic absorption may carry a lower risk for MALA in patients with renal insufficiency, in whom metformin therapy may presently be contraindicated.

Nilotinib-Associated Destructive Thyroiditis.

Protein tyrosine kinase inhibitors are currently an important drug class in the treatment of leukemia. They represent targeted cancer therapy and have become the treatment of choice in chronic myeloid leukemia. Tyrosine kinases are enzymes expressed in multiple tissues and are involved in several signaling pathways influencing cellular growth. Below we describe a patient who developed an unusual complication of tyrosine kinase inhibitor therapy: thyrotoxicosis due to destructive thyroiditis. We review the pathophysiology of tyrosine kinase inhibitor-induced thyroid dysfunction particularly with regard to new second-generation tyrosine kinase inhibitors.

Megace Mystery: A Case of Central Adrenal Insufficiency.

Megestrol acetate (MA) is a synthetic progestin with both antineoplastic and orexigenic properties. In addition to its effects on the progesterone receptor, MA also binds the glucocorticoid receptor. Some patients receiving MA therapy have been reported to develop clinical features of glucocorticoid excess, while others have experienced the clinical syndrome of cortisol deficiency-either following withdrawal of MA therapy or during active treatment. We describe a patient who presented with clinical and biochemical features of central adrenal insufficiency. Pituitary function was otherwise essentially normal, and the etiology of the isolated ACTH suppression was initially unclear. The use of an exogenous glucocorticoid was suspected but was initially denied by the patient; ultimately, the culprit medication was uncovered when a synthetic steroid screen revealed the presence of MA. The patient's symptoms improved after she was switched to hydrocortisone. Clinicians should be aware of the potential effects of MA on the hypothalamic-pituitary-adrenal (HPA) axis.