16th Annual Southern Hospital Medicine Conference Abstracts

Rachel Apple, MD; Internal Medicine and Pediatrics, Vanderbilt University, Nashville, TN
Rosette Chakkalakal, MD, MHS; Department of General Internal Medicine, Vanderbilt University, Nashville, TN

Case Presentation: A 48-year-old male with a history of intravenous drug use presented with 2 weeks of back pain radiating from his buttocks to his shoulders. Review of symptoms was positive for night sweats, anorexia, and intermittent difficulty voiding requiring self-catheterization. He was afebrile with elevated heart rate and blood pressure and was noted to be in moderate distress secondary to pain. Examination revealed a II/VI systolic murmur at the left lower sternal border, no nuchal rigidity, intact strength and reflexes, and normal perineal sensation and rectal tone. On his arms and legs were scattered petechiae and track marks. Initial studies were significant for leukocytosis of 13,000 with 82% neutrophils; opiates, tricyclics, and antidepressants on urine drug screen; erythrocyte sedimentation rate of 58; and C-reactive protein of 235. CT of the back demonstrated multiple abscesses in the right iliopsoas, paraspinal, and abductor musculature; MRI of the cervical, thoracic, and lumbar spine revealed extensive subdural empyema (SDE) filling the lumbar through cervical canal, as well as loculated fluid within the cauda equina region. The patient, who at the time of admission was neurologically intact, was deemed a poor surgical candidate because his extensive SDE would require multilevel neurosurgical intervention that would place him at significant risk for spinal instability and neurologic compromise. He was therefore treated with antibiotics alone. Initial therapy included vancomycin, cefepime, metronidazole, bactrim, and rifampin. Blood, urine, and muscle abscess cultures were positive for methicillin-sensitive Staphylococcus aureus, and antibiotics were tailored to nafcillin, bactrim, and rifampin. Repeat MRI after 2 weeks demonstrated marked improvement in the lumbar SDE, with slight or no decrease in the SDE elsewhere. The patient remained stable without neurologic deficit and was transferred to a nursing facility for prolonged antibiotic therapy. At 8-week follow-up, the patient remained neurologically intact with continued improvement in the extent of his SDE and scattered muscular abscesses.

Discussion: Spinal SDE is an extremely rare condition with high rates of morbidity and mortality. Surgical drainage followed by systemic antibiotics is the treatment of choice, but when surgery is contraindicated, patients may be treated with antibiotics alone. Outcomes of medical management for SDE are largely unknown.

Conclusion: Standard therapy for spinal SDE is emergent surgery and antibiotics, but situations may arise, such as with this patient, in which surgical risk outweighs its benefits, necessitating treatment with antibiotics alone. When patients with SDE must be managed medically, early identification of the causative organism to guide antibiotic choice and close monitoring in the inpatient setting for incident neurologic compromise and response to therapy are critical to reducing the morbidity and mortality associated with this rare condition.

Aimee Wehber, MD; Department of Internal Medicine, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN
Kimberley Morris, MD; Department of Internal Medicine, University of Tennessee Medical Center, Knoxville, TN

Case Presentation: An 80-year-old male presented with a 1-week history of weakness, lightheadedness, nausea, vomiting, and minor nonproductive cough. His hematocrit was 23% with a positive fecal occult blood test. He denied abdominal pain, fevers, melena, rectal bleeding, or hematemesis. Significant medications included aspirin and naproxen. Early in his hospital stay, he developed abdominal distension and required a blood transfusion. CT of the abdomen revealed hyperdense thickening of the bilateral rectus abdominis muscles, consistent with bilateral rectus sheath hematomas. He then developed large flank bruising bilaterally. His abdomen remained nontender throughout his hospitalization. He eventually required embolization of the left inferior epigastric artery to stabilize his hematocrit.

Discussion: Rectus sheath hematoma is an uncommon diagnosis in patients presenting with symptomatic anemia. It results from insult to the epigastric arteries, typically from abdominal trauma, anticoagulant use, or extreme abdominal muscle contraction. The most common presentation is abdominal pain, tenderness, guarding, nausea, vomiting, and fever. Treatment approaches are typically conservative but sometimes require invasive management with embolization of offending vessels or surgery. This patient's lack of abdominal pain, tenderness, or palpable mass placed spontaneous rectus sheath hematoma lower on our differential; however, the diagnosis was made in a timely manner upon exploration using CT of the abdomen that is the first-line test. Understanding the sensitivity and specificity of imaging tests for this condition is prudent depending on index of suspicion. Rectus sheath hematomas are increasingly common among hospitalized patients given the frequent use of abdominally injected medications, including insulin and anticoagulants used for prophylaxis. The mortality is significantly higher among patients receiving anticoagulation, and thus, early diagnosis is essential.

Conclusion: This case illustrates the importance of considering a wide differential diagnosis for any chief compliant, including anemia and abdominal pain. While rectus sheath hematomas are uncommon diagnoses for the above chief complaints, it is important to recognize the condition early, as it is associated with significant mortality.

Martin Cerda, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Jean Touchan, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Doug Chapman, MD; Department of Cardiology, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 55-year-old female presented from home with acute onset of radiating substernal chest pain of an hour duration associated with shortness of breath, nausea, vomiting, and dizziness. The patient reported that she had been at home prior to the presentation of her pain and that the pain radiated to her shoulders and moved up her back and into her jaw. Upon arrival to the ED, she was found to have hypertensive urgency. It was treated, and her vital signs stabilized. On physical examination, she had unequal pulses of 2+ bilaterally in the lower extremity and right upper extremity and 1+ in the left upper extremity. Cardiac examination was unremarkable for any murmurs, rubs, or gallops. She underwent CT of the chest, concerning for dissection protocol, that showed focal dissection of the left proximal subclavian artery beginning just distal to the origin and extending 2.2 cm. Vascular surgery was consulted for possible surgical intervention; however, surgery was deferred to address the non-ST-elevation myocardial infarction (NSTEMI). Cardiac biomarkers were trended and showed initially a total creatine kinase (CK) of 101, CK-MB of 5.2, and troponin of 0.022. Upon admission to the coronary care unit, the patient underwent a left heart catheterization for subclavian stenting and was found to have nonobstructive coronary artery disease. Successful stenting of the left proximal subclavian artery was achieved with Omnilink stents 8 × 29 and 9 × 39.

Discussion: Spontaneous subclavian artery dissections (SAD) are rarely reported. Incidences of SAD have been primarily reported during catheterization with coexisting anomalies of the aortic arch or trauma. The exact underlying mechanism has yet to be clearly defined; however, it has been associated with drug use, trauma, uncontrolled hypertension, and vasculopathies. There are no known reported cases of a spontaneous SAD presenting as an NSTEMI. Scheffler et al report a 58-year-old female who presented with left upper extremity ischemic pain after playing golf that resulted in a left proximal SAD. Another case by Ananthakrishnan describes a 62-year-old female who spontaneously presented with left arm pain with absent left-sided pulses. Garewall et al report a case of a 54-year-old male with uncontrolled hypertension who presented with vertigo and intrascapular pain and was found to have multifocal infarctions involving the bilateral cerebellar hemispheres. All of these cases had favorable outcomes using fibrinolytics, anticoagulation, and endovascular treatment.

Conclusion: We present a case of a 55-year old female who presented as an NSTEMI and was found to have a proximal left SAD. SADs are rarely reported in the medical literature and usually are associated with direct trauma, heart catheterization, or anomalous aortic arch. To our knowledge, no cases report spontaneous SAD presenting as an NSTEMI in nonpregnant, healthy females.

Martin Cerda, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Brittany Bissell, PharmD; Department of Pharmacy, University of Florida-Jacksonville, Jacksonville, FL
Rafik Jacob, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: An African American female presented to the hospital with a complaint of intermittent, lower abdominal pain over the course of 3-4 days that was associated with nausea and nonbloody vomiting. The patient's medical history consisted of acute intermittent porphyria and iron deficiency anemia diagnosed in 2006. The patient had a history of multiple positive blood cultures, including Burkholderia cepacia, Pantoea agglomerans, and Staphylococcus lugdunensis. Each of these line infections was treated with removal of the PORT-A-CATH; however, the line was eventually replaced each time because of extremely poor intravenous access. Because of this extensive history, the patient had previous exposure to multiple broad-spectrum antiinfective agents. Blood cultures grew Brevundimonas in 1 of 2 blood culture samples. After 1 full day of therapy with cefepime, antibiotic therapy was changed to piperacillin-tazobactam due to one known case of cefepime resistance in the literature. Antibiotic susceptibility was performed, and the isolate was susceptible to ciprofloxacin, levofloxacin, and piperacillin-tazobactam. The patient improved after administration of Zosyn. Repeat cultures were negative. The PORT-A-CATH was removed on day 14 of her hospital stay, and the levofloxacin was continued for 14 days from port removal.

Discussion: Brevundimonas species previously belonged to the Pseudomonas family; however, a separate genus was categorized in 1994. Brevundimonas species are aerobic, nonsporulating, nonfermenting gram-negative bacilli. Brevundimonas species have a global distribution and have been isolated from water, soil, plants, and, infrequently, from clinical specimens. Human infections involving Brevundimonas species are rarely observed. The portal of entry remains largely undetermined in patients with Brevundimonas bacteremia. Studies have reported that most blood cultures of Brevundimonas species have been drawn from patients with in-dwelling catheters. Of those with Brevundimonas bacteremia, roughly 40% had implanted vascular catheters at the time of the diagnosis. Due to the infrequent isolates of Brevundimonas in human clinical samples, it remains unclear if these microbes are contaminants or true pathogens.

Conclusion: While Brevundimonas species are common isolates in soil, water, and plants, they remain rare pathogens causing bacteremia in human clinical samples. Previous studies showed varied susceptibility to antibiotics; however, piperacillin-tazobactam and carbapenems remain the suggested antibiotics for Brevundimonas infections. Our case is unique as we report the presence of Brevundimonas bacteremia in an immune-competent patient. Fortunately, our patient was able to tolerate treatment with piperacillin-tazobactam with subsequent oral levofloxacin therapy for a favorable outcome.

Alexander Leasure, BS; The University of Queensland, Ochsner Clinical School, New Orleans, LA
Badr Alsaleh, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA

Case Presentation: A 69-year-old male with a medical history of coronary artery disease and stroke without residual deficits presented with stroke-like symptoms. The patient had a history of intermittent neurological spells for the past 2 years. The spells consisted of altered mental status, left-sided hemiparesis with left tongue deviation, left gaze preference, and aphasia. The spells lasted 20-40 minutes and resolved spontaneously. He had no pain or aura, and episodes occurred weekly with no precipitating factor ever identified. During his first ED visit, he initially received a score of 17 on the National Institutes of Health stroke scale, indicating a high likelihood of stroke. He was subsequently imaged and given tissue plasminogen activator. CT of the head, CT perfusion, and CT angiography were all negative. The next day, he had no residual neurological deficits and was discharged home on optimized medical therapy. After initial presentation, the patient had numerous investigations including MRIs and magnetic resonance angiograms, all of which were unremarkable. On 2/26/15, investigators had a stroke of luck when an episode occurred during a cerebral angiogram. They were investigating vertebrobasilar insufficiency exacerbated by head turning. During the procedure but before any dynamic head turns, the patient had an episode lasting approximately 20 minutes. The CT angiogram showed patent vessels and good flow throughout the entire episode. He recovered spontaneously in approximately 45 minutes. At this point, the neurology team suspected a migraine subtype and added verapamil SR 240 mg/d and SLOW-MAG 2 tablets daily for prophylaxis.

Discussion: Stroke-like symptoms are common and often do not indicate a true stroke. Up to 19% of suspected ischemic strokes diagnosed by a neurologist actually have noncerebrovascular causes. Common stroke mimics include seizure, systemic infection, brain tumor, metabolic disorder, electrolyte derangement, and transient ischemic attack (TIA). Hemiplegic migraine is a rare subtype that includes a hemiplegic aura. A survey estimated the total prevalence of hemiplegic migraine in Denmark to be 0.01%. Hemiplegic migraine is diagnosed if the patient has fully reversible unilateral motor weakness with anarthria that completely resolves within 72 hours, the condition cannot be better accounted for by another International Classification of Headache Disorders-3 diagnosis, and TIA and stroke must be excluded. In rare instances, imaging with SPECT/PET has been used to diagnose hemiplegic migraine. Treatment for hemiplegic migraine is aimed at preventing future attacks. No particular prophylactic strategy has been shown to be superior. Options include beta blockers, tricyclic antidepressants, anticonvulsants, and calcium channel blockers. Modest evidence in the form of a small randomized controlled trial supports the efficacy of verapamil. Triptans and ergotamines should be avoided because of their potential to cause cerebral vasoconstriction.

Conclusion: Stroke-like symptoms are common and often do not indicate a real stroke. Hemiplegic migraine is a rare disorder characterized by aura and motor weakness that generally lasts less than 72 hours and is completely and spontaneously reversible. The 3 most stroke-specific features are facial palsy, upper limb hemiparesis, and dysarthria. Diagnostic challenges often present when investigation results are negative but the patient is still having neurological symptoms. The fortunate observation of an episode during diagnostic imaging elucidated an otherwise elusive disease.

Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Russell Cullinane, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Abdulwahab Hritani, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Amit Babbar, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: An 84-year-old male with a history of adenocarcinoma of the prostate (treated with proton radiotherapy and chemotherapy 8 years prior), coronary artery disease (non-ST-elevation myocardial infarction 1 week prior), and hypertension presented to our institution with painless hematuria and scrotal swelling for the past 4 weeks after traumatic Foley removal at another institution. On examination, his vital signs were stable; however, he had massive nontender scrotal and penile swelling. Foley catheter placed on admission collected dark red blood with clots. Aspirin and clopidogrel (Plavix) were held because of the significant hematuria. Urinalysis showed large blood, 200 mg/dL protein, and small leukocytes. Coagulation panel was normal. Serum creatinine was elevated at 1.24 mg/dL (baseline 0.88 mg/dL). Hemoglobin was 7.4 g/dL on admission (baseline 9-10 g/dL); platelets and leukocytes were normal. Vitamin C level was low 0.1 mg/dL (baseline 5.6 μmol/L). Renal ultrasound showed minimal prominence of the left renal pelvis inferiorly. Abdominal pelvis CT showed irregular and nodular bladder wall thickening and mild bilateral hydroureteronephrosis. Cystoscopy and biopsy were performed with fulguration of the biopsy area and clot evacuation (15 mL). Friable prostatic vessels were noted, as well as thickened bladder mucosa at the dome and posterior bladder. Biopsies were negative for malignancy but showed reactive urothelium with ulceration, granulation tissue, and acute and chronic inflammation. Continuous bladder irrigation did not improve hematuria. Frequent blood transfusions were required despite medical/surgical management. Hyperbaric oxygen therapy was recommended by urology for hemorrhagic cystitis in the setting of prior radiation exposure. However, the patient was unable to obtain this because of a urinary tract infection. He was started on daily vitamin C, and hematuria resolved within 2 weeks. To date, he has had no further episodes of hematuria.

Discussion: Scurvy is one of the oldest diseases known to mankind and is caused by vitamin C deficiency. Nowadays, it exists primarily within certain vulnerable populations such as patients with neurodevelopmental disabilities or psychiatric illnesses, elderly subjects, and patients with unusual dietary habits. Measurement of the ascorbic acid concentration is usually not helpful to ascertain a diagnosis of scurvy because values tend to reflect recent intake rather than actual tissue stores of vitamin C. Typical symptoms, along with a history of dietary deficiency of vitamin C, are usually sufficient to establish the diagnosis. Nevertheless, guidelines suggest that a fasting serum vitamin C concentration >34.1 μmol/L rules out scurvy and <11.4 μmol/L shows deficiency. The human body is unable to synthesize ascorbic acid and depends on dietary sources to meet its needs. A daily intake of between 15 mg (young children) and 120 mg (lactating women) is recommended. The body store of vitamin C is roughly 1,500 mg³ and its roles include support of collagen formation; involvement in the metabolism of carnitine, tyrosine, and neurotransmitters; and action as a redox agent by removing free radicals and protecting blood vessel walls. In developed countries, scurvy is seldom seen, although it can occur in individuals whose diets lack fresh fruit and vegetables. Our case demonstrates hematuria complicated by vitamin C deficiency. Although our patient had other risk factors for hematuria, the low vitamin C may have exacerbated and prolonged the bleeding. When vitamin C was repleted, the hematuria resolved, showing the importance of vitamin C deficiency as a complicating factor in bleeding.

Conclusion: It is important to continue acknowledging the role of nutrition in health to promote healthy lifestyles and help prevent serious life-threatening illnesses.

Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Russell Cullinane, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Abdulwahab Hritani, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Andreea Poenariu, MD; Department of Nephrology, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 23-year-old African American female with a history of lupus nephritis presented with worsening bilateral pedal edema and a 20 lb weight gain within the past 2 weeks. Her current medications included daily prednisone 60 mg and lisinopril 10 mg. On examination, her vital signs were stable, and physical examination was significant only for bilateral pitting pedal edema extending to mid-thigh. Blood tests revealed normal creatinine and blood urea nitrogen, elevated phosphorus at 6.0 mg/dL, low albumin at 0.8 g/dL, and low calcium at 7.8 mg/dL. Corrected calcium was 10.4 mg/dL. Lipid panel showed elevated triglycerides (1,225 mg/dL), elevated total cholesterol (404 mg/dL), elevated low-density lipoprotein (268 mg/dL), and low high-density lipoprotein (40 mg/dL). She also had a low complement (C3) level. Urine protein/creatinine ratio was 2.7. Vitamin D level was also low at 5 ng/mL. Her pedal edema responded to furosemide therapy. She was also started on hydroxychloroquine, and prednisone therapy was continued. Simvastatin and fenofibrate were used to manage the dyslipidemia. By the following day, her triglyceride level had decreased to 417 mg/dL with a repeat normal phosphorus level at 4.1 mg/dL, low albumin of 1.4 g/dL, and low calcium of 8.2 mg/dL. Corrected calcium was 10.3 mg/dL. She was discharged after her weight returned to her baseline 4 days later.

Discussion: The large number of disorders in which phosphate metabolism is disturbed and the acute and chronic clinical sequelae that may follow such disturbances are indicative of the clinical importance of phosphate levels. Multiple factors, including nutritional intake, medications, renal or intestinal excretion, and cellular redistribution, are potential etiologies of hyperphosphatemia. The clinical manifestations of mild hypophosphatemia or hyperphosphatemia are typically minor and nonspecific (myalgias, weakness, anorexia). When the imbalance is severe, critical complications may occur (tetany, seizures, coma, rhabdomyolysis, respiratory failure, and ventricular tachycardia). Hyperlipidemia can cause a variety of errors in the biochemical analysis of serum. Spurious depression of serum electrolyte concentrations can occur due to a space-occupying effect of the lipids in the sample. It has been demonstrated that if the lipemic serum is not dialyzed prior to colorimetric analysis or if the absorbance of the unreacted serum is not taken into account, a predictable technique-dependent overestimation of the serum in organic phosphorus level can occur. The laboratory at our institution does not take this into account, and hence, the pseudohyperphosphatemia in our case was the result of elevated triglyceride level. However, from the literature, the magnitude of this error is unable to be determined based on the level of hypertriglyceridemia. From our case, physicians should be aware of lipemia-induced hyperphosphatemia when elevations in the serum inorganic phosphorus concentration are encountered. Thus, a spuriously normal level of serum inorganic phosphorus in a patient with hyperlipidemia might also mask true hypophosphatemia. Treatment with phosphate-binding agents would be inappropriate in these cases.

Conclusion: It is important to be aware of pseudohyperphosphatemia from hypertriglyceridemia to avoid inappropriate investigation and treatment of patients.

Rediet Gebeyehu, MD; Atlanta Medical Center, Atlanta, GA
Tanna Lim, MD; Atlanta Medical Center, Atlanta, GA
Eltirmezy Mohammed, MD; Atlanta Medical Center, Atlanta, GA
Jennifer Guzman, MD; Atlanta Medical Center, Atlanta, GA
Jobira Woldemichael, MD; Atlanta Medical Center, Atlanta, GA

Case Presentation: A 38-year-old African American male who was a nonsmoker, nondiabetic, chronic alcoholic presented with hemoptysis of 2 days' duration. The patient reported dry cough of 1-year duration with weight loss and night sweats. Initial examination was normal except for decreased breath sounds with crepitation on the left upper posterior chest. Laboratory examination showed mild hyponatremia but was otherwise normal. Initial chest x-ray showed patchy consolidation in the mid and upper lobes with superimposed cavitation, concerning for an atypical infectious process. CT of the chest showed bilateral cavitary lesions with areas of adjacent atelectasis or infiltrates. Abdominal CT was noncontributory. Because of the results of the initial assessment of the pulmonary upper lobe cavitation, the patient was started on broad-spectrum antibiotics. Sputum culture and acid-fast bacilli smear with culture were negative. Streptococcus pneumoniae Ag, urine Legionella, human immunodeficiency virus rapid test, and polymerase chain reaction were also negative. Voriconazole was initiated empirically following no signs of improvement. Antigen and antibody testing for fungal etiologies was negative excluding Aspergillus. Autoimmune markers, including antinuclear antibody, perinuclear antineutrophil cytoplasmic antibody, and cytoplasmic antineutrophil cytoplasmic antibody, were negative. Bronchoscopy with bronchoalveolar lavage, brushing, and tissue biopsy from the cavitary lesion were sent for culture and histopathology and showed no atypical cells but possibly yeast. Transbronchial biopsy from the left upper lobe showed mixed inflammation with granulomatous changes and no atypical cells. The tissue culture showed mold that was sent to a regional laboratory for identification. The patient showed relative improvement on antifungal treatment. Tissue and bronchial wash culture finally revealed Rhizopus and Aspergillus niger species. The surprising tissue finding of Rhizopus in addition to Aspergillus species mandated additional treatment with amphotericin B.

