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- Pulmonary Hyalinizing Granuloma in a Veteran With Latent Tuberculosis and Agent Orange Exposure. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):409A.
ILD Student/Resident Case Report PostersSESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Pulmonary Hyalinizing Granuloma (PHG) is a rare fibronodular process associated with autoimmune, infectious and neoplastic disease. An association between PHG and exposure to Agent Orange (AO), a dioxin-containing compound, has not previously been described. We report a case of PHG in a patient with latent tuberculosis infection (LTBI) and AO exposure.CASE PRESENTATION: A 57 year-old male with a five-year history of a productive cough with brown/black sputum and an unintentional 5.4-kg weight loss over one month was found to have a new right upper lobe soft tissue density on chest radiograph. He did not endorse fever, night sweats, or hemoptysis. He was an active thirty-nine pack-year smoker and reported exposure to AO during his military service. Computerized tomography revealed a non-calcified 3.3 cm lobulated soft tissue mass in the apical segment of the right upper lobe with numerous satellite lesions. Positron emission tomography showed isolated mild 18F-fluorodeoxyglucose avidity. Pulmonary function tests were normal. Endemic fungal serologies and sputum cultures were negative. QuantiFERON-TB Gold assay was positive. Airway was normal on flexible fiberoptic bronchoscopy. Cultures and stains from bronchoalveolar lavage were negative for pathogens. A CT-guided core biopsy of the apical mass was consistent with PHG. A course of isoniazid with pyridoxine was completed for LTBI. No specific therapy was initiated for PHG. His productive cough improved and his weight stabilized. At one year, imaging showed decreased size of the right upper lobe mass and there was complete interval resolution of his symptoms.DISCUSSION: Dioxin (DX) is a cell-cycle deregulator that promotes derangements in translation. Kuwatsuka et al and Peltier et al independently reported markedly increased concentrations of pro-inflammatory cytokines (e.g. IL-17, IL-23, IL-1β, TNF-α, PGE2, COX2) and decreased concentrations of the anti-inflammatory markers (IL-22 and IL-10) in DX-exposed patients and organisms. An exaggerated pro-inflammatory state, such as those seen in DX exposure, is the current understanding of PHG pathogenesis. Thus, exposure may increase the chance of developing PHG.CONCLUSIONS: Spontaneous resolution of PHG without PHG-specific treatment has been described in the literature. LTBI cannot be excluded as the etiology of PHG in this patient, as treatment yielded interval radiographic and clinical improvement. However, only minimal radiographic improvement was seen. Dioxin-containing compounds promote vigorous inflammatory responses that may promote PHG. This report is the first to associate dioxin-containing compounds and PHG.Reference #1: Kuwatsuka Y, et al., "Yusho patients show increased serum IL-17, IL-23, IL-1B, and TNFa levels more than 40 years after accidental polychlorinated biphenyl poisoning.", J Imm. Oct 2013Reference #2: Peltier MR, et al., "2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) enhances placental inflammation." J Rep Imm. Jun;98(1-2):10-20. 2013DISCLOSURE: The following authors have nothing to disclose: Jonathan Dell Pena, Scott Oh, Jaime BetancourtNo Product/Research Disclosure Information.
- Case of Potential Treatment Gone Rogue. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):401A.
