United States

Background: Primary infection with varicella zoster virus (VZV) causes varicella (chickenpox), while herpes zoster (shingles) is a secondary infection that occurs when latent VZV is reactivated. Both primary and secondary VZV infections can cause central nervous system manifestations, including encephalitis, which is rare and often fatal.

Case Presentation: A 66-year-old woman with history of rheumatoid arthritis, psoriasis, and coronary artery disease presented to our hospital with sudden-onset altered mental status. She was found naked, confused, and covered in feces and urine at home. At presentation, she was afebrile, tachycardiac (106 bpm), tachypneic (24 breaths/min), saturating 97% breathing ambient air. Labs were unremarkable. Non-contrast head CT revealed disproportionately enlarged ventricles and temporal lobe volume loss. Brain MRI confirmed ventriculomegaly. Blood cultures were drawn, and IV vancomycin, ceftriaxone, and ampicillin were started empirically. Initial blood cultures were negative. On Day 3, lumbar puncture with cerebrospinal fluid (CSF) analysis showed elevated WBC (1,077 cells/mcL) with 97% lymphocytes, low glucose (21 mg/dL) and elevated protein (298 mg/dL). CSF viral PCR panel was positive for VZV, necessitating initiation of IV acyclovir. Given no significant improvement despite treatment, lumbar puncture was repeated on Day 8, with similar findings as the initial CSF analysis. Ampicillin was discontinued because repeated blood cultures and CSF analysis were negative for Listeria. By Day 17, she had completed a 14-day course of IV acyclovir but remained febrile and confused. The patient’s family decided to transition her to comfort care measures, and she expired on Day 23.

Discussion: Nervous system manifestations of VZV include meningitis, encephalitis, cerebellar ataxia, vasculopathy, and myelopathy. Unlike encephalitis caused by herpes simplex virus type-1 and enteroviruses, VZV encephalitis is uncommon, occurring in one out of every 33,000 to 50,000 cases of VZV infection. VZV encephalitis is associated with intense inflammation, and often has an acute presentation. Studies report higher median CSF protein levels and higher CSF lymphocytosis in VZV encephalitis compared to enterovirus encephalitis. Even with appropriate treatment, VZV encephalitis is almost 100% fatal in immunocompromised hosts. A high index of suspicion and early initiation of appropriate treatment for VZV encephalitis is essential, especially in immunocompromised hosts.

AMA Research Challenge 2022

A Case of Varicella Zoster Virus Encephalitis – A Rare but Often Fatal Cause of Encephalitis

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Charles Lopresto, DO

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Welcome to the largest national, multi-specialty research event featuring research from 750 medical students, residents and fellows, and international medical graduates.


poster

Abstract Title: Difficult case of refractory hypertension 

Background: Refractory hypertension is a rare but challenging disease to treat. The most updated phenotype helps distinguish it from white coat syndrome, resistant or secondary hypertension. However, controlling blood pressure, in this case, is likely a frustrating process for the patient and doctor alike. 



Case Presentation: 34 years old Caucasian male with a ten-year history of uncontrolled hypertension was referred by his primary care physician's office to a cardiology office for blood pressure (BP) management. On his first visit, his BP was 180s/110s. in addition to the high BP, his history and physical exam were positive for chest pain and palpitation; otherwise, unremarkable. Blood work, echo, and kidney ultrasound results excluded secondary causes and were only significant for hyperlipidemia. Therefore, the patient was started on a statin. Over the course of five months, the patient followed up every 1-3 weeks. Multiple medication adjustments were made by either increasing the dose or switching to another group of medications. He has always been on seven antihypertensive agents, including chlorthalidone and spironolactone. Nevertheless, his BP has always been high (150s -210s/100-150 mmHg). 