Discussion: Pulmonary coinfection with Rhizopus and Aspergillus has rarely been described. Rhizopus principally occurs in immunocompromised individuals with involvement of the orbits and sinuses in 66% and of the lungs in 16% of cases. Aspergillus is a ubiquitous fungus that causes a variety of clinical syndromes in the lung, ranging from aspergilloma to chronic necrotizing aspergillosis in patients who are mildly immunocompromised or have chronic lung disease. We report an unusual case of pulmonary coinfection of Aspergillus and Rhizopus with lung cavitation in an immune-competent host. Based on our clinical search, coinfection with Rhizopus and Aspergillus has been described only in very few case reports and with immunocompromised hosts. Major risk factors include uncontrolled diabetes mellitus, hematologic malignancy–associated neutropenia, and immunosuppression linked with transplantation.

Conclusion: Our patient, despite chronic alcohol use, was otherwise immune competent. This case allows us to recognize and sheds light on the possibilities of disease entities outside of the commonly listed spectrum. By thoroughly investigating patients, one can direct appropriate treatment targeting a complete cure.

Jeffrey Winder, DO; Department of Medicine, University of Florida-Jacksonville, Jacksonville, FL
Francois Jo-Hoy, MD; Department of Medicine, University of Florida-Jacksonville, Jacksonville, FL
Rommy Issa, MD; Department of Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 48-year-old Caucasian male with a medical history of multiple myeloma (chemotherapy started 6 months prior), anemia of chronic disease, uric acid stones, and hypertension presented with a chief complaint of generalized weakness. He was hyperkalemic (7.5 mmol/L) and hyponatremic (123 mmol/L). He denied smoking, alcohol, and drug use. Family history was noncontributory. His home medications included allopurinol, aspirin, carvedilol, potassium citrate, and dexamethasone. On examination, his vitals were stable. He was alert and oriented. Cardiovascular, pulmonary, abdominal, and neurologic examinations were unremarkable. The patient was treated with albuterol nebulizers, calcium chloride, regular insulin with dextrose, and normal saline. His sodium level increased and plateaued at 131 mmol/L. Further workup revealed a proteinemia secondary to multiple myeloma, with a corrected sodium of 135 mmol/L, indicating pseudohyponatremia. The hyperkalemia ensued, for which the following laboratory workup was obtained: serum osmolality was 329 mOsm/kg, urine osmolality was 656 mOsm/kg, osmolar gap was 21, serum bicarbonate ranged between 17-22 mmol/L, urine sodium was 150 mmol/L, urine potassium was 15.7 mmol/L, urine chloride was 89 mmol/L, urine pH was 5.3, urine anion gap was 77, and transtubular potassium gradient (TTKG) was calculated at 1.6. Given these findings, the hyperkalemia was attributed to type 4 renal tubular acidosis (RTA). His low TTKG was suggestive of hypoaldosteronism. Serum aldosterone level was 4.9 ng/dL (range 1-30 ng/dL), and his renin level was elevated in both upright and supine positions, essentially confirming our diagnosis of type 4 RTA. He was started on fludrocortisone, and his hyperkalemia resolved.

Discussion: RTA is a group of diseases characterized by a hyperchloremic non–anion gap metabolic acidosis as the result of an inability of the renal tubules to secrete hydrogen ions (H+) or retain bicarbonate (HCO3). There are 4 types of RTA. Type 1 (distal) RTA is due to the inability of the distal convoluted and collecting tubules to increase H+ elimination via urinary ammonium (NH4+) excretion despite the presence of metabolic acidosis. Type 2 (proximal) RTA is due to impaired reabsorption of HCO3 in the proximal tubules. It is rarely seen in isolation, whereby failure of HCO3 reabsorption is related to a decreased renal threshold for reabsorption. It is commonly found in association with Fanconi syndrome. Type 3 RTA is a mixture of types 1 and 2. Type 4 RTA is caused by decreased NH4⁺ production as a result of aldosterone deficiency or resistance. Laboratory assessment of RTA includes calculating the serum/urine anion gaps, measuring serum/urine potassium and urine pH, and calculating urine osmolar gap.

Conclusion: Multiple myeloma has historically been associated with type 2 RTA in the setting of Fanconi syndrome. Based on our literature review, only one case of type 4 RTA has been published about patients with multiple myeloma. Our patient had known multiple myeloma and was found to have type 4 RTA, perhaps indicating the possibility of a more common association between the 2 conditions.

Jeffrey Winder, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Martin Cerda, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Julio Perez-Downes, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Ozdemir Kanar, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Khyati Baxi, MD; Department of Cardiology, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation 1: A 69-year-old African American female presented for evaluation of syncope. Her medical history was significant for hypertension. She had been working outside, and her husband found her unconscious. She did not recall preceding symptoms and denied prior syncopal episodes. Family and social history were noncontributory. She took no home medications. On arrival, she was alert and oriented. She was hypertensive, but vitals were otherwise stable. Neurologic, cardiovascular, pulmonary, and abdominal examinations were unremarkable. CT scan of the head was negative for hemorrhage. ECG demonstrated left ventricular hypertrophy. Cardiac enzymes were negative. She underwent left heart catheterization that revealed nonobstructive coronary disease. Left ventriculogram showed a beak-shaped morphology, suggestive of apical hypertrophic cardiomyopathy (HCM). Transthoracic echocardiogram (TTE) revealed a preserved ejection fraction (EF) and confirmed apical HCM. During her stay, no abnormalities were seen on telemetry. Her syncope was attributed to a mechanical fall. She was discharged on carvedilol.

Case Presentation 2: A 65-year-old African American male presented complaining of left arm numbness. He had been recently discharged from the hospital after presenting in cardiac arrest and being successfully resuscitated. He was diagnosed with an ST elevation myocardial infarction that was treated with a drug-eluting stent in the left anterior descending artery. Regarding his left arm numbness, he denied any preceding trauma. He had full range of motion, and strength was intact. Family and social histories were noncontributory. His home medications were aspirin, ticagrelor, lisinopril, carvedilol, amlodipine, hydrochlorothiazide, and atorvastatin. He was alert and oriented, and vitals were stable. Neurologic, cardiovascular, pulmonary, abdominal, and musculoskeletal examinations were unremarkable. X-ray of the arm showed degenerative changes but no acute process. Ultrasound of the arm was negative for clots. ECG was unchanged compared to those from his recent admission. Cardiac enzymes were negative. TTE was negative for a left ventricular aneurysm and showed preserved EF but was remarkable for a new finding of apical HCM not seen on prior echocardiogram. His carvedilol was switched to metoprolol tartrate. He was discharged on the same medications.

Discussion: Apical HCM is commonly seen in the Asian population but is rarely documented in African Americans. Our patients were diagnosed after acute events, illustrating how apical HCM might go undetected for years. The diagnosis is established on echocardiogram, and first-line treatment is calcium channel blockers or beta blockers. Ablation does not play a role because of its nonobstructive nature.

Conclusion: Our cases illustrate how apical HCM in other ethnicities might be more prevalent than presumed. Early recognition of familial prevalence leading to counseling and interventions may serve as a critical component in diagnosis, thus helping to decrease risk of future events.

Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Lauren Stemboroski, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Julio Perez-Downes, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
William Cullinane, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Pham Dat, MD; Department of Medical Oncology, University of Florida-Jacksonville, Jacksonville, FL
Anwer Siddiqi, MD; Department of Pathology, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 50-year-old Vietnamese male presented for evaluation of an anterior chest wall mass that had been gradually increasing in size for the past 5 months. He denied prior chest wall trauma and had no constitutional symptoms. He denied alcohol and tobacco use. He had emigrated from Vietnam in 2011. Examination revealed an anterior chest wall mass that was fixed to the manubrium. It was mildly tender, and the overlying skin was erythematous and warm. Both CT and MRI confirmed an enhancing mass measuring 8.6 × 6.0 × 3.5 cm that was centered within the manubrium with extension through the anterior and posterior cortex and into the upper portion of the sternum. He underwent CT-guided needle biopsy that showed a diffuse infiltrate comprised predominantly of plasma cells. Flow cytometry showed a population of bright CD38-positive and CD20-positive cells. Serum protein electrophoresis revealed a monoclonal spike in the gamma region corresponding to a lambda light chain, and serum immunofixation electrophoresis showed elevated lambda light chain 1741 and beta-2 microglobulin 6.1. His 24-hour urine protein was elevated at 7760 mg/24 h. Metastatic bone survey was negative. Bone marrow biopsy was consistent with marrow involvement by plasma cell myeloma. He was subsequently started on bortezomib 1.3 mg/m² SC/week and oral dexamethasone 40 mg weekly. After 3 months of treatment, the mass was clinically smaller, and lenalidomide 15 mg/d on days 1-21 of a 28-day cycle was added. Follow-up serum protein electrophoresis revealed decreased gamma globulins.

Discussion: Plasma cell dyscrasias are a group of entities characterized by the neoplastic proliferation of a single clone of plasma cells, typically producing a monoclonal immunoglobulin that can present as a single neoplasm (plasmacytoma) or multiple lesions (multiple myeloma). Primary tumors of the sternum represent about 1% of all bone tumors and are usually malignant. A solitary plasmacytoma (SP) is composed of monoclonal plasma cells that are cytologically, immunophenotypically, and genetically identical to those seen in multiple myeloma. They are uncommon localized osseous lesions that account for <5% of all plasma cell neoplasias. Plasmacytomas may be primary or secondary to the disseminated multiple myeloma and may arise from the osseous (medullary) or nonosseous (extramedullary) sites. The most common sites are in the marrow areas of the most active hematopoiesis, such as the axial skeleton and pelvic girdle. Rib and sternal involvement accounts for 10%-15% of cases. Plasmacytomas almost always destroy bone. The diagnostic criteria of SP of the bone require the presence of a solitary bone lesion confirmed by skeletal survey; plasma cell infiltration proven by biopsy; the absence of myeloma cells in the bone marrow; and a lack of anemia, hypercalcemia and renal involvement.

Conclusion: Patients with an SP of the sternum diagnosed on incisional biopsy mandate further investigation to exclude the presence of multiple myeloma. Localized SP has been considered curable with surgical resection plus radiotherapy vs multiple myeloma that is managed with systemic therapy and stem cell transplant in the appropriate patient.

Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Lauren Stemboroski, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Julio Perez-Downes, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Zaiden, MD; Department of Medical Oncology, University of Florida-Jacksonville, Jacksonville, FL
Anwer Siddiqi, MD; Department of Pathology, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 65-year-old African American female with a history of chronic anemia presented with worsening symptomatic anemia. She also noted a 35 lb weight loss 2 months prior. Examination revealed a pale, cachectic female with bilateral pitting pedal edema. Admission hemoglobin was 5.9 g/dL. She was transfused 2 units of packed red blood cells. The patient had been previously investigated for multiple colonic polyps. She had had a colonoscopy 2 years prior that revealed multiple sessile polyps, averaging 6-12 mm in size, found in the entire colon. Biopsy then was positive for tubular adenomas. She was planned for subsequent surveillance colonoscopy but defaulted from follow-up. Both of her children were diagnosed with colon cancer before the age of 40 years; however, the circumstances of diagnosis and treatment were unclear. Repeat colonoscopy on this admission revealed multiple small to medium sessile polyps from the rectum to the distal transverse colon. A lateral spreading polypoid lesion was found in the rectosigmoid colon but was negative for malignancy. Another suspicious mass was found in the distal transverse colon. It was villous and circumferential, almost completely obstructing the colon and preventing further interrogation of the colon. Biopsy of this mass was positive for invasive adenocarcinoma. Genetic testing revealed a deletion at exon 15 that was identified as a deleterious mutation consistent with the diagnosis of familial adenomatous polyposis (FAP). Staging CT was negative for metastatic disease. Despite counseling by the surgical oncology team, the patient declined operative intervention, opting for outpatient follow-up with surgical and medical oncology.

Discussion: FAP is an autosomal dominant syndrome characterized by the presence of hundreds to thousands of adenomatous polyps within the colon and rectum. The condition is attributed to truncating mutations of the APC gene on chromosome 5q. Inheritance is autosomal dominant; however, there is phenotypic heterogeneity ranging from severe disease to mild attenuated disease with few polyps. All patients with FAP should be offered genetic counseling and mutation analysis. If a pathognomonic mutation is identified, first-degree relatives should also be offered testing. Endoscopic surveillance of the large bowel is recommended to commence from the early teens. Because the natural history of FAP averages 15-20 years from the first development of adenomas to progression of malignancy, 2-year sigmoidoscopies are satisfactory once normal; however, annual colonoscopy is recommended once adenomas are discovered and should continue until colectomy is planned. Lifelong endoscopic surveillance is recommended for family members with an identified mutation as penetrance is virtually 100%. For those high-risk family members without an identified APC mutation, surveillance can be discontinued at age 50. The mainstay of surgical prophylaxis for the large bowel is colectomy with ileorectal anastomosis or proctocolectomy with ileal pouch-anal anastomosis.

Conclusion: FAP is responsible for <1% of all colorectal cancer cases, but evolution to large bowel malignancy approaches 100% in the absence of prophylactic surgery. As such, strict adherence to screening protocols should be emphasized, with appropriate prophylactic surgical intervention and lifelong surveillance thereafter.

Lauren Stemboroski, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
William Cullinane, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Elisa Sottile, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 34-year-old female with a history of migraine headaches and nephrolithiasis presented with coryzal symptoms of 4 days. She complained of a cough productive of yellow sputum with mild pleuritic chest pain but no dyspnea. Rhinovirus was positive on nasal swab. Examination was significant for subcentimeter, discrete, nontender cervical lymph nodes and gingival hypertrophy. Petechiae were also noted at the blood pressure cuff site. No other bleeding diatheses were noted, and cardiac and pulmonary examinations were unremarkable. Routine laboratory workup revealed leukocytosis of 183,000 with 87% blasts. The patient was thrombocytopenic with 67,000 platelets. Lactate dehydrogenase and D-dimer were elevated at 1,212 and >20, respectively, and fibrinogen was decreased at 96. Haptoglobin, international normalized ratio, and bilirubin levels were within normal limits. Chest x-ray (CXR) was unremarkable. Intravenous fluid hydration, hydroxyurea, and allopurinol were initiated. Urgent bone marrow biopsy was highly suggestive of acute monocytic leukemia (AML-M5). Echocardiogram showed a normal left ventricular size and wall thickness with an ejection fraction of 70%. Immediate induction chemotherapy was deferred due to the ongoing rhinovirus and concern for starting myelosuppressive therapy during an active infection. The following day, she developed worsening right-sided chest pain. CXR showed diffuse interstitial opacities, more focal at the right upper lobe. She was started on empiric vancomycin and cefepime. CT scan revealed multifocal areas of consolidation within the bilateral lung fields; however, they were peripherally located. The next day, the patient became acutely hypoxic with an arterial partial pressure of 45 mmHg on room air. The hypoxia was oxygen responsive, and saturations improved to 100% on a 50% venturi mask. Voriconazole was added, and she was admitted to the medical intensive care unit. Diuresis and noninvasive positive pressure ventilation were attempted without improvement, necessitating intubation. Induction chemotherapy was commenced on the day of intubation with cytarabine and idarubicin. The following day, she became hypotensive, requiring pressor support; however, she improved, was liberated from the ventilator 3 days later, and completed her course of induction chemotherapy. Follow-up CXR showed almost complete resolution of the opacities.

Discussion: We describe a case of an adult patient who presented with rhinovirus and AML-M5 who developed acute respiratory distress syndrome (ARDS) with respiratory failure due to leukemic infiltration. In this case, rhinovirus was positive; however, her pulmonary infiltrates were peripheral on CT and appeared more consistent with the appearance of leukostasis than infection.

Conclusion: Many times, ARDS is attributed to infection or pulmonary hemorrhage; however, it is important to recognize the underlying cause so appropriate induction chemotherapy is not delayed. It was not until induction chemotherapy was completed that these infiltrates resolved. Respiratory events in AML patients must be treated with a multidisciplinary approach, including cytoreduction with early chemotherapy.

Amanda Cruz-Cruz, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA
Laura Bateman, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA

Case Presentation: A 62-year-old African American female with a medical history of diabetes mellitus type 2 and recent stroke presented unresponsive from a rehabilitation facility. Upon arrival, she was immediately intubated for airway protection and placed on mechanical ventilation. Hemodynamic stabilization was obtained via pressors and empiric broad-spectrum antibiotics following the early goal-directed therapy model for treatment of sepsis. Laboratory workup was significant for moderate anemia, lactic acid of 3.9 mmol/L, troponin-I <1 ng/mL, and thyroid-stimulating hormone of 4.1 uIU/mL with normal free T4. ECG showed normal rate and sinus rhythm but was notable for T wave flattening and poor R wave progression. The patient was subsequently diagnosed with septic shock secondary to a left empyema. The empyema was drained via chest tube as she was not a candidate for a video-assisted thoracoscopic surgery. A bedside 2-dimensional echocardiogram done 2 days after presentation showed normal wall thickness and normal valves but a severely depressed left ventricular function with 20%-25% ejection fraction, a huge change from prior echocardiograms in which preserved left ventricular function was observed. Six days after initiation of treatment and successful source control, a repeat bedside 2-dimensional echocardiogram showed a low normal left ventricular systolic function consistent with 55% ejection fraction. Repeat ECG showed complete resolution of T and R wave abnormalities. We concluded that her acute myocardial dysfunction was directly correlated with the development of sepsis.

Discussion: The pathophysiology, management, and long-term cardiovascular treatment for patients who experience sepsis-induced cardiomyopathy are poorly understood. No known cohort studies have followed these patients long term. Causative associations that have been proposed include a combination of global ischemia in conjunction with the release of cytokines, prostanoids, and nitric oxide that results in a transient decrease in myocyte oxygenation. These assaults can “stun” the heart, resulting in global hypokinesis until sepsis is controlled. Although we lack sufficient data to support this theory, some studies have shown that 6-7 days after initiation of appropriate treatment for sepsis, systolic function can return to baseline. Risk stratification based on degree of sepsis, type of microorganism, or risk factors for atherosclerotic cardiovascular disease is unknown.

Conclusion: Acute cardiomyopathy is a poorly recognized and potentially fatal complication of sepsis. Its presence can increase mortality to up to 90% compared to those without cardiovascular dysfunction. Little data support its pathophysiology, but it remains a common, preventable complication. The high frequency of sepsis and cardiac-related deaths in the hospital setting presents significant opportunities for further investigation. This case emphasizes how early identification of sepsis can be directly linked to decreased patient morbidity and mortality.

Amar Parikh, MD; Department of Internal Medicine, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN
Carlos Rollhauser, MD; Department of Gastroenterology, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN
Mark Rasnake, MD; Department of Infectious Disease, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN

Case Presentation: A 34-year-old female presented to the ED complaining of melena, dyspnea, palpitations, and near syncope. She reported intermittent epigastric pain and a 15 lb weight loss during the previous 3 months. The patient denied fever, diaphoresis, or irregular menses. Her hemoccult was positive, and laboratory workup was remarkable for hemoglobin of 4.6. Initial evaluation with right upper quadrant ultrasound showed a 5 cm mass near the gallbladder fossa, and follow-up CT of the abdomen demonstrated a pancreatic head mass suggestive of solid neoplasm. It caused intrahepatic and extrahepatic biliary ductal dilation along with displacement of the hepatic portal vein, superior mesenteric vein, and artery. The patient was transfused with 4 units of packed red blood cells (RBC) and placed on intravenous Nexium. Subsequent upper endoscopy did not reveal a bleeding ulcer, and gastroduodenal biopsy was negative for malignancy. Colonoscopy and small bowel follow-through were unremarkable as well. Surgical oncology assessed the resectability of the patient's tumor and planned to perform an elective Whipple procedure in 2 weeks. As her hemoglobin remained stable at 9.5 on day 3, she was discharged with appropriate follow-up. Within 2 days, she returned to the hospital with prior symptoms of overt gastrointestinal bleed, dyspnea, and a hemoglobin drop of 3 units. She was admitted to the ICU, and RBC nuclear scan showed an active bleeding site in the proximal duodenum adjacent to the ampulla of Vater. The surgical oncologist advised against interventional radiology angiography with embolization because of the concern for duodenal necrosis that would preclude her Whipple. She was taken to the operating room promptly, and pathology studies of the resected pancreatic mass revealed an extramural gastrointestinal stromal tumor (GIST) originating from the duodenum.