ILD Student/Resident Case Report PostersSESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Anti-tumor necrosis factor (Anti-TNF) medications are accepted therapeutic armamentarium for treating refractory sarcoidosis. 1 We describe a case of anti-TNF associated pulmonary sarcoidosis and review the potential etiopathogenesis of this association.Fifty four year old Caucasian male with psoriasis was referred by his dermatologist for evaluation of positive quantiferon gold test. Notably he was on adalimumab for his psoriasis over the preceding year. He reported a prior negative PPD about a year previously. He had no dyspnea, cough, chest pain or constitutional symptoms. His examination was unremarkable. Comprehensive metabolic panel and Complete blood count were normal. Chest radiography revealed left hilar adenopathy which was new compared to a study done on unrelated visit. CT scan revealed bilateral hilar and mediastinal adenoapthy with nodules in bronchovascular distribution. Bronchoscopic transbronchial biopsy revealed peribronchovascular non-caseating granuloma consistent with sarcoidosis. The samples were negative for Acid fast bacilli and cultures negative for mycobacteria and fungi. It was also negative for malignancy. The adalimumab was stopped and the lymphadenopahty regressed.Anti-TNF associated sarcoidosis has been documented. The chronology of adalimumab therapy, occurrence of adenopathy and resolution of the adenopathy with stopping this therapy support the diagnosis of antiTNF related sarcoidosis. This patient's course is within the median time of 11 months described by Daı¨en in the French series. 2 The exact mechanism of antiTNF induced granuloma formation is not well defined. Since TNF activity is central in the formation of granuloma, antiTNF would intuitively counteract formation of granuloma and promote its resolution. A possible explanation is that anti-TNF may modulate the cytokines to point of restoring Th1 response which is the primary mechanism for granuloma formation.3 An alternative theory is that soluble TNF receptors may allow sufficient TNF activity with these medications to support granuloma formation. Thirdly, anti-TNF may promote reactivation or infection of yet unidentified infectious pathogen responsible for causing sarcoidosis. Treatment is stopping the inciting anti-TNF agent.Clinicians should be aware of anti-TNF associate sarcoidosis. Reference #1: Pritchard C, Nadarajah K: Tumor necrosis factor alpha inhibitor treatment for sarcoidosis refractory to conventional treatments: a report of five patients. Ann Rheum Dis 2004; 63: 318-20. Reference #2: Daien CI et al. Sarcoid-like granulomatosis in patients treated with tumor necrosis factor blockers: 10 cases. Rheumatology. 2009;48:883-6.Reference #3: Maurice MM et al. Treatment with monoclonal anti-tumor necrosis factor alpha antibody results in an accumulation of Th1 CD4þ T cells in the peripheral blood of patients with rheumatoid arthritis. Arthritis Rheum 1999;42:2166-73.The following authors have nothing to disclose: Pius Ochieng, Frank Genese, Doroota Korta, Donald FishmanNo Product/Research Disclosure Information.
- Cocaine Blues: A Case of Drug-Induced Methemoglobinemia. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):318A.
Critical Care Student/Resident Case Report Posters IIISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Acquired methemoglobinemia has been associated with various substances including benzocaine and nitrates. We present a case of cocaine-associated methemoglobinemia attributed to an adulterant used to "cut" it.CASE PRESENTATION: A 22 year old female presented to the Emergency Department with blue skin after using intranasal cocaine. Initial exam was notable for tachycardia, tachypnea, and cyanosis. Oxygen saturation (SaO2) remained low at 86% despite supplemental oxygen. Co-oximetry measured a methemoglobin (metHb) level of 69.8%. Methylene blue was administered in addition to usual supportive care. The metHb level dropped to 8.3% within one hour and 1.2% by day 2, and she was discharged on hospital day 3.DISCUSSION: Methemoglobinemia may be hereditary or triggered by exposure to an offending agent. Ferrous iron (Fe2+) is oxidized to the ferric state (Fe3+) forming metHb which is unable to bind oxygen. Manifestations reflect the degree of impaired oxygenation and include dyspnea, hypoxia, headache, coma, and hemodynamic compromise. MetHb renders pulse oximetry inaccurate as it normally absorbs light at both 660 and 940 nm, whereas metHb has a peak of 631 nm. SaO2 tends to be fixed at about 85% at metHb levels >20% irrespective of oxyhemoglobin levels (1). Chocolate brown and blue blood which does not change when exposed to oxygen has been reported with metHb (2). A saturation gap, the difference between SaO2 and PaO2, is indicative of elevated metHb (3). Methemoglobinemia associated with cocaine is due to diluting adulterants employed to maximize profits, rather than to the cocaine itself (1-3). Local anesthetics such as benzocaine and phenacetin implicated in methemoglobinemia are utilized as they mimic the local effects of cocaine. Methylene blue is indicated for a symptomatic patient or a metHb level >20%, in addition to usual supportive care. It is administered intravenously at 1-2 mg/kg over 5 minutes and can be repeated at 1 mg/kg after 20-30 minutes. Hyperbaric oxygen and exchange transfusion may also be helpful (3). Patients should be monitored for rebound phenomenon based on exposure pharmacokinetics.CONCLUSIONS: Acute acquired methemoglobinemia is a potentially fatal condition precipitated by various medications including diluents used to adulterate cocaine. A saturation gap may provide a characteristic diagnostic clue prompting confirmation with co-oximetry. Intravenous methylene blue should be considered for symptomatic patients or high levels of metHb.Reference #1: Hunter L, Gordge L, Dargan PI, et al. Methaemoglobinaemia associated with the use of cocaine and volatile nitrites as recreational drugs: a review. Br J Clin Pharmacol. 2011. 72(1): 18-26.Reference #2: McKinney CD, Postiglione KF, Herold DA. Benzocaine-adulterated street cocaine in association with methemoglobinemia. Clin Chem. 1992; 38(4): 596-597.Reference #3: Weichert I. Acute Management of Cocaine-Associated Methaemoglobinaemia. Case Reports in Medicine. 2011; 2011: Article ID 136396, 1-3.DISCLOSURE: The following authors have nothing to disclose: Brent Tatsuno, Scott Oh, Jaime BetancourtNo Product/Research Disclosure Information.
