SESSION TYPE: Surgery Student/Resident Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Angina occurs when myocardial oxygen demand exceeds oxygen supply; the clinical manifestation is often chest discomfort. Several non-atherosclerotic conditions have been studied and reported in literature that cause angina in rarity.

CASE PRESENTATION:

A 40 year old Chinese healthy male presented to the emergency department with chest pain described as heavy, retrosternal, non-radiating, constant for 30 minutes associated with dizziness, nausea and palpitations which started while lifting a weight of 40 pounds. It relieved gradually with rest. His physical activity was limited due to the chest discomfort (CCS Class II angina). He had a smoking history of 10 packs per day without alcohol or illicit substance use and an insignificant family history. His physical exam was positive for grade II/VI continuous murmur at the left sternal border, with clear lungs and normal jugular venous pressure. His exercise stress test which was terminated at 7 minutes as he developed dizziness, ST segment depression in the lateral leads along with non-sustained ventricular tachycardia and a transient left bundle branch block. Cardiac catheterization showed insignificant coronary artery disease but revealed a fistula leading from the Left anterior descending (LAD) to the main pulmonary artery. This was confirmed by Coronary CT angiogram coursing within the epicardial fat along the lateral aspect of the pulmonary outflow tract. An attempt to coil the fistula via the pulmonary circulation was unsuccessful. Robotic arm assisted ligation in the operating room showed a 1-cm long feeding vessel coming off the LAD with only one visualized branch, which was isolated and ligated close to the LAD. TEE was used to confirm the presence and absence of flow. This resulted in patient recovery without any complications.

DISCUSSION:

A coronary artery fistula (CAF) is an abnormal communication between an epicardial coronary artery and a cardiac chamber or a major vessel. They may present at any age and are mostly congenital. Whether or not a patient will develop symptoms depends on the degree of volume overload and severity of the left to right shunt. Coronary angiography still remains the gold standard for diagnosis. Surgical ligation and transcatheter embolization are known treatment options for CAF.

CONCLUSIONS:

Our patient presented with symptoms of stable angina, further unmasked during exercise stress testing. His symptoms are explained by the "steal" phenomenon where coronary blood flow is shunted to the pulmonary artery at the expense of myocardium, resulting angina. Symptoms abated after successful ligation of the fistula using a robotic arm.1) Heart failure with transient left bundle branch block in the setting of left coronary fistula. Juraschek SP, Kovell LC, Childers RE, Chow GV, Hirsch GA. Source Department of Medicine, Johns Hopkins Bayview Medical Center, Johns Hopkins University School of Medicine, 4940 Eastern Avenue, Baltimore, MD 21224, USADISCLOSURE: The following authors have nothing to disclose: V Subbarao Boppana, Sravanthi Nandavaram, Sidharth Jogani, Robert CarhartNo Product/Research Disclosure InformationSuny Upstate Medical Center, Syracuse, NY.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Chest pain is an important symptom of myocardial infarction (MI) and this is why it alerts the health care team. AHA guidelines say that the presence of any 2 of the 3 cardinal features of acute coronary syndrome, i.e. chest pain, EKG changes and positive & rising cardiac enzymes, are enough to diagnose MI. But a false diagnosis of MI may lead the patient to unnecessary invasive procedures that might be associated with morbidity and mortality.

CASE PRESENTATION:

40 year old female with history of diabetes mellitus presented to the ED with 10/10 left-sided chest pain radiating to left arm with numbness of left arm and palpitations & anxiety. The pain increased on deep inspiration. Physical examination revealed over-weight female with no other significant positive finding. Troponin I and CK-MB were elevated. 12 lead EKG showed ST segment elevation in leads I, II, avR, avL & V2-V6 with no reciprocal changes. Patient had a history of URI 1 week back. Based on this scenario, she was diagnosed with acute pericarditis. Repeat troponin levels showed rise. Diagnoses of myocarditis or myocardial infarction were also considered at this point. Considering the risk factors (weight, diabetes mellitus, ST elevation, Troponin rise) and unavailability of a catheterization laboratory at our hospital, it was decided to transfer the patient for PCI. At the other hospital, trans-thoracic echocardiogram done prior to catheterization revealed no cardiac wall motion abnormalities that might be present due to MI. It was decided not to proceed with catheterization but instead manage the patient conservatively due to risk-benefit analysis of the procedure and more likelihood of acute pericarditis. The patient improved with conservative management. Patient was followed clinically and with serial TTE.