Discussion: Extramural GISTs present frequently with abdominal pain, bleeding, weight loss, anemia, and early satiety. These tumors are highly vascular and fragile, making it difficult to perform a biopsy without the risk of spreading tumor cells and causing peritoneal metastasis. Pancreatic tumor workup per the American Gastroenterological Association guideline favors resection if concern for distant metastasis is low on imaging and the patient is a good surgical candidate. Resection of the tumor with free margins and negative regional lymph node involvement is considered curative. Diagnosis of GIST in our patient was based on histology and immunohistochemistry. GIST tumors overexpress c-KIT, DOG-1, CD34, and CD117 proteins. Because of the tumor's large size (>5 cm) and highly mitotic features, the National Comprehensive Cancer Network guidelines and our interdisciplinary team determined that 3 years of adjuvant imatinib therapy will provide our patient a 70% chance of 5-year relapse-free survival status post complete surgical resection.

Conclusion: Postoperatively, our patient did well on imatinib 400 mg daily, and serial CT of the abdomen every 6 months has not shown evidence of disease reoccurrence. The majority of pancreatic neoplasms are adenocarcinomas and have high mortality because of late presentation with advanced metastasis. This rare case, however, highlights the importance of early diagnosis and prompt treatment of a pancreatic mass as a few carry a good prognosis.

Amar Parikh, MD; Department of Internal Medicine, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN
Avi Das, MD; Department of Internal Medicine, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN
Mark Rasnake, MD; Department of Infectious Disease, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN
Daniel Ely, MD; Department of Internal Medicine, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN

Case Presentation: Our patient presented with dyspnea, fever, chills, and productive cough of clear thick sputum for 2 weeks. His history was significant for end-stage renal disease on hemodialysis and liver disease secondary to sarcoidosis, status post liver transplant 1 year prior. Initial evaluation was significant for white blood cell count of 12,400, creatinine of 3.97 mg/dL, and chest x-ray consistent with left lower lobe opacity. Bacterial pneumonia was suspected, and he was started on intravenous ceftriaxone and levofloxacin. He improved temporarily but declined rapidly on day 4 with confusion and lethargy. He was nonverbal, opened his eyes occasionally, and did not follow commands. Lumbar puncture revealed elevated cerebrospinal fluid protein and elevated glucose. Repeat chest CT showed bilateral multifocal consolidation consistent with pneumonia. In lieu of worsening pneumonia and rapid decline, bronchoscopy was performed, and pathology revealed blastomycosis. Amphotericin B liposomal formulation was initiated, and the patient quickly improved over the following few days.

Discussion: Respiratory tract infections are primarily of viral or bacterial etiology. Blastomycosis, however, is a rare fungus that can cause pneumonia with systemic involvement of bone, skin, and the central nervous system (CNS) upon dissemination. Blastomycosis is an infectious disease that we rarely come across in clinical practice. It is caused by inhalation of the dimorphic fungus Blastomyces dermatitidis and most commonly affects people living in midwestern, southeastern, and south central states. The epidemiology of this illness is unclear because of the lack of an antigen marker for skin testing, but it is estimated to have an annual incidence rate of 1 case per 100,000 based on historical outbreaks. CNS involvement happens in 1% of blastomycosis infections but can be as high as 45% in the immunocompromised population, including transplant recipients and individuals with human immunodeficiency virus. Delay in diagnosis causes significant morbidity and mortality in half of the individuals with CNS involvement.

Conclusion: With prompt diagnosis and treatment, our patient made a remarkable and quick recovery from his disseminated blastomycosis episode. Within days, he showed marked improvement in his mental status and pneumonia. After completing 6 weeks of induction therapy with amphotericin, he will take lifelong oral itraconazole. This case illustrates that we must keep a high index of suspicion for blastomycosis and other fungal infections, especially in immunocompromised patients when antibiotics fail.

Jobira Woldemichael, MD; Atlanta Medical Center, Atlanta, GA
Ngozika Orjioke, MD, FCCP; Atlanta Medical Center, Atlanta, GA
Eltrimizi Mohammed, MD; Atlanta Medical Center, Atlanta, GA
Milena Vukelic, MD; Atlanta Medical Center, Atlanta, GA
Rediet Gebeyehu, MD; Atlanta Medical Center, Atlanta, GA

Case Presentation: A 51-year-old African American female developed seizures post repair of a brain aneurysm 3 years ago. She had a history of alcohol abuse and noncompliance with her antiseizure therapies. She was admitted to the ICU with fever, encephalopathy, and status epilepticus requiring mechanical ventilator support. The patient was started on empiric antibiotic therapy and levetiracetam. Sedation was initiated with continuous propofol infusion. Initial laboratory data were significant for leukocytosis, non–anion gap metabolic acidosis, and subtherapeutic phenytoin levels; blood and urine cultures showed Escherichia coli. CT of the head was normal except for remote aneurysm clipping with postoperative encephalomalacia in the right anterior temporal lobe. Initial electroencephalogram (EEG) showed a 10 Hz posterior dominant background rhythm with an occasional sharp and slow wave seen over the right parietal region consistent with partial onset epilepsy. Because the patient was having nonremitting seizures, 24-hour EEG monitoring was initiated. She remained in status epilepticus. Valproic acid, midazolam infusion, and lacosamide were added, and a phenobarbitone coma was induced. The patient was in nonconvulsive status epilepticus for a total of 6 days based on continuous EEG monitoring. Once seizure activity was adequately suppressed, all infusions were weaned while maintaining the patient on high doses of lacosamide, levetiracetam, and valproic acid. She remained in a state of coma with preserved brainstem reflexes for 2 weeks. EEG was suggestive of anoxic injury with background slow cortical activity. Neurology suggested that recovery was unlikely, and end-of-life discussions were initiated with the family. However, 8 days after her last seizure, the patient started to show some responsiveness and was able to obey 1-step commands. The patient was more alert and was able to make her needs known with nonverbal communication at the time of discharge to a long-term acute care hospital for ventilator weaning and low-level rehabilitation.

Discussion: Status epilepticus that continues for more than 24 hours and is resistant to antiepileptic and anesthetic drugs is known as malignant refractory status epilepticus (MRSE). It accounts for 15% of all cases of status epilepticus in patients admitted to the hospital. Several case series report variable outcomes after weeks of iatrogenic coma with MRSE. Our case represents one of the uncommon cases of MRSE. Despite the high morbidity and mortality rate, our case demonstrates that survival with meaningful functional and cognitive recovery is still possible after prolonged MRSE.

Conclusion: Medical complications among survivors of MRSE are unpredictable because of the exposure of the brain to continuous seizure activity and the need for prolonged anesthesia. The factors that predict and influence possible recovery are unknown. Because of limited data, more studies and case reports are needed to evaluate and study factors that may help in prognostication of MRSE.

Abdulwahab Hritani, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Pujan Patel, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Alan B. Miller, MD; Department of Cardiology, University of Florida-Jacksonville, Jacksonville, FL
Timothy Paterick, MD, JD, MBA; Department of Cardiology, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation 1: A 70-year-old male with a medical history of chronic obstructive pulmonary disease (COPD) on O₂ was intubated in the field after being found in tripod position. He was brought to the ED where he was found to be in circulatory shock with bilateral wheezes. Troponin I level was elevated at 0.204 ng/mL. ECG revealed ST segment elevation in V3 and V4. A transthoracic echocardiogram (TTE) revealed global left ventricular (LV) dysfunction with an ejection fraction (EF) of 15%. He received COPD exacerbation and non-ST-elevation myocardial infarction (NSTEMI) therapy. By day 3, the patient was weaned off pressors and was extubated. On day 5, left heart catheterization (LHC) revealed no obstructive coronary artery disease. TTE on day 5 showed EF of 65%. The patient was discharged with the diagnosis of global stress-induced cardiomyopathy in the setting of COPD exacerbation.

Case Presentation 2: A 63-year-old female with a medical history of COPD presented to the ED with shortness of breath (SOB). Physical examination revealed bilateral wheezes. Troponin T level was elevated at 0.08 ng/mL, and the ECG showed T wave inversions in V3-V6. She was started on NSTEMI and COPD exacerbation therapy. On day 2, TTE showed apical stress-induced cardiomyopathy with an EF of 35%. On day 3, the patient underwent LHC that showed no coronary artery disease. Patient was discharged home with the diagnosis of stress-induced cardiomyopathy due to COPD exacerbation.

Case Presentation 3: A 53-year-old male with a medical history of COPD presented to our ED in respiratory distress. Physical examination revealed bilateral wheezing. ECG showed sinus tachycardia. Troponin I levels were elevated at 0.32 ng/mL. TTE showed global LV dysfunction, with akinetic septal wall motion abnormalities and an EF of 25%-30%. He received COPD and NSTEMI therapy. On day 5, the patient had LHC that showed no coronary artery disease and preserved EF. A TTE on day 6 showed resolution of the LV dysfunction with an EF of 60%.

Case Presentation 4: A 50-year-old female with a medical history of asthma presented to our ED with SOB and cough. She was in respiratory distress and became unresponsive in the ED and had to be intubated. She was tachycardic and hypertensive, had O₂ saturation of 88% on room air, and had coarse breath sounds bilaterally. Troponin was <0.05 ng/mL. ECG showed sinus tachycardia. TTE showed reversed Takotsubo cardiomyopathy with an EF of 35%-40%. She received asthma and heart failure therapy. On day 9, a repeat TTE showed a normalization of the LV function and an EF of 65%. She was discharged with the diagnosis of stress-induced cardiomyopathy secondary to asthma exacerbation.

Discussion: Takotsubo or stress-induced cardiomyopathy is defined as a reversible LV regional dysfunction in the absence of coronary artery disease. We present 4 cases of stress-induced cardiomyopathy in the setting of obstructive pulmonary disease (OPD) exacerbation. The first 3 patients had COPD and the fourth patient had asthma. The pathophysiology of stress-induced cardiomyopathy is thought to be coronary vasospasm secondary to catecholamine excess, but recent reports suggest that the cause of Takotsubo cardiomyopathy might be secondary to coronary microvascular dysfunction. The pathophysiology of the coexistence of stress-induced cardiomyopathy and OPD exacerbation is stress-induced cardiac dysfunction due to exaggerated sympathetic activation, and the use of sympathomimetic bronchodilators instigates myocardial stunning in such patients. Furthermore, the emotional and physiological stresses associated with OPD exacerbation are thought to be a trigger for cardiomyopathy.

Conclusion: Stress-induced cardiomyopathy should always be suspected when troponins are elevated in patients with severe OPD.

John Wang, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA
Sixto G. Giusti-Torres, MD; Department of Nephrology, Ochsner Clinic Foundation, New Orleans, LA
Damodar R. Kumbala, MD; Department of Nephrology, Ochsner Clinic Foundation, New Orleans, LA
Shirisha Bodana, DO; Department of Nephrology, Ochsner Clinic Foundation, New Orleans, LA

Case Presentation: A 41-year-old African American male without known medical history presented to the hospital with the chief complaint of a 1-week history of gradual, incapacitating, bilateral lower extremity edema. High-risk conduct for sexually transmitted disease was identified during the history. Physical examination revealed a maculopapular rash on his palms and soles. Initial laboratory workup showed rapid plasma reagin dilution of 1:128, serum creatinine of 1.2 mg/dL, and spot urine to protein creatinine ratio of 5.7. Kidney biopsy was consistent with membranous nephropathy. After 4 weeks of antibiotic treatment for secondary syphilis, the patient had complete resolution of his nephrotic picture.

Discussion: Membranous nephropathy, a glomerular disease characterized by deposits in the subepithelial space, is one of the most common causes of nephrotic syndrome in the adult population. Although in the majority of cases an inciting event cannot be identified, in about one-third of cases an association with autoimmune disease, drugs, or infections is usually found. Syphilis is a rare infectious cause of membranous nephropathy and usually presents with nephrotic-range proteinuria. Healthcare providers must remain aware of the association of syphilis with renal disease and its possible presentations.

Conclusion: During the past 15 years, we have seen a reemergence in cases of primary and secondary syphilis in the United States, and this increase in cases could lead to a greater number of patients affected by this sexually transmitted disease who present with renal involvement. History and physical findings suggestive of this sexually transmitted disease in a patient presenting with proteinuria and/or nephrotic syndrome should point toward accurate diagnosis. Resolution of the associated nephropathy and its clinical manifestations is seen after antibiotic treatment against Treponema pallidum.

Bryan S. Blase, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA

Case Presentation: A 40-year-old female presented to the hospital with the chief complaints of dyspnea upon walking only a few steps, paroxysmal nocturnal dyspnea, and lightheadedness. She had a medical history significant only for Sheehan syndrome after a postpartum hemorrhage complicated her last pregnancy. Echocardiography demonstrated a normal sized left ventricle and an ejection fraction of 10%. Her laboratory studies were significant for thyroid-stimulating hormone of 6.8 μU/mL and B-type natriuretic peptide of 1,400 pg/mL. Cardiac catheterization demonstrated nonobstructive coronary artery disease. She was started on a regimen of milrinone and dobutamine. She was subsequently diuresed with furosemide and started on nitroprusside to reduce afterload. The patient was evaluated by the heart failure team for a possible heart transplant. Further laboratory testing demonstrated a decreased cortisol level. Luteinizing hormone, follicle-stimulating hormone, prolactin, estradiol, and insulin-like growth factor 1 were also decreased. Cortisol stimulation test was positive, and the patient was diagnosed with secondary adrenal insufficiency. MRI of the pituitary demonstrated an empty sella. She was subsequently started on stress dosing of hydrocortisone and was also started on levothyroxine. Once the hydrocortisone and levothyroxine were titrated, her laboratory abnormalities began to normalize. She also saw an increase in her energy levels and improvement in her shortness of breath. In subsequent months, her cardiac function improved dramatically, and she was weaned off inotropic medications. More recent echocardiography has demonstrated ejection fractions of 55%-65%, and the patient no longer has any symptoms of heart failure.

Discussion: Cardiomyopathy is a disease of weakened or defective heart muscle that often leads to heart failure. The many causes of cardiomyopathy include genetic, toxic, infectious, and inflammatory etiologies. Rarely, cardiomyopathies can be of endocrine etiology. This clinical vignette describes a case of severe dilated cardiomyopathy caused as a result of Sheehan syndrome. The patient presented with symptoms of severe cardiomyopathy caused by a hormonal deficiency.

Conclusion: This case demonstrates an unusual etiology of cardiomyopathy. Genetic, infectious, toxic, and ischemic causes of cardiomyopathy are well documented and seen frequently in the cardiology and general medicine services. Endocrine abnormalities causing severe cardiomyopathy are far less common. What makes this case even more unusual is the dramatic improvement the patient experienced over a very short period of treatment. This case demonstrates the importance of keeping a broad differential and considering endocrine etiologies when evaluating cardiomyopathies and also demonstrates the dramatic improvement that is possible with appropriate hormone replacement.

Bryan S. Blase, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA
Laura Bateman, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA

Case Presentation: A 38-year-old female with a history significant only for diabetes mellitus type 2 presented to the hospital as a transfer for evaluation of a left eye retinal hemorrhage. Ten days prior to admission, she had been hospitalized for fatigue and diagnosed with iron deficiency anemia. During that hospitalization, she received 4 units of packed red blood cells and was started on a regimen of iron supplementation. On present admission, she was incidentally found to have a platelet count of 15,000/microL. She had no personal or family history of any hematologic abnormalities other than iron deficiency anemia. Review of systems and physical examination were significant only for a recent history of easy bruising. A platelet antibody screen revealed reactivity in 11 of the 12 wells for platelet-specific antibodies. The patient was diagnosed with posttransfusion purpura. She was started on a course of prednisolone that allowed her platelet count to recover without the need for plasmapheresis. She was, however, left with the sequela of retinal hemorrhage.

Discussion: Thrombocytopenia is a common finding in hospitalized patients with an extensive differential. Depending on the context and severity, the risks associated with thrombocytopenia can range from harmless bruising to life-threatening hemorrhage. The most common causes of thrombocytopenia include drug reactions, infections, immunologic pathways, and malignancy-related conditions. Posttransfusion purpura is a rare but serious cause of thrombocytopenia. It generally presents 7 to 10 days after a blood transfusion. Patients exposed to human platelet antigens (HPAs) in donor blood can develop antibodies to HPA that result in the destruction of their own platelets. Anti-PLA1 is the most frequently identified antibody, which in turn reacts with platelet antigen HPA-1a. The antibody binds to the platelet and is then removed via the liver or spleen. Platelet transfusions will not increase platelet counts and are not a treatment for posttransfusion purpura. Intravenous steroids are the first-line treatment. Patients who have developed posttransfusion purpura in the past are advised to use autologous donations or antigen-matched components for all further blood transfusions.

Conclusion: This case demonstrates one of the potentially dangerous complications associated with blood transfusions. Although the complication is rare, patients with no prior hematologic pathology can become critically thrombocytopenic following a routine blood transfusion, placing them at risk for a variety of complications. To prevent increased morbidity and mortality, familiarity with the side effects of transfusions is necessary, and blood products should always be administered with caution. This case not only reports an unexpected case of thrombocytopenia but also highlights the importance of early recognition of the inciting events that may lead to thrombocytopenia and the role of conservative stewardship of blood products.

Lauren Stemboroski, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville FL
Jeffrey Winder, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville FL
Elisa Sottile, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville FL

Case Presentation: A 54-year-old female with a medical history significant for atrial fibrillation, coronary artery disease, chronic obstructive pulmonary disease (COPD), and tobacco abuse presented with a 4-day history of right-sided facial rash, with severe pain and a worsening productive cough during the previous week. The rash was over the right V1 and V2 dermatomes, was hypersensitive to touch, and had one large subcentimeter darkened lesion on the right cheek and scattered smaller lesions with diffuse erythema. Physical examination revealed poor dentition, diffuse rhonchi, bibasilar rales, and scant wheezing. She also had conjunctival injection of the right eye with crusting of the upper and lower lashes. Her temperature was 100.9°F, and she was hypoxic on room air. Complete blood count was remarkable for 83% neutrophils. Chest x-ray demonstrated a left lung base hazy opacification and right middle lobe interstitial prominence. She was treated for her rash with intravenous acyclovir for possible herpes zoster and with clindamycin for secondary cellulitis. Clindamycin was discontinued, and the patient was treated with levofloxacin for the community-associated pneumonia, along with steroids, inhalers, and nebulizers for her COPD. On day 3, blood cultures showed gram-positive cocci, and intravenous vancomycin was initiated. After prolonged incubation with complex media, the culture grew Rothia mucilaginosa, Abiotrophia species, and vancomycin was discontinued. Sputum cultures reported mixed flora. Varicella zoster IgM, viral panels, and urine antigens for Streptococcus and Legionella were negative. The patient also had a negative antinuclear antibody, human immunodeficiency virus, and acute hepatitis panel with no signs of a compromised immune system. Her symptoms and chest x-ray improved, and repeat blood cultures were negative. The patient's facial rash began to resolve after 3 days of treatment. Echocardiogram was negative for endocarditis.

Discussion: R mucilaginosa, a gram-positive coccus of the family Micrococcaceae, is considered part of the normal flora of the oropharynx and upper respiratory tract. It is an opportunistic, nutritionally variant organism that grows well on nonselective media. This bacterium has been well documented as a cause of culture-negative endocarditis; our patient did not have any evidence of a murmur on physical examination or vegetations on echocardiogram. The likely source of infection in this case was odontogenic. The patient's multifocal pneumonia could have been caused by this organism; however, we did not have an adequate respiratory culture. Very few cases of lower respiratory tract infection caused by R mucilaginosa have been diagnosed by bronchoscopic, blood, or sputum specimens.

Conclusion: R mucilaginosa is reported primarily in severely immunocompromised, neutropenic hosts. It is important to increase awareness of this emerging pathogen because it is fastidious in nature, is underreported, and lacks current recommendations for optimal treatment.