- Aorto-Left Atrial Fistula. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):317A.
Critical Care Student/Resident Case Report Posters IIISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Aorto-atrial fistula is a rare but devastating complication of aortic valve endocarditis. We report a case of 58 year old woman who presented with altered mentation and lower extremity weakness. Detailed evaluation revealed bilateral embolic strokes, aortic valve endocarditis, severe aortic regurgitation and aorto-left atrial fistula. She subsequently underwent successful surgical repair.CASE PRESENTATION: A 58 year old female with hypertension and diabetes mellitus was admitted with twelve hours of lower extremity weakness and confusion. Initial evaluations revealed acute renal failure, new-onset atrial fibrillation and pulmonary edema. Computed tomography and magnetic resonance imaging of the brain showed bilateral acute and subacute embolic infarcts. Blood cultures grew beta streptococcus group B and antibiotic therapy was initiated. Transesophageal echocardiography demonstrated large mobile vegetations on the aortic valve leaflets, severe aortic regurgitation, and a fistula between the aortic root and left atrium. The patient required immediate cardiac surgery. Intra-operative findings included fungating vegetations invading the aortic valve leaflets and annulus, an aorto-left atrial fistula, mitral valve leaflet vegetations, a tricuspid valve abscess, and thrombus of the left atrial appendage. An extensive operative repair included: aortic root replacement with a homograft patch repair of the right and left atria, septal leaflet of the tricuspid valve, reconstruction of the aorto-mitral curtain, and left atrial appendage ligation. After recovering from post-operative cardiogenic shock, she was successfully extubated, and ultimately had a favorable outcome.DISCUSSION: Infective endocarditis is an infection of the endocardial surface of the heart and can involve cardiac valves, the mural endocardium, or a septal defect. Acute native valve endocarditis typically involves normal valves and usually has an aggressive course. Staphylococcus aureus and group B streptococci are the usual causative agents of this type of endocarditis. Major complications include valvular insufficiency, congestive heart failure, embolic episodes, sinus of valsalva aneurysm and intra-cardiac fistulas. Treatment is focused at eradication of infectious agent, addressing valvular complications and treatment of underlying congestive heart failure. Approximately 15-25% patients require surgery for indications such as refractory heart failure, persistent sepsis after 72 hours of appropriate antibiotic treatment, conduction abnormalities, rupture of aneurysm of sinus of valsalva or fungal endocarditis.CONCLUSIONS: An aorto-atrial fistula is an extremely rare but devastating complication of endocarditis that requires immediate attention and repair.Reference #1: Archer TP, Mabee SW, Baker PB, Orsinelli DA, Leier CV. Aorto-left atrial fistula. A reversible cause of acute refractory heart failure. Chest. 1997 Mar;111(3):828-31.The following authors have nothing to disclose: Muhammad Adrish, Deborah OrsiNo Product/Research Disclosure Information.
- Rhabdomyolysis Induced Renal Failure Secondary to Dual Infection With Influenza A and Legionella pneumophilia. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):281A.
