The Journal of the Louisiana State Medical Society : official organ of the Louisiana State Medical Society最新文献

A 27-year-old man was admitted to the coronary care unit because of chest pain and an electrocardiogram (ECG) read by the computer as an inferior infarct and left ventricular hypertrophy (Figure).

A 57-year-old man presented to the surgical oncology clinic with a mildly tender mass under his right arm. Four years prior, the patient had a melanoma removed from his right shoulder along with an ipsilateral right axillary sentinel lymph sampling. Computed tomography (CT) scan was negative for metastatic disease at that time. The patient did not undergo completion axillary node dissection and was lost to follow-up. The patient was originally from Australia, did not tan but reported multiple sunburns before age 18. He was of Irish ancestry. He denied weight gain, fever, fatigue, anorexia, or night sweats. The patient had a medical history of atrial fibrillation, hypertension, gout, melanoma, and benign prostatic hypertrophy. His surgical history included an appendectomy and a facial laceration repair. His brother died at 16 years old from leukemia and his mother died from colon cancer. He consumed 3 alcoholic beverages per day and denied tobacco or illicit drug use. On physical exam, the patient's temperature was 98.8° Fahrenheit, heart rate of 73 beats / minute, blood pressure of 121 / 59 mm Hg, respiratory rate of 18 / min. He appeared to be healthy and in no apparent distress. Cardiovascular, respiratory, breast, gastrointestinal, musculoskeletal, and neurological exam were unremarkable. His right axillary lymph node exam revealed a firm mass roughly 2.5 cm tall by 1.5 cm wide. This mass was biopsied and findings were consistent with metastatic melanoma. CT scan revealed small volume mediastinal adenopathy and a 4.5 cm right axillary mass. There was a 4.7 cm lesion within the anterior left lower lobe of the liver and periportal node conglomerate measuring 3.9 cm consistent with metastatic disease (Figure 1). He was negative for the BRAF V600E mutation. The patient was consented for treatment with combination immune checkpoint inhibition with ipilimumab and nivolumab. After two cycles the patient showed good response, but temporarily stopped treatment after complications related to a ST segment elevation myocardial infarction. He developed mild pneumonitis felt to be related to nivolumab, and recovered after a short course of glucocorticosteroids. Restaging CT scans were ordered after two cycles of therapy (Figure 2), which showed decrease in the size of the axillary and hepatic metastases. At six months, CT scans showed continued durable response (Figure 3).

A 39 year-old male with a history of diabetes, retinitis pigmentosa, and genital warts presented with intractable occipital headaches accompanied with nausea and vomiting. The patient had markedly depressed CD4 counts. Furthermore the patient tested negative for HIV and HTLV 1/2 and had normal immunoglobulin levels. During hospital course the patient underwent a lumbar puncture and multiple imaging exams, including both CT and MR. Except for occasional nausea and vomiting controlled by therapeutic lumbar punctures, phenergan, and dilaudid the patient's hospital course was uncomplicated.

Since its introduction in 1986, propofol ( two, 6-diisopropylphenol) , an intravenous sedative-hypnotic agent, has been utilized for the induction and maintenance of general anesthesia and conscious sedation in over 80 percent of cases; largely replacing thiopental ( sodium pentothal) over a decade ago. Unrestricted as a controlled substance, propofol's abuse potential emerged quickly and was highlighted by the death of pop singer, Michael Jackson, in 2009. In order to assess the epidemiological features of fatal propofol abuse, a descriptive analysis of the scientific literature was conducted using Internet search engines. Well-documented cases of fatal propofol abuse were stratified as unintentional or accidental deaths and as intentional deaths by suicides or homicides. Continuous variables were compared for differences by unpaired, two-tailed t-tests with statistical significance indicated by p-values less than 0.05. Of 21 fatal cases of propofol abuse, 18 (86 percent ) occurred in healthcare workers, mostly anesthesiologists and nurse anesthetists (n=14, 67 percent ). One case occurred in a layman who purchased propofol on the Internet. Seventeen deaths (81 percent ) were accidental; two were suicides (9.5 percent ) and two were homicides (9.5 percent ). Blood levels in intentional death cases were significantly greater than in accidental death cases (p less than 0.0001) all of which reflected initial therapeutic induction-level doses in the ranges of 2.0-2.5 mg/kg. Though lacking in analgesic effects, the abuse of propofol by young healthcare professionals, particularly operating room workers, has been significant; and likely underreported. Propofol is a dangerous drug with an evident abuse potential which often results in fatalities.

Introduction: Chronic pancreatitis by definition is a recurrent episode of acute pancreatitis and is commonly associated with alcoholism in the US. Another cause of chronic pancreatitis is hypertriglyceridemia (HTGP);, occurring in 1-5 percent of cases. The incidence of HTGP is higher in patients with diabetes and HIV, usually requiring triglyceride levels > 1000 mg/dL.