Amanda Theppote, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA
Laura Bateman, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA

Case Presentation: A 56-year-old female with a history of cocaine abuse and prior acute renal failure secondary to ibuprofen abuse presented as a transfer with a 4-month history of epistaxis and hemoptysis. She was initially admitted at an outside hospital for severe anemia with hemoglobin of 4 and required multiple blood transfusions to stabilize. Her renal function had dramatically worsened from a baseline creatinine of 1.8 to 3.7, and dialysis was initiated. Laboratory workup at that time showed positive hemolysis markers; however, peripheral blood smears were negative for schistocytes. An initial rheumatological workup showed negative direct antiglobulin test, antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), human immunodeficiency virus, and antiglomerular basement membrane. On admission to our facility, her physical examination was pertinent for complete breakdown of the nasal septum, scleral icterus, labored breathing with diffuse rales, systolic murmur, and mild abdominal tenderness. CT of the chest showed scattered asymmetric ground-glass opacities. A second rheumatological workup showed positive ANA and atypical c-ANCA (cytoplasmic-antineutrophil cytoplasmic antibody), accompanied with a negative double-stranded DNA, myeloperoxidase, and proteinase 3 (PR3). Renal biopsy showed p-ANCA (perinuclear-antineutrophil cytoplasmic antibody) pauci-immune necrotizing glomerulonephritis. She was diagnosed with granulomatosis with polyangiitis (GPA), and her symptoms stabilized with prednisone and rituximab.

Discussion: GPA is a rare autoimmune disease of small- to medium-sized vessels that classically presents with granulomatous inflammation of the respiratory tract and necrotizing vasculitis of the kidneys. Common manifestations include hemoptysis, glomerulonephritis leading to renal failure, and nasal septum perforation resulting in saddle nose deformity. The presence of c-ANCA and PR3 in conjunction with a renal biopsy showing crescentic necrotizing glomerulonephritis is pathognomonic for GPA. This case highlights the difficulty of diagnosing a patient with a myriad of symptoms and evolving laboratory values, namely the presence and absence of c- and p-ANCA and PR3, respectively. Additionally, our patient had several factors that confounded her diagnosis. Her nasal septum perforation may have been secondary to either GPA or chronic cocaine use. Also, the patient's prior ibuprofen-related renal failure may have masked the original onset of glomerulonephritis. To our knowledge, no case in the literature has described GPA with both positive p- and c-ANCA and a negative PR3, with corresponding renal histological changes consistent with GPA.

Conclusion: This case demonstrates the collective work of hospitalists throughout the State of Louisiana and illustrates the challenging process of diagnosing a patient with atypical features of a disease. Our patient's diagnosis would not have been formed accurately without the teamwork and coordination of hospitalists at several different facilities.

Syed Rafay Ali Sabzwari, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Carol Ma, MD, FACC; Florida Heart Group, Orlando, FL

Case Presentation: A 73-year-old male who had recently been diagnosed with metastatic squamous cell carcinoma of the right lung presented with worsening pressure-like nonpositional central chest pain associated with some shortness of breath for the past 2 weeks. His other pertinent medical history included chronic obstructive pulmonary disease, mild coronary artery disease, myasthenia gravis, and medically resolved nonischemic cardiomyopathy; his recently diagnosed metastatic disease involved the right cerebellum and the left lobe of the liver identified on MRI of the brain and MRA of the chest. Repeat chest x-ray and laboratory data were stable; echocardiogram showed normal left ventricular function and no effusion. However, ECG demonstrated inferior lead ST elevations with cardiac enzymes repeatedly negative, nuclear stress test 6 months ago with no reversible ischemia, and a prior heart catheterization with mild coronary artery disease. Given the extensive metastatic disease and the cardiovascular findings, a PET-CT was done that identified a focus of hypermetabolism in the apex of the left ventricular wall consistent with an infiltrative process representing a metastatic lesion along with metastatic involvement of the right adrenal gland and proximal sigmoid colon. Because the patient desired aggressive treatment, he underwent gamma knife radiation for the cerebellar metastasis and is enrolled palliatively in the Abound study (with abraxane/carboplatin chemotherapy).

Discussion: Diagnosis of cardiac metastasis can be challenging because of nonspecific symptoms. In one of the largest autopsy series of more than 1,900 cancer patients, 8% had metastatic heart disease. The literature contains rare reports of myocardial metastasis presenting with myocardial infarction and stroke due to embolization, worsening congestive heart failure due to abnormal contractility, or valvular abnormality and conduction defects. In our patient, it was quite plausible that the isolated ST elevations were not ischemic changes and were attributed to ion channel disruption by mass lesion, causing ECG repolarization abnormalities. This case is unique in that despite widespread metastasis to the brain, adrenals, and liver, cardiac metastasis was not detected by routine imaging. PET-CT had to be utilized. Usually an echocardiogram and cardiac MRI and CT noninvasively provide high-resolution images; however, MRI is preferred.

Conclusion: Lung cancer is the most common cause of cardiac metastasis. Although the most commonly involved area is the pericardium, very rarely the myocardium can also be involved. It is important to keep cardiac metastasis as part of differential when working up cardiac causes of chest pain in the presence of ST elevations or conduction defects when advanced imaging in the form of PET-CT needs to be utilized.

Julio Perez-Downes, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Amie Leon, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 31-year-old African American female with a medical history significant for acquired immune deficiency syndrome (AIDS) and noncompliance with highly active antiretroviral therapy (HAART) presented with pleuritic chest pain. She described the pain as midsternal, squeezing, nonradiating, gradual in onset, and intermittent over 9 hours; associated with palpitations, fatigue, and dyspnea on exertion; exacerbated by movement; and relieved by arm elevation. Physical findings revealed tachycardia (rate 125), fever (101.3°F), and tachypnea (29). Her CD4 count was 6 (1%). Because of findings consistent with sepsis, blood cultures were obtained, revealing methicillin-resistant Staphylococcus aureus bacteremia. Transthoracic echocardiogram (TTE) revealed a trivial pericardial effusion. Subsequent TTE was ordered 9 days after initial findings, confirming the increase in size of the effusion with inflammatory exudates and constrictive physiology. After 5 days of treatment, repeat TTE revealed resolution of the pericardial effusion along with related symptoms and signs.

Discussion: Pericardial effusion is a known entity in patients with AIDS. Prior to the use of HAART, pericardial effusion was the most common manifestation of AIDS-related cardiovascular disease. The incidence of pericardial effusion has been identified as an independent predictor of mortality. In patients with AIDS, most detected effusions are small and asymptomatic and are incidentally found during evaluation. The most common physical examination finding is sinus tachycardia, with overt ECG changes and chest x-ray findings being uncommon. The average CD4 count in patients with pericardial effusion is 59, with a range of 18-10. Additional findings included increased mortality at 6 months from onset of effusion, with a rate of 62% in patients with effusion vs 7% in patients without effusion. The etiology of pericardial effusion in the setting of AIDS remains elusive. In our patient, HAART was instituted 2 days before evidence of pleural effusion because of the development of AIDS nephropathy. Echocardiographic evidence of resolution of pericardial effusion was noted 19 days after initiating treatment. HAART has been proven to greatly reduce the rate of effusions, and such decline has a concomitant decrease in mortality rates. Despite the decline of pericardial effusion, it is important to continue to try to elucidate the mechanism of this occurrence in uncontrolled AIDS.

Conclusion: This case illustrates how despite available resources and treatment for HIV-AIDS, pericardial effusion is still found in a portion of the HIV-AIDS population. This finding portends a poor prognosis. The etiology of pericardial effusion in patients with AIDS remains elusive. Our case illustrates how institution of HAART contributes to the resolution of pericardial effusion. Further studies are required to fully understand the development of pericardial effusion in AIDS and how HAART contributes to its resolution.

Julio Perez-Downes, DO; Department of Internal Medicine, University of Florida-Jacksonville, FL
Abdulwahab Hritani, MD; Department of Internal Medicine, University of Florida-Jacksonville, FL
Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, FL
Patrick Antoun, MD; Department of Cardiology, University of Florida-Jacksonville, FL

Case Presentation: A 35-year-old African American female with no prior cardiac history experienced sudden onset of exertional chest discomfort. The patient became unresponsive after arrival in the ED and was subsequently found to be in ventricular fibrillation (V-fib). The patient was in V-fib for 6 minutes; cardiopulmonary resuscitation was done with conversion after electrical cardioversion. Repeat ECG after return of spontaneous circulation demonstrated inferolateral ST elevation myocardial infarction. Toxicology screen was positive for amphetamines. Left heart catheterization showed 99% thrombotic occlusion of the mid-distal left anterior descending coronary artery (LAD). Two drug-eluting stents were placed in the distal LAD. Transthoracic echocardiogram (TTE) showed an ejection fraction (EF) of 10%-15%. The patient's cardiac function recovered during the course of her complicated stay with appropriate medical management. Subsequent TTE revealed improved EF to 60%-65% after 11 days with normal contraction of all myocardial segments but persistent left ventricular apical thrombus. Her neurological status improved significantly, and on interview, she denied any use of amphetamines or illicit drugs. She reported that during the past couple of months, she had been supplementing with a natural weight loss dietary supplement.

Discussion: Amphetamine use is strongly associated with coronary artery disease. The mechanism of myocardial injury as a result of amphetamine use is believed to be acute coronary vasospasm, with subsequent decreased perfusion and development of an acute coronary syndrome. Chronic use of amphetamines can also lead to accelerated atherosclerosis and increased thrombogenicity, both of which can lead to thrombo-occlusive acute coronary syndromes in young individuals. One of the side effects of amphetamine use is decreased appetite, a side effect that is desirable to some patients trying to lose weight. In view of the positive toxicology screen for amphetamines and the lack of history of abuse or use by our patient, we propose the notion that weight loss dietary supplements in fact may contain amphetamines or amphetamine-like substances.

Conclusion: Our case illustrates how inadvertent use of amphetamines by patients with no history or risk factors can be the culprit for life-threatening events. Patients often struggle with weight management and look for alternatives to supplement their efforts to lose weight. Without proper disclosure and in light of the recent trend of the addition of amphetamines to dietary supplements, it is important to educate patients and maintain a high index of suspicion when young adults present with acute coronary syndromes and have no history or family history of coronary disease.

Gopi Patibandla, MD; Hospitalist Service, Western Maryland Health System, Cumberland, MD Meghan Crum, PharmD; Western Maryland Health System, Cumberland, MD
Rohit Jain, MD; Hospitalist Service, Western Maryland Health System, Cumberland, MD

Case Presentation: A 39-year-old Caucasian male presented to the ED complaining of urinating blood for approximately 12 hours. He also developed midabdominal and back pain, as well as nausea and vomiting. He had a medical history significant for seizures; hepatitis C; bipolar disorder; anxiety; and alcohol, tobacco, and substance abuse. Initial red blood cells were 14.7 × 10¹²/L, hemoglobin was 14.7 g/dL, hematocrit was 43.7%, and point-of-care serum creatinine was 1.3 mg/dL. Aspartate transaminase and alanine transaminase were elevated at 2,197 U/L and 400 U/L, respectively. Initial creatine kinase (CK) was 343,482 U/L. CT of the abdomen and pelvis revealed no abnormal findings. Urinalysis revealed large amounts of blood. Urine toxicology screen was positive for benzodiazepines, tetrahydrocannabinol, and methadone. Home oral medications included clonazepam 1 mg twice daily, lithium carbonate 150 mg twice daily, and methadone 120 mg daily. The patient's symptoms were precipitated by working out in a gym with concentration on his upper body and then mowing the grass upon returning home. A repeat CK taken 4 hours later was 2,242,407 U/L; later that day, after hydration and sodium bicarbonate administration, his CK level decreased to 152,170 U/L. The patient's CK level continued to decrease until it was 400 U/L at discharge.

Discussion: Rhabdomyolysis is a breakdown of striated muscle causing a release of intracellular components including myoglobin. Causes include direct trauma or injury to the muscle, excessive muscle activity, hereditary muscle enzyme defects, medications, and infection. The most familiar causes of medication-induced rhabdomyolysis are the HMG-CoA reductase inhibitors, more commonly referred to as the statins. The range of rhabdomyolysis comprises subclinical elevations in CK to obstruction in the kidneys leading to acute renal failure that may lead to death.

Conclusion: A literature search does not show any case reports of elevations in CK anywhere near our reported level. In fact, severe rhabdomyolysis is only defined as a CK of ≥5,000 U/L, a level 400 times less than in this patient. Causes of the severe elevation in CK in this patient are probably multifactorial and are unclear at this time. Evaluating this patient for hereditary causes of rhabdomyolysis should be considered if similar symptoms recur in the future.

Russell Cullinane, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 44-year-old African American male with diabetes mellitus and bipolar type 1 disorder (on lithium) presented with incoherent rapid and pressured speech after being arrested for a verbal altercation. On admission, his vital signs were stable, and the rest of his physical examination was unremarkable. During hospitalization, he had a large daily urine output of approximately 6-7 liters. On further interrogation of the patient and family members, he was noted to have had polydipsia during the week prior to admission. Blood tests showed elevated serum creatinine and sodium levels of 1.8 mg/dL and 159 mmol/L, respectively. His lithium was discontinued on admission in light of his elevated creatinine. Serum osmolality was 311 mOsm/kg with a urine osmolality of 131 mOsm/kg, indicating diabetes insipidus. Desmopressin 10 mcg was administered intranasally, and repeat urine osmolality 1.5 hours later was 215 mOsm/kg, a >60% increase from preadministration levels, consistent with central diabetes insipidus. After the patient was started on nightly intranasal desmopressin, serum sodium levels returned to normal, and urine output decreased to 1-2 liters daily. MRI of the brain showed no masses or lesions. Remarkably, the patient's speech improved to normal, and he was discharged to a mental health facility. Lithium was never restarted.

Discussion: Diabetes insipidus is characterized by the production of large volumes of dilute urine with urine production usually >50 mL/kg/d total body weight with an osmolarity <300 mOsmol/L. Clinical signs of dehydration are uncommon, likely secondary to an associated rise in plasma osmolarity that stimulates thirst-causing polydipsia. Diabetes insipidus resulting from decreased secretion of arginine vasopressin (AVP) is termed central diabetes insipidus. If the diabetes insipidus results from sensitivity to AVP, it is termed nephrogenic diabetes insipidus. AVP is located in the supraoptic and paraventricular nuclei of the hypothalamus and released in the posterior pituitary. AVP release is regulated by the osmotic pressure of body fluids detected by osmoreceptors that are extremely sensitive to small changes in serum osmolarity but seem to be insensitive to solutes like urea and glucose. AVP then causes selective permeability of water in cells located in the distal tubule and medullary collecting ducts of the kidney. In our case, the patient's serum osmolality was 311 mOsm/kg, a level sufficient to produce maximal stimulation of AVP release from the posterior pituitary and therefore negating the need for water deprivation prior to vasopressin administration. The patient's change in urine osmolality of >60% after vasopressin administration was consistent with central diabetes insipidus, an unforeseen result considering the patient's history of prolonged lithium use of more than 2 years that proposed nephrogenic diabetes insipidus as a more likely diagnosis. Central diabetes insipidus can be caused by congenital, acquired, and genetic disorders but is idiopathic in nearly half of all adult cases, as demonstrated in our case.

Conclusion: In patients who use lithium chronically, central diabetes insipidus can also develop. This case highlights the importance of proper diagnosis of diabetes insipidus as either central or nephrogenic, even if the history highly favors one over the other, to ensure timely and effective management.

Kannan Thanikachalam, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Chioma Nwagbara, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Krishna Venkata, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Jyoti Samant, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 40-year-old African American female with a medical history of diabetes mellitus, end-stage renal disease on hemodialysis, and multiple dialysis catheter infections was admitted with the chief complaint of purulent discharge from an arteriovenous (AV) fistula. The patient was afebrile and underwent excision of the infected AV graft on the day of admission. Blood cultures and wound cultures grew methicillin-resistant Staphylococcus aureus with a vancomycin minimum inhibitory concentration of 2. Epsilometer test was sensitive. The patient was started on vancomycin with the goal of obtaining therapeutic levels of 15-20 mcg/mL. She received vancomycin for 6 days but remained persistently bacteremic. The patient's antibiotics were changed to daptomycin on day 7 of hospitalization. Gentamicin and rifampin were added for synergy and more penetration, respectively. The patient remained persistently bacteremic for 11 days despite antibiotics. CT of the chest with contrast was done to look for alternative sources of infection and revealed filling defects in the innominate vein, concerning for deep venous thrombosis–septic thrombophlebitis, and also showed a hypodense lesion in the spleen with the possibility of a septic infarct. The patient was started on anticoagulation, and her antibiotics were continued. On day 14 of hospitalization, the patient's bacteremia cleared. She was discharged on oral anticoagulation and daptomycin.

Discussion: Suppurative thrombophlebitis should be suspected in patients with persistent bacteremia after 72 hours of appropriate antimicrobial therapy, particularly in the setting of an intravascular catheter. The most common causes of suppurative thrombophlebitis are Staphylococcus aureus, coagulase-negative staphylococci, and Candida. Risk factors for the development of the disease are total parenteral nutrition via a central venous catheter, multiple previous antibiotic therapies, prolonged venous catheterization, and immunosuppression. While ultrasonography can help detect venous thrombosis, CT scanning is of great benefit to also assess the presence of peri-venous fluid, soft tissue abscesses, or additional organ involvement. Complications of suppurative thrombophlebitis include septic pulmonary emboli, secondary pneumonia, infective endocarditis, or any other metastatic seeding. Treatment of central venous catheter–related septic thrombophlebitis includes prompt removal of the focus of infection (intravenous catheter), administration of intravenous antibiotics, and consideration regarding surgical intervention and/or anticoagulation. Patients who do not respond to conservative medical management may require surgical intervention. Options include mechanical thrombectomy and endovascular thrombolysis.

Conclusion: Persistent bacteremia is a common presentation during hospitalist medicine practice and requires further evaluation to rule out septic thrombophlebitis. This case also describes the need for the hospitalists to be aware of further surgical interventions for patients who do not respond to medical management.

Talha Nawaz, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Kannan Thanikachalam, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Adrian Noriega, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Jewell Halanych, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 25-year-old African American male was admitted after being involved in a motor vehicle accident and sickle cell crisis. His medical history was significant for sickle cell disease and congenital biliary atresia. On his second day of admission, 1 unit of packed red blood cells was transfused for worsening anemia. During the transfusion, the patient spiked a fever of 101.5°F. After 4-6 hours, he started complaining of a fullness sensation in his throat and dysphagia. Upon examination, a significant swelling of the uvula with pale appearance was appreciated, and uvula angioedema or Quincke edema was diagnosed. Treatment with intravenous methylprednisolone, diphenhydramine, and famotidine was started. The next morning, complete resolution of the angioedema was seen. At that time, the patient was receiving hydromorphone infusion pump, morphine PRN, hydroxyurea, methocarbamol, and ursodiol. Blood work showed a normal C4, C1 esterase inhibitor, negative Coombs test, absent eosinophil count, and a throat culture that grew group B streptococcus. After 24 hours, the steroids and antihistamines were stopped, and the patient did not develop further episodes. The patient was followed up as an outpatient, and he was still taking the same medications. No more episodes have been reported.

Discussion: Isolated uvular angioedema, or Quincke disease, is a relatively rare presentation of angioedema of the upper airway. It is most commonly idiopathic but can also be a consequence of trauma, infection, medication reaction (most commonly with angiotensin-converting enzyme inhibitors), or hereditary angioedema. Our patient had a negative Coombs test, ruling out an immune reaction but not an allergic reaction mediated by mast cells. Although medications, including narcotics, have been reported to cause isolated uvula edema, medications were not likely the cause because they were not stopped after the patient developed the reaction. Also, the steroid and antihistamine were only given for 24 hours because the edema completely resolved. Although group B streptococcus grew in the throat culture, it is also unlikely to be the etiology because infection presents as uvulitis, and group B streptococcus is not considered a common throat pathogen. Uvulitis manifests with odynophagia, sore throat, and a red swollen uvula—not a pale uvula as in this case. Uvula edema usually manifests as fullness of the oropharynx and difficulty in talking. It can also cause shortness of breath and respiratory failure, so prompt treatment is necessary to avoid complications.

Conclusion: Adverse reactions after blood transfusions are common in hospitalist practice. The literature includes case reports about facial angioedema related to blood transfusion, but an exhaustive search did not reveal any cases isolated to the uvula. Before stopping crucial medications, physicians should consider other causes of angioedema.