Due to the failure of medical management to control the patient's BP, He was referred to Providence hospital/Simplicity study for sympathetic denervation. Unfortunately, he did not meet the study criteria. Furthermore, a recent stress test showed that his refractory hypertension is now complicated by cardiomyopathy with an EF of 35%. Thus, he was switched from Telmisartan to Entresto 49/51 mg twice daily. 



Discussion: The most updated refractory hypertension definition is a failure to control BP after a routine clinical follow-up of ≥3 visits for ≥ 6 months despite being adherent to a regimen of >5 classes of antihypertensive agents, including chlorthalidone 25 mg daily and spironolactone 25 mg daily or eplerenone, 50 mg twice daily and without evidence of underlying secondary causes of hypertension. However, the clear definition of refractory hypertension is not necessarily associated with a clear management plan or promising outcomes for this group of patients. 



A difficult case of refractory hypertension

Background
Inferior Vena Cava (IVC) filters are a versatile tool used in prevention of pulmonary embolism but face many challenges in complications, most notably fracturing. This complication can be as high as 38% depending on the model and remains a significant concern in long term risk-benefit viability of the device. We present the unique case of a patient with a history of sarcoidosis, surgical complications from prior hysterectomy, and fractured IVC filter resulting in multiple repeat pulmonary emboli.

Case Presentation
In July 2021, a 52 year old Caucasian female with history of hysterectomy, sarcoidosis, bariatric surgery and 8 year history of IVC filter placement presented with back pain and on evaluation was found to have filter fracturing. Her filter was prophylactically placed around 2013 after a past provoked pulmonary embolism following a hysterectomy for endometriosis.

Retrieval of fractured IVC filter parts was attempted with 3 struts remaining. CT angiogram evaluation revealed presence of multiple pulmonary emboli in the right upper and left lower lobes. The patient was hemodynamically stable and was discharged on 10mg Eliquis BID.

One month later, she presented to the ED with severe fatigue and was found to have new emboli in the left lower lateral segmental lobe. Patient was hemodynamically stable and was started on heparin, eventually transitioning to Eliquis outpatient management.

Discussion
Recurrent emboli following IVC fracture is a novel event. We postulate this phenomenon is attributable to compounded risk of thrombosis in those with prior risks of hypercoagulability.

The pathophysiology of IVC filter fracturing is not well documented. Fracturing is related to metal fatigue from tilting and repetitive flexion. It is possible that recurrent emboli following filter fracture is secondary to underlying hypercoagulability disorders such as sarcoidosis. Sarcoidosis compounds the risk of embolism through inflammatory mediators and increased turbulence within vessel lumens from extrinsic lymphadenopathy compression. Combined with endothelial damage from fractured parts, these risk factors intensify embolism risk.

Although filters may be used for prevention of embolisms, they paradoxically may also increase the risk. Thus, usage is cautioned, and timely removal is highly advised.

A patient with sarcoidosis and multiple pulmonary embolism from IVC filter fracture: A Rare Case Report

A rare case of anti-tubercular drug induced cardiomyopathy

Abstract Title: 
A Rare Case of Infective Endocarditis caused by Serratia marcescens

Background: 
Serratia marcescens is a gram-negative bacillus that usually causes respiratory and CNS infections but it rarely can cause infective endocarditis.

Case Presentation: 
A 62-year-old male with PMH of intravenous drug use and Hepatitis C presented to the ED with palpitations and back pain for three weeks with no reported fevers. In the ED, his vitals were: temperature 103.9° F, BP 105/72, HR 125, RR 20 and O2 saturation 100% on room air. The remainder of his examination revealed bilateral subconjunctival hemorrhages and multiple track marks; there were no neurological deficits, petechiae, or murmurs. Laboratory studies revealed WBC 12.82, bandemia of 13%, and lactic acid 4.1. An MRI brain revealed scattered acute infarcts; subsequent spinal MRIs were negative for abscesses. He was admitted for sepsis possibly secondary to endocarditis and started on broad spectrum antibiotics; an initial TTE was negative for vegetations, and blood cultures later grew S. marcescens. The patient subsequently developed an intermittent AV block. Repeat TTE revealed a linear echo-density on the aortic leaflets; TEE showed a 2cm vegetation on the aortic valve with perforation. He was transferred to a tertiary center for further care; he underwent aortic valve replacement, which was complicated by aortic root rupture. He also developed sick sinus syndrome and required a pacemaker. The remainder of his hospitalization was unremarkable and he was discharged on a prolonged antibiotic course.