Critical Care Global Case ReportsSESSION TYPE: Global Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Rhabdomyolysis is characterized by elevated creatine phosphokinase levels and can cause renal failure if not recognized promptly. Numerous precipatiting factors have been identified for this condition including injury, drug toxicity and infections. Here we report a case of severe rhabdomyolysis caused by dual infection with Influenza and Legionella. This case novel in the fact that both infectious agents are known to cause rhabdomylosis independantly however co-infection with both leading to rhabdomyolysis has not been reported earlier.CASE PRESENTATION: 47 year-old male presented with fever, sore throat, cough, myalgias and dark urine ongoing for the past 4 days. He denied any nausea, vomiting, diarrhea or recent trauma. Past medical history was unremarkable and he denied any medication use. On examination he was febrile(100.8F) and tachypneic. Air entry was decreased in the left lower lung zones along with crepitations. Lower extremity muscle groups were tender to palpation. Remainder of the examination was normal. Laboratory investigation showed leukocytosis with neutrophil predominance, elevated serum creatine(3.2mg/dl), increased blood urea nitrogen(60mg/dl) and markedly high levels of creatine phosphokinase(140,000IU/L). Urinanalysis showed presence of large amount of blood however red blood cell count was normal on microscopic examination. Urine myoglobin test was positive. Chest radiography demonstrated left lower lobe consolidation with mild effusion. Given clinical picture of rhabdomyolysis secondary to pneumonia an intensive infectious workup was initiated. Influenza viral swab and urine antigen for legionella both returned positive. Appropriate antibiotic therapy and aggressive fluid therapy was initiated. His respiratory status worsened the following day necessitating transfer to the intensive care unit for closer monitoring. Serum urea nitrogen and creatine levels continued to rise with declining urine output necessitating renal replacement therapy. Following two weeks of intensive theraepy his condition improved with near complete recovery of kidney function.DISCUSSION: Infections account for around 5% of rhabdomyolysis cases1. Though Legionnaire's disease is more common among the elderly population, rhabdomyolysis complicating pneumonia has been more commonly reported among younger males. It is usually from infection with serogroup 1. Bacterial endotoxin mediated muscle injury is thought to be responsible in such cases. Presence of severe uremia is recognized as a marker for increased morbidity and mortality in such patients. Among viral etiologies, influenza A is the most common agent associated with rhabdomyolysis2. Invitro studies have demonstrated viral invasion of muscle fibers as possible mechanism for muscle injury. Renal failure is more common among patients with influenza as compared to other infectious etiologies and is found to occur in around 50% of cases. Other possible bacterial, viral etiologies of rhabdomyolysis include streptococcus, shigella, salmonella, coxsackie virus and human immunodeficiency virus3. Though uncommon fungal and atypical parasitic infections can also cause elevated creatine phosphokinase levels, though not to the degree found with viral or bacterial infections. Management usually involves aggressive fluid therapy along with use of appropriate antimicrobial agents. Prognosis is usually good for lower levels of uremia and complete recovery of renal function is generally the norm. Our case is novel in the fact that it is the first one to demonstrate presence of both legionella and influenza infection in a patient with atraumatic rhabdomyolysis.CONCLUSIONS: Rhabdomyolysis in the setting of infection needs to be recognised early. Legionella and Influenza are the most common infectious agents associated with rhabdomyolysis and as demonstrated can occur concomitantly. Treatment consists of intravenous hydration and control of infection. Early recognition allows for prompt institution of appropriate therapy and helps to minimize renal complications associated with this disorderReference #1: Gabow PA et al. The spectrum of rhabdomyolysis.Medicine 1982; 61:141Reference #2: Foulkes W etal. Influenza A and rhabdomyolysis. J Infect 1990; 21:303Reference #3: Upinder S et al. Infectious etiologies of rhabdomyolysis: Three case reports and review. Clin Infect Dis 1996; 642: 9DISCLOSURE: The following authors have nothing to disclose: Amith George Jacob, Amrutha Mary George, Teny JohnNo Product/Research Disclosure Information.
- Holy Moly! Severe Serotonin Syndrome Associated With a Recreational Agent. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):248A.
