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Chest pain [keywords]
- Impact of copeptin on diagnosis, risk stratification, and intermediate-term prognosis of acute coronary syndromes. [JOURNAL ARTICLE]
- Clin Res Cardiol 2013 May 23.
BACKGROUND:The aim of the current study was to evaluate the diagnostic and intermediate-term prognostic impact of C-terminal portion of provasopressin (copeptin) in combination with troponin I.
METHODS:In this prospective single-center study we recruited a total of 230 unselected patients with suspected recent acute coronary syndrome (ACS) presenting consecutively at our chest pain unit. Troponin I and copeptin levels were determined at presentation and after 3-6 h. Follow-up was performed after 180 days.
RESULTS:Acute myocardial infarction (AMI) was the final diagnosis in 107 patients (STEMI: 24, NSTEMI: 83). The median copeptin level was significantly higher in patients having AMI than in those without (20.83 vs. 12.2 pmol/L, p < 0.0001). A troponin I level <0.04 ng/mL in combination with copeptin <14 pmol/L at admission ruled out AMI with an negative predictive value (NPV) of 97.3 %. p = 0.0045 for the added value of copeptin to troponin I. Kaplan-Meier analysis showed that copeptin levels above the diagnostic cut-off were associated with an elevated intermediate-term (180 days) mortality (p = 0.019), while no patient with copeptin values below the cut-off died. Univariate Cox regression analysis identified copeptin as strong predictor of intermediate-term mortality (HR 4.28, 95 % CI 1.58-11.6, p = 0.004). The predictive performance for prediction of 180-day mortality was significantly better if copeptin was included (C-index of 0.80) compared with that of troponin alone (C-index 0.78, p = 0.01 for the added value of copeptin to troponin I).
CONCLUSIONS:Additional assessment of copeptin allows a rapid and reliable exclusion of AMI and improves diagnostic accuracy in myocardial ischemia. This study showed for the first time that copeptin provides valuable predictive information for risk stratification and intermediate-term outcome in ACS patients.
- Histoplasma and Pneumocystis Coinfection in an HIV-Negative Patient. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):247A.
SESSION TYPE: Infectious Disease Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Disseminated histoplasmosis can rarely be found in patients without known underlying immunodeficiency.
CASE PRESENTATION:58 year-old woman presented for evaluation of progressive dyspnea with non-productive cough and generalized weakness for eight months. She also reported intermittent fever, pleuritic chest pain, dysphagia, and easy bruisability. Her past medical history was unremarkable. She was not taking immunosuppressive medications. She did not have sick contacts nor did she have outdoor activities such as camping or travelled recently. At presentation, she was febrile, tachycardic, tachypneic, and hypotensive. She had diffuse crackles on lung auscultation. Initial laboratory tests showed hemoglobin of 9.1 g/dL, platelet count of 82 x 10^9/L, and WBC count of 3.9 x10^9 /L with 4% lymphocytes and CD4 count of 78. High resolution chest CT revealed bilateral nodular and ground-glass peribronchiolar infiltrates, cavitary lesion in left upper lobe, hilar and mediastinal adenopathy. She was admitted and empiric antibacterial therapy was initiated. Viral serology for HIV, EBV, and Influenza, RSV and Parvovirus PCR, urine Legionella antigens, Mycobacterium TB QuantiFERON were negative. Fungal serology was positive for histoplasma. The patient's hypoxic respiratory failure worsened and required intubation. Bronchoscopy with bronchoalveolar lavage was negative for malignancy, but positive for both Histoplasma and Pneumocystis by PCR. Blood cultures grew Histoplasma capsulatum. Urine histoplasma antigen was detected at high levels. Bone marrow biopsy was performed and extensive involvement by histoplasma was determined to be the cause of her pancytopenia. Antimicrobial therapy was changed to amphotericin B and sulfamethoxazole/trimethoprim along with methylprednisolone for treatment of disseminated histoplasmosis and Pneumocystis pneumonia. She improved significantly shortly after initiation of appropriate treatment. She tolerated extubation and ultimately was discharged from the hospital in good condition.