DISCUSSION:

Although classical physical exam findings are diagnostic of acute pericarditis, ST segment elevation with increasing cardiac biomarker levels create a suspicion of MI. Diffuse ST segment elevation is one of the most important diagnostic characteristics of acute pericarditis. J point elevation and diffuse ST elevation help in differentiating MI from pericarditis. Our patient was unique that she didn't have pericardial rub and didn't have ST elevation in all the leads, and this might otherwise been suggestive of massive anterior wall MI. Troponin and CK-MB elevation were found in 38 patients in a study involving 118 patients (32%) of acute pericarditis. These patients are supposed to have myopericarditis. The 90 minute door-to-balloon window prompts us to take the patient for PCI in case of ST elevation and Troponin elevation.

CONCLUSIONS:

Cardiac catheterization is an invasive procedure that is associated with significant risks and risk-benefit ratio should always be analyzed before sending the patient for it.1) Imazio M, Demichelis B, Cecchi E, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol 2003; 42:2144DISCLOSURE: The following authors have nothing to disclose: Kovid Trivedi, Pranay Trivedi, Hasnain Bawaadam, Nitesh Jain, Aman Sethi, Rashid NadeemNo Product/Research Disclosure InformationChicago Medical School/Rosalind Franklin University of Medicine & Science, North Chicago, IL.

SESSION TYPE: Critical Care Student/Resident CasesPRESENTED ON: Monday, October 22, 2012 at 01:45 PM - 03:00 PM

INTRODUCTION:

Sinus histiocytosis with massive lymphadenopathy is a rare histiocytic disorder (1969). The etiology is unknown although suspected occult infection or exaggerated immune response to infectious agent is possible.

CASE PRESENTATION:

A 27 yo AA female presenting with 1 week of worsening dyspnea & chest pressure. She reports having similar episodes for 1year. She reports palpitations, nausea and cough. CT Chest demonstrated a pericardial effusion, right pleural effusion, and extensive bilateral air space opacity in a tree and bud configuration and enlargement of the medisastinal and bihilar soft tissue mass impinging on the pulmonary artery. TTE showed markedly dilated RA/RV & reduced systolic function. PA systolic pressure was 85-90mmHg. She was treated with IV steroids and required high concentration oxygen. VAT with lymph node and lung biopsy was performed before pulmonary artery stenting and radiation therapy without significant therapeutic response. Pathology concluded "sinus histiocytosis with massive lymphadenopathy". Histiocytes showed emperipolesis and were CD68+, variably S100+, and CD1a negative.

DISCUSSION:

SHML occurs in any age group but most frequently in young children/adults, Males> Females, in those of African or Caribbean decent. Potential causative agents include Post-viral (HHV6 or EBV), Hodgkins/non-hodgkins, and auto-immune disease although exact etiology is unclear. Typically SHML presents as massive bilateral cervical lyphadenopathy with fever, night sweats, & weight loss. Common extranodal sites include skin, upper respiratory tract, and bone but rarely include lung, spleen and bone marrow. Kidney, lower respiratory tract and liver involvement are poor prognostic factors. These patients typically have leukocytosis, elevated ESR, and polyclonal hypergammaglobulinemia. On pathology lymph nodes show pericapsular fibrosis with dilated sinuses, heavily infiltrated with large histiocytes, lymphocytes and plasma cells. Emperipolesis is the engulfment of lymphocytes and erythrocytes by histiocytes that express S100 and is considered the hallmark of SHML/RDD. Cells stain positive for S100, CD68 and negative for CD1a. We report a rare presentation of sinus histiocytosis with massive lymphadenopathy which presents as a mediastinal mass with lung involvement. Majority of patients have a benign course and do not require treatment. Therapy is reserved for patients with extranodal disease with vital organ involvement causing life-threatening complications. Systemic corticosteroids can decrease nodal size and symptoms. Radiotherapy and chemotherapy have limited efficacy.