William Cullinane, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Robert Ali, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Lauren Stemboroski, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Elisa Sottile, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 46-year-old African American male with sickle cell trait and a remote history of intravenous drug abuse (last use approximately 1 year ago) presented with worsening right knee pain and calf swelling for the past 5 months. He denied prior sexually transmitted infections or puncture wounds to the skin. He worked as a mason. Examination revealed a tender, edematous right knee and calf without warmth or erythema. Abrasions and vitiliginous changes were noted at both knees. Venous Doppler ultrasound showed avascular complex fluid collections in the right popliteal fossa and right calf. CT scan of the knee showed a large knee effusion with thickened synovium and concomitant multiloculated peripherally enhancing fluid collections extending between the gastrocnemius and soleus muscles. MRI further revealed synovitis and maceration of the medial meniscus. The patient underwent right knee arthrotomy with partial synovectomy. Turbid fluid and marked reactive tenosynovitis were visualized. Separation of the soleus and gastrocnemii muscles revealed a firm, gelatinous substance hardened between the 2 muscles, as well as multiple adhesions and a significant amount of necrosis. Cultures were positive for Pseudomonas aeruginosa, and the patient was treated for 2 weeks with combination cefepime and ciprofloxacin, followed by ciprofloxacin alone for an additional 2 weeks. Negative workup included human immunodeficiency virus (HIV), antinuclear antibody, rheumatoid factor, rapid plasma reagin, gonorrhea/Chlamydia screen, and blood cultures; however, hepatitis C was positive with a viral load of 266,000 IU/mL.

Discussion: Acute bacterial joint infections usually involve a single joint. Subacute or chronic monoarthritis is suggestive of mycobacterial or fungal infection, with episodic inflammation usually seen in Lyme disease and syphilis. Bacteria usually enter the joint directly from surgery or from the bloodstream, a contiguous site of infection such as bone or soft tissue, injection, animal bites, or trauma, with large joints more commonly involved than small joints. Joint damage begins within the first 48 hours and is secondary to increased intraarticular pressure, proteases, cytokines, synovial macrophages, and various inflammatory cells. Risk factors include rheumatoid arthritis, diabetes mellitus, glucocorticoid therapy, hemodialysis, malignancy, alcoholism, HIV, and hemoglobinopathies. Arthrocentesis is the test of choice, with cell counts of 25,000/mL to 250,000/mL and >90% neutrophils being typical of infected joints. Definitive diagnosis requires identification of the pathogen in smears, cultures, or nucleic acid amplification. P aeruginosa is a nonfastidious, motile, gram-negative rod that rarely initiates an infectious process in the absence of host injury or compromise.

Conclusion: P aeruginosa is an uncommon cause of bone and joint infections but is well documented to cause vertebral osteomyelitis and sternoclavicular joint arthritis in the setting of intravenous drug abuse. Although hematological seeding of joints can occur in healthy persons, a host predisposition is usually present. Hepatitis C infection in tandem with the sickle cell trait may have sufficiently dampened the humoral immunity of our patient, resulting in the insidious knee septic arthritis with eventual extracapsular involvement.

Marcum W. Collins, MD; Department of Internal Medicine, University of Tennessee Medical Center, Knoxville, TN
Gary L. Klipple, MD; Department of Rheumatology, University of Tennessee Medical Center, Knoxville, TN

Case Presentation: A 23-year-old African American male recently diagnosed with heart failure presented to the ED with complaints of progressive dyspnea and lower extremity edema. Two months prior, he presented to an outside facility with similar complaints, was diagnosed with cardiomyopathy, and was sent home with medical management for systolic heart failure. On admission, the patient was noted to be diaphoretic, lethargic, and dyspneic. He confirmed dry cough, bilateral lower extremity edema, and 40 lb weight gain during the past month. He denied chest pain, fever, sick contacts, arthralgias, rashes or nodules, and drug or alcohol use. Upon further questioning, he confirmed odynophagia with cervical lymphadenopathy and subjective fever 1 month before his original heart failure diagnosis, prior to which he was in good health. Initial evaluation including ECG and troponin was negative for cardiac ischemia but showed a brain natriuretic peptide of 1,823, with an erythrocyte sedimentation rate of 27. Urinary drug screen and blood alcohol were both negative. Transthoracic echocardiogram showed severe global hypokinesis, moderate to severe mitral regurgitation, and left ventricular ejection fraction of 15%-20%. Workup for causes of acute carditis, including group A streptococcus (GAS), revealed an antistreptolysin O titer of 1,419 with a DNase-B antibody of 1,500. In addition, coxsackie A viral titers were elevated at 1:1600. The patient was diagnosed with acute rheumatic heart disease (RHD), was started on evidence-based heart failure medications and daily prednisone, and was sent home with a LifeVest defibrillator.

Discussion: Acute rheumatic fever (ARF) is an inflammatory disease that occurs following GAS pharyngitis. RHD is a manifestation during ARF, resulting in pancarditis. Although RHD is still endemic in countries such as Africa, Asia, and South America, it is infrequently seen in developed countries such as the United States. According to Tibazarwa et al, an incidence of ≤10/100,000 cases per year was found in America and Western Europe. Traditionally, adherence to the Jones criteria is necessary for the diagnosis of ARF. However, according to the Guidelines for the Diagnosis of Rheumatic Fever, a presumptive diagnosis of ARF can be made in a patient presenting with indolent carditis as the only manifestation months after an acute GAS infection. As presented here, damage caused by GAS can lead to severe valvular heart disease and nonischemic cardiomyopathy and may be associated with acute cardiac decompensation. When coupled with other causes of carditis, including coxsackie virus, the disease burden can be severe.

Conclusion: With few causes of acute cardiomyopathy in young adults, recognizing infectious etiologies that can independently or concomitantly lead to a severe, debilitating cardiac manifestation in a young, previously healthy patient is of paramount importance. Failure to recognize such etiologies can lead to progression of the disease process and further cardiac decompensation.

Kathryn Nelson, MD; Department of Family Medicine, Atlanta Medical Center, Atlanta GA
Nomi Traub, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta GA
Haider Alwash, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta GA

Case Presentation: A 51-year-old female presented with a diffuse rash consisting of ulcerations and black/purple necrotic plaques. She noted that the rash first appeared on her arms 3-4 weeks earlier before spreading to her chest, ears, and lower extremities. The lesions, initially red, became itchy and eventually darkened to the current blackish plaques. The patient reported a history of a similar but less-severe rash on 2 previous occasions during the past few years. The patient initially denied any drug abuse but later admitted to snorting cocaine. Urine drug screen was only positive for cocaine. Her partner used the same cocaine without incident. CT scan of the lower extremity showed fasciitis, subcutaneous cellulitis, and subcutaneous emphysema. The patient emergently underwent an extensive excisional debridement of her bilateral lower extremities and a transmetatarsal amputation of the left foot because of gangrenous changes. Extensive serologic tests revealed only elevated C-reactive protein and erythrocyte sedimentation rate and positive antinuclear antibody (ANA) and hypocomplementemia. A skin biopsy performed a few weeks prior to admission demonstrated thrombotic vasculopathy and leukocytoclastic vasculitis. Outside records from 1 year earlier, when the patient portrayed similar but less-severe lesions, demonstrated positive ANA and a positive perinuclear antineutrophil cytoplasmic antibody (p-ANCA). Additional treatment during hospitalization included low-dose steroids, analgesics, and antibiotics for 2 weeks. The patient clinically improved during the course of the 16-day hospitalization and was discharged. She required a below-knee amputation 1 year later for nonhealing wounds.

Discussion: During the past 5 years, numerous publications have described a syndrome of cutaneous vasculitis surmised to be associated with cocaine that is contaminated with levamisole. The US Food and Drug Administration withdrew levamisole from the US market in 2000 after cases of agranulocytosis were associated with its use in patients with rheumatoid arthritis and cancer. The US Drug Enforcement Administration first noted levamisole-contaminated cocaine in 2003, and adulteration rates reportedly have risen dramatically since then. Nevertheless, cases of levamisole-associated vasculitis in patients who use cocaine remain rare. In case reports of presumed levamisole-induced vasculitis, patients present with purpuric lesions and hemorrhagic bullae and eschars, particularly on the face, ears, and lower extremities. Common laboratory findings include neutropenia, positive ANA, positive antineutrophil cytoplasmic antibodies (ANCAs), and lupus anticoagulant. The histology of cutaneous lesions often shows leukocytoclastic vasculitis and thrombotic vasculopathy. Spontaneous resolution of the lesions usually occurs once exposure to levamisole ceases. However, occasionally, patients sustain extensive tissue damage, as in our case, and amputation ensues—or death. Our case provided an unusual opportunity to view the laboratory abnormalities with 2 separate bouts of vasculitis. During the second occurrence, our patient did not have positive ANCAs and neutropenia that are reportedly almost ubiquitous. We did not test the patient for human elastase antibody, reported as a sensitive and specific test by some authors.

Conclusion: Hospitalists should familiarize themselves with the features of vasculitis associated with levamisole and remain cognizant of the broad spectrum of illness linked to levamisole-contaminated cocaine.

Jobira Woldemichael, MD; Atlanta Medical Center, Atlanta GA
Nomi Traub, MD; Atlanta Medical Center, Atlanta GA
Adugnaw Bekele; Atlanta Medical Center, Atlanta GA
Rebecca Jones; Atlanta Medical Center, Atlanta GA
Mulualem Teferi; Atlanta Medical Center, Atlanta GA

Case Presentation: A 56-year-old African American female with diabetes presented with a 3-week history of headache and vomiting. She noted tenderness on the right side of her face and jaw, diplopia, and blurred vision. She had been evaluated at 2 other hospitals where head CT had been normal and she was told “it was all in her head,” implying a psychiatric cause. The patient had been diagnosed with stage III endocervical adenocarcinoma after a cervical biopsy 1.5 years earlier and had received radiation treatments and cisplatin. She and her oncologist had initiated a drug holiday 2 months prior to her neurologic symptoms. Physical examination revealed no fever or meningeal signs. Neurologic examination showed normal motor and sensory examinations and a right abducens nerve palsy. Initial brain MRI demonstrated microvascular disease. The patient received steroid treatment for possible temporal arteritis; a right temporal artery biopsy was negative. Cerebrospinal fluid analysis demonstrated elevated protein, low glucose, white blood cells 28/μL, and red blood cells 133/μL with negative cytology. MRI of the internal auditory canal further evaluated the base of the brain and showed meningeal enhancement with a 5 mm right parietal lesion and a 5 mm cerebellar lesion. The patient developed seizures and encephalopathy. A second lumbar puncture (LP) exhibited malignant cytology. CT of the chest, abdomen, and pelvis revealed intraabdominal lymphadenopathy, consistent with underlying cervical cancer. While medical records were sought and treatment options were being considered, the patient declined cognitively and expired from respiratory arrest within 2 weeks of admission.

Discussion: Leptomeningeal metastasis (LM) clinically comes to light in 5% of solid tumors, most commonly in breast cancer, lung cancer, melanoma, or gastrointestinal tumors. Gynecologic cancers rarely metastasize to the meninges; cervical cancer is the least likely to do so. Patients with LM most often present with headache associated with nausea and vomiting from increased intracranial pressure, altered mental status, and cranial nerve palsies. Diplopia occurs most frequently as a symptom of cranial nerve invasion by a tumor in the subarachnoid space. Cerebellar dysfunction, radiculopathy, and seizures may occur. Gadolinium-enhanced MRI of the brain and spine, a sensitive modality for LM, usually is pursued initially. LP with positive cytology, although less sensitive, is more specific. Yield improves with a sample of at least 10 mL, prompt processing, and sampling close to the site of symptoms. However, sensitivity is only approximately 70% for the initial LP and 86% if a second LP is performed.

Conclusion: We present this case for its rarity but more significantly to illustrate several important principles for hospitalists. Attribution of a patient's symptoms to psychiatric causes must be done very cautiously in a patient with advanced cancer. When radiologic studies fail to show expected abnormalities, personal review with the radiologist often reveals subtle findings that provide clues to a diagnosis. In this case, we pursued the possibility of central nervous system vasculitis when the initial MRI of the brain did not show evidence of tumor. Ultimately, repeated studies and diligent pursuit of a second LP revealed this rare diagnosis.

Chioma Nwagbara, MD, MPH; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Kannan Thanikachalam, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Krishna Venkata, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 37-year-old female with thalassemia-HbS disease, cerebrovascular disease with left hemiplegia, and aphasia presented with a complaint of abdominal pain. She described a severe right upper quadrant abdominal pain with associated nausea but no vomiting. On physical examination, the patient was normotensive and afebrile. Abdominal examination revealed tender hepatomegaly and increased bowel sounds. She had leukocytosis with neutrophilic predominance, anemia, and thrombocytosis. Her total bilirubin and alkaline phosphatase were elevated. CT of the abdomen showed multiple hepatic lesions consistent with metastatic disease and a left upper quadrant mass that appeared to be within the pancreatic tail, favoring primary pancreatic neoplasm with metastases to the liver. Percutaneous liver biopsy pathology report described metastatic neuroendocrine neoplasm. The patient was started on octreotide for treatment of the neuroendocrine tumor (NET).

Discussion: Pancreatic NETs have an incidence of approximately 1 per 100,000 individuals per year and account for 1%-2% of all pancreatic tumors. They may manifest at any age. The majority of patients with advanced pancreatic NETs have liver metastases. Most tumors (50%-75%) are nonfunctioning and not associated with a hormonal syndrome. Functioning tumors may include insulinoma, glucagonoma, VIPoma, and gastrinoma. Clinical presentation depends on the type of the tumor and the functionality. Because of lack of functionality, nonfunctioning pancreatic NETs present late in the course of disease with features of local compression and metastatic disease. When symptomatic, the most common presenting symptoms of a nonfunctioning pancreatic NET are abdominal pain (35%-78%), weight loss (20%-35%), and anorexia and nausea (45%). CT and MRI are highly sensitive for identification of primary pancreatic NETs, as well as liver metastases. Early arterial phase imaging is valuable for detection of hypervascular primary tumors and liver metastases. For those who have potentially resectable metastatic disease, resection may provide prolonged control of symptoms and tumor growth. However, the majority of patients have a recurrence even if resection is complete. For patients with unresectable disease, options to control tumor growth and symptoms related to tumor bulk or hormonal hypersecretion include somatostatin analogs, nonsurgical liver-directed therapy, and systemic antitumor therapy.

Conclusion: Abdominal pain as a symptom in a patient with a history of sickle cell disease should not be considered as just another sickle cell crisis pain. Thorough evaluation is required to look for all possible etiologies.

Radhwan Alrubaye, MD; Atlanta Medical Center, Atlanta, GA
Zohra S. Chaudhry, MD; Atlanta Medical Center, Atlanta, GA
Yonathan Negew; Atlanta Medical Center, Atlanta, GA
Lall Thomas; Atlanta Medical Center, Atlanta, GA

Case Presentation: A 77-year-old female presented to the ED with a 1-day history of nausea and vomiting accompanied by upper abdominal pain. Her medical history was significant for dementia, seizure, cerebral vascular accident, hypertension, hyperlipidemia, peripheral vascular disease, and right AKA. Her current medications included metoprolol, furosemide, atorvastatin, levetiracetam, citalopram, and buspirone. She denied the use of alcohol. The patient was not in acute distress, but her abdomen was distended, she had tenderness over the epigastric region, and she had positive bowel sounds. Laboratory workup was significant for leukocytosis 23.1, creatinine 2.1, bilirubin 1.7, alanine aminotransferase 132, aspartate aminotransferase 206, alkaline phosphatase 157, and lipase >1,800. We reviewed her medications list and stopped furosemide. CT of the abdomen revealed enlargement of the pancreatic head with a central collection of 3 cm debris that suggested impeding duodenal diverticula into the pancreatic head. A 2-3 cm diverticulum rose from the proximal duodenum and extended inferiorly to the pancreatic head. The gastrointestinal service was consulted and approved conservative management. Diverticula perforation was excluded by MRI with contrast; therefore, no surgical innervation was needed. The patient's clinical condition improved, with white blood cells and liver function tests trending dramatically down.

Discussion: Duodenal diverticula are acquired pouches in the mucosa and submucosa. They are rare in patients younger than 40 years. Most are solitary and within 2.5 cm of the ampulla of Vater. Patients with juxtapapillary diverticula have a high incidence of gallstone disease. The majority of duodenal diverticula are asymptomatic. Clinical presentation may be characterized by nonspecific abdominal symptoms, but complications are responsible for presentation in most cases. When drainage in the neck is inadequate or the neck is narrow, these conditions favor inflammation and may even lead to hemorrhage or perforation. Compression of the common bile duct, dysfunction of the ampulla, or a poorly emptying diverticulum with a narrow neck can all lead to pancreaticobiliary disease and possible pancreatitis. The treatment of duodenal diverticula is mainly supportive. Surgical or endoscopic interventions should be reserved for symptomatic diverticula and for complicated duodenal diverticula refractory to medical treatment.

Conclusion: Our patient had direct compression of the duodenum to the head of the pancreas that explained the cause of pancreatic inflammation. We suggest excluding the diverticulum initially when determining the idiopathic cause of pancreatitis. However, when a duodenal diverticulum is found in the absence of any additional pathology, only then should the symptoms be attributed to the diverticulum.

Sumant Aroraa, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Adrian Noriegaa, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Alvin Mendozaa, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 56-year-old female was admitted to the hospitalist service with worsening productive cough, fever, chills, and night sweats. Her medical history included asthma and paroxysmal atrial tachycardia. She denied smoking and history of travel outside of the United States. Her symptoms had started several months prior and required multiple ED visits. She was treated with antibiotics for presumed pneumonia. On the current admission, she had scattered wheezing in bilateral lung zones. Laboratory workup was notable for white blood cell count of 16,200/μL with 14% eosinophils. Chest x-ray showed patchy peripheral opacities in the left upper and lower lung fields. Initially, the patient was started on levofloxacin and vancomycin for presumed bacterial pneumonia. However, she developed a diffuse papular rash on her upper extremities and back. Because blood and sputum cultures were negative, empiric antimicrobials were discontinued. Autoimmune workup including antinuclear antibody, rheumatoid factor, cytoplasmic antineutrophil cytoplasmic antibody, and perinuclear antineutrophil cytoplasmic antibody was normal. Serum level of total IgE was 234 IU/mL (normal <114), erythrocyte sedimentation rate was 55 mL/hr (normal 0-29), and C-reactive protein was 13.82 mg/dL (normal 0-29). CT of the chest revealed multiple subpleural bilateral ground glass opacities. Bronchoalveolar lavage (BAL) showed bronchial epithelial cells and macrophages without eosinophilia. Left lower lobe transbronchial lung biopsy (TBLB) revealed significant interstitial eosinophilic infiltration. We diagnosed chronic eosinophilic pneumonia (CEP) based on the clinical, radiologic, and pathologic findings. Therapy was changed to 80 mg/d of intravenous methylprednisolone, and the patient's symptoms and pulmonary opacities resolved by day 7. She was discharged home on a tapered dose of oral prednisone.

Discussion: CEP is an idiopathic disorder characterized by marked accumulation of eosinophils in the pulmonary interstitium and alveolar spaces. It usually affects patients aged 30-50 years. Diagnosis is made by clinical presentation, predominantly peripheral or pleural-based mid to upper lung zone opacities on chest imaging and eosinophilia (≥25%) on BAL, with eosinophilic predominance in interstitial infiltrates and alveolar exudates on lung biopsy. However, biopsy is usually not required for diagnosis unless the patient lacks eosinophils on BAL or fails to improve with steroids. Our patient underwent TBLB that was diagnostic. Patients typically have productive cough, dyspnea, fever, weight loss, and fatigue for months to years as in our case. However, because of lack of awareness among hospitalists and internists alike, most CEP patients receive multiple courses of antibiotics for presumed bacterial pneumonia. These antimicrobials are associated with several side effects, including dermatologic side effects. Our patient had a diffuse papular rash, likely secondary to levofloxacin, that was confirmed as spongiotic dermatitis on skin biopsy.

Conclusion: CEP must always be included in the differential diagnosis of recurrent pneumonia. Diagnosis requires a high index of clinical suspicion, as CEP is often mistaken as bacterial pneumonia both by internists and hospitalists. Early diagnosis of CEP is important to prevent undesired adverse effects of antimicrobial therapy.

Sumant Aroraa, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Rehan Sarmada, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Khalid Rasheeda, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 65-year-old male presented with diffuse abdominal pain, nausea, and vomiting. He had a known history of multiple malignancies (renal cell carcinoma, Hodgkin lymphoma, adenocarcinoma of the colon) and a recent repair for iatrogenic colonic perforation. His cancers were in remission as per annual PET scans. He had diffuse abdominal tenderness with hypoactive bowel sounds. Unenhanced CT of the abdomen revealed small bowel obstruction. Initial conservative management failed, and exploratory laparotomy was performed. On postoperative day 1, the patient developed abdominal distension with hypotension and tachycardia that persisted despite intravenous hydration. Repeat CT scan of the abdomen suggested ongoing intraabdominal bleed. At this time, his hematocrit was 22% (normal 40%-51%) with activated partial thromboplastin time (aPTT) of 43 seconds (normal 24-33 seconds) and a platelet count of 118,000/uL (normal 140,000-400,000). Prothrombin time, international normalized ratio, fibrinogen level, and liver function tests were normal. He received packed red blood cells followed by exploratory laparotomy for hematoma evacuation, but no actively bleeding site was identified. His abdominal symptoms and signs resolved; however, he started oozing blood from the surgical laparotomy site that continued despite repeated hemostasis attempts. His hematocrit dropped to 18.7% with aPTT of 73 seconds that failed to correct on mixing study. Hematology was consulted, and further workup revealed factor VIII (FVIII) activity of 6% (normal 50%-150%), FVIII inhibitor titer of 5.5 Bethesda units (BU) (reference range <0.8 BU), normal platelet function and von Willebrand factor levels, and a Russell viper venom test of 50 seconds (normal <44 seconds). These findings suggested a diagnosis of acquired hemophilia A (AHA). We started treatment with FEIBA (factor eight inhibitor bypassing activity) and high-dose corticosteroids. Bleeding from the surgical site resolved, the FVIII inhibitor disappeared, and aPTT (38 seconds) returned to the normal level.