DISCUSSION:The presented patient did not have history of immunosuppression. She underwent extensive negative evaluation by immunologists for underlying immunosuppressive disorders such as cellular or humoral immunodeficiencies. Nevertheless, she developed severe disseminated histoplasmosis with bone-marrow involvement. This caused pancytopenia with a low CD4 count which ultimately predisposed her to pneumocystis infection. This case is an example of disseminated histoplasmosis with subsequent co-infections in apparently immunocompetent host.
CONCLUSIONS:Histoplasmosis should be in the differential diagnosis when a patient presents with pulmonary infiltrates, adenopathy, cytopenia, even when he/she is not from the Mississippi and Ohio River valleys.1) Disseminated histoplasmosis: clinical and pathologic correlations. Goodwin RA Jr, Shapiro JL, Thurman GH, Thurman SS, Des Prez RM. Medicine (Baltimore). 1980;59(1):1DISCLOSURE: The following authors have nothing to disclose: Benyam Addissie, Joseph SkalskiNo Product/Research Disclosure InformationMayo Clinic, Rochester, MN.
- Diffuse Lung Disease and Neurofibromatosis-1-Recurrent Association, Uncertain Relationship. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):1038A.
SESSION TYPE: Miscellaneous Cases IIIPRESENTED ON: Wednesday, October 24, 2012 at 11:15 AM - 12:30 PM
INTRODUCTION:Neurofibromatosis-1 (NF-1) is an autosomal-dominant neurocutaneous disorder with major clinical manifestations involving the nervous system, skin and bones (1). Since the early 1960s, there have been multiple reports noting coexistence of diffuse lung disease and NF-1 (2). Currently, no consensus exists regarding the clinical entity neurofibromatosis with diffuse lung disease (NF-DLD).
CASE PRESENTATION:A 31-year-old black male with NF-1 was admitted to the hospital with complaints of worsening cough, pleuritic chest pain and shortness of breath. No fever, chills, weight loss, hemoptysis, night sweats, joint pains, or previous environmental/occupational exposures were reported. He developed shortness of breath and cough at age 25 being diagnosed with chronic obstructive pulmonary disease with no further workup performed; frequent exacerbations requiring hospitalization have plagued him since. He began smoking at age 17, approximately half pack per day with no drug or alcohol use. On examination, chest had symmetric expansion with quiet but clear sounds bilaterally. Plain chest x-ray showed hyperinflation and upper lobe bullae bilaterally; comparison from 2007 showed bullae and hyperinflation with slight progression on new imaging. CT chest revealed giant upper lobe bullae and paraseptal-predominant emphysema diffusely; no interstitial disease was noted. Pulmonary function testing revealed normal vital capacity with moderately-severe obstructive defect. Laboratory workup was negative for HIV with normal alpha-1 antitrypsin level. The patient was treated with antibiotics and short-acting bronchodilators, discharged home with instruction for smoking cessation with follow-up in pulmonary clinic.
DISCUSSION:This patient developed impressive lung disease at age 25 with a 5 pack-year smoking history. Of note, his clinical history and CT chest are consistent with giant bullous emphysema (vanishing lung syndrome), an association not reported previously with NF-1. The question arises whether NF-1 contributed or predisposed our patient to developing lung disease. Two large patient series have looked at the relationship of NF-1 and diffuse lung disease with differing conclusions made with regards to the existence of NF-DLD (2,3).
CONCLUSIONS:We propose that NF-1 predisposes to the development of bullous emphysema beyond the effect of smoking alone. Future investigation is required searching for mechanisms by which smoking and environmental exposures contribute to early and accelerated development of bullous emphysema. The possible association of smoking with bullous emphysema should be included in counseling and treatment of patients with NF-1 and nicotine dependence.1) Ferner, Rosalie. Lancet Neurol 2007; 6:340-512) Zamora et al. Eur Respir J 2007; 29:210-2143) Ryu et al. Chest 2005; 128:2381-2386DISCLOSURE: The following authors have nothing to disclose: Timothy Nokes, Ahmed AwabNo Product/Research Disclosure InformationUniversity of Oklahoma Health Science Center, Oklahoma City, OK.
- Examination of Stat Response Team Data Investigating Mortality, Increased Level of Care, and Change in DNR Status at the University of Louisville Hospital. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):380A.