Case: A 33 year old man with uncontrolled type 1 diabetes and recurrent pancreatitis, first diagnosed 5 years prior, presented as a transfer from an outside hospital for a recurrent episode of HTGP. He reported recurrent pain episodes, requiring 6-9 hospitalizations within the last year for pancreatitis. He reported poor compliance with his insulin regiment at home. Other home medications included gemfibrozil, lisinopril, niacin, and omega-3 fatty acid. On transfer, his glucose was 296, triglyceride level was >3600, and A1C of 12.4. Transfer report lab work showed a triglyceride level >7000 and a lipase of 600. The patient had severe, diffuse abdominal tenderness on examination. He was diagnosed with pancreatitis secondary to hypertriglyceridemia due to a lipoprotein metabolism disorder and long-standing uncontrolled DM1. An intensive insulin drip was started on this patient, with goals of correcting his TG to less than 500 along with lowering his glucose. After 13 days, mostly on insulin drip, his TG decreased to 995 and pain was controlled, eventually tolerating a diabetic diet. He was encouraged to modify his diet and take his medications as directed at discharge.

Discussion: The relationship between hypertriglyceridemia and pancreatitis is poorly understood. In HTGP, a decrease in triglyceride concentration is a management priority. Rapid triglyceride concentration lowering is managed by insulin or plasmapheresis. As HTGP often presents in patient with uncontrolled diabetes, insulin is frequently used as treatment to lower both blood glucose and triglycerides; insulin decreases serum triglyceride levels by enhancing lipoprotein lipase activity and inhibiting hormone sensitive lipase, accelerating metabolism and decreasing adipocyte breakdown. Patients should be educated on the importance of compliance with drug therapy and lifestyle modifications.

Case: A 40 year old woman with a history of HIV, congestive heart failure secondary to an unknown congenital heart defect, and hypertension presented to our emergency department with worsening edema. On room air, oxygen saturation was 55 percent . On 5L of oxygen via nasal cannula, oxygen saturation was 88 percent . Physical examination was notable for central cyanosis, facial and lid edema, a II/VI holosystolic murmur across right chest radiating to entire right back hemithorax, decreased breath sounds at bases with pulmonary crackles, clubbing of fingers and edema of bilateral lower extremities. The patient related lifelong knowledge of a congenital heart defect, but had not been seen by a cardiologist as an adult. She was asymptomatic, yet sedentary until one year ago when she had the first of multiple hospitalizations for acute decompensated heart failure. A chest x-ray showed massive cardiomegaly with right-sided calcified aortic arch and patchy bilateral infiltrates. Transthoracic echocardiogram revealed severe right ventricular hypertrophy, ventricular septal defect, overriding aorta, and ejection fraction of 50 percent , consistent with unrepaired ToF. We utilized multimodality imaging techniques including CT angiography and Cardiac MRI which further defined her cardiac anatomy. Findings were consistent with unrepaired ToF with pulmonary atresia. The pulmonary arteries arose directly from the aorta in a confluent fashion via a large patent ductus arteriosus, major aortopulmonary collateral artery. The arterialized pulmonary arteries were aneurysmal with dissection and mural thrombus formation.

Discussion: This case illustrates how a patient with a rare presentation of unrepaired ToF with pulmonary atresia can go undiagnosed into adulthood. Early recognition utilizing a multimodality imaging approach can lead to proper diagnosing and hopeful surgical repair which can provide considerable improvement in functional status and long-term survival.

Introduction: Immunotherapy has been approved for treatment of melanoma. Autoimmune endocrinopathies have been reported in trials involving immunotherapy but autoimmune diabetes has not been definitively linked to them. Here we describe a case of autoimmune diabetes presenting with DKA after receiving combined immunotherapy with anti-CTLA4 and anti-PD1 monoclonal antibodies.

Case: A 47year old gentleman with metastatic melanoma presented to our institution with confusion, abdominal pain and decreased oral intake. The patient had a history of diabetes on metformin which was discontinued two years prior. He was started on Novilumab/Iplimumab for metastatic melanoma. He had received two cycles of immunotherapy and treatment was initially well tolerated. However, eight days after the second cycle the patient developed lethargy, confusion, vomiting and abdominal pain. CT of the head was negative for intracranial abnormalities and without evidence of brain metastasis. His laboratory results included: serum sodium 126 mmol/L, potassium 6.7 mmol/L, BUN 55 mg/dL, creatinine 3.5, bicarbonate 5 mmol/L, chloride 94 mmol/L, albumin 3.2 g/dL. Serum beta-hydroxybuterate was elevated (4.7 mmol/L, N: 0.0-0.5 mmol/L) and the calculated anion gap was 43 mmol/L. Serum lipase elevated (535 u/L, N: 4-60 u/L). The diagnosis of diabetic ketoacidosis was made and he was started on intravenous fluids and insulin therapy. Given his history of metastatic melanoma, his DKA was initially thought to be secondary to pancreatic metastasis especially considering the elevated lipase level. A non-contrast CT of the abdomen showed no evidence of pancreatic metastasis. Interestingly, further investigation identified high serum titers of anti-glutamic acid decarboxylase (anti-GAD) antibodies (0.43 nmol/L, N: less than 0.02 nmol/L), a low C-peptide level (0.2 ng/ml, N: 0.9-5.5 ng/ml), supporting an autoimmune etiology of the diabetes. Other islet autoantibodies were not elevated and his Hemoglobin A1C was 8.0 percent .

