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Altered mental status [keywords]
- 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.
- "Bath Salts": Bad New Kids on the Block. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):984A.
SESSION TYPE: Miscellaneous Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Psychoactive "bath salts" are a relatively new group of designer drugs that mimic the effects of substances like cocaine and methamphetamine. Although cardiovascular complications have been reported, respiratory consequences of their use are not well described.
CASE PRESENTATION:We report the case of a 43-yo-male with history of obesity, hypothyroidism, diabetes, hypertension and chronic obstructive pulmonary disease (COPD) who presented with altered mental status and hypoxia. Symptoms of dyspnea, agitation followed by obtundation progressed rapidly over a period of 24 hours. There were no preceding symptoms or illness. He was admitted to the intensive care unit and diagnosed with acute respiratory distress syndrome (ARDS) with the presence of hypoxia and bilateral pulmonary infiltrates. He required non-conventional ventilation with airway pressure release ventilation (APRV), inhaled epoprostenol and systemic steroids for refractory hypoxemia. Thorough diagnostic investigation was performed including multiple body fluid cultures, bronchoalveolar lavage, toxicology screen and respiratory viral panel. They were all unrevealing. There was no history of exposures. However eventually a family member reported that patient had been inhaling "bath salts" right before his illness. Little was known about "bath salts" by our team and further investigation revealed that they were the likely cause of his ARDS.
DISCUSSION:"Bath salts" are stimulants that were sold as tablets, capsules, or powder and easily purchased in places such as convenience stores, gas stations, and the Internet. The most common are mephedrone and methylone. The drugs cause intense stimulation, and symptoms may include euphoria, pleasurable "rush", tachycardia, and hypertension. They are not detected on common drug screens making it difficult to be identified without a history of use. The prevalence of use increased in the United States in the past 2 years. Several adverse events were reported including deaths. U.S. Drug Enforcement Administration recently named the key ingredients in "bath salts" as Schedule I, thereby making them illegal to possess or sell in the United States.
CONCLUSIONS:This case illustrates the potential severe respiratory complications caused by drugs called "bath salts". High index of suspicion is necessary as they are not detected with common drug screens.1) Fass JA, Fass AD, Garcia AS. Synthetic Cathinones (Bath Salts): Legal Status and Patterns of AbuseThe Annals of Pharmacotherapy 2012 March, Volume 46, 436-441DISCLOSURE: The following authors have nothing to disclose: Humberto Choi, Manuel Ribeiro NetoNo Product/Research Disclosure InformationCleveland Clinic Foundation - Respiratory Institute, Cleveland, OH.
- Bipolaris Brain Abscess in a Patient Treated With Steroids for Neurosarcoidosis. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):259A.
SESSION TYPE: Infectious Disease Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Neurosarcoidosis, treated with steroids, leads to immunocompromised state. This can cause opportunistic infections. Our case demonstrates brain abscess with rare biplolaris pathogen.
CASE PRESENTATION:35-year-old African American male presented with three-day history of altered mental status, dysarthria and disequilibrium. Fifteen months prior, he was evaluated for dizziness, headache, chest pain and hearing loss. Work-up reveled abnormality on brain magnetic resonance imaging (MRI) along with multiple pulmonary nodules and hilar lymphadenopathy. Bronchoscopy revealed non-caseating granulomas. Stage 2 pulmonary and neurosarcoidosis was diagnosed and treatment with dexamethasone was initiated and maintained. Examination reveled right facial drooping and right-sided hearing deficit. MRI revealed six ring-enhancing lesions in the cerebral cortex (Figure 1). Work-up included lumbar puncture, blood cultures, and investigations for toxoplasma, cryptococcus, and tuberculosis, all yielding negative results. Biopsy of the lesions revealed yellow purulent fluid showing septate hyphae identified as Bipolaris species. Patient responded to intravenous (IV) voriconazole and was discharged on oral voriconazole. Repeat MRI showed interval increase in lesion size. Patient was readmitted and started on IV voriconazole and liposomal amphotericin B. Intracerbral abscesses were drained by neurosurgery. Patient improved with IV therapy over 15 days and was discharged on oral voriconazole for a time course presumed to be months to be managed based on improvement of clinico-radiological features.
DISCUSSION:Genus bipolaris, usually found in plant debris and soil, causes phaeohyphomycosis. Most isolated species are bipolaris specifera, biploaris austaliensis, and bipolaris hawaiiensis(1). Reported infections with bipolaris include sinusitis, keratitis, endophthalmitis, and peritonitis(1). Though an infection of immunocompromised host, cases of bipolaris infection have been reported in immunocompetent host as well. In a review of 101 CNS cases of phaeohyphomycosis, 6 were caused by bipolaris: 2 brain abscesses, 3 meningitis and 1 encephalitis. From the 6: 2 immunocompromised, 1 head trauma, and 1 had neurosurgical intervention, 2 immunocompetent (brain abscesses) (2) . CNS phaeohyphomycoses has a mortality of 100% if untreated and 65% for those who are treated3. The current treatments available include surgical debridement, combination anti-fungal therapy and immunotherapy(3).
CONCLUSIONS:This potentially fatal but treatable disease must be kept in mind when investigating an immunocompromised patient.1) Revankar SG, Sutton DA. Melanized fungi in human disease. Clin Microbiol Rev. 2010 Oct;23(4):884-9282) Revankar SG, Sutton DA, Rinaldi MG. Primary central nervous system phaeohyphomycosis: a review of 101 cases. Clin Infect Dis. 2004 Jan;38(2):206-163) Li DM, de Hoog GS. Cerebral phaeohyphomycosis-a cure at what lengths? Lancet Infect Dis. 2009 Jun;9(6):376-83.DISCLOSURE: The following authors have nothing to disclose: Monaliben Patel, Nayan Desai, Alicia Menezes, Anuradha MookerjeeNo Product/Research Disclosure InformationCooper University Hospital, Camden, NJ.
- Disseminated Blastomycosis Involving the Peritoneum Following a Kidney Transplant. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):262A.
SESSION TYPE: Infectious Disease Student/Resident CasesPRESENTED ON: Tuesday, October 23, 2012 at 11:15 AM - 12:30 PM
INTRODUCTION:B. dermatitidis, the etiologic agent for Blastomycosis, is a dimorphic fungus that is endemic to the Ohio-Mississippi River Valley. Annual incidence of infection ranges from 0.43-1.40 patients per 100,000 (1). Human infection typically occurs through inhalation of conidia causing pulmonary disease. In solid organ transplant recipients, B. dermatitidis infection is rare and is associated with high mortality and morbidity. Here we present a case of disseminated Blastomycosis in a renal transplant patient.
CASE PRESENTATION:The patient was a 68 year old male with a history of a single nonrelated living kidney transplant three months prior to presentation with a post-operative course notable for CMV encephalitis and a perinephric lymphocele three weeks prior to admission. He was admitted for altered mental status, fevers and abdominal pain. Admission exam was significant for confusion, respiratory accessory muscle usage, and diminished breath sounds at the lung bases. An abdominal CT showed evidence of recurrence of a perinephric lymphocele, diffuse reticular nodularities, and a confluent consolidation in the right lower lobe. Subsequent fluid from the lymphocele grew VRE. Despite treatment with Daptomycin, he developed acute hypotension. A repeat CT showed worsening bilateral reticular 3-4 mm lung nodules, ascities, and portal hypertension. A paracentesis and bronchoscopy were performed. Both the ascitic fluid and BAL showed broad based buds later identified as Blastomycosis dematitidis. Subsequent urinary B. dermatitidis antigen was also above the limit of quantification. Therapy with Liposomal Amphotericin B was started but progressive multiorgan failure ensued. The patient's mental status improved to permit participation in treatment decisions, and the patient elected to proceed with palliative measures.
DISCUSSION:Disseminated Blastomycosis is a rare complication following solid organ transplant. By one case series, the cumulative incidence is 0.14% (8/9104) (1) with an associated mortality of up to 67% in patients with ARDS. Median time of disease onset following transplant is 24 months. Cutaneous disease is the most frequently encountered form of dissemination. There have been only four prior reports of peritoneal Blastomycosis in the literature (2), and dissemination was attributed to hematogenous spread.