SESSION TYPE: ICU Safety and Quality PostersPRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM
PURPOSE:Recent studies have failed to show a mortality benefit after the institution of Stat Response Teams (SRTs). To our knowledge, no systematic review has examined if the reason for stat response was associated with specific outcomes (increased level of care, mortality, and change in Do Not Resuscitate (DNR) status). We propose that respiratory distress accounts for the majority of changes in these outcomes.
METHODS:A retrospective review of 177 SRT summaries from January 2010 to August 2011 was conducted. Reasons for activating SRT were grouped into eight categories: respiratory distress, systolic blood pressure less than 90, chest pain, dysrhythmia, acute bleeding, acute change in neurologic status, hypoglycemia, and other. Statistical analysis used Chi-Square or Fisher's Exact Test to identify which of the eight categories were associated with outcomes of requiring increased level of care, mortality, and change in DNR status. P-values of ≤0.05 were significant.
RESULTS:The data showed a statistically significant increased level of care (P = 0.0047), mortality (P = 0.0185), and change in DNR status (P = 0.0089) in the respiratory distress category. Also, increased level of care was seen in the dysrhythmia category (P = 0.0065). 46% of patients requiring increased level of care were in the respiratory distress category and 18% were in the dysrhythmia category. Respiratory distress accounted for 60% of mortality after stat response, and 61% of those that changed DNR status. One interesting finding was that those with increased level of care were actually less likely to have acute change in neurologic status (P = 0.0002), hypoglycemia (0.0080), or other category (P = 0.0185).
CONCLUSIONS:Respiratory distress was associated with a need for increased level of care, higher mortality, and change in DNR status. Also, there was a significant increased level of care in the dysrhythmia category.
CLINICAL IMPLICATIONS:SRT calls for respiratory distress or dysrhythmia should raise clinical concern. These patients are at higher risk for deterioration, should receive more vigilant care, and deserve earlier consideration for transfer to higher level of care. These findings suggest that stat responses for respiratory distress or dysrhythmia should be examined individually to see if these categories of stat responses result in a mortality difference.DISCLOSURE: The following authors have nothing to disclose: Michael Scott, Patton Thompson, Timothy Wiemken, Sajjad Jameel, Linda Hummel, Linda Goss, Rodrigo Cavallazzi, Mohamed SaadNo Product/Research Disclosure InformationUniversity of Louisville, Louisville, KY.
- Transpulmonary Chemoembolization (TPCE) for Leiomyosarcoma Lung Metastases Using Doxorubicin Soaked Drug-Eluting-Beads (DEB). [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):585A.
SESSION TYPE: Cancer Student/Resident Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Leiomyosarcoma is a rare malignancy which responds poorly to systemic chemotherapy and radiation. Dew, et al. demonstrated a 5 year survival rate of 31% after surgical resection of the primary tumor. We present a 48 yo patient with leiomyosarcoma metastases to the lung treated with transpulmonary chemoembolization (TPCE).
CASE PRESENTATION:A 48 year old man presented with lower extremity edema and was diagnosed with leiomyosarcoma of the IVC. After surgical resection of the primary tumor and systemic chemotherapy and radiation, the patient developed lung and liver metastasis not amenable to surgical resection. His liver metastases are well controlled with transarterial chemoembolization. His lung metastases continue to progress despite systemic chemotherapy. He has undergone two treatments of segmental TPCE using doxorubicin beads (image 1). He had minimal fatigue the week after the second procedure. He had no other systemic side effects such as nausea, vomitting, or mucositis. He has no worsening cough or chest pain related to embolization of the pulmonary artery. Image 2 demonsrates post-procedural appearance of his left lung. He will undergo further TPCE for continued treatment.
DISCUSSION:Leiomyosarcoma of the IVC is a rare malignancy with less than 300 cases reported. Our patient in this study has disease recurrence to the lungs and liver after primary surgical resection and systemic chemotherapy administration. Given the poor response of leiomyosarcoma to chemotherapy and radiation, alternate therapies were considered to treat his nonresectable pulmonary disease. Vogl, et al. performed a study from 2001-2005 demonstrating the use of TPCE for pulmonary metastatic disease in 52 patients. 27 of the 52 cases demonstrated partial response or stable disease and all patients had minimal side effects from the procedure. Our patient has undergone 2 treatments of TPCE for his pulmonary disease. The patient has experienced no significant side effects from the embolization or local chemotherapy administration; he has had no complications since his initial treatment approximately 45 days ago.