Discussion: There are few case reports about diabetes and immunotherapy. Autoimmune mechanism was suggested as the culprit, although not all cases reported with positive antibodies. Moreover, it is unlikely that patient developed latent autoimmune diabetes (LADA); and not related to immunotherapy due to the course of LADA is quite more gradual and our patient presented with acute DKA few days post the second cycle. Physicians and patients should be aware that autoimmune disorder such as DKA may be a rare but important immunotherapy related adverse events.

A 56 year old African-American man presented to the emergency department with dyspnea and dysphagia with drooling. On his initial evaluation, disproportionate obesity of the face, neck and shoulders were noted. The patient's history was significant for obstructive sleep apnea, end-stage renal disease, alcoholic liver disease, pulmonary hypertension and alcoholic cardiomyopathy. He had multi-decade history of heavy alcohol abuse, but quit drinking two years previously.

Case: A 54 year old woman with hypothyroidism presented with right flank pain that began acutely one week prior to presentation. She was told initially she had a urinary tract infection and treatment resulted in mild symptomatic improvement. The pain returned and she presented to another Emergency Department (ED); and was told the pain was due to constipation. She returned to the ED the next day when her pain worsened and her labs were notable for WBC of 19,000/uL, BUN/Cr of 28/0.75 mg/dL, AST of 31 U/L, ALT of 92 U/L and total bilirubin of 0.6 mg/dL. RUQ ultrasound was notable for dilation of the common bile duct. Given concern for choledocholithiasis, she was started on cefepime and metronidazole. MRCP demonstrated a distended gallbladder without stones and a small amount of pericholecystic fluid. Also noted were two areas of increased signal in the right kidney, concerning for neoplasia or infarction. Contrasted abdominal Computed tomography showed a moderate size area of hypodensity, consistent with renal infarct. Workup for embolic source of the infarction was unrevealing. Renal artery angiogram demonstrated a spontaneous dissection of the superior branch of the right renal artery. PCI was not performed due to risk of jeopardizing the other vessels and so she was managed medically with rivaroxaban along with hydrochlorothiazide and metoprolol succinate to keep her systolic blood pressure below 140 mmHg. The morning after the procedure, the patient told the treatment team that her grandson liked to jump from a height and she would catch him on her right side. This was felt to be a likely etiology of her spontaneous dissection. At the time of discharge, her pain was improved and repeat angiogram performed eight weeks later noted healing of the dissection.

Discussion: Spontaneous renal artery dissection is a rare cause of abdominal pain and often presents a diagnostic and therapeutic challenge. This case highlights the importance of considering alternate etiologies of localized abdominal pain when other common pathologies have been excluded.

Introduction: Left main coronary artery (LMCA); thrombus with an acute myocardial infarction identified with coronary angiography is a clinically rare condition with an extremely high mortality rate. We present a case of LMCA thrombus that presented as a non-ST elevation myocardial infarction (NSTEMI);.

Case: A 45-year-old woman with a history of tobacco use and hyperlipidemia presented with a complaint of 10/10 "hard pain" across her chest radiating to her left shoulder and breast which woke her from sleep. The pain was constant and severe, with no alleviation with rest. She had not experienced anything like this before. Workup revealed an upward trending troponin (1.98.989.79);, and an EKG with some tachycardia but no ST elevation or T wave changes. Her CBC, CMP and coagulation studies were unremarkable. A toxicology screen was positive for opiates and benzodiazepines, medications she was on for pain and anxiety respectively. ACS protocol was started with DAPT, LMWH, Statin, ACEi, and Beta-blocker. An angiogram revealed a large thrombus in the LM coronary artery extending into the aorta with concomitant 99 percent stenosis of distal LAD. 2D Echo w/ bubble contrast was significant for PFO, akinetic apical inferior and anterior wall. The mid antero-septum and apical lateral wall were hypokinetic. Interventional Cardiology and CTS recommended conservative management with medical optimization (Continue DAPT, heparin);, watchful waiting for the thrombus to resorb.

Discussion: Left main coronary artery thrombosis (LMCAT); identified during coronary angiography is a rare and challenging condition. It is a life threatening condition with an approximate incidence rate of 0.8 percent . It is thought to be secondary to plaque rupture with subsequent thrombus formation that is associated with persistent hypercoagulable state, cocaine induced plaque rupture or coronary vasospasm, post-partum state and embolization of intra-cardiac masses. The patient presentation can vary from sudden cardiac death to STEMI, NSTEMI, unstable angina and cardiogenic shock. Standardized therapy has not been developed due to the small number of reported cases.