CONCLUSIONS:

We report an aytpical presentation on a rare histiocytic disorder of biopsy proven Rosai-Dorfman disease (SHLM) resulting in hypoxic respiratory failure and death.1) Y. Shi et al. Sinus histiocytosis with Massive Lymphadenopathy (Rosai-Dorfman Disease): A case report and review of 49 cases with fine needle aspiration cytology. Cytojournal 2011:8:3DISCLOSURE: The following authors have nothing to disclose: Sajeet Sawhney, Edison Gavilanes, George Haralambou, Melvin HochmanNo Product/Research Disclosure InformationNew York Hospital Queens, Flushing, NY.

SESSION TYPE: Cardiovascular Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Cor-triatriatum sinister is a rare congenital disorder, where left atrium is divided into two chambers by a fibromuscular membrane. It occurs in 0.1-0.4% of all patients with congenital heart disease (1). We report a case where isolated cor-triatriatum sinister was incidentally diagnosed in a patient with new onset atrial fibrillation.

CASE PRESENTATION:

53-year-old Hispanic female with past medical history of diabetes mellitus and hypertension presented with complaint of palpitations. There was associated intermittent sub-sternal chest pain, lasting for 3 to 4 minutes with no specific aggravating and relieving factors. She refused shortness of breath, diaphoresis, dizziness, syncope or any previous similar symptoms. Home medications included losartan and metformin. There was a strong family history of coronary artery disease and stroke and she smoked 3 cigarettes per day. On examination, she had pulse rate of 130 bpm with irregularly irregular rhythm. Rest of the physical examination was normal. Electrocardiogram showed atrial fibrillation with rapid ventricular response. Initial laboratory data including two set of cardiac enzymes and thyroid function tests were normal. Chest radiograph was normal. She was admitted to telemetry floor for rate control and anticoagulation therapy. Transesophageal doppler echocardiogram revealed cor-triatriatum sinister and a concomitant jet of blood across the orifice (Image 1) and confirmed absence of thrombus. Subsequently, a cardiac MRI was performed which showed a larger proximal chamber measuring 3.9 x 5.4 cm with all four pulmonary veins draining into it. The distal chamber measured 4 x 4 cm and the orifice (Image 2) measured approximately 1.5 cm in diameter. The patient was referred for cardiothoracic surgery and was continued on anticoagulation.

DISCUSSION:

Isolated cor-triatriatum presenting as new onset atrial fibrillation in an adult patient is rare since most cases are diagnosed in infancy. The age and severity of presentation depends on the size of the communicating orifice. If the defect is large, patients may remain asymptomatic until adulthood (2). Symptoms occur mainly due to fibrosis and calcification of the orifice or development of atrial fibrillation.

CONCLUSIONS:

Presentation of cor triatriatum as new onset atrial fibrillation in an adult patient is an uncommon finding. Corrective surgery is required to provide the relief of symptoms in majority of cases (3).1) Krasemann Z, Scheld HH, Tjan TD, Krasemann T. Cor triatriatum: short review of the literature upon ten new cases. Herz. 2007; 32(6):506-510.2) Chen Q, Guhathakurta S, Vadalapali G, Nalladaru Z, Easthope RN, Sharma AK. Cor triatriatum in adults: three new cases and a brief review. Tex Heart Inst J. 1999; 26(3):206-210.3) Lam CR, Green E, Drake E. Diagnosis and surgical correction of 2 types of triatrial heart. Surgery. 1962; 51:127-137.DISCLOSURE: The following authors have nothing to disclose: Priyank Shah, Vipin Mittal, Nishant Gupta, Sharad Bajaj, Fadi Alattar, Aderemi Soyambo, Mahesh Bikkina, Fayez ShamoonNo Product/Research Disclosure InformationSt. Joseph's Regional Medical Center, Pateron, NJ.

SESSION TYPE: Cardiovascular Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

We describe a case of an asymptomatic young female who presents with hemiplegic stroke with successful thrombolysis and left atrial myxoma resection.