Discussion: AHA is an underrecognized (1 to 4 cases per million) but potentially life-threatening (mortality 8%-22%) hemorrhagic disorder. Affected patients usually have no previous or family history of spontaneous bleeding. Etiologies include chronic inflammatory disorders, autoimmune diseases, malignancy, pregnancy, medications, or surgery. In our patient, his history of multiple malignancies and abdominal surgery likely predisposed him to AHA. Diagnosis of AHA is challenging for internists and hospitalists alike without expert input from a hematologist, especially in postoperative conditions because of the overlap with other coagulopathies such as disseminated intravenous coagulation and thrombocytopenia. The diagnosis is suggested by isolated prolongation of aPTT that fails to correct on mixing study and detection of the FVIII inhibitor. Treatment goals include immediate hemostasis followed by inhibitor eradication. Low inhibitor titers (<5 BU/mL) respond to recombinant FVIII replacement, while higher titers (>5 BU/mL) require activated prothrombin complex concentrate as a bypassing agent. Corticosteroids and cyclophosphamide have been used with remission rates of 60%-80%, while rituximab is reserved for resistant cases.

Conclusion: Hospitalists commonly encounter patients with unexplained bleeding. In such cases, AHA must be included in the differential. This consideration is especially important in unexplained postoperative bleeding with a prolonged aPTT, as reoperation is dangerous.

Ozdemir Kanar, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Ciel Harris, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Jeffrey Winder, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Rahman Nakshabendi, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Win Aung, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 28-year-old African American male with a medical history of recently diagnosed human immunodeficiency virus (HIV) but who was not on highly active antiretroviral therapy (HAART) presented following a seizure at home. He stated the seizure began as a jerky movement on the left side of his body, and then he had a witnessed loss of consciousness with a tonic-clonic seizure. He denied any incontinence or tongue biting and said the seizure was his first episode. Another witnessed grand mal seizure was observed in the ED. Review of systems included a 10 lb weight loss in the past month and total body myalgia. The patient reported taking no medications at home except for street estrogen to try and make himself more feminine. He admitted to smoking 1 pack per day and drinking socially but denied any illicit drug use. CT of the head showed symmetric hypodensities within the bilateral basal ganglia. T2-weighted/FLAIR imaging showed hyperintense signal in the right postcentral gyri. Prothrombin time, partial thromboplastin time, and international normalized ratio were within normal limits. Toxicology, cryptosporidium, rapid plasma reagin, parvovirus, and cytomegalovirus tests were negative. Lumbar puncture showed no abnormalities. CD4 count was 3, and viral load was 174,000. ADAMTS13, anticardiolipin, factor V, and protein C were within normal limits. D-dimer was 1.26, and protein S was low at 42. In consultation with nephrology and infectious disease, it was determined the patient had had a stroke from HIV-induced protein S deficiency along with estrogen and tobacco. The patient was started on HAART and given anticoagulation until his CD4 count was >200. He will be followed up in an outpatient HIV clinic.

Discussion: HIV infection is a well-known risk factor for thromboembolic phenomena; this connection has been proven by a large number of studies, with a reported venous thromboembolism frequency of 0.19%-7.63% per year. HIV infection is associated with a 2- to 10-fold increased risk of venous thrombosis in comparison with a general population of the same age. In fact, protein S deficiency is the most regularly detected coagulation abnormality seen in HIV-infected patients, with a reported prevalence ranging from 27%-76%, with 12% of those patients having a venous thromboembolism. The cause of this deficiency is likely multifactorial, leading to the current pursuit of the underlying cause. Proposed causes include direct endothelial cell, hepatocyte, and megakaryocyte damage by the virus, while other authors suggest that tumor necrosis factor alpha can lower the levels of active protein S, downregulating protein S synthesis in the endothelial cells. It is also useful to note that these abnormalities correlate directly with the severity of the immunosuppression as measured by CD4 counts and importantly with the presence of malignancy, inflammatory/autoimmune responses, HAART, or infection.

Conclusion: The mechanisms involved in an HIV-infected patient's hypercoagulable state include abnormalities of blood flow, of blood composition, and of the blood vessel wall as defined by Virchow. However, patients with HIV are at higher risk for developing thromboembolic phenomena because they are predisposed to malignancy and infection and also because of the presence of antiphospholipid antibodies, lupus anticoagulant, and deficiencies of protein C and S.

Krishna Venkata, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Hardik Satashia, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Kannan Thanikachalam, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Talha Nawaz, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Ashish Manne, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: An 87-year-old Caucasian female with a history of hypertension, coronary artery disease, and bradycardia with an automatic implantable cardioverter defibrillator presented to the hospital with altered mental status after ingesting more than 100 carvedilol (3.125 mg) and amlodipine (5 mg) tablets each. Her initial vitals were temperature 98.3°F, heart rate (HR) 62 bpm, respiratory rate 16 breaths per minute, blood oxygen saturation 99%, and blood pressure (BP) 82/50 mmHg. She received normal saline (bolus), glucagon, and high-dose insulin with dextrose. Later, norepinephrine, epinephrine, insulin (with dextrose), and calcium gluconate drips were started, after which her HR and BP dropped to 48 bpm and 62/39 mmHg, respectively. Phenylephrine and lipid emulsion therapy were added, and her pacemaker was interrogated to reset the pacing rate at 80. The next day, her mental status continued to worsen, and she developed acute kidney injury, hypoxemic respiratory failure, and metabolic acidosis with a pH of 7.25, partial pressure of carbon dioxide of 27, partial pressure of oxygen (PO₂) of 68, and bicarbonate of 12. The patient was eventually intubated. Her chest x-ray showed bilateral pulmonary infiltrates suggestive of acute respiratory distress syndrome (ARDS), and echocardiogram showed ejection fraction of 55%-60%. No significant improvement on chest x-ray was noted even while the patient was on intravenous furosemide for the next 3 days. By day 6, although the patient was hypotensive, her renal function started to improve, but her ARDS continued to worsen with PO₂ of 65 on fraction of inspired oxygen 100% and positive end-expiratory pressure of 8. The family decided to withdraw care per the patient's living will, and the legal department was consulted. Care was withdrawn on day 8, and the patient passed away.

Discussion: Amlodipine, a dihydropyridine calcium channel blocker (L-type) with a long half-life of 30-50 hours and a large volume of distribution (21 L/kg), has a predominant effect on vascular smooth muscles compared to cardiac cells, but this selectivity is lost in overdose, creating a negative dromotropic and inotropic effect on cardiac cells. Carvedilol produces peripheral vasodilation because of its alpha 1 blocking property and bradycardia from beta 1 blockade. Together they can produce severe hypotension and bradycardia as observed in our patient. Severe amlodipine overdose can be complicated by refractory hypotension, acute kidney injury, metabolic acidosis, and ARDS with difficulty to wean ventilator dependence that leads to a prolonged ICU stay and increased overall mortality. Our patient showed worsening respiratory failure despite improvement in hemodynamics after 7 days of aggressive medical management with vasopressors, cardiac pacing, ventilator support, calcium gluconate, insulin, glucagon, and lipid emulsion therapy. One case report of combined amlodipine and carvedilol poisoning has been published to date, with the patient surviving after extracorporeal membrane oxygenation and temporary pacemaker placement.

Conclusion: Combined amlodipine and carvedilol overdose can produce severe life-threatening toxicity complicated by circulatory failure, ARDS, and acute kidney injury. ARDS should be suspected early with respiratory distress, and timely ventilator support should be considered.

Krishna Venkata, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Kannan Thanikachalam, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Talha Nawaz, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Ashish Manne, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Jewell Halanych, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 40-year-old Caucasian male with a history of cervical bulging disc presented with the complaint of right-sided extremity numbness and weakness following a coughing spell. Other associated symptoms included transient blurriness of the vision in his right eye, shaking movements in his right arm, and headache. His symptoms resolved within 1 hour, even prior to arrival at the hospital. The patient denied any loss of consciousness, head injuries, facial drooping, chest pain, palpitations, or lower extremity swelling. On examination, the patient was alert and oriented with regular heart rate and rhythm, normal motor and sensory examination, and intact cranial nerves. Pertinent laboratory findings included low-density lipoprotein of 151 mg/dL, but his complete blood count and electrolytes were normal. CT scan of the brain and carotid Doppler ultrasound were normal. MRI of the brain without contrast showed low-lying cerebellar tonsils (7 mm inferior to the foramen magnum) consistent with Chiari type I malformation. Although transthoracic echocardiogram was normal, transesophageal echocardiogram (TEE) showed patent foramen ovale (PFO). No arrhythmias were noted on telemetry during his entire hospitalization. Considering the risks and benefits of surgical closure of the PFO, the cardiologist advised antiplatelet therapy. Neurology recommended conservative management of his symptoms with clinical and MRI surveillance of the Chiari malformation rather than surgical decompression of the foramen magnum. The patient was started on aspirin and a statin and was discharged on the same medications.

Discussion: PFO, a congenital cardiac lesion, is found in at least 1 of 4 people, with high prevalence in people <55 years who present with cryptogenic stroke. Stroke symptoms are attributed to the paradoxical embolism that can happen during Valsalva maneuvers such as coughing and sneezing. Identification of PFO does not prove a causal relationship for the stroke. TEE or agitated saline contrast echocardiogram can be used for the diagnosis of PFO. Incidentally detected PFO does not require follow-up or treatment unless it is considered to be causally related to the embolic events. In that case, antiplatelet therapy is advised compared to percutaneous PFO closure or anticoagulation therapy unless the patient has deep vein thrombosis or recurrent strokes. Chiari malformations are classified into 4 types. Chiari type I malformation has low-lying cerebellar tonsils >5 mm below the level of the foramen magnum. Clinical manifestations are mainly due to the elevated intracranial pressure, cranial neuropathies, brainstem compression, cerebellar atrophy, and myelopathy. Symptoms are exacerbated by physical activity or Valsalva maneuvers. Chiari malformations are best evaluated by MRI brain. Conservative management with clinical and MRI surveillance is recommended for asymptomatic patients with an incidental diagnosis of Chiari type I malformation without syringomyelia. For symptomatic patients with lower cranial nerve palsies, severe neck pain, cerebellar symptoms, syringomyelia, or occipital headache, surgical decompression of the foramen magnum is recommended.

Conclusion: Both PFO and Chiari malformation can manifest as transient weakness or numbness following a coughing spell. Taking a careful history and physical examination is necessary, and the risks and benefits of treatment options should be considered before starting the patient on treatment for PFO or Chiari type I malformation.

Talha Nawaz, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Kannan Thanikachalam, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Krishna Venkata, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 27-year-old male presented with productive cough, dyspnea, and subjective fever for 1 week. He reported having chronic bronchitis since childhood and having multiple episodes of acute bronchitis and pneumonia for approximately 7 years. Physical examination was significant for a temperature of 100.4°F, room air oxygen saturation of 93%, clubbing in fingers, diffuse wheezing, and crackles and bilateral rhonchi on chest auscultation. Chest x-ray showed multiple bilateral cystic opacities in the lungs. CT of the chest confirmed extensive cystic bronchiectasis with mid and basilar predominance and air levels compatible with active pneumonia. Sputum culture grew Pseudomonas aeruginosa that was successfully treated with intravenous piperacillin/tazobactam. Because the acute infectious process did not explain the CT findings, further workup was pursued that revealed normal sweat chloride test; immunoglobulin IgA, IgG, and IgM levels; antinuclear antibody; rheumatoid factor; anti-cyclic citrullinated peptide antibody; anti-SSA/SSB; Scl 70 (anti-topoisomerase I); and alpha-1 antitrypsin levels. Fungal and acid-fast bacilli smears/cultures were negative. At that point, the diagnosis of Williams-Campbell syndrome (WCS) was made.

Discussion: WCS is a rare congenital syndrome characterized by the absence of cartilage in the subsegmental bronchi (most commonly between the 4th to 6th order bronchial divisions) leading to formation of bronchiectasis distal to the affected bronchi. It usually manifests in childhood, but diagnosis can be challenging and may take several years, as in this patient. Patients are commonly labeled with asthma because bronchiectasis occurs after multiple airway infections. Multislice spiral CT and CT bronchoscopy are the tests of choice to study cystic lung diseases. Cystic fibrosis can often be confused in patients with multiple cysts and recurrent childhood airway infections. However, this patient had multiple cystic bronchiectasis in the central and lower areas of the lung, and cystic fibrosis usually has upper lobe predominance. The diagnosis was made based on history, physical examination, and multislice spiral CT and by ruling out all other causes. Inspiratory/expiratory CT bronchoscopy to show the airway collapse typically seen around the areas with missing cartilage has been recommended by some experts but is not a definitive test. Histopathology can be helpful when done in the right location but is invasive and often misses the areas of missing cartilage. Differential diagnosis of cystic bronchiectasis is broad and includes cystic fibrosis, allergic bronchopulmonary aspergillosis, alpha-1 antitrypsin deficiency, immunoglobulin deficiency, mycobacterial infections, immotile cilia syndrome, Mounier-Kuhn syndrome, and WCS. Treatment is similar to that for cystic fibrosis, including pulmonary hygiene and breathing treatments, but disease-specific treatments such as inhaled DNase I or ivacaftor are not effective.

Conclusion: It is important to have a high index of suspicion for WCS in patients who present with recurrent respiratory infections, bronchiectasis, productive cough, and dyspnea.

Aartee Deshpande, MD, MPH; Department of Internal Medicine, University of Alabama-Huntsville, Huntsville, AL
Parekha Yedla, MD; Department of Internal Medicine, University of Alabama-Huntsville, Huntsville, AL

Case Presentation: A 54-year-old African American female presented to the ED for progressive lethargy and generalized weakness for 5 months. In the ED, initial blood tests showed severe anemia and elevated troponins. The patient was treated for non-ST-elevation myocardial infarction with aspirin, metoprolol, and low molecular weight heparin (LMWH). Upon further evaluation by the primary team, the patient reported weakness in her arm and legs and low back pain that occasionally radiated to her legs that started after a fall 5 months prior. She was unable to get up from a chair without assistance and was also unable to comb her hair. Review of symptoms was positive for significant weight loss, night sweats, and leg swelling. She denied chest pain, fever, chills, bleeding, rashes, nausea, vomiting, or dyspnea. On examination, she appeared cachectic and pale. Bilateral lower extremities showed severe pitting edema. Cardiopulmonary examination was otherwise normal. On musculoskeletal examination, marked proximal muscle weakness in shoulder and hip was noted bilaterally. Abdomen-pelvic examination showed a small palpable suprapubic mass and vaginal bleeding. When asked again, the patient reluctantly mentioned that she had had intermittent vaginal bleeding for 1 year. LMWH was discontinued, and further investigations were obtained. She had severe iron deficiency anemia; elevated creatine kinase (CK) (5,548 U/L), CK-MB (236.9 ng/mL), and troponin T (1.11 ng/mL); and mild transaminitis with normal pro b-type natriuretic peptide and basic metabolic panel. CT of the abdomen and pelvis showed a 10 cm heterogeneous uterine mass with pleural effusion, pericardial effusion, several liver lesions, and abdominal and pelvic lymphadenopathy. Pathology of uterine curetting showed papillary serous-type high-grade endometrial carcinoma. Meanwhile, CPK levels and troponin levels were trended and were unchanged on the second day (CPK 3,839 U/L and troponin 1.0 ng/mL) and on the seventh day (CPK 3,205 U/L and troponin 1.08 ng/mL) even after intravenous fluids, without any symptoms of chest pain or ST changes on ECG. Electromyography confirmed inflammatory myopathy. Aldolase and lactate dehydrogenase (LDH) were elevated, and antinuclear antibody and myositis antibodies were negative. The patient was diagnosed with polymyositis (PM) along with primary endometrial malignancy. She was started on oral prednisone, and she felt symptomatically better.

Discussion: The patient had highly characteristic proximal muscle weakness and pain with elevated CK, LDH, troponin T, aldolase and transaminases, prompting the diagnosis of PM. In her previous medical encounters before the index hospitalization, these symptoms were attributed to her fall and back injury. Elevated troponin T, CK, and CK-MB are common entities in hospital medicine. When evaluating acute coronary syndromes, uncommon causes should also be considered such as inflammatory myositis. Although the incidence of PM is low, association with malignancy is present in a significant number of cases. Prompt diagnosis will assist with early detection and treatment of associated malignancy.

Conclusion: Complete history and examination are crucial. A high index of suspicion is required to diagnose PM. When elevated CK, CK-MB, and troponin T are not associated with chest pain or dyspnea, other causes should be evaluated.

Zohra S. Chaudhry, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta, GA
Miriam Parker, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta GA
Samuel Payne; Medical College of Georgia, Augusta, GA

Case Presentation: A 53-year-old homeless African American male presented with a 2-week history of progressively worsening generalized pruritus associated with a painful vesiculobullous rash involving >30% of his body surface area. His medical history included type 2 diabetes mellitus with peripheral neuropathy, hypertension, syphilis, and cocaine-induced myocardial infarction. His current medications included metformin, insulin, lisinopril, and clonidine. He had no known allergies. Physical examination revealed a well-nourished male with numerous flaccid and tense bullae of different sizes and stages of maturation on his hands, interdigital web spaces, forearms, axilla, genitals, groin, and feet. The bullae were fluid filled, with some draining clear, nonpurulent fluid. Nikolsky sign and skin scraping tests were negative. No mucosal lesions were present. The physical examination was otherwise was unremarkable. The patient was started on intravenous fluids, antipruritics, and analgesics along with 5% permethrin cream for presumed scabies. Given the extensive nature of disease, oral ivermectin was initiated at 200 mcg/kg on days 1, 5, 8, 9, and 15. Human immunodeficiency virus and rapid plasma regain tests were negative. Immunoglobulin studies were all within normal limits. A skin punch biopsy revealed Sarcoptes scabiei mites, confirming our diagnosis. Immunofluorescence studies were not done as our index of suspicion for scabies was high. The bullae gradually resolved with reepithelialization of the skin.

Discussion: Caused by the human mite Sarcoptes scabiei, scabies is a common infection with more than 300 million cases reported annually. Subcutaneous burrows are pathognomonic and typically present as a pruritic papulovesicular rash involving the flexor surfaces of the wrists, interdigital web spaces, axillary folds, belt line, scrotum in males, and areolar area of the breasts in females. Bullous scabies is a rare presentation that mimics bullous pemphigoid and can even induce the formation of true bullous pemphigoid lesions. Only 33 cases of bullous scabies have been reported in the literature to date. Bullous scabies is a rare presentation of a common disease. The pathogenesis of bullae formation is unknown, although several theories have been proposed. Because this condition can mimic bullous pemphigoid quite closely, a high index of suspicion is needed to diagnose the disease. Bullous scabies should always be considered in a patient with suspected bullous pemphigoid that is not responding to immunosuppressive therapy. Various treatments of bullous scabies have been used. For localized disease, treatment is identical to that of classical scabies, including 5% permethrin cream, 10% crotamiton lotion, or lindane lotion. For more extensive involvement, oral ivermectin may be added. Oral steroids along with immunosuppressive agents have also been used in select cases with varying success.

Conclusion: Timely diagnosis of bullous scabies is important not only for the patient but also to ensure that an outbreak of scabies does not occur among healthcare workers. Physicians must be aware of the varying presentations of scabies infection, including the bullous type, so appropriate isolation and treatment measures are taken.

Ryan Kunjal, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Ria Ramadoo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Shahid Mohammed, MD; Department of Pathology and Laboratory Medicine, University of Florida-Jacksonville, Jacksonville, FL
Rafaat Makary, PhD; Department of Pathology and Laboratory Medicine, University of Florida-Jacksonville, Jacksonville, FL
Leighton R. James, MD; Department of Medicine, Division of Nephrology and Hypertension, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 25-year-old female was admitted for an elective renal biopsy to investigate persistent postpartum proteinuria. Her medical history was significant for type 1 diabetes mellitus (diagnosed at age 13) and hypothyroidism. During her recent first pregnancy, she developed preeclampsia with significant proteinuria (3.15 g/24 h) and required emergent cesarean section at 31 weeks for impending eclampsia. Renal ultrasound at the time was unremarkable. However, at a 4-month follow-up visit, she still had features of nephrotic syndrome. Elective renal biopsy was consistent with diabetic nephropathy but was also noted to have a subcapsular micro focus (0.1 cm) of tumor with histologic and immunohistochemical features favoring a microscopic perivascular epithelioid cell tumor (PEComa) positive for HMB-45. She was scheduled to have further radiologic investigation and close follow-up, but she defaulted.