Critical Care Case Report Posters ISESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Serotonin syndrome is a potentially life-threatening drug reaction that may occur following therapeutic drug use, inadvertent interactions between drugs, overdose of particular drugs, or the recreational use of certain drugs . It is caused by drug induced excess of intrasynaptic 5-hydroxytryptamine (5-HT) . We report a case of severe serotonin syndrome caused by interaction between a serotonin-norepinephrine reuptake inhibitor (SNRI) and street drug- `Molly'.CASE PRESENTATION: A 41-year-old male with history of bipolar disorder was brought to ED for evaluation of extreme combativeness for one day. He was on risperidone and desvenlafaxine (an SNRI) and admitted to taking a "street drug -Molly". Vitals revealed temperature of 40⁰C, pulse of 108bpm and blood pressure of 155/122mmhg. The patient was extremely agitated, diaphoretic and tremulous. Despite multiple intravenous lorazepam boluses, he remained combative. He was subsequently intubated and placed on a mechanical ventilator. Laboratory workup was significant for sodium of 118 meq/L, creatinine kinase (CK) of 3543U/L and myoglobin of 16,261ng/ml. Based on his clinical presentation, severe serotonin syndrome was diagnosed and managed with aggressive fluid hydration, cessation of serotonergic agent, sedation and neuromuscular blockade with cisatracurium. He subsequently developed massive rhabdomyolysis followed by acute renal failure requiring initiation of hemodialysis. With supportive care, his renal and neurological function improved and he was successfully extubated on day 19. He was discharged to a subacute facility on day 35.DISCUSSION: "Molly" colloquially refers to MDMA(3,4-methylenedioxy-N-methylamphetamine) that is relatively free of adulterants. MDMA is a ring-substituted amphetamine derivative which indirectly stimulates the release and inhibits the reuptake of 5-HT . Its use especially in association with SSRIs or SNRIs has been associated with severe serotonin syndrome [1,3] requiring immediate and aggressive medical intervention.CONCLUSIONS: Clinicians should be aware about the dangerous interaction between serotonergic agents and recreational drugs which could result in potentially lethal serotonin syndrome.Reference #1: Boyer EW, Shannon M.The serotonin syndrome. N Engl J Med. 2005 Mar 17;352(11):1112-20.Reference #2: Gillman PK. The serotonin syndrome and its treatment. J Psychopharmacol 1999;13:100 - 9.Reference #3: Parrott AC. Recreational Ecstasy/MDMA, the serotonin syndrome, and serotonergic neurotoxicity. Pharmacol Biochem Behav. 2002 Apr;71(4):837-44.DISCLOSURE: The following authors have nothing to disclose: Srijana Rai, Pranabh Shrestha, Ram Katpally, Marc AdelmanNo Product/Research Disclosure Information.
- The Discontinuation Dilemma: Which Vasopressor Should Be Weaned First in Patients Recovering From Shock? [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):238A.
Sepsis & Septic ShockSESSION TYPE: Original Investigation SlidePRESENTED ON: Sunday, October 26, 2014 at 04:30 PM - 05:30 PMPURPOSE: There is a paucity of data on which order to wean vasopressors in patients recovering from shock. A single study with a small sample size has shown a higher incidence of hypotension when vasopressin (VP) was discontinued before norepinephrine (NE). This study aimed to evaluate possible adverse outcomes associated with the order of vasopressor discontinuation.METHODS: A retrospective cohort study was performed in shock patients who were concomitantly treated with NE and VP. Sample sizes were calculated to have at least 60 patients in NE group and 30 in VP group, taking conservative figures from a prior study. Patients were divided into two groups depending on whether NE or vasopressin was discontinued first in weaning vasopressors. The primary outcome was the incidence of hypotension within 24 hours of discontinuation of the first vasopressor and before the discontinuation of the remaining agent. The secondary outcome was length of hospital stayRESULTS: Of 195 patients identified eligible, NE was discontinued first in 148 patients (NE group) and VP discontinued first in 47 patients (VP group). There was no difference in incidence of hypotension between the groups (44 patients [30%] in NE group vs. 14 patients [30%] in VP group, p=0.994). No difference in hypotension was also observed in a subgroup analysis in 150 patients with septic shock (33 out of 117 patients in NE group [28%] vs. 10 out of 33 patients in VP group [30%], p=0.814). There was no difference in the secondary outcome, length of hospital stay, between the two groups (25 days in NE group vs. 26 days in VP group, p=0.619).CONCLUSIONS: In patients recovering from shock concurrently treated with NE and VP, there was no difference in incidence of hypotension either when NE or VP was discontinued before the other during vasopressor weaning. There was no difference in length of hospital stay between the groups. The same findings were observed in a subgroup of septic patients.CLINICAL IMPLICATIONS: Our study showed no difference in outcomes when one vasopressor is discontinued over another. Hence, the order of vasopressor discontinuation in patients recovering from shock may be based on a practitioner's preference, ease of dosage or an institutional medication shortage.The following authors have nothing to disclose: Hyeong Kim, Pooja Desa, Edwin Avallone, Thomas Weart, David AdkinsNo Product/Research Disclosure Information.
- Safety of Oral Midodrine as a Method of Weaning From Intravenous Vasoactive Medication in the Medical Intensive Care Unit. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):224A.
Non Pulmonary Critical Care PostersSESSION TYPE: Original Investigation PosterPRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PMPURPOSE: We evaluated the safety of oral midodrine administered to medical intensive care unit (MICU) patients as a method of weaning from intravenous vasoactive medication (IVM).METHODS: For a six-month period starting in March 2013, we monitored use of oral midodrine in an 18-bed MICU. Patients who continued to require low to moderate doses of a single IVM but who could not be weaned from the agent, were started on oral midodrine in order to reduce IVM dose. Midodrine dose was increased until IVM was no longer required. Following transfer from MICU, midodrine was reduced as tolerated by the regular floor team. Data was collected prospectively on a daily basis by one investigator and entered into a standard de-identified data sheet for safety assessment.RESULTS: Fifty patients (age 69.3+/-17, male/female 30:20, SAPS II score 57.6+/-16.5) received oral midodrine. IVM used: phenylephrine (19), norepinephrine (17), dopamine (11), dobutamine (2), and vasopressin (1). Average length of stay (LOS) in MICU was 7.6+/-5.2 days; 17 patients had central intravenous access (CIVA), removed when weaned off IVM; initial and maximal doses of midodrine in MICU were 30.5+/-18.5 and 66.6+/-41.4 mg/day respectively with no adverse effects observed; 27 (54%) patients were discharged from the hospital on a midodrine dose of 17.8+/-31.6 mg/day.CONCLUSIONS: Oral administration of midodrine at the reported doses is safe in the MICU. Its use may reduce the need for IVM, thereby decreasing MICU LOS and need for CIVA. Our results suggest that in patients who continue to require low to moderate doses of a single IVM may be safely converted to oral midodrine. This report is preliminary, as it remains to be determined how to define the patient population for whom midodrine is appropiate.Use of oral midodrine may reduce the duration of IVM administration, allowing both earlier MICU transfer and discontinuation of CIVA. This approach may have potential for risk reduction in the MICU.DISCLOSURE: The following authors have nothing to disclose: Jose Luis Cardenas-Garcia, Micah Withson, Lauren Healy, Seth Koenig, Managala Narasimhan, Paul MayoNo Product/Research Disclosure Information.
- Factors Affecting Recurrence of Clostridium difficile. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):217A.
ICU InfectionsSESSION TYPE: Original Investigation SlidePRESENTED ON: Monday, October 27, 2014 at 01:30 PM - 02:30 PMPURPOSE: Clostridium-difficile-Associated-Diarrhea (CDAD) has been increasing in incidence with limited data on possible risk factors for recurrence.METHODS: This IRB-approved retrospective study included 3010 patients (pts), out of which 2019 were admitted between 1/2007 and 11/2013 and had adequate follow up. CDAD was defined as >3 episodes of loose stools in <24 h with a positive Clostridium difficile stool toxin assay. Recurrence was defined as a 2nd positive stool test within 90 days following complete resolution of previous diarrheal episode and cessation of treatment comprising a ten-day period. Severe CDAD was suggested by WBC >15,000 cells/microL or a serum creatinine level ≥1.5 times with a correlated clinical picture. Pts medical records were reviewed for demographics, hospital length of stay, laboratory blood work, co-morbidities, medication used, presenting complaint and CDAD treatment. Recurrence of CDAD was sub-analyzed based on each comorbid condition, medication and treatment given (vancomycin, metronidazole, fidaxomicin or any combination).2019 patients were diagnosed with CDAD, 798 males, average age 67 and average length of hospital stay was 10 days. 233 pts had severe CDAD, 51 pts with malignancy. 268 recurrences identified in the study population. In univariate line regression, definitive correlation exists between recurrence and PPI and steroid however, other parameters of the cohort were mostly non significant, including age (p=0.2478), male gender (p=0.368), length of hospital stay (p=0.899). In multivariate analysis using Cox regression, adjusting for age, sex, length of hospital stay and treatment used, there was definitive correlation between patients with PPI (P=0.0331), steroid (P=0.0305) and recurrence of CDAD.CONCLUSIONS: PPI, steroids and Clostridium-difficile pharmacological agent used in treatment had statistically significant effect on recurrence of CDAD.CLINICAL IMPLICATIONS: CDAD is one of the most common and serious complications in intensive care units, Intensivists should watch for recurrence in patients on PPI or steroids.DISCLOSURE: The following authors have nothing to disclose: Mohamed Abdelfatah, Rabih Nayfe, Ala Nijim, Kathleen Enriquez, Richard WatkinsNo Product/Research Disclosure Information.