CONCLUSIONS:TPCE is a promising treatment option for patients with unresectable pulmonary metastatic disease. Our patient has had no significant complications or side effects after treatment. Although no conclusions can be drawn on one case, the lack of significant side effects after local doxorubicin administration suggests that further research is warranted using TPCE as a tolerable treatment for nonresectable pulmonary metastatic disease.1) J. Dew, K. Hansen, J. Hammon, T. McCoy, E. A. Levine, and P. Shen, "Leiomyosarcoma of the inferior vena cava: surgical management and clinical results," American Surgeon, vol. 71, no. 6, pp. 497-501, 2005.2) Vogl TJ, Lehnert T, Zangos S, Eichler K, Hammerstingl R, Korkusuz H, Lindemayr S. Transpulmonary chemoembolization (TPCE) as a treatment for unresectable lung metastases. Eur Radiol. 2008;18:2449-2455.DISCLOSURE: The following authors have nothing to disclose: Andrew West, Drew Sessions, Mollie MeekTranspulmonary Chemoembolization of pulmonary metastases is a procedure that has been rarely reported in literature. It is still likely considered a research procedure/technique. This will not discuss any products used.UAMS, Little Rock, AR.
- The Use of Endobronchial Ultrasound in the Diagnosis of Subacute Pulmonary Histoplasmosis. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):222A.
SESSION TYPE: Respiratory Infections Posters IIPRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM
PURPOSE:Physicians often rely on multiple tests to establish a diagnosis of pulmonary histoplasmosis. Subacute pulmonary histoplasmosis (SPH) is characterized by infection with Histoplasma casulatum and the presence of symptoms for > 1 month with a localized pulmonary opacity and/or hilar and mediastinal adenopathy. SPH is particularly challenging to diagnose, as it often affects immunocompetent individuals in whom identification of the organism and antigen detection are often negative. Endobronchial ultrasound (EBUS) with transbronchial needle aspiration (TBNA) is a useful tool in the investigation of hilar and mediastinal adenopathy but it is not known if EBUS-TBNA provides useful information that can aid in the diagnosis of SPH. We hypothesized that EBUS would provide additional confirmatory information for diagnosis in individuals suspected of SPH.
METHODS:We retrospectively reviewed patients with mediastinal and/or hilar adenopathy referred to our institution for EBUS who were believed to be suffering from SPH. We collected information on symptoms, physical exam findings, EBUS findings, cultures, pathology, serology and antigen detection.
RESULTS:Six patients were reviewed. All had symptoms (fever, sweats, chest pain, cough) for > 1 month. One patient had hilar adenopathy alone, 5 had had mediastinal and hilar adenopathy. Pathology examination of the nodal material revealed granulomatous inflammation in 5 and necrosis in 1. None of the material demonstrated fungal organisms. All patients had positive serology. One patient had antigenuria and one had antigenemia. Culture material was negative in all patients.
CONCLUSIONS:EBUS-TBNA provided findings that are consistent with SPH but not confirmatory in this small case series. SPH was always associated with positive serology, but infrequently associated with antigen detection. Histoplasmosis was not detected by pathology or culture in any patient.
CLINICAL IMPLICATIONS:EBUS-TBNA does not confirm a diagnosis of SPH but can provide information that is consistent with the diagnosis. EBUS-TBNA may be useful in eliminating other causes of hilar and mediastinal adenopathy.DISCLOSURE: The following authors have nothing to disclose: J. Ferguson, Katarine Egressy, Mohammed MohammedNo Product/Research Disclosure InformationUniversity of Wisconsin, Madison, WI.
- History and Physical Exam and Simple Math Go a Long Way in Developing a Diagnostic Differential: A Case of Methanol Poisoning. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):361A.
SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Patients who present to the ER with altered mental status due to toxic ingestion or attempted suicide are difficult to treat because of unknown social and clinical factors. We present a case of methanol ingestion that highlights the importance of obtaining a good history and physical exam.