Discussion: PEComas are rare, potentially malignant mesenchymal neoplasms composed of histologically and immunohistochemically distinctive perivascular epithelioid cells (PEC). These cells that stained the melanosome marker HMB-45 were first identified in 1992 and were then further described as a group of mesenchymal tumors in 1996. Since then, approximately 250 cases have been reported and include angiomyolipoma, pulmonary clear cell “sugar” tumor, and others. They are usually asymptomatic, causing vague abdominal pain if they are large enough. Diagnosing them radiologically is challenging because of the high variability of their components. PEComas have significant overlap in morphology with other more common neoplasms of the kidney, such as clear cell renal cell carcinoma. Once the appropriate diagnosis is made, they are stratified by risk of progression. It has been proposed that those displaying 2 or more of a group of features—large size (>5 cm), infiltrative growth, high nuclear grade and hypercellularity, mitoses ≥1 per 50 hpf, necrosis, or vascular invasion—should be regarded as potentially malignant. There is no standard recommended treatment as the natural history is unpredictable. Most tumors described in the literature were treated by either excisional biopsy or surgical resection of the primary tumor. Metastatic tumors tend to be highly aggressive with little efficacy of chemotherapy.

Conclusion: As physicians, we must be aware of this rare family of tumors because of their unpredictability and aggressive potential. Our patient defaulted from follow-up in spite of best efforts. Her management plan would have included further radiologic and pathologic definition of the tumor to guide treatment and prognostication.

Maruf Ali, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta, GA
Forrest M. Toca, MD, FACP; Department of Internal Medicine, Atlanta Medical Center, Atlanta, GA

Case Presentation: A 59-year-old male with a history of ischemic heart disease on medical therapy presented with progressive dyspnea, intermittent dizziness, and near-syncopal episodes. On examination, the patient was alert and fully oriented. His pulse rate was 58 bpm, blood pressure was 125/70 mmHg, respiratory rate was 16 breaths per minute, and oxygen saturation was 98% while breathing ambient air. The patient's breath sounds were normal. Heart sounds were heard with soft systolic murmur at the left sternal border. The remainder of the examination was unremarkable. On the day of admission, he developed cardiac arrest with documented ventricular fibrillation and was successfully resuscitated. Transthoracic echocardiogram revealed a moderately enlarged left ventricle with severely depressed systolic function (left ventricular ejection fraction of 15%). A large protruding fixed thrombus was attached to the left ventricular apex. Thrombus was also seen in the right ventricle apex. Optimal medical therapy was continued for heart failure. Because of the clinical findings, an implantable cardioverter defibrillator (ICD) was indicated. He received a subcutaneous ICD because of the presence of thrombus in the right ventricle. The patient was discharged without any further event.

Discussion: An entirely subcutaneous ICD has been demonstrated to be a reliable and effective system for detecting and terminating ventricular arrhythmias and for potentially avoiding many of the complications associated with transvenous ICDs. This case illustrates one of the several advantages of the subcutaneous ICD that may make it a preferred treatment rather than simply an alternative to the transvenous route. In our literature search, we found no report of the use of subcutaneous ICD for right ventricle thrombus. It is well documented that transvenous device leads may result in thromboembolic complications. Placement of a transvenous defibrillator lead in the presence of a right ventricle thrombus would potentially have deleterious consequences. The subcutaneous ICD has several limitations, principally because of the absence of pacing ability. It cannot be used in patients requiring pacing for bradyarrhythmias, resynchronization therapy for heart failure, and antitachycardia pacing. However, these conditions were not present in this case. Future studies and observations will better define patient target groups and establish the therapeutic potential of the subcutaneous device technology.

Conclusion: This case illustrates the preferable use of a subcutaneous ICD in select clinical presentations, one of which is the presence of right ventricle thrombus.

Joanne Wyrembak, MD; Department of Internal Medicine, Duke University Medical Center, Durham, NC

Case Presentation: An 82-year-old female with diet-controlled type 2 diabetes and dementia presented to the ED with altered mental status. She was brought in by her son who noted that her mental status had become progressively worse during the past 2 days, but on the day of presentation, she developed odd, uncontrolled movements. She was found to have hyperosmolar hyperglycemic state (HHS) with a blood glucose of 653. She was started on an insulin infusion with resolution of her HHS and improvement in her mental status. Her hemoglobin A1c was notably 13.4%, up from 7.2% just 6 months prior. She was transitioned to a subcutaneous insulin regimen with good glucose control. However, despite the improvement in her mental status and blood sugars, her uncontrolled movements persisted. They were predominantly left sided, involving both her arm and leg. She was able to temporarily suppress the movements on command, and they ceased during sleep but were exacerbated by activity. The movements were choreiform in nature and were violent enough that the patient sustained several abrasions from repeated trauma against bedrails. Her creatine kinase also notably increased to a peak of 883, thought to be related to her continuous movements. She was diagnosed with chorea-hemiballism secondary to decompensated type 2 diabetes. MRI of the brain did not demonstrate evidence of an acute stroke, but the study was limited by movement despite attempts to sedate the patient. Neurology was consulted, agreed with the diagnosis, and recommended starting risperidone and clonazepam to help suppress the movement. Her movements improved on the medication regimen, and she was ultimately discharged to a skilled nursing facility.

Discussion: Review of the literature demonstrates that HHS is the one of the most common acquired causes of hemiballism. It predominantly affects older women, with the hypothesis that the postmenopausal state leads to increased dopamine sensitivity and predisposes patients to developing hemiballism. Imaging with MRI typically reveals lesions in the contralateral striatum. The mechanism remains unclear, although it is hypothesized that the hyperosmolar state leads to hyperviscosity and the resulting acute infarct. Symptoms generally resolve with treatment of hyperglycemia, although some studies report symptoms that last weeks to months. In situations with persistent symptoms, antipsychotics such as haloperidol or risperidone can be used, sometimes in conjunction with benzodiazepines, to manage movements until their resolution.

Conclusion: Our patient fit the classic presentation of an older female presenting with HHS and unilateral choreiform movements. Her MRI did not demonstrate a lesion, although the poor quality of the study may be the reason. Her symptoms persisted despite resolution of her hyperglycemia, but they were well managed with the addition of risperidone and clonazepam. Given that HHS is a common entity in hospital medicine, it is prudent to recognize this rare but important sequela of the condition, as well as the appropriate treatment strategies for the residual movement disorder that can persist following the resolution of HHS.

Bhagyashree Shastri, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta, GA
Maruf Ali, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta, GA
Riyadh Al Rubaye, MD; Department of Internal Medicine, Atlanta Medical Center, Atlanta, GA

Case Presentation: A 17-year-old African American female presented to our hospital after she woke up with a headache that morning followed by multiple grand mal seizures. One week prior, she had had an emergent cesarean section for pregnancy-induced hypertension. On arrival to the ED, she was confused and had visual disturbances. Physical examination showed a heart rate of 110 bpm, blood pressure of 180/100 mmHg, respiratory rate of 30 breaths per minute, and temperature of 37.1°C. On neurologic examination, she moved all extremities spontaneously and withdrew to painful stimuli. The fundoscopic examination was normal, and bilateral pitting pedal edema was present. White blood cell count was 18,800/mcl. Based on the clinical picture, her differential diagnosis included postpartum eclampsia, meningoencephalitis, seizure disorder, intracranial hemorrhage, and metabolic encephalopathy. She was started on magnesium sulfate, empiric antibiotics, and antiepilepsy and antihypertensive medications. Lumbar puncture and cerebrospinal fluid analysis were unrevealing. CT scan of the brain was consistent with hypertensive encephalopathy with minimal hemorrhage in the left posterior occipital lobe. MRI of the brain with contrast showed areas of signal void in the parieto-occipital and fronto-parietal regions bilaterally with abnormal edema involving both the gray and white matter. The diagnosis of posterior reversible encephalopathy syndrome (PRES) was established with these radiologic findings. Her blood pressure was optimally controlled, and antibiotics were discontinued. She recovered with no residual deficits and was discharged on antiepilepsy medications after 1 week of hospitalization. MRI of the brain repeated 1 month later showed near resolution of the parieto-occipital and frontal signal alterations.

Discussion: PRES is a clinical and radiographic syndrome with insidious onset of encephalopathy, seizures, and characteristic radiologic findings. This case illustrates the importance of keeping a high index of suspicion based on these radiologic findings to prevent unwarranted evaluation. Early recognition of PRES in eclampsia is critical because prompt control of blood pressure will cause reversal of the syndrome. The MRI findings of white matter vasogenic edema predominantly affecting the posterior occipital and parietal lobes of the brain will confirm the diagnosis. In most cases, PRES is reversible in days to weeks, and radiologic recovery lags behind clinical recovery.

Conclusion: PRES continues to be discussed widely since it was first recognized in 1996. Its clinical picture can mimic numerous entities, in this case, eclampsia. Delay in diagnosis and initiating appropriate treatment may result in permanent damage to the brain.

Chioma Nwagbara, MD MPH; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL
Kannan Thanikachalam, MD; Department of Internal Medicine, University of Alabama at Birmingham Montgomery Health Center, Montgomery, AL

Case Presentation: A 27-year-old female with no known medical history presented to the ED complaining of back pain and productive cough with coffee-colored sputum associated with dyspnea. She described a severe, intermittent, sharp pain radiating around the chest wall that was worse with coughing and taking a deep breath, was relieved by narcotics, and had been ongoing for 2 weeks. She denied prior contact with persons with similar illness, history of deep vein thrombosis, recent long-distance travel, night sweats, or weight loss. On physical examination, she was tachycardic and hypertensive. The rest of the physical examination was unremarkable except for diffuse wheezes on chest examination and tenderness in the upper thoracic spine. She had leukocytosis with neutrophil predominance. Chest x-ray showed a right perihilar pneumonia and possible underlying mass. CT angiography of the chest showed an 8.7 × 3.3 cm mass in the posterior mediastinum. The biopsy pathology report suggested a pulmonary sequestration cyst with organizing pneumonia. Antibiotics treatment was instituted with resolution of her cough, dyspnea, and hemoptysis. The pain was controlled with narcotics. She was referred to cardiothoracic surgery.

Discussion: Bronchopulmonary sequestration (BPS) is a rare congenital malformation of the lower respiratory tract that consists of a nonfunctioning mass of lung tissue that lacks normal communication with the tracheobronchial tree and that receives its arterial blood supply from the lower thoracic or abdominal aorta. It comprises 0.15%-6.4% of all congenital pulmonary malformations. BPS is often associated with other congenital anomalies including congenital diaphragmatic hernia, congenital heart disease, vertebral anomalies, pulmonary hypoplasia, colonic duplication, and congenital pulmonary airway malformation. The 3 groups, based on location, are intralobar, extralobar, and bronchopulmonary foregut malformation. The intralobar variant is the most common form and accounts for 75%-90% of cases. It is often asymptomatic and an incidental finding prenatally or in the immediate postnatal period. However, respiratory distress is commonly present in symptomatic children. In adolescents and adults, it presents with recurrent pneumonia, hemoptysis, chest pain, and rarely heart failure. Treatment is surgical resection that is often reserved for patients with symptoms. Surgical intervention has good outcomes in these patients and often leads to resolution of most symptoms. Serial monitoring is recommended for asymptomatic patients.

Conclusion: BPS, although common in children, can present with complications in adults.

Farah Al-Saffar, MD, MPH; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Saif Ibrahim, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Jeff Winder, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Julio Perez-Downes, DO; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Case Presentation: A 49-year-old male with a medical history of diabetes, hypertension, metastatic melanoma (status resection of brain metastasis 2 months prior to admission), and recent admission for shingles presented to the ED for right thoracic rash and skin lesions. Physical examination revealed a middle-aged gentleman who was not in apparent distress; staples marks were seen on right side of his scalp. Skin examination was significant for dark red papular skin rash in the right thoracic area roughly at the 4th and 5th intercostal areas extending to the posterior axilla where multiple hard lumps were seen in groups. Lesions were weeping with pus. Given the patient's recent history of possible herpes zoster and his immunocompromised status, he was started empirically on acyclovir. The same history of malignancy prompted our team to proceed with skin biopsy. All the patient's previous admissions had been at an outside facility, so further information was obtained from the patient's family as well as medical records that were faxed later. The patient had had the initial lesion (melanoma) 2 years ago in the right scapular area, it was resected, and he had one cycle of chemotherapy, but he was not willing to continue treatment. He had a recent admission for another skin lesion in the same area that was also resected. Skin biopsy of the lesions demonstrated that the lesional cells were strongly positive for S-100 and Melan-A immunostains, while negative for CK AE1/AE3 immunostain. These findings supported the diagnosis of metastatic amelanotic melanoma. CT of the chest showed evidence of subcutaneous invasion, lung metastasis, and metastatic bony lesions. Given the patient's poor functional status and the minimal benefit of pursuing further treatment, palliative care was consulted and the patient elected hospice care without further interventions.

Discussion: Skin rash is a common entity encountered by internists in clinics and in inpatient practice as well. The physician's clinical experience and familiarity with different skin lesions are important factors in the production of the diagnostic label. In this case, the patient's skin lesions were highly suggestive of herpes zoster, yet the true diagnosis was metastatic amelanotic skin melanoma. Few cases document the recurrence of melanoma in zosteriform transformation, and our case is one of them. It delineates the importance of routinely carrying out skin biopsy—an underperformed, yet easy-to-do and highly diagnostic bedside tool.

Conclusion: Skin rashes are frequently encountered in general medicine practice. Even in the face of typical zoster lesions, physicians should take into account the whole clinical picture. Skin biopsy is an important diagnostic tool that can be performed at bedside with an excellent diagnostic yield.

Asad ur Rahman, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Aamer Abbass, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Umair Majeed, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Udayakumar Navaneethan, MD; Center for Interventional Endoscopy, Florida Hospital Orlando, Orlando, FL

Case Presentation: A 69-year-old male with a history of Clark III malignant melanoma that was completely excised from the right flank 3 years ago presented with a 3-week history of worsening headache and dizziness. MRI of the brain revealed a right-sided cerebellar bleed adjacent to a 1 cm nodule. A suboccipital craniectomy with resection was done, with biopsy showing malignant melanoma. A staging PET scan revealed areas of increased uptake in the left lower lung and left upper quadrant of the abdomen abutting the small bowel. Enteroscopy revealed a 40 mm cratered jejunal ulcer with heaped edges, and biopsy revealed malignant melanoma. Because the patient had widespread disease, abdominal surgery was deferred. Treatment with ipilimumab and radiotherapy to the brain was initiated, but he presented 3 months later with acute abdominal pain and diarrhea. He had completed 3 cycles of ipilimumab and prednisone. CT of the abdomen revealed peritoneal free air, and an exploratory laparotomy revealed a mass at the antimesenteric border of the duodenum. Biopsy was consistent with melanoma. The perforated area was resected, and an end-to-end anastomosis was performed. However, the patient had a postoperative intracranial bleed and was referred to hospice care.

Discussion: Gastrointestinal (GI) involvement of melanoma is rare in symptomatic patients (1%-4%); however, it is a frequent autopsy finding (60%) in patients with primary cutaneous melanoma. Our case portrays how malignant melanoma may insidiously metastasize widely but ultimately may present with a catastrophe. In this case, metastatic cutaneous melanoma with initial asymptomatic jejunal involvement was found on a PET scan, with subsequent secondary duodenal perforation. The small bowel is the most common location for GI metastasis (35%-97%), followed by the stomach/duodenum (5%-50%).Vague chronic abdominal pain is the most common presentation, followed by GI bleed and weight loss. Acute abdomen as a result of perforation is a rare presentation, and only 8 cases have been reported in the literature thus far. Metastases on endoscopy may take the form of ulcers, nodules, or polyps, while serosal or mesenteric involvement is less common. Unfortunately, our patient had evidence of disease in the brain, lung, bowel, and liver, making him a poor candidate for resection on initial presentation. GI involvement of melanoma is a marker of poor prognosis, with a 5-year survival rate of 14% and a median survival of 12.5 months.

Conclusion: Malignant melanoma has been termed the “syphilis of modern oncology” and can have myriad presentations. It underscores the importance of clinical suspicion in patients with a history of melanoma who present with any GI symptom.

Aadil Maqsood, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Asad ur Rahman, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Jonhong Gui, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
George Everett, MD;Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL

Case Presentation: A 41-year-old African American male with a history of human immunodeficiency virus (HIV), a CD4 count of 126, and cocaine abuse presented to the ED with complaints of acute left leg pain and swelling for 1 week. Venous Doppler showed no deep vein thrombosis but revealed a collapsed popliteal vein. No evidence suggested infection. Peripheral pulses were very weak but palpable. He was discharged on oral analgesics for nonspecific muscular pain. Two weeks later, an obvious discrepancy of 10 cm was noticed in the diameter of both legs, and peripheral pulses were no longer palpable. Venous Doppler was again unrevealing. Noncontrast CT of the leg showed hemorrhagic bursitis vs hematoma, with compression of popliteal vessels. CT angiography (CTA) of the aorta and lower extremities showed left popliteal fossa hematoma with associated mass effect upon the popliteal vessels and occlusion of the popliteal artery suspicious for popliteal artery rupture. CTA of other arteries distal from abdominal aorta was normal. The patient was taken to surgery and was found to have a popliteal artery rupture with a missing 1 cm piece of popliteal artery. There was no evidence of aneurysm, inflammation, or atherosclerosis, although the proximal and distal ends were thrombosed. Five hundred milliliters of blood was evacuated, and the artery was repaired with Artegraft. Arterial biopsy showed benign vascular histology. The patient's blood culture was negative. He recovered uneventfully postoperatively and was discharged home after 5 days.

Discussion: While popliteal artery rupture is rare, it is the most common peripheral artery rupture. Most of the cases are preceded by an aneurysm or pseudoaneurysm due to atherosclerosis; however, other nonaneurysmal causes include mycotic embolism, sepsis, and being postsurgical. HIV and cocaine are associated with systemic arterial aneurysms and arteritis. Ours is the first reported case of spontaneous nonaneurysmal rupture of the popliteal artery without prior trauma or surgery in a patient with HIV and cocaine abuse. Popliteal artery rupture is a life- and limb-threatening condition because of the distal ischemia caused by bleeding and/or compartment syndrome. The popliteal artery can rupture with or without a preceding aneurysm and should always be considered as the underlying etiology of acute painful limb swelling, with or without compartment syndrome. Suspicion of popliteal artery rupture should be especially high when the patient does not have deep vein thrombosis or clinical signs to suggest cellulitis. The risk is further heightened in the presence of risk factors for HIV, cocaine abuse, and other vascular aneurysms.

Conclusion: HIV and cocaine are known risk factors for aneurysm formation and aneurysm rupture, but they may also lead to arterial rupture without preceding aneurysm. Possible explanations can be direct HIV infection or an autoimmune response due to molecular mimicry. Cocaine may also contribute to arterial deterioration. The definitive etiology of arterial rupture remained unclear in this case.

Aadil Maqsood, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Arooj Tabassum, MD
Khalid Abusaada, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL

Case Presentation: A 27-year-old previously healthy Asian female presented to the ED with the complaint of sudden-onset palpitations when she woke up in the morning. Her palpitations worsened with physical activity and were associated with mild lightheadedness when she walked. She reported never having had palpitations before. Extensive review of symptoms was negative. The patient denied the use of nicotine products or contraceptives. Her family history was positive for her father having had a myocardial infarction at age 58. Physical examination was unremarkable except for a heart rate of 118 bpm while supine, with orthostatic increase to 128 bpm on standing. ECG revealed sinus tachycardia (ST) but otherwise normal morphology. D-dimer was negative. The patient's ST continued despite receiving intravenous fluids, so she was admitted with telemetry monitoring. Extensive blood workup and chest x-ray were normal. Transthoracic echocardiogram revealed a structurally normal heart. Overnight telemetry revealed an average heart rate of 105 bpm in sinus rhythm. She continued to have palpitations and was discharged on propranolol with a diagnosis of inappropriate sinus tachycardia (IST). The patient continued to have palpitations with mild limitation of physical activity on treatment trials of verapamil and beta blockers. After 3 years, she visited a physician's office for right ear pain and was found to have a broken piece of earring in her ear with surrounding inflammation. She had lost the earring around the time of symptom onset. After removal of the earring, the patient's symptoms of palpitations completely resolved and her pulse returned to normal 80s without medications.