- Acute Eosinophilic Pneumonia: A Rare Side Effect of Daptomycin. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):179A.
Infectious Disease Student/Resident Case Report Posters IIISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Daptomycin is a cyclic lipopeptide antimicrobial agent having bactericidal activity. It has been marketed as a strong antibacterial agent against a wide spectrum of Gram-positive pathogens including MRSA and VRE and bacteria's resistant to Methicillin and Vancomycin. Antibiotics and NSAIDs are commonly associated with eosinophilic pneumonia. There have been a few case reports of pulmonary complications associated with Daptomycin published recently.A 65-year-old female with a history of severe bilateral knee osteoarthritis with total knee replacement, complicated by septic arthritis is admitted with symptoms of fever, chills and cough after 2 week treatment with Daptomycin. She underwent bilateral resection arthroplasty with antibiotic spacer insertion and was started on IV Vancomycin initially. After 3 week treatment with Vancomycin, patient developed Interstitial Nephritis; hence was switched to Daptomycin. At admission, patient had a fever 101.9F and oxygen saturation of 89% on room air. Her WBC at admission was 12,700 μL with eosinophil 12%, ESR 72 mm/hr, CRP 24.9mg/dl. Chest radiography revealed patchy bilateral infiltrates. CT scan showed ground glass opacity in bilateral lung field. Patient failed to improve on antibiotics and extensive workup including blood cultures, sputum culture and streptococcus urine antigen test came back negative. After ruling out other etiologies, Daptomycin was stopped and Prednisone was immediately started. Patient's symptoms improved with in 24 hrs. Her hypoxic respiratory failure improved, oxygenation improved from 89 % to 98% on room air. Patient denied lung biopsy for a tissue diagnosis.DISCUSSION: Daptomycin is a new drug with widespread usage. It has a safe side effect profile with very few cases reported of Daptomycin causing Eosinophilic Pneumonia. Daptomycin, a lipophilic molecule, has a unique calcium dependent mechanism of action. It binds to synthetic surfactant irreversibly, thus reducing its efficacy. Accumulation of daptomycin in alveolar epithelium could also explain its pulmonary complication. However, the exact mechanism is still unknown. Eosinophilic pneumonia due to Daptomycin is a diagnosis of exclusion. It has a rapid onset with fever, hypoxemia, bilateral pulmonary infiltrates, and eosinophilia in bronchoalveolar lavage fluid. Drug related etiology should always be suspected in patients with acute eosinophilic pneumonia, in absence of an infectious or alternative cause of pneumonia. Clinical improvement is seen after cessation of the drug.CONCLUSIONS: Hypoxic respiratory failure can occur due to Daptomycin-induced eosinophilic pneumonia. Early recognition is important, since it can cause significant morbidity and mortality if it goes un-diagnosed.Reference #1: Kalogeropoulos AS, Tsiodras S, Loverdos D, Fanourgiakis P, Skoutelis A. Eosinophilic pneumonia associated with daptomycin: a case report and a review of the literature. J Med Case Reports. 2011;5( 1):13 DISCLOSURE: The following authors have nothing to disclose: Muhammad Azam, Sarah Asghar, Rita Jain, David Aggen, Khalid Zakaria, Sarwan KumarNo Product/Research Disclosure Information.