CONCLUSIONS:This appears to be the first reported case of peritoneal Blastomycosis in a solid organ transplant recipient.1) Gauthier GM, Safdar N, Klein BS, Andes DR.Blastomycosis in solid organ transplant recipients. Transpl Infect Dis. 2007 Dec;9(4):310-7.2) MacDonald HJ, Fong IW, Gardiner GW, Soutter DI. Splenic abscess caused by Blastomyces dermatitidis in association with peritoneal involvement: case report and review. Clin Infect Dis. 1992 Jan;14(1):348-9.DISCLOSURE: The following authors have nothing to disclose: Srinath Sriram, Mohammed Mohammed, David SonettiNo Product/Research Disclosure InformationUniversity of Wisconsin, Madison, WI.
- Severe Hypoxemic Respiratory Failure and Thrombotic Thrombocytopenic Purpura. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):317A.
SESSION TYPE: Critical Care Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy characterized by hemolytic anemia and thrombocytopenia. Common microthrombi-related ischemic symptoms include cerebral, renal, cardiac, and gastrointestinal; reports indicate that dyspnea is an uncommon complaint and severe, life-threatening hypoxemia in the setting of TTP is extremely rare (1).
CASE PRESENTATION:A 24 year old black male developed altered mental status while exercising, culminating in syncope. Paramedics found him awake but confused. In the emergency department, patient was intubated due to altered mental status. The blood pressure was 241/137, oxygen saturation of 100%with clear lungs. Hemoglobin was 9.3g/dL, platelet count 46,000/ mm3, and peripheral smear showed 30 schistocytes/HPF. CT brain showed diffuse cerebral edema; MRI revealed bilateral cortical and leptomeningeal enhancement. Upon arrival to the tertiary center, patient remained hypertensive 168/110, heart rate 140 with temperature 38.1 C. Platelet count decreased to 22,000/ mm3, LDH 2105 u/L, and blood, urine and CSF studies were all negative for infection. Shortly after arrival gradual worsening hypoxemia ensued. Chest x-ray showed no infiltrate. PaO2 on blood gas was 42-45 mmHg despite paralytics and PEEP 15-20cmH2O on the ventilator; inhaled nitric oxide was ordered to bedside. Emergent plasma-exchange and steroids were instituted for presumptive TTP. Oxygenation improved with plasma-exchange and extubation occurred early morning day 3. Platelet counts had normalized to 210,000/mm3. Malignant hypertension was considered as the etiology of the thrombotic microangiopathy. However, significant fall of platelet counts from day 6 through day 8 of hospitalization with lack of hypertensive pressures necessitated repeat plasma-exchange and course of steroids resulting in rapid improvement and remission. ADAMST13 levels were <5% with presence of inhibitor.
DISCUSSION:A few case reports and series have proposed respiratory failure as a feature of TTP (2-3). However, confounding factors included co-diagnoses known to mimic findings of TTP and respiratory failure. A large patient registry indicates that on presentation, pulmonary symptoms are infrequent and significant infiltrates on chest x-ray are rare (1).
CONCLUSIONS:Our patient met clinical and laboratory criteria for the diagnosis of TTP having severe hypoxic respiratory failure without significant pulmonary infiltrates. We hypothesize that our patient's respiratory failure was related to occlusion of the pulmonary microvasculature with resolution as appropriate therapy was provided. Profound hypoxemia without pulmonary infiltrates has not been widely reported as part of the TTP symptom complex.1) George, James. Blood 2010;116:4060-40692) Panoskaltsis et al. Am Journal of Hematology 2000; 65:50-553) Chang et al. Am Journal Medical Sciences 2001; 321(2):124-128DISCLOSURE: The following authors have nothing to disclose: Timothy Nokes, Ahmed Awab, James George, Qiaofang ChenNo Product/Research Disclosure InformationUniversity of Oklahoma Health Science Center, Oklahoma City, OK.
- A Case of Anti-NMDA Paraneoplastic Neurologic Syndrome in a Patient Presenting With Autonomic Instability and Altered Mental Status. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):359A.
SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:A 27 yo previously healthy female was brought in for altered mental status (AMS) and autonomic instability (AI). Two weeks before presentation she had a seizure after taking tramadol for a broken metacarpal bone and started on Levetiracetam. Shortly thereafter, she developed severe behavioral changes and agitation requiring an admission to an inpatient psychiatric unit, where she received a course of Haldol, Benztropine, and Thorazine. She subsequently developed severe hyperthermia, AMS, AI, and diffuse rigidity and was sent to the emergency department for evaluation.