Discussion: ST is perhaps the most common dysrhythmia and can be caused by a wide spectrum of diseases, from physiologic response, dehydration, anxiety, and pain to myocardial infarction, myocarditis, sepsis, hyperthyroidism, and pulmonary embolism. IST is persistent ST without underlying etiology. IST has been linked to autonomic dysregulation due to unknown etiology in multiple studies. Studies have shown that external ear stimulation can lead to sinus bradycardia; however, ours is first reported case of ST due to ear irritation. Appropriate otoscopic examination is considered part of the workup for IST. A likely explanation may be inhibition of the auricular branch of the vagus nerve caused by a gold foreign body; however, further reports and studies are needed to establish this causality. Similarly, other branches of the vagus nerve may also play role, but data are lacking in the field.

Conclusion: The complete resolution of the patient's ST after removal of a foreign body from her ear suggests that the two were most likely related. In support of this hypothesis, she lost the earring piece around the same time of symptom onset.

L. Wesley Aldred, MD; Department of Medicine, University of Mississippi Medical Center, Jackson, MS
Seth Parham, MD; Department of Medicine, University of Mississippi Medical Center, Jackson, MS
Jeremy Taylor, MD; Department of Medicine, University of Mississippi Medical Center, Jackson, MS
Stephen Leblanc, MD; Department of Medicine, University of Mississippi Medical Center, Jackson, MS
Andy Wilhelm, DO; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Mississippi Medical Center, Jackson, MS

Background: Hospital policies are ever changing as hospital administration chooses new areas to focus on for improvement. Nationwide, there has been a continual focus placed on hospital-acquired infection. Recently, our institution implemented a policy that mandates better documentation of indwelling urinary catheters. Policy changes frequently have unintended consequences, and we sought to determine if the policy change requiring increased documentation of indwelling urinary catheters and tight monitoring of catheter-associated urinary tract infections (CAUTIs) served as a disincentive to order urine cultures.

Methods: We performed a quality improvement project at an academic medical center in Jackson, MS. We included all patients admitted to the medical intensive care unit (MICU) in July 2014 and January 2015. We compared the number of urine cultures ordered on those patients in July 2014, prior to the policy change, to the number of urine cultures ordered on patients in January 2015, after the policy change. A two-tailed t test was used for all continuous data and a P-value <0.05 was considered statistically significant.

Results: The prechange group included 144 patients, and the postchange group included 176 patients. Prior to the policy change, 29 of 144 patients (25.2%) had urine cultures ordered, whereas after the policy change, 29 of 176 patients (19.7%) had urine cultures ordered (P=0.4662).

Conclusion: This change in policy yielded a 5.5% reduction in the total number of urine cultures ordered, as postulated, although the difference was not statistically significant. However, we believe this trend is concerning and warrants further investigative studies. Our data included all MICU patients, not just the patients who had fever of unknown origin, met systemic inflammatory response syndrome criteria, or had signs and symptoms of urinary tract infection. We recommend that any further studies include more patients for greater power, as well as more specific data.

Jinendra Satiya, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Asad ur Rahman, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Umair Majeed, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Shengchuan Dai, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Vikram, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Debby Sentana, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Vladimir Pech, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL
Sally Litherland, PhD; Principal Research Scientist, Florida Hospital Cancer Institute, Orlando, FL
Xiang Zhu, PhD; Principal Research Scientist, Florida Hospital Cancer Institute, Orlando, FL
Khalid Abusaada, MD; Department of Internal Medicine, Florida Hospital Orlando, Orlando, FL

Background: In the geriatric population, outcomes of gastrointestinal (GI) bleed are affected by the nature of the underlying etiology of the bleed as well as the comorbidities that increase the risk of complications. The outcomes and the utility of endoscopic procedures in the very old patients who present with GI bleed are not well known. The aim of this study was to assess the outcomes of patients >80 years who presented with a GI bleed regarding their clinical characteristics, complications, outcomes, and the need for therapeutic endoscopic intervention.

Methods: We retrospectively reviewed charts of patients >80 years who presented to the ED at Florida Hospital Orlando from 2007-2012 with GI bleed. We excluded patients who had known esophageal or gastric varices or known cirrhotic liver disease. We obtained patient characteristics, clinical course, and outcomes from the charts.

Results: We screened 600 charts for inclusion and exclusion criteria, and 90 patients were included in the study. The average age was 85.8 years. Sixty-three (70%) of the 90 patients had an upper GI bleed. The mean Charlson Comorbidity Index (CCI) was 6.9, and the mean Blatchford score was 8.5. Forty-one (66.13%) patients underwent an esophagogastroduodenoscopy (EGD), 8 (12.9%) underwent a colonoscopy, 11 (17.74%) did not undergo an EGD or colonoscopy, and 2 (3.23%) underwent both procedures. Two (2.22%) of the total 90 patients died during the hospitalization. One patient had several comorbidities and the decision was to not proceed with the endoscopic procedure; the other patient died after a complicated hospital stay because of colonic perforation during colonoscopy. Of the total cohort of 90 patients, in 85 (94.44%) the endoscopic procedure did not result in a change of management. Of the 5 patients who needed intervention (5.56%), 2 (2.22%) required it to control the bleeding (one patient required cauterization of an arteriovenous malformation and another needed small bowel resection to control a bleed from a hemorrhagic polyp) and 3 (3.33%) needed it as treatment for the diagnosis made by endoscopy (one patient with a pancreatic cancer diagnosis was discharged to hospice care, one patient had colon cancer, and another patient had a large villous adenoma that resulted in hemicolectomy).

Conclusion: The very elderly (>80 years) patients presenting to the ED with GI bleeding have high scores on the CCI and high Blatchford scores on admission. However, most of the patients stopped bleeding without the need for an endoscopic procedure. We suggest a higher threshold for endoscopy in the very old population as they are at a significantly higher risk than the general population for developing postprocedure complications. Further research is needed to identify the clinical and historic characteristics of patients in this age group who would benefit from endoscopic investigation.

Garry McCulloch, MD; Department of Cardiology, University of Florida-Jacksonville, Jacksonville, FL
Abdulwahab Hritani, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Melissa Dakkak, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Ambar Patel, MD; Department of Cardiology, University of Florida-Jacksonville, Jacksonville, FL
Harendra Patel, MD; Department of Cardiology, University of Florida-Jacksonville, Jacksonville, FL
Candice Baldeo, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Christopher Klassen, MD; Department of Radiology, University of Florida-Jacksonville, Jacksonville, FL
Steven Lavine, MD; Department of Cardiology, East Tennessee State University, Johnson City, TN

Background: The presence of coronary artery calcium (CAC) reflects total atherosclerotic burden. With the increased use of thoracic CT for lung cancer screening, assessment of coronary artery disease (CAD) is being explored on non-gated thoracic CT (NGCT). The results obtained from NGCT are comparable with dedicated calcium scoring CT but are not sufficiently accurate to replace the ECG-gated noncontrast cardiac CT. In our study, we tested the correlation between CAC scoring and myocardial perfusion imaging (MPI) results to rule out ischemia based on data from our institution. The premise of this study was that a CAC score in the 0-400 range would correlate with the absence of ischemia on subsequent MPI. Thus, once this is statistically significant, the need for further costly cardiac investigations may potentially be eliminated in future admissions for recurrent nonspecific chest pain.

Methods: A total of 180 patients with no known CAD were retrospectively screened and identified as having had NGCT and MPI within 6 months between 1/1/2006 and 10/31/2011. Coronary artery calcifications were quantified, and measurements were performed using the standard Agatston CAC algorithm. Total calcium scores were classified into two categories: 0-400 and >400. MPI scans were categorized as normal vs abnormal. Abnormal MPIs were subclassified based on the amount of ischemia as mild, moderate, and severe.

Results: Of the 180 patients, 10 had ischemia on MPI, and 6 of these patients had moderate/severe ischemia. Mean CAC was significantly higher in patients with any amount of ischemia (548 + 579 vs 159 + 392, P=0.004) as well as moderate/severe ischemia (622 + 579 vs 165 + 402, P=0.008). Receiver operating characteristic curve to diagnose moderate/severe ischemia had an area under the curve of 0.79. A CAC score of 0 had a negative predictive value (NPV) of 98%, sensitivity of 83%, and specificity of 52%. A CAC score of 400 had an NPV of 98%, sensitivity of 50%, and specificity of 87%. Multivariate analysis revealed that a CAC >400 trends towards being an independent predictor for ischemia (P=0.055, OR=5.49).

Conclusion: This institutional retrospective study shows that a CAC score of 0 on NGCT may be used to predict the absence of ischemia on MPI.

Francois Jo-Hoy, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Farah Al-Saffar, MD, MPH; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Rahman Nakshabendi, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL
Rohini Ramtahal, MD; University of the West Indies College of Medicine,Trinidad and Tobago
Rama Hritani, MD; University of Aleppo College of Medicine, Aleppo, Syria
Abdulwahab Hritani, MD; Department of Internal Medicine, University of Florida-Jacksonville, Jacksonville, FL

Background: Takotsubo cardiomyopathy (TCM) is a transient cardiomyopathy that can mimic the presentation of acute coronary syndrome. The severe cardiac dysfunction that can be associated with TCM and the vulnerable nature of the postpartum period prompted us to review those cases associated with cesarean section (CS) delivery.

Methods: A literature review was conducted utilizing PubMed, Cochrane, and Google Scholar databases using the terms Takatsubo, Takotsubo, Tako-tsubo, ballooning, stress-induced, and transient cardiomyopathy and the terms C-section and cesarean section. All articles published through July 30, 2014 were included.

Results: Nineteen cases were found. The patients' ages ranged from 24-50 years with the mean age being 32 years. The majority of the CS deliveries were elective procedures (68%, n=13). The onset of TCM occurred within 24 hours for each of the 19 reviewed cases. Dyspnea was the most common presenting symptom (68%, n=13), followed by chest pain (57 %, n=11). Eighty-nine percent (n=17) of patients had elevated troponins, with 2 patients having no increase. The most common ECG finding was T wave inversion. Three patients had ST segment elevations. Echocardiogram findings were varied with no predominance in affected segments. Ninety-four percent (n=18) of the reviewed cases documented specific affected left ventricular segments. Fifteen percent (n=3), 21% (n=4), and 15% (n=3) had isolated apical, midsegment, and basal segment involvement, respectively. Concomitant apical and midsegment dysfunction occurred in 26% (n=5). The basal segment and midsegment were both affected in 15% (n=3) of cases. Fifteen cases documented depressed ejection fractions (EF) ranging from 14%-46%, with a mean EF of 31%. Management varied depending on patient presentation and encompassed conservative therapy with diuresis to more aggressive therapy with mechanical ventilation, the use of inotropes and vasopressors, and even the need for intraaortic balloon pump. Most of the patients developed pulmonary edema (78%, n=15). Seven patients developed cardiogenic shock, and 1 patient's course was complicated by cardiac arrest. In our review, 9 patients had left heart catheterization, and all demonstrated nonobstructive lesions. All of the cases documented a complete recovery for all patients. Recovery time ranged from 1-90 days, with the mean recovery time being 18 days.

Discussion: The exact pathophysiology of TCM is not fully understood; emotionally and physically stressful events are thought to be precipitating factors, with catecholamine surges playing an imperative role. It is postulated that such surges lead to myocardial stunning. Classically, ECG demonstrates akinesis or hypokinesis of the midsegment and apical segment with sparing of the basal segment. However, 4 variants have been described: apical, midventricular, basal, and focal TCM. The absence of obstructive coronary artery disease (CAD) was once thought to be necessary to make the diagnosis of TCM, but recently it has been found that because of the prevalence of CAD, both commonly coexist. Treatment with beta blockers and angiotensin-converting enzyme inhibitors is commonly utilized as is furosemide if diuresis is needed. Left ventricular systolic function typically recovers, with <10% of patients having a recurrence of TCM.

Conclusion: While still relatively uncommon, TCM is being increasingly identified. The stress that the female body undergoes during a CS can predispose to the development of TCM. Because of the limited number of cases reported, this review cannot be generalized to the general population.

Ross M. Hoffman, MBBS; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA
Matthew L. Clark, MBBS; The University of Queensland, Ochsner Clinical School, New Orleans, LA
Renee Y. Meadows, MD; Department of Hospital Medicine, Ochsner Health System, New Orleans, LA

Background: Without a do not resuscitate (DNR) order, a patient who experiences in-hospital cardiac arrest receives cardiopulmonary resuscitation. However, <20% of patients who receive CPR survive to hospital discharge, and only half of the survivors are discharged without neurologic deficits. Patients significantly overestimate their chances of survival to discharge after successful resuscitation. Similarly, physicians' predictions of survival are no more accurate than random chance. Discussions about goals of care should occur at the time of admission. Goals of care should be shaped by the patient's preferences, including review of an advance health directive (AHD) if one exists. Code status discussions (CSDs) should include the patient's predicted survival with likelihood for a good outcome. The Good-Outcome-Following-Attempted-Resuscitation (GO-FAR) score, a prearrest point score that predicts a patient's chance of neurologically intact survival to discharge following successful resuscitation, was validated in 2013. This clinical decision rule may be used during CSDs to assist patients with shared decision-making in partnership with their healthcare providers.

Methods: In a 473-bed academic tertiary care hospital, preintervention DNR note content was obtained by retrospective review of 155 convenience sampled patient charts containing DNR orders. Provider notes written 2 days before and after the date of the DNR order were included. A qualitative pilot study surveyed 75 internal medicine residents (PGY 1-3) via anonymous questionnaire by convenience sample. The residents' experiences with CSDs were assessed in October 2014 (response rate 47%). The GO-FAR score and essential components of an AHD review were incorporated into a note template (CSD Note) that was made available to residents in the electronic medical record. Perceived usefulness and adoption of the CSD Note were assessed in May 2015 (response rate 48%) following a 15-week intervention period. Based on Rogers' diffusion of innovations model, 16% of residents (innovators and early adopters) were expected to use the CSD Note during this pilot phase.

Results: Preintervention chart review found explanations for DNR orders in only 33 (21%) records, 88 (57%) lacked explanation, and 34 (22%) lacked any mention of code status despite the order for DNR status. Among PGY 3 and PGY 2 residents, 77% reported “usually” or “always” having a CSD during each admission, while 36% of interns reported the same frequency. Only 50% of residents reported “usually” or “always” verifying documentation of patient preferences when entering a DNR order. Six respondents (17%) used the CSD Note during the 15-week intervention period. All respondents rated it as “easy” or “not difficult” to use, 67% found it helpful in choosing the content of their CSDs, and 83% reported that the CSD Note led them to include more detail in their documentation.

Conclusion: This project aimed to optimize decision-making about code status and improve documentation of inpatient CSDs through validated postresuscitation outcome prediction and review of patients' AHDs and goals of care. The CSD Note enhanced both content and documentation of CSDs with inpatients. Adoption of the CSD Note in our hospital is expected to follow general principles for dissemination of healthcare innovations.

Drey A. Pavlov, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA
Ross M. Hoffman, MD; Department of Internal Medicine, Ochsner Clinic Foundation, New Orleans, LA
Fiona Winterbottom, APRN; Ochsner Clinic Foundation, New Orleans, LA
Teresa Nash, PharmD; Department of Pharmacy, Ochsner Clinic Foundation, New Orleans, LA
Lucas Shum, MAcct; Ochsner Clinic Foundation, New Orleans, LA
Erik Sundell, MD; Department of Emergency Medicine, Ochsner Clinic Foundation, New Orleans, LA
Leonardo Seoane, MD; Department of Pulmonary/Critical Care, Ochsner Clinic Foundation, New Orleans, LA

Background: Sepsis affects more than 800,000 patients per year in the United States alone. Many studies support early aggressive therapy as crucial to improving outcomes, but early therapy hinges on accurate diagnosis and classification of sepsis. Recent clinical trials and expert opinion identify timely treatment as being more important than goal-oriented protocol in achieving better outcomes.

Methods: A total of 1,051 consecutive patients admitted with a diagnosis of severe sepsis or septic shock (SS&SH) to the medical intensive care unit (MICU) at a single center from July 1, 2008 to June 31, 2012 were enrolled as part of a quality improvement initiative. Subgroup analysis of mortality and length of stay (LOS) in patients who were transferred to the MICU from the floor within 6, 12, 24, and 48 hours of admission was performed. Patients with cardiopulmonary arrest on presentation were excluded from analysis. The primary endpoint was inhospital mortality.

Results: A total of 979 patients met inclusion criteria, of whom 325 (33.3%) were transfers from the floor to the MICU. Of these, 150 (46%) were transferred within 48 hours of admission (early floor admit [EFA]): 38 (25.3%) in <6 hours, 29 (19.3%) in 6-12 hours, 45 (30%) in 12-24 hours, and 38 (25.3%) in 24-48 hours. Baseline characteristics were similar across all groups, including average Acute Physiology and Chronic Health Evaluation (APACHE) scores (>48 hours, 27.1±8.3; 24-48 hours, 26.7±7.8; 12-24 hours, 25.4±7.5; 6-12 hours, 24.1±7.9; <6 hours, 26±9.6; P=0.62). In-hospital mortality was similar among EFA patients (24-48 hours, 26.3%; 12-24 hours, 22.2%; 6-12 hours, 24.1%; <6 hours, 23.7%; P=0.98). Aggregate mortality for EFA patients was worse than that of patients admitted directly from the ED (24.0% vs 17.9%, P=0.041). The mortality for patients transferred from the floor to the MICU after 48 hours (late floor admit [LFA]) was associated with substantially increased mortality (31.4%, P<0.001). Overall cohort mortality was 27.9%. LOS followed similar trends, with a significantly longer LOS (in days) in floor-to-ICU admits compared to ED admits (ED: 9.6±8.3; EFA: 13.9±12.1; LFA: 14.9±13.3; P<0.001). Subgroups of EFA patients did not have statistically significant differences in LOS (<6 hours: 15.4±15.4; 6-12 hours: 13.3±8.3; 12-24 hours: 13.6±12.6; 24-48 hours: 13.3±10.7; P=0.90).

Conclusion: At a single center, nearly half of patients eventually diagnosed with SS&SH yet admitted first to the floor were transferred “early” to the MICU. As hypothesized, patients transferred from the floor to the MICU had higher mortality than those admitted directly from the ED to the MICU. Unexpectedly, mortality in the first group did not vary with time to transfer up to 48 hours, regardless of whether early goal-directed therapy goals were met. Nosocomial infection was not likely the cause of sepsis in this group, further demonstrating the need for early aggressive therapy in SS&SH. Accurate diagnosis of SS&SH on initial presentation to the ED is thus crucial to improving mortality.

Anjali Grandhige, MD; Emory Palliative Care Center, Emory University, Atlanta, GA
Danielle Moulia, MPH; Emory Palliative Care Center, Emory University, Atlanta, GA
Zachary Binney, MPH; Emory Palliative Care Center, Emory University, Atlanta, GA

Background: It is well documented that patient preferences about care at the end of life are not often elicited, especially during an acute admission. This omission can lead to unwanted aggressive interventions at the end of life. In 2014, our health system began to proactively identify hospital medicine patients with high-risk diagnoses who would qualify for a palliative care (PC) consultation that includes discussion of treatment preferences. We then evaluated if early intervention with PC led to increased documentation of treatment preferences.

Methods: Using informatics, a daily trigger list of patients admitted to the hospital medicine service who potentially met PC criteria was sent to the PC team beginning in August 2014. The PC team reviewed the list and contacted the patient's attending physician to discuss whether PC was appropriate for the patient. Data on all patient encounters that met or would have met the trigger criteria and had a PC consult between January 2014 and June 2015 were collected. We calculated the proportion of patient encounters with a do not resuscitate (DNR) order or advance directive (AD) in the electronic medical record (EMR) on or before discharge, including previous hospitalizations. To see if our trigger program had any effect on high-risk hospital medicine patients, we compared the proportion of patient encounters with a documented DNR or AD before (January 2014-July 2014) and after (August 2014-June 2015) implementation of the triggers using chi-square tests.

Results: There were 1,078 patient encounters that met trigger criteria and were seen by the PC team during the study period. Of these, 208 patient encounters occurred before the implementation of the trigger list and 869 occurred after implementation. There was a statistically significant (P<0.05) increase in the proportion of patient encounters with a DNR filed in the EMR after implementation of the trigger list, 12.3% vs 20.4%. There was also a small increase in the proportion of patient encounters with an AD filed in the EMR after the implementation of the trigger list, 8.9% vs 10.2%.

Conclusion: Early identification of patients with serious life-limiting illness is crucial so that they have the opportunity to express their desires about the type of care they want for themselves. All too often, we wait until a medical crisis to elicit patient preferences—if we ask at all. Our project focused on patients at highest risk for a crisis event, and we proactively had these crucial conversations. Through a partnership with hospital medicine, we increased documentation of their treatment preferences such as DNR status and ADs to ensure that individual patient wishes were honored by the healthcare teams.