CASE PRESENTATION:

A 49-year-old female presents to the emergency department with new onset left sided weakness, slurred speech, and left facial droop. She denied any constitutional symptoms. She was hemodynamically stable. Neurological examination revealed left hemiplegic weakness. Her examination was otherwise benign. Her EKG and laboratory tests were unremarkable. CT scan of the brain was normal. Tissue plasminosgen activator (t-PA) was administered and the patient was admitted to the intensive care unit. MRI of the brain showed an acute infarction involving the right frontal, temporal lobe, and basal ganglia. Transesophageal echocardiogram showed a large mobile mass in the left atrium measuring 4.5 cm x 3.8 cm, fixed to the atrial septum by a stalk located superior to the mitral annulus (Fig.1). Surgical resection was performed (Fig.2), revealing a mass with a smooth grey, brown surface suggestive of atrial myxoma. Histopathology was confirmatory showing characteristic polygonal and stellar tumor cells.

DISCUSSION:

Atrial myxoma is the most common benign tumor of the heart and has a greater predilection to the left atrium.1 Embolic phenomena is thought to be caused by either tumor detachment or clot embolization.1 Patients can present with dyspnea on exertion, palpitations, or congestive heart failure. Autoimmune features include: constitutional symptoms, fatigue, fever, myalgia, arthalgia, muscle weakness, rash, and weight loss. Activation of pro-inflammatory cytokines such as: IL-6 and Tumor Necrosis Factor alpha (TNFa) have been implicated.2 Often thrombolysis is given to patients presenting with stroke prior to diagnosing atrial myxoma. Although, randomized clinical data is lacking, managing this challenging scenario has resulted in variable results including: clinical improvement, persistent neurological deficits, or death.3

CONCLUSIONS:

This case describes an uncommon presentation of stroke in a young patient with left atrial myxoma. Her course resulted in successful clinical outcomes following thrombolysis and surgical resection. Echocardiography should be considered when entertaining sources of thrombo-emboli presenting with stroke.1) Reynen, K. (1995). "Cardiac myxomas." N Engl J Med 333(24): 1610-1617.2) Mendoza, C. E., M. F. Rosado, et al. (2001). "The role of interleukin-6 in cases of cardiac myxoma. Clinical features, immunologic abnormalities, and a possible role in recurrence." Tex Heart Inst J 28(1): 3-7.3) Nagy, C. D., M. Levy, et al. (2009). "Safe and effective intravenous thrombolysis for acute ischemic stroke caused by left atrial myxoma." J Stroke Cerebrovasc Dis 18(5): 398-402.DISCLOSURE: The following authors have nothing to disclose: Fahad Alsindi, Vijay Duggirala, Andrew VillanuevaNo Product/Research Disclosure InformationLahey Clinic, Burlington, MA.

SESSION TYPE: Cancer Student/Resident Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Spontaneous pneumothorax can be caused by lung tissue weakness - rupture of thin cysts called blebs on lung surface. Chest pain, dyspnea and occasionally palpitations are classical symptoms of pneumothorax but it can also present silently.

CASE PRESENTATION:

A 58 year old Caucasian male working as a chemical engineer presented with palpitations and rapid heart rate of 190 per minute which was resolved with valsalva maneuver in ER. He did not have any chest pain or dyspnea. Chest X ray followed by CT scan of the chest showed large left pneumothorax. Patient had previous small 15% pneumothorax before 1 year discovered incidentally during coronary calcium scoring imaging study. At that time, patient was asymptomatic and pneumothorax got resolved without any interventions. He had no problems in the interim. After one year, patient again presented with left sided hydropneumothorax. Patient underwent thoracoscopy which eventually converted into small thoracotomy with lysis of adhesions, stapling of apical bleb and resection of lingular bleb and associated calcified nodule and talc Pleurodesis. Pathology report did not show any malignant cells. He underwent thoracentesis multiple times for recurrent left sided pleural effusion but still the cause for his recurrent pneumothorax, hydropneumothorax and pleural effusions was a mystery. Fluid cytology was negative for any malignancy. Bronchoscopy also did not show any abnormalities. Eventually, patient underwent decortication procedure due to recurrent pleural effusion, and to our surprise, cytology results showed malignant mesothelioma with epitheloid variant

DISCUSSION:

Malignant pleural mesothelioma is a neoplasm with most common clinical presentation being nonpleuritic chest pain and dyspnea. Common radiological findings include unilateral pleural effusion. Our patient presented with pneumothorax which is a rare presentations to begin with. He also had recurrent pneumothorax and hydropneumothorax. The pleural mesothelioma is accounted for 11 % spontaneous pneumothorax. The patient in the case, never had any known asbestos exposure. The incidence of atypical presentation of malignant mesothelioma is increasing in recent years but the overall rate of malignant mesothelioma is slowly decreasing since 1990s. Histopathological investigation should always be considered in recurrent pneumothorax.

CONCLUSIONS:

Awareness of malignant pleural mesothelioma presenting as a recurrent spontaneous pneumothorax or hydropneumothorax would increase the rate of early diagnosis and treatment.1) Sheard JD, Taylor W, Soorae A, Pearson MG. Pneumothorax and malignant mesothelioma in patients over the age of 40. Thorax. 1991;46:584DISCLOSURE: The following authors have nothing to disclose: Mihir Patel, Hetvi Joshi, Jayantilal MehtaNo Product/Research Disclosure InformationEast Tennessee State University, Johnson City, TN.

SESSION TYPE: ILD Student/Resident Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Pulmonary Alveolar Microlithiasis (PAM) is a rare disease characterized by microliths throughout the alveolar space, which are composed of calcium phosphate.

CASE PRESENTATION:

A 29-year-old Honduras male presented with complaints of severe dyspnea, burning pleuritic chest pain (7/10), and palpitations that began the previous morning. These symptoms were intermittent and worsened over 24 hours. His chest pain resolved shortly after presentation to the hospital. He denied sputum production, fever, cough, and chills; and he had no other accompanying symptoms. The patient was generally healthy and had no significant past medical history or family history. The patient did not have any allergies and did not take any medications. He immigrated to the United States from Honduras at the age of 25 and worked as a painter. The patient was in no acute distress. Vital signs: Temperature 99.7 Deg.F, heart rate 110bpm, blood pressure 128/96mmhg, respiratory rate 15/min, oxygen saturation 96% on room air. Physical exam was only significant for bilateral crackles on lung auscultation. The remainder of the physical exam was markedly normal. Laboratory data was significant for normal-high hemoglobin and hematocrit, 15.9 gm/dl and 45.4%, respectively. Chest x-ray showed so-called "Sand Storm Appearance." Chest CT scan demonstrated pleural densities suggesting calcification and scattered interstitial prominence (Fig. 1). Pulmonary function tests demonstrated restrictive ventilatory defects. The patient subsequently underwent video assisted thoracic surgery with biopsy. The pathologic diagnosis was PAM (Fig. 2).

DISCUSSION:

PAM is a rare disease, which can be either sporadic or inherited. Puhr first described it in 1933 with over 500 cases reported worldwide to date (3). Typical presentations are similar to the above findings of "sandstorm" lungs and diffuse reticulonodular appearance (1). Most patients are asymptomatic despite striking radiographic findings with symptoms beginning around the third/fourth decades of life. Recent reports describe the role of mutation in Type IIB Sodium-Phosphate co-transporter gene (SCL34A2) in disease pathogenesis (2). Usually no treatment is required for the asymptomatic patients but in advanced cases lung transplantation and disodium etidronate have been tried with varied results.

CONCLUSIONS:

PAM is a rare disease with characteristic radiographic picture that needs to be considered in differential diagnosis of interstitial lung disease.1) Fuhrman, Carl R., Siddiqui, Nasir, A. Pulmonary Alveolar Microlithiasis. RadioGraphics 2011. 31:585-590.2) Huquin, Izumi S., et. al. Mutations in the SLC34A2 gene are associated with pulmonary alveolar microlithiasis. Amer. Journal Resp. Crit. Care Medicine. 2007 Feb 1;175(3):263-8.3) Puhr L. Microlithiasis alveolaris pulmonum. Virchows Arch Pathol Anat Physiol Klin Med 1933;290:156-160.DISCLOSURE: The following authors have nothing to disclose: Brent Acker, Igor AksenovNo Product/Research Disclosure InformationMemorial University Medical Center, Savannah, GA.

SESSION TYPE: Arrhythmias PostersPRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE:

The stroke risk factors (RF), congestive heart failure(CHF), advanced age, hypertension(BP), diabetes(DM) and coronary artery disease(CAD) are also the RF for atrial fibrillation/flutter (AF). The incidence of stroke in AF pts is well known and is related to the presence of the stroke RF. Pts with AF without these RF rarely have strokes and are usually not anticoagulated. The incidence of AF in stroke pts is unclear because AF is often transient, episodic, asymptomatic, not present on the pts stroke admission and is frequently not diagnosed. It is likely that AF is caused by the RF and is a common mechanism whereby these RF cause stroke.

