Background: Several medical conditions require chronic anticoagulation, but there are potential long-term complications, including intracranial hemorrhages. Pituitary apoplexy (PA), caused by infarction or bleeding into the pituitary gland, is a rare condition that commonly occurs in the setting of a pituitary adenoma. However, several reports have shown an increased risk of PA associated with anticoagulation therapy. Recent case reports have shown that even the newer oral anticoagulants may increase the risk of PA. Typically patients present with an acute headache, visual disturbances and pituitary hormonal deficiencies. Management is controversial and includes either a conservative medical treatment versus a more aggressive surgical approach. We present a case of a PA induced by Apixaban, an orally active factor Xa inhibitor. Clinical Case: This is the case of a 45 years-old male patient with prior medical history of hyperthyroidism treated with radioiodine ablation, systolic heart failure and atrial fibrillation, receiving Apixaban for stroke risk reduction. The patient presented initially to the ER after developing an acute, pulsatile frontal headache, associated with nausea and vomiting. He was treated for a suspected acute gastroenteritis and was discharged home. Two days later the patient returned to the ER, with persistent headaches unresponsive to oral analgesics. This time, the patient also complained of decreased energy, difficulty concentrating, and memory problems. He denied visual changes, galactorrhea, decreased libido or polyuria. Vital signs were unremarkable and there was no orthostatic hypotension. Physical examination showed a male in mild distress due to pain. There were no visual field defects on confrontation, no neurological deficits, and an intact mental status. Brain imaging showed hemorrhage within the pituitary gland with associated edema, compatible with PA. There was no obvious evidence of a pre-existing pituitary adenoma. Laboratory workup did not reveal any hormonal deficiencies. The patient was managed conservatively with close neurological follow up and empiric high dose dexamethasone. Headaches improved significantly after treatment and eventually resolved. After clinical improvement, the patient was discharged home on physiologic replacement of glucocorticoids with outpatient follow up and plans for re-evaluation of hormonal axis. Conclusion: Oral anticoagulants can increase the risk of PA, even in the absence of a pre-existing pituitary adenoma, as other case reports have shown. Management is controversial, and although there are agents for reversal of Apixaban effects (recombinant factor Xa), their use in PA has not been described. This case was managed conservatively with excellent results. Although we cannot exclude a pre-existing pituitary adenoma in this patient, this case shows that Apixaban increases the risk of PA.
WITHIN recent years a great number of determinations (which need not be mentioned in detail) have given the impression that the ferricyanide method of oxygen estimation has yielded lower results for the oxygen capacity of blood than the Van Slyke pump. This difference existed between the Van Sly k e pump and both forms of ferricyanide apparatus as currently used-Hal dane's constant pressure model and B ar croft's differential model. Such a difference has been explained: (1) onthe assumption that reducing substances in the plasma, as shown by Douglas(), Parsons and Parsons2), and also by Litarczek(3), use up oxygen during the time in which the blood is being equilibrated in the apparatus; (2) that reducing substances in the corpuscles do the same, Mo rawit z and Rohmer(4), Douglas(5); (3) that the corpuscles are incompletely laked, Haldane(6), the unlaked portions not yielding their oxygen and (4) the blood may be contaminated with organisms, Haldane(6), which have an appreciable respiration.All these explanations possess an element of truth, the first awo certainly apply to blood of anaemic individuals and probably of rabbits. Harro p (7) has drawn a general relation between the rate of oxidation in blood and the number of reticulated red cells. Nevertheless they do not cover the whole ground, because, although they are not applicable to fresh hiemoglobin solutions (as opposed to blood), such hsemoglobin solutions on occasions exhibit the phenomenon which it is sought to explain. 19-59 (3) The figure given is in each case the average of a number of determinations, the number being stated in brackets. Thus for solution I the Haldane's apparatus(s) gave 16-42, 16*42, 15.91, 16-35, 15-91, while the Van Slyke pump gave 17-15 and 16-77.
Introduction Sodium-glucose cotransporter type 2 inhibitors (SGLT2-i) have proven to be a gamechanger for patients with diabetes, cardiovascular, and renal disease. However, this class of medications confers an increased risk for adverse side effects such as genitourinary infections and, rarely, euglycemic diabetic ketoacidosis (EDKA). Studies have shown that the risk of euglycemic DKA from SGLT2 inhibitors increase sevenfold in patients with type 2 diabetes mellitus (T2DM) with an overall incidence of approximately 0.1%. These side effects need to be taken into consideration when prescribing this type of therapy. Case Description Case of a 61-year-old male, with hypertension, type 2 diabetes mellitus on glargine, insulin lispro and empagliflozin, adherent to his regimen. Also, patient had a history of CAD s/p PCI (2015), and urethral stricture with self-catheterization who presented to the ED complaining of genital pain of 4 days evolution. Patient had been treated at home with clindamycin without improvement of symptoms. Upon evaluation at ED, laboratories were remarkable for WBC: 25.90, glucose: 144mg/dL, sodium: 134mmol/L, potassium: 5.3mmol/L, CO2: 10mmol/L, ketones: large. Arterial blood gases with metabolic acidosis and anion gap: 26.3. [LAG1] Glycated hemoglobin was 6.8%. Urinalysis was significant for glucosuria 1000 mg/dL, SG 1. 036, 30 mg/dL of protein, negative for nitrites and leukocyte esterase, and few bacteria. Blood glucose levels remained between 145-194 the first 24 hours after admission. Urology service performed a penile exploration with the finding of bilateral corpus cavernosum abscesses that were drained and cultured. Patient was diagnosed with EDKA and started therapy with IV insulin infusion as per DKA protocol, however 10% dextrose infusion was required to continue insulin IV infusion until ketoacidosis resolution. Broad spectrum IV antibiotics were initiated. However, his clinical condition deteriorated and developed respiratory failure requiring mechanical ventilation. After 36 hours of insulin infusion, IV antibiotics and fluids, his anion gap normalized. Abscess and blood cultures reported Candida Glabrata. Antifungal therapy was started and after seven days, the patient's clinical condition improved with resolution of his sepsis and DKA, and was successfully extubated. Patient was discharged to a rehabilitation facility. Conclusion EDKA presents a diagnostic and treatment challenge. It should be suspected in patients with metabolic acidosis, ketonemia and under treatment with a SGLT2-i, even in the absence of hyperglycemia. Prompt treatment initiation with IV insulin infusion along with IV dextrose is important for resolution of DKA. Five-percent dextrose solution should be started and titrated as needed, but if ketoacidosis does not resolve, 10% dextrose can be considered to maintain the insulin infusion. Prescribing this class of hypoglycemic medication should be avoided in those who are clearly at high risk of this well-known complications. Patient education regarding early recognition and to seek early medical evaluation are essential. [LAG1]Anadir unidades Presentation: No date and time listed
Introduction Cushing's Disease (CD) denotes a pathologic endogenous hypercortisolism secondary to excessive adrenocorticotropic hormone (ACTH) production. Cushing Disease is a rare condition with an estimated incidence of approximately 1.2-1.4 new cases / 1. 000. 000 per year. Although surgical intervention is the gold standard in the management of CD, many patients may present persistence or recurrence of disease despite surgical intervention, resulting in significant deterioration of their quality of life (QoL). For those in whom pituitary surgery is not an option or has not been curative, medical therapies have been developed. One of these newer treatments is the drug Osilodrostat, an inhibitor of the enzyme 11-beta-hydroxylase, responsible for the final step of cortisol biosynthesis in the adrenal glands. Case Discussion Case of a 21 year-old female patient with history of Cushing's Disease status post-transsphenoidal surgery (TSS) in 2017, obesity and oligomenorrhea who presented to our clinics showing signs and symptoms of hypercortisolism despite previously documented post-surgical remission in 2017. Patient reported recent development of acne, weight gain, round face, elevated blood pressure and mood changes. At the moment of evaluation, her most recent MRI showed post-surgical changes without a discrete lesion. Work-up was compatible with recurrence of Cushing's with an ACTH at 75pg/mL (nl, 10-60pg/mL), urinary free cortisol (UFC) at 1,122mcg/24h (nl, 4-50mcg/24h) and serum morning cortisol at 24. 0mcg/dL (nl, 5-20mcg/dL). In view of a negative MRI for a pituitary lesion, a Bilateral Inferior Petrosal Sinus Sampling (BIPSS) was performed. The BIPSS procedure revealed a pituitary source with a right pituitary lateralization suggestive of a right ACTH-producing tumor. The patient was consulted to Neurosurgery Service, but while waiting for repeat surgery, control of hypercortisolism was needed. The patient was started on Osilodrostat 2mg twice a day and was able to achieve normalization of UFC to 4mcg/24h, serum morning cortisol 5mcg/dL and late-night salivary cortisol (LNSC) of 30ng/dl (<90ng/dL) with significant improvement in her QoL, depression and clinical manifestations. The patient tolerated therapy well. Conclusion Cushing's Disease is a complex condition with potential serious complications if untreated. Even though TSS is the first line therapy, approximately 25% of patients show persistence of disease, and a similar proportion may experience recurrence. When surgery fails, medical treatment such as Osilodrostat, can temporarily suppress excessive cortisol production and ameliorate its clinical manifestations improving patients’ QoL while more definitive therapy is established. Presentation: No date and time listed
Introduction Adrenocortical carcinoma (ACC) is a rare malignancy of the adrenal glands, but often presents an aggressive behavior with variable prognosis. Median age of diagnosis is in the fifth to sixth decade of life with a median survival rate of 3-4 years. Complete surgical resection is the first line and only curative therapy. In patients with high-risk ACC, adjuvant therapy with mitotane, alone or in combination with other cytotoxic agents, may be used. Case description Case of a 33-year-old female with history of thyroid nodules presenting with a one year history of amenorrhea and hirsutism. One year prior to evaluation, the patient developed an intense right flank pain requiring abdominal-pelvic CT. It showed a solid heterogeneous right flank mass measuring 16×16×12 cm, 44Hounsfield units without enhanced contrast washout. Hormonal workup at that time resulted with DHEA-S > 10,000ng/mL(nl 350-4300), androstenedione 10.7 ng/mL (nl 0.35–2.78), total testosterone 3.21 ng/mL (nl < 0.52), midnight salivary cortisol at 14 nmol/L (nl < 3.6) and normal FSH, ACTH and serum morning cortisol. Staging chest CT exhibited bilateral pulmonary embolisms. Patient underwent right open total adrenalectomy of a necrotic/hemorrhagic mass measuring 20×16×9 cm with complete resection. Histology consistent with a low-grade ACC with a mitotic rate 18/50 HPF, with capsular invasion but no lymphovascular invasion and clear margins. It was stratified as stage T2N0M0. Immunohistochemistry's were positive for Melan-A, calretinin, synaptophysin, and inhibin. Ki67 was 80%. She was started on hydrocortisone replacement. PET/CT scan showed hypermetabolic focus at the right thyroid lobe (previously biopsied with benign findings), but otherwise no pathologic 18 FDG uptake related to known oncologic disease. Due to her high risk of recurrence, the patient was started on mitotane 2 g daily as adjuvant therapy but had to discontinue therapy after 1 month due to lack of availability. One year after initial presentation, she was evaluated at our clinics and after discussion with Oncology Service restarting mitotane was recommended. However, marked transaminitis was noted along with right abdominal discomfort. Abdominal MRI revealed hepatic hypo-enhancing masses suggestive of liver metastases, with the largest measuring 6.7cm. Patient underwent right partial hepatectomy and was found with extensive metastatic carcinoma and lymph node involvement. Therapy with mitotane was restarted, pending chemotherapy initiation. Conclusion The goal of any therapy for ACC is to alleviate symptoms and prolong survival. Mitotane, an adrenolytic drug used as palliative treatment, is among therapeutic options. Due to the rarity of the disease, data regarding its use is mixed due to limited randomized controlled trials. Nevertheless, it supports improvement in recurrence-free and possibly overall-survival after complete radical resection in stage I, II or III ACC. Unfortunately, there is still marked individual variation in outcomes. Presentation: No date and time listed
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