CASE PRESENTATION:A 46-year-old male was brought to the ER with complaints of altered mental status, abdominal pain, and alcohol intoxication. The family reported that the patient had a history of alcohol dependence but had been sober for 2 years. However, recently, he developed severe depression and had been consuming large quantities of alcohol. The family also admitted he had possibly consumed household substances for their alcohol content. On examination, the patient was in moderate distress and had altered mental status. Except for severe right upper quadrant tenderness, the physical exam was unremarkable. Laboratory results showed WBC 10,200/dL. Electrolytes were sodium 139, potassium 4, chloride 110, bicarbonate 16, creatinine 1.4, total bilirubin 0.4, aspartate transaminase 64, alanine transaminase 56. Serum osmolality was 381. Ethanol level was less than 10 mg/dL. His calculated anion gap was 13, ABG pH 7.27, and calculated serum osmolality was 295, indicating anion gap metabolic acidosis with an increased osmolar gap of 86. As a precaution, the patient was started on intravenous fomepizole. At that time, additional questions were asked of the patient which resulted in admission of ingestion of a household product, but the specifics were not known. Methanol and ethylene glycol levels were ordered. Isopropyl alcohol, ethylene glycol, salicylate and acetaminophen levels were found to be within normal limits. The patient's methanol and acetone levels were 154 mg/dL and 80mg/dL, respectively. As a result, emergent hemodialysis was initiated and within 24 hours, methanol levels were less than 10mg/dL.
DISCUSSION:Methanol poisoning is one of the most common types of alcohol related toxicities and can mimic ethanol intoxication because it causes central nervous depression. In 2010, there were 719 possible methanol exposures (excluding automotive products and cleaning agents) and 12 deaths.
CONCLUSIONS:A detailed history, recognition of abnormal lab parameters, application of simple calculations can narrow down the differential diagnosis in cases of possible overdose or suicide attempt. In this case, initial clinical exam and history increased suspicion of toxic ingestion. Appropriate lab tests were ordered based on the possible substances and timely identification and intervention with fomepizole and emergent dialysis played a significant role in preventing complications related to methanol toxicity including permanent loss of vision, multi-system organ failure, and subsequent death.1) AAPCC (American Association of poison control centers) 2010 Annual Report of the NPDS (National Poison Data System)DISCLOSURE: The following authors have nothing to disclose: Jason Lambrecht, Madhu Kalyan Pendurthi, Vijaya Gogineni, Thomas Rayl, Anna MaioNo Product/Research Disclosure InformationCreighton University Medical Center, Omaha, NE.
- Acinetobacter baumanii De Novo Soft Tissue Infection Causing Higher Cervical Spinal Cord Compression - A Case Report. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):352A.
SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Acinetobacter baumannii is generally considered an opportunistic nosocomial pathogen and is rarely encountered as a pathogen causing community-acquired soft tissue infection.
CASE PRESENTATION:A 54 year old female presented with bilateral hand pain followed by all four extremity weakness and urinary incontinence over a period of two months. She has h/o well controlled hypertension, diabetes mellitus type 2 and arthritis. No h/o previous surgery. She denied smoking, alcohol drinking and illicit drug use. Here vitals were stable and neuro examination showed loss of touch sensations on right side of the face and body, right flaccid hemiplegia and left spastic hemiplegia. There was lymphadenopathy. Her routine blood workup was with in normal limits with negative HIV testing. PPD was positive, AFB sputum smear time three came back negative and chest Xray was negative. There was an extradural circumferential mass causing compression at the level of C1, C2 and C3 on contrast enhanced MRI of the cervical spinal cord. CT guided core biopsy of the mass was done. Gram staining showed rare WBC and gram negative rods, AFB smear was negative while culture grew abundant gram negative rods- Acinetobacter baumanii. After treatment with antibiotics clinically patient improved.
DISCUSSION:Acinetobacter baumannii is an aerobic gram-negative coccobacillary rod with a natural reservoir in soil and water sources around the world. It is generally considered an opportunistic nosocomial pathogen , affecting especially patients receiving treatment in the intensive care unit setting and immunocompromised patients. This is the first reported case of community-acquired A. baumannii denovo soft tissue infection causing higher cervical spinal cord compression resulting in quadriplegia. The evidence is now mounting that A. baumannii can no longer be exclusively considered a nosocomial pathogen, and is capable of causing profound clinical disease in the absence of traditional nosocomial risk factors.