METHODS:

To determine the incidence of AF in ischemic stroke pts and to relate the stroke RF to AF we reviewed the clinical records, all the 12 lead ECGs in a 13 year institutional data base and the 2D echocardiograms of 985 consecutive pts with a diagnosis of ischemic stroke over 3 years.

RESULTS:

AF was found in 31.3% (95% CL 28.5, 34.2) of the ischemic stroke pts. In the 784 pts with BP, 33.7% had AF; higher than the 21.9 % in the pts without BP*. Of the 168 pts with CHF 61.9% had AF, more than the 25.0 % in those without CHF**. Of 527 pts >/= 75 years old, 45.2% had AF, more than the 15.3% in those < 75**. CAD was present in 240 pts ; 33.4% had AF vs 27.5%**. DM pts had 32.8 % AF*. Pts with LA enlargement had a higher incidence of AF than those without LAE, 47.3% vs 11.7%**; as did pts with EF<50%, 49.0% vs 28.3%**. *P<.01 **P<.0001

CONCLUSIONS:

Although the extensive ECG data base made it less likely that we would miss AF, recording of ECGs was random, related to ER, clinic visits and hospital admissions. Diagnosis of AF from the data base was frequently fortuitous and serendipitous. Even so, with probably many episodes of AF missed, we found a higher incidence of AF in stroke pts than previously reported. We also found that stroke pts with the risk factors had significantly more AF than those without the RF suggesting that these RF may cause the AF and that AF is frequently the mechanism whereby these risk factors cause stroke.

CLINICAL IMPLICATIONS:

These findings 1) support that any stroke pts with these risk factors who are not diagnosed with AF should be meticulously studied for AF so anticoagulation can be administered to prevent a subsequent stroke, and 2) any pt with these risk factors who complains of palpitations should be investigated to diagnose AF so anticoagulation can be considered to prevent a first stroke.DISCLOSURE: The following authors have nothing to disclose: Jacob Haft, Louis TeichholzNo Product/Research Disclosure Information.

SESSION TYPE: Cardiovascular Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

The World Health Organization divides pulmonary hypertension (PH) into five groups [1]. This case describes a unique presentation of Group V PH resulting from lymphomatous compression of the pulmonary arteries.

CASE PRESENTATION:

A 38 year-old African American male with a history of HIV (CD4 count 516, undetectable viral load) and stage three Hodgkin's Lymphoma (HL) presented with complaints of dyspnea and palpitations. On exam he had jugulovenous distension and was hypotensive; TTE revealed cardiac tamponade. Emergent pericardiocentesis resulted in drainage of 1.5L of serosanguinous fluid from his pericardial sac. However, he continued to complain of dyspnea and post-procedural TTE still suggested elevated right-sided pressures and a possible mediastinal mass. A TEE revealed compression of both main branches of the pulmonary arteries after the bifurcation (Images 1A and 1B). CT chest confirmed extensive mediastinal lymphadenopathy resulting in mass effect on both pulmonary arteries (Image 2A). Emergent chemotherapy was initiated with ifosfamide, carboplatin and etoposide (ICE) and one month later, he was asymptomatic with complete resolution of the lymphadenopathy on follow-up CT (Image 2B).

DISCUSSION:

There are several case reports in the literature of right ventricular outflow tract obstruction by mediastinal lymphadenopathy (usually non-HL) resulting in elevated right-sided pressures [2]. However, compression of the pulmonary arteries after their bifurcation with HL is a novel etiology. Although literature on this topic is limited, short term outcomes appear to be good with chemotherapy if the initial hemodynamic insult is tolerated.

CONCLUSIONS:

Although the causes of dyspnea in a patient with lymphoma are myriad, pulmonary hypertension must be recognized and appropriately investigated so that outcomes may be optimized.1) McLaughlin VV et al. American College of Cardiology Foundation Task Force on Expert Consensus Documents. American Heart Association. American College of Chest Physicians. American Thoracic Society, Inc. Pulmonary Hypertension Association ACCF/AHA 2009 expert consensus document on pulmonary hypertension a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association developed in collaboration with the American College of Chest Physicians; American Thoracic Society, Inc.; and the Pulmonary Hypertension Association. J Am Coll Cardiol 2009. Apr;53(17):1575-78. doi: 10.1016/j.jacc.2009.01.004.2) Russell, JC and Lowry, KG. Presentation of non-Hodgkin's Lymphoma as acute hypoxia caused by right ventricular compression. Anesth Analg 2003;96:1768 -71.DISCLOSURE: The following authors have nothing to disclose: Sandeep Krishnan, Bashar Staitieh, A. Maziar Zafari, Gautam KumarNo Product/Research Disclosure InformationEmory University, Atlanta, GA.

SESSION TYPE: Critical Care Global Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Centipedes are multisegmeted arthropods with a single pair of legs per segment and one pair of antennae .Centipede stings occur in the warmer climates throughout the world. The species of medical importance is Scolopendra Sp which has been described as the longest and the most aggressive tropical centipede. Centipede stings often occur as the victim is putting on clothes or while in bed.

CASE PRESENTATION:

A 19 yr old female arrived in our tertiary care emergency room at 5:30am after being treated at a local hospital for an unknown insect bite on her right arm 6 hrs prior while asleep.She had complaints of vomiting,dyspnea and local pain.She received antihistamines,steroids,epinephrine and analgesics for anaphylactic shock and pain prior to arrival.Her presenting vitals were a heart rate of 145 beats per minute, BP 60/40 mmHg ,respiratory rate of 35/min and oxygen saturation of 85% on room air. She had bilateral crackles and her hemoglobin,WBC count,electrolytes and PT,INR were normal. EKG revealed ST depression in V3,V4,V5,V6 leads (>2mm).Chest radiograph showed pulmonary edema and echocardiogram showed global hypokinesia of the left ventricle with EF of 40%,while troponin-t(2.98)was slightly elevated . Treatment was initiated with digoxin,carnitine and dobutamine infusion to support her cardiac output and furosemide was given for pulmonary edema along with non-invasive ventilation.She improved with therapy and a repeat echocardiogram two days later showed EF of 62% with normal LV function.Subsequent history and bystander observation confirmed the visual appearance of the insect to be a centipede.

DISCUSSION:

Gomes et al (1)used animal models to demonstrate significant cardiovascular effects of Scolopendra venom, mediated by histamine and a cardiodepressant factor designated as Toxin-S. Most authorities recognize the cardiodepressant Toxin-S to be the lethal factor (predatory), and the histamine/serotonin components to be pain mediators (defensive)(2). Systemic symptoms due to centipede bite may include anxiety, fever, dizziness, palpitations, and nausea. Extensive myonecrosis with subsequent compartment syndrome, rhabdomyolysis, and acute renal failure has been seen after a centipede bite.Japanese Scolopendra species have been reported to cause psychological disturbances and Korsakoff syndrome. A recent study suggests possible myocardial ischemia after a nonfatal centipede sting as a mechanism that could lead to death(3)

CONCLUSIONS:

There have been only a few cases of centipede envenomation causing myocardial ischaemia reported. Our case was notable due to the acute presentation of pulmonary edema with cardiac injury with raised cardiac enzyme levels. This complication should be considered when treating such patients, and appropriate diagnostic studies should be obtained.1) Gomes A, Datta A, Sarangi B, Kar PK, Lahiri SC. Occurrence of histamine and histamine release by centipede venom. Indian J Med Res. 1982;76:888.2) Stankiewicz M, Hamon A, Benkhalifa R, et al. Effects of a centipede venom fraction on insect nervous system, a native Xenopus oocyte receptor and on an expressed Drosophila muscarinic receptor. Toxicon.1999;37:1431-1445.3) Ozsarac M, Karcioglu O, Ayrik C, Somuncu F, Gumrukcu S. Acute coronary ischemia following centipede envenomation: Case report and review of the literature. Wilderness Environ Med. 2004;15:109-12DISCLOSURE: The following authors have nothing to disclose: Munta Kartik, Sai Praveen Haranath, Rahul Amte, Palepu GopalNo Product/Research Disclosure InformationApollo Hospitals, Department of Critical Care Medicine, Jubilee Hills, Hyderabad, India.