Discussion: 
Infective endocarditis with S. marcescens is rare; some studies report only 0.14% of IE cases are caused by Serratia. Although IV drug users typically have higher rates of right-sided valvular endocarditis, S. marcescens tends to involve left-sided valves. S. marcescans is rapidly progressive. Typical symptoms include fever, myalgias, or dyspnea. Exam findings can include cardiac murmurs, splinter hemorrhages, Janeway lesions, Osler nodes, and Roth spots. IE diagnosis is made via positive blood cultures and vegetations on echocardiography. Surgical intervention is recommended within 7-10 days; mortality is as high as 85% in patients with Serratia who only received medical therapy. After prompt surgical intervention, antimicrobial treatment includes combination therapy of B-lactam and an aminoglycoside or fluroquinolone for at least six weeks. 


A Rare Case of Infective Endocarditis by Serratia Marcescens

Drug-Induced Interstitial Lung Disease (DILD) describes an inflammatory response to various drugs that can result in fibrosis of the lung. It can present with dose-dependent toxicity or as an immune-mediated response, with respiratory illness ranging from benign infiltrates to debilitating respiratory fibrosis. This report describes a patient with a history of chronic, recurrent pneumonia suspected to be gabapentin-induced pneumonitis and severe gastroesophageal reflux disease (GERD). Respiratory symptoms initially improved after abstinence from gabapentin but then recurred postoperatively, after a GERD-related hiatal hernia repair. Diagnosis of DILD remains difficult and a diagnosis of exclusion, and our case may provide evidence for a relationship between gabapentin, GERD, and DILD: chronic aspiration combined with depressed cough reflexes characteristic of drugs like gabapentin may contribute to lung injury. Future research may provide a better understanding of how GERD may act to exacerbate DILD and give insight into a mechanism of similar adverse drug interactions.

A Rare Presentation of Suspected Gabapentin-Induced Idiopathic Pneumonitis

Background: Multiple studies have shown that a majority of community-acquired pneumonia (CAP) associated mortalities are due to cardiovascular disorders. Up to 30 % of patients with CAP are at risk of cardiovascular complications during the first thirty days of hospital admission, especially older than 65 years or with underlying cardiac conditions. However, mechanisms involved in this pathogenesis are not fully understood in younger healthy patients. We are presenting a case of acute onset of systolic heart failure in the setting of community-acquired pneumonia.

Case Presentation: A 45-old male patient presented to the emergency department with a complaint of upper respiratory tract infection symptoms of 4 days duration. He received oseltamivir but worsening of symptoms, including nausea and vomiting, were noted. Vital signs were normal except for tachycardia, and the physical exam was non-focal. FLU A and B and COVID-19 testing were negative. Chest x-ray (CXR) revealed right lower lobe infiltrates. The patient was started on Levofloxacin for CAP coverage. The patient was stable, but on day three, oxygen desaturation (85%) with tachycardia and dyspnea were found. Physical examination revealed bilateral coarse crackles, especially lower lobes. CT angiography Chest ruled out pulmonary embolism but revealed diffuse bilateral alveolar and interstitial infiltrates suspicious for vascular congestion with superimposed pneumonia. Echocardiography revealed dilated cardiomyopathy, systolic heart failure (HF) with reduced left ventricular ejection fraction to 15%, and mild to moderate mitral regurgitation. Guideline-directed medical therapy for HF was initiated. Left heart catheterization excluded significant coronary artery disease.

Discussion: We present a case of acute onset of systolic heart failure in a young immunocompetent male patient who presented with CAP. The workup for CAP includes sputum cultures, blood cultures, methicillin-resistant staphylococcus aureus PCR, legionella antigen testing, cytomegalovirus, Epstein-Barr virus IgM, herpes simplex virus type I and II, and human immunodeficiency virus were negative.


Acute Onset of Systolic Heart Failure in The Setting of Community-Acquired Pneumonia in an Immunocompetent Patient

Background
Atypical hemolytic uremic syndrome (aHUS) is a rare condition characterized by hemolytic anemia, thrombocytopenia and acute renal failure. The mechanism of aHUS consists of a genetic mutation in complement regulation incited by a strong trigger leading to uninhibited activation of the complement system. Trigger events include infection, medications, malignancy or a systemic illness that initiates inflammatory reaction like pancreatitis. We present a case of a patient that presented in an extreme hyperglycemic state with acute pancreatitis and was subsequently diagnosed with aHUS. 
Case Presentation
38-year-old obese Hispanic male with no past medical history who presented to the emergency department with altered mental status. On physical exam, he was lethargic and hemodynamically unstable. Initial labs showed metabolic acidosis with anion gap, acute kidney injury, glucose of 1500, moderate serum acetone and a hemoglobin A1C of 11.9. Lipase was 1766 (upper limit of normal 60) and computed tomography of the abdomen without contrast revealed multiple loculated fluid collections around the pancreas. His renal function progressively worsened, requiring hemodialysis. On hospital day 2, his platelet count decreased to 20 and peripheral blood smear revealed schistocytes. Heparin-induced thrombocytopenia, disseminated intravascular coagulation and viral infections from Hepatitis B, C and human immunodeficiency virus were all ruled out. Also, shiga-like toxin antigen and stool culture were negative. Given the fevers, renal failure, hemolytic anemia, thrombocytopenia and altered mental status; thrombotic thrombocytopenia purpura (TTP) was suspected and immediate plasmapheresis was initiated. He completed 11 sessions of plasmapheresis in conjunction with 11 days of methylprednisolone 40 mg every 8 hours. ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) level resulted at 43%, making aHUS more likely. The patient was then started on eculizumab with improvement in his mental status and renal function. 
Discussion
Although rare, patients can develop both TTP and aHUS, with hemolytic anemia, thrombocytopenia and acute renal dysfunction following pancreatitis. Due to the high mortality of TTP, patients should be promptly treated with plasmapheresis while awaiting results of ADAMTS13 levels. If ADAMTS13 is normal, the physician should consider aHUS as a possible diagnosis and start eculizumab as soon as possible to salvage renal function.

Acute pancreatitis causing aHUS in a patient with new-onset diabetes mellitus

Association between statin use and Morbidity-Mortality outcome in stroke patient with LDL <70 mg/dl: A retrospective study from a stroke registry

Background 
Encountering direct complications of absorbable antibiotic carriers is rare. When treating prosthetic joint infections, absorbable antibiotic calcium-sulfate beads have a superior elution profile to other traditional antibiotic loaded beads which eventually require removal. In a case of persistent polymicrobial post-operative infection, an unexpected turn of events manifested with heightened serum calcium after carrier insertion.

Case Presentation 
A 74-year-old woman with advanced osteoarthritis of the hip presented with progressive right hip pain. Right total hip arthroplasty (THA) was successfully performed; however, she developed a hip abscess, fever, and chills shortly after staple removal. Abscess cultures resulted positive for methicillin-resistant Staphylococcus aureus and Finegoldia magna. Rifampin and vancomycin were initiated, and she underwent arthroplasty revision. Despite implant exchange, continued polymicrobial infection necessitated a second revision.
A second THA revision was performed with the insertion of Stimulan calcium-sulfate antibiotic carriers to optimize control of the persisting polymicrobial infection. Rifampin therapy was continued, and daptomycin substituted vancomycin due to acute kidney injury. Post-operative day five, she was found to be hypercalcemic with corrected serum calcium peaking at 12.6 mg/dL; prior labs confirmed serum levels within normal limits. Only notable symptoms were nausea and features of delirium. A broad differential was explored for this acute abnormality. Suppressed parathyroid hormone (PTH) and vitamin D metabolites favored a PTH-independent process. Granulomatous disease was suspected as a bone biopsy showed non-caseating granuloma. Hypercalcemia of malignancy was considered, with raised suspicion for multiple myeloma as elevated monoclonal protein were found. 
Serum calcium levels and delirium improved with fluids and bisphosphonate therapy. We suspected calcium-sulfate antibiotic bead spacers as the most likely calcium source after immunofixation showed no overt evidence of monoclonal proteins, diagnostics of granulomatous disease origins remained negative, and repeat PTH, vitamin D metabolites, and PTHrP remained inconsistent with primary parathyroid or paraneoplastic-mediated processes. She was discharged with downtrending inflammatory markers and normal calcium levels.

Discussion 
Calcium-sulfate antibiotic beads are effective for managing surgical site and prosthetic joint infections; however, the risk of transient hypercalcemia remains. Further studies are necessary to determine if there is a threshold amount of calcium-sulfate antibiotic beads which correlates with higher risk of developing hypercalcemia. 


Beads of Calcium, the Culprit of Confusion

Background
Syncope is the result of cerebral hypoperfusion with underlying etiologies classified as neurally mediated, cardiac, or orthostatic hypotension. Risk stratification based on etiology of syncope is crucial since cardiac syncope is associated with increased morbidity and mortality and may have specific treatment options, whereas neurally mediated syncope and orthostatic hypotension are often benign and are treated with supportive care. It is estimated that 5-21% of syncope is of cardiac etiology. Signs and symptoms, listed with the associated positive likelihood ratio (+LR) that predict increased risk of cardiac syncope include age >35 at initial episode of syncope (3.3), history of existing heart disease (2.7-7.3), exertional syncope (1.4-15), syncope while supine (1.1-4.9), prodromal chest pain, dyspnea, or palpitations (1.9-3.8), cyanotic during episode (6.2), and abnormal ECG (2.3).

Case Presentation
A 50-year-old woman presented with syncope while walking up a flight of stairs. Syncope was preceded by palpitations, dizziness, and dyspnea. ECG demonstrated sinus rhythm, 1st degree AV block, RBBB, and LAFB without ischemic changes. CT Coronary revealed multiple perilymphatic pulmonary nodules with hilar lymphadenopathy concerning for sarcoidosis. Transthoracic echocardiogram showed normal LVEF of 66% and proximal septal wall thickening. On hospital day 2, the patient experienced syncope while supine with bradycardia to the 20s and hypotension to 70s/40s. Repeat ECG and showed complete heart block. The patient received emergent transvenous pacing along with IV dopamine and norepinephrine infusions. On hospital day 3, she received a permanent dual chamber pacemaker-defibrillator. She underwent fluorodeoxyglucose positron emission tomography (FDG-PET) and biopsy confirming the diagnosis of cardiac sarcoidosis.

Discussion
This case demonstrates the importance of recognizing signs and symptoms associated with high-risk cardiac syncope, which should prompt hospital admission and further diagnostic evaluation. After identifying cardiac syncope, it is important to determine the underlying cause which can be due to arrythmias or structural heart disease. This patient’s arrhythmogenic cardiac syncope was due to cardiac sarcoidosis, an infiltrative granulomatous disease that impacts multiple organs. Clinical manifestations of cardiac sarcoidosis occur in only 5% of patients and typically presents as conduction abnormalities, ventricular arrythmias, and heart failure. Diagnosing cardiac sarcoidosis is crucial to identify patients that will benefit from appropriate treatment.


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