CONCLUSIONS:We described a patient who is from community, non smoker, and non alcoholic, had well controlled DM -2 and had no h/o trauma/surgery. The case raises concerns that this highly adaptable organism may soon evolve into a significant community pathogen, too.1) Glew, R. H., Jr., R. C. Moellering, and L. J. Kunz. 1977. Infection with Acinetobacter calcoaceticus (Herellea vaginicola): clinical and laboratory studies. Medicine 56:79-95.2) Jimenez, P., A. Torres, R. Rodriguez-Roisin, J. P. de la Bellacasa, R. Aznar, J. M. Gatell, and A. Agusti-Vidal. 1989. Incidence and etiology of pneumonia acquired during mechanical ventilation. Crit. Care Med. 17:882-885.DISCLOSURE: The following authors have nothing to disclose: Qammar Abbas, Hafiz Imran, Ameer RasheedNo Product/Research Disclosure InformationTBHC New York, Brooklyn, NY.
- Respiratory Failure With Diaphragmatic Palsy: A Rare Complication of Relapsing Polychondritis. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):992A.
SESSION TYPE: Miscellaneous Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Relapsing Polychondritis (RP) is a unique and rare autoimmune disorder in which the cartilaginous tissues are the primary targets of destruction. Though reported, involvement of non cartilaginous structures and neurological complications are rare. Although, neurological manifestations with cranial nerve palsies have been reported, we are aware of no previously reported case of phrenic nerve palsy in RP. We present a case of RP manifested as respiratory failure with diaphragmatic/ phrenic nerve palsy.
CASE PRESENTATION:65 yr old relatively healthy African American male was admitted with 3 weeks history of ear pain, hoarseness of voice and dry cough. On admission, he was noted to be in hypercapnic respiratory failure with blood gas : pH :7.28, pCo2:64 and pO2:84 on 2 lit of oxygen. Other laboratory data was significant for leucocytosis (WBC: 30,000 ) and anemia (Hb:9 gm/dl). Head and neck examination showed swollen right ear (Fig 1) with erythema, tenderness and flattening of the nasal septum. Respiratory examination revealed diminished breath sounds at the left base. CXR showed left diaphragm elevation. A bronchoscopy was performed showing vocal cord dysfunction with failure to abduct on inspiration and tracheobronchial inflammation (Fig 2). Inflammatory markers were elevated with ESR:130 and CRP:237. Vasculitic screening including ANCA, ANA was negative. Based on the clinical and bronchoscopic findings, suspicion of RP was high which was later confirmed on ear lobe biopsy (Fig 3, 4). He was started on steroids and azathioprine with clinical improvement. A sniff test was performed which confirmed the unilateral diaphragm palsy.
DISCUSSION:Diagnostic criteria that distill the most common clinical features of relapsing polychondritis were put forth in 1976 by McAdam et al. 1, but have since been modified. Reported neurologic manifestations in RPC include cranial neuropathies of the second, sixth, seventh, and eighth nerves, hemiplegia, seizures, myelitis, peripheral neuropathy, rhombic encephalitis, or limbic encephalitis. These symptoms are presumed to be due to (local) vasculitis2. Phrenic nerve involvement with diaphragmatic palsy is a rare manifestation and we hypothesize that the underlying mechanism is probably a vasculitic phenomenon.
CONCLUSIONS:In the absence of other etiologies of phrenic nerve palsy in our patient, underlying RP is the probable causative factor.1) McAdam LP, O'Hanlan MA, Bluestone R, et al.: Relapsing polychondritis: prospective study of 23 patients and a review of the literature. Medicine (Baltimore) 19762) Sundaram MB, Rajput AH (1983) Nervous system complications of relapsing polychondritis. NeurologyDISCLOSURE: The following authors have nothing to disclose: Sridhar Badireddi, Mohammad SiddiquiNo Product/Research Disclosure Information, Little Rock, AR.
- Left Atrial Compression Secondary to a Thymoma Mimicking a Ventricular Aneurysm: A Case Report. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):1008A.
SESSION TYPE: Miscellaneous Student/Resident Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM