Presentation: This is a 51-year-old male with a history of Graves disease who presented to the ED with worsening proptosis and 10/10 eye pain. He reported being unable to shut his eyes, photophobia, decreased vision, and extreme eye sensitivity to touch. He was initially diagnosed with Graves disease 3 months ago, after which he was started on Methimazole 15mg 3x a day. Patient has a history of multiple sclerosis treated with an Alemtuzumab infusion 6 months ago. He additionally reports a history of depression, smoking, and alcoholism. Hospital Course: The patient presented with stable vitals signs with T: 36.5 C, HR: 97, BP: 117/68, O2 Sat 98% on RA. Physical exam was notable for Va: 20/100 OD, 20/200 OD with near card Sc. The R pupil was dilated Nr OU. EOM exam was notable for restricted ductions in all fields of gaze OU. IP was 20 mmHg OD and 22mmHg OS with Toponen 95%. Significant Proptosis OS more than OD with resistance to retropulsion. Bilateral conjunctival erythema with clouded corneas. Labs were significant for Hgb 12.2, MCV 80, Plt 342, ANC 12.1, Creatinine 0.69, albumin 2.8, Alk Phos 158, CK 41, FT4 0.53, TSH 0.318, and FT3 1.63. An US of the thyroid was significant for thyromegaly and a 5mm right thyroid nodule. A CT Orbit/Sella was significant for thyroid associated orbitopathy with greater exophthalmos on the left and maxillary sinusitis. The patient received 1000mg Rituximab infusion and IV Decadron every 4 hours with referral for possible thyroidectomy, orbital decompression as per ophthalmology, and continued multiple sclerosis management as per neurology. Discussion This complex case highlights worsening Graves orbitopathy as a rare side effect of Alemtuzumab. This orbitopathy persisted despite high dose methimazole. Urgent IV Decadron with orbital decompression should be considered in the acute setting with thyroidectomy for symptom resolution. Presentation: No date and time listed
Patient is a 29-year-old female with PCOS and morbid obesity and recent admission for abdominal pain is found to have bilateral adrenal hemorrhage and prolonged PTT. Patient was found to be anemic with hemoglobin of 6.1 a week prior to presentation, attributed to dysfunctional uterine bleeding and was treated with subsequent transfusion. She presents a week after her initial presentation with recurrent constant sharp pulsating abdominal pain, and reported pain was worse in mid-epigastric area radiating into her back, with a temperature of 38.2 and heart rate of 135, troponin level 2.64, with a negative CT for PE, but incidental bilateral adrenal hemorrhage absent on CTA from last week, with a CBC showing WBC 21.7 RBC 3.5 Hgb 8.6 MCV 76.9 MCH 24.7 RDW 17.6, with normal folate and B12. Patient was monitored closely and was started on IV hydrocortisone 50 mg every six hours, her PTT was found to be 88 and PT of 17.5, so antiphospholipid syndrome was suspected and confirmed with positive lupus anti-coagulant (LAC) and anticardiolipin IgG ab, and B2 glycoprotein. Patient had no evidence of adrenal infract that could have converted to hemorrhage. Objectives Antiphospholipid syndrome (APS) is an autoimmune systemic disorder characterized by persistent antiphospholipid antibodies including lupus anticoagulant, anticardiolipin or anti B2- glycoprotein I antibodies, presenting with arterial venous or small vessel thrombosis or recurrent early pregnancy loss. Other manifestation including livedo reticularis, cutaneous ulceration, thrombocytopenia, and hemolytic anemia, valvular heart disease and nephropathy. In our case, the patient APS was confirmed by the presence of the markers, but no evidence of adrenal infracts what could have converted to hemorrhage was found. Conclusions Although APS leads to a hypercoagulable state which can lead to adrenal vein thrombosis, leading to adrenal hemorrhage which can be fatal. Screening for antiphospholipid antibodies should be considered in all patients with unknown etiology of adrenal hemorrhage to promote diagnosis and timely management. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
Presentation: A 25-year-old man presented to the ED with intentional multi-drug overdose onset 9PM on the night prior to admission. PMHx is significant for seizures, hypothyroidism, resting tremors, and smoking. The patient expressed frustration over his persistent hand tremors with depressed mood and took 25 tablets of 500mg Keppra, 30-40 tablets of 150 mcg Levothyroxine, and 25 tablets of 10mg propranolol. The patient denied any chest pain, SOB, nausea, vomiting, lightheadedness, fever, focal weakness, numbness or tingling, prior SI, rash, dysuria, or bleeding. Hospital Course: Vitals were T: 37 Celsius, HR: 92 BPM, 135/87 BP, RR: 18, and SpO2: 93%. Initial EKG showed sinus rhythm with 80 heart rate. The physical exam was significant for profuse diaphoresis and generalized tremors. There were no ST or T wave abnormalities indicating ischemia. The patient had a lab workup that was significant for a TSH of 0. 006, FT4 of >5, FT3 of 7. 09, and T4 of 22.77, after which he was placed on plasmapheresis. The FT4 trended downward to 2.56 after plasmapheresis. The patient experienced transient elevations in creatine kinase and bilirubin, but lab workup was otherwise unremarkable. The patient met admission criteria for inpatient psychiatry and discharged to a psych facility. Discussion Given the 7-day half-life of Levothyroxine, plasmapheresis was considered the best option to prevent fatal thyroid storm. This case also demonstrates the importance of how a multi-drug overdose can present more benign presentation with stable vitals. In this case, the effects of propranolol masked the initial symptoms of hyperthyroidism and decreased FT3 levels, indicating the importance to conduct a thorough history to manage polypharmacy drug overdoses. This case highlights plasmapheresis as an effective treatment modality for thyroid storm. Presentation: No date and time listed
Case Presentation A 27-year-old female with a history of T1DM presented to the ED for continued visual changes onset the past 10 days. The patient states that she was driving from Wisconsin to Arizona when she developed blurry vision localized to her right eye. She was previously evaluated by outpatient ophthalmology where she was diagnosed with R abducens palsy with no evidence of retinopathy. Associated symptoms included nausea, dizziness, and right sided HA localized behind her right eye and the base of her head. This HA was not relieved by Excedrin or Tylenol. Over the past 3 months, her menstrual periods have been lighter and irregular. Additionally, she has been lactating ever since the birth of her child 2.5 years ago. Hospital Course: Pt had stable vitals: T: 36.4 C, HR: 97, BP: 130/76, RR: 23, SPO2: 100%. Physical exam was WNL other than CN6 palsy. Lab workup was notable for: Na: 138, Cr: 1. 02. FT4 0.94, TSH 3.281, AM Cortisol 8.5, Random Cortisol 7.5, FSH 3.4, FG Glucose 329, and Prolactin 60.4. An MR Brain with and without contrast revealed an enlarged pituitary with a posterior 7mm lesion with small amount of hemorrhage given the high T1 signal. The patient was admitted for concerns of apoplexy and started on Hydrocortisone 50mg IV q12 x2 followed by Hydrocortisone 15mg qAM and 5mg qPM. 18 units of Lantus were started q24 hours along with Cabergoline 0.5mg tabs qhs Wednesday and Sunday. Discussion Pituitary Apoplexy is an endocrine emergency characterized by cortisol levels insufficient for normal body homeostasis. However, not all presentations of Apoplexy are typical. This case highlights isolated abducens palsy as the presenting feature of pituitary apoplexy. Due to the nature of the anatomy of the cavernous sinus, ocular palsies can be a simple physical findings that may have important clinical correlates that should be investigated further. Presentation: No date and time listed
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