CASE PRESENTATION:On presentation her MAP ranged from 40-140 within 10-minutes, with large variations in HR. She showed no focal neurologic deficits on exam. The patient was admitted to the ICU and intubated for airway protection. An extensive serum, CSF, and CNS radiographic work up was unrevealing. Differential diagnosis included Neuroleptic Malignant Syndrome (NMS) and tetanus given the recent hand trauma, and treatment was started for both with bromocriptine and metronidazole respectively without improvement. Eventually, her anti-NMDA receptor antibody test returned positive. She received a 5 day course of IVIG without improvement and was switched to steroids with very gradual symptomatic improvement. CT and MRI of abdomen/pelvis did not show signs of malignancy. A Transvaginal ultrasound showed a cystic right ovary and she underwent a unilateral oophorectomy but pathology was negative for teratoma. After 7 weeks, she was able to talk in sentences, eat independently, but had impaired short term memory.
DISCUSSION:Patients with Anti-NMDA limbic encephalitis (LE) have symptoms which often include insomnia, anxiety, bizarre behavior, hallucinations, memory deficits, seizures, catatonia, autonomic instability, dystonia, rigidity, and hypoventilation. Our patient had the majority of these symptoms. About half of female patients older than 18 have an ovarian teratoma associated with A-NMDA, and removal of the malignancy usually results in improvement of symptoms(1). Alternative treatment includes IVIG, steroids, and plasmapheresis. LE can be secondary to both auto-immune and paraneoplastic encephalitides. An extensive serologic exam is required to establish the diagnosis (Table 1,2). Response to treatment can be dramatic but is highly variable. The differential diagnosis includes, NMS, Creutzfield-Jakob disease, CNS infections, cerebrovascular disease, psychiatric disorders, and toxic metabolic encephalopathy.
CONCLUSIONS:Patients who present with autonomic instability, AMS , and aforementioned symptoms, should be considered for LE syndromes such as Anti-NMDA. If not identified in a timely manner, the disease can be progressive and fatal.1) Vitaliani R, et al. Paraneoplastic encephalitis, psychiatric symptoms, and hypoventilation in ovarian teratoma. Ann Neurol 2005; 58:594.DISCLOSURE: The following authors have nothing to disclose: Milan Patel, Nima Ghasemzadeh, Aalok Patel, Ram SubramanianNo Product/Research Disclosure InformationEmory University, Atlanta, GA.
- A Rare Cause of Neurologic Devastation in the ICU. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):318A.
SESSION TYPE: Critical Care Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Undifferentiated neurologic dysfunction represents an opportunity to expand the differential diagnosis. This case illustrates the importance of considering intravascular large B-cell lymphoma (IVLBCL) in patients with undiagnosed neurologic complaints.
CASE PRESENTATION:A 69 year old man presented to the emergency department with progressive lower extremity weakness and paresthesias. He was in good health three months prior when these symptoms began in his feet and ascended. He underwent evaluations at local hospitals that included imaging and two lumbar punctures. No etiology was determined, but he was treated with intravenous corticosteroids and initially had mild improvement in symptoms. He was sent to rehabilitation where his symptoms progressed with loss of bowel and bladder control and paraplegia. In the emergency department, his neurologic exam was significant for lower extremity paresis, areflexia, sensory deficits to the level of T6, and altered sensorium. His mental status worsened requiring transfer to the intensive care unit for mechanical ventilation. Repeat brain magnetic resonance imaging (MRI) demonstrated progressive, diffuse white matter signal abnormalities. Spine MRI did not demonstrate cord lesions. Electromyography demonstrated a mild sensory neuropathy without evidence for inflammatory demyelination. Cerebral spinal fluid was significant for protein of 100 mg/dL (15-45 mg/dL) and oligoclonal bands. Complete blood counts, liver function tests, and metabolic panels were all normal. The patient's hospitalization was complicated by venous thromboembolism, prolonged mechanical ventilation with ventilator associated pneumonia, seizures, and worsening mental status. He was transitioned to comfort care and subsequently expired. Autopsy revealed IVLBCL in the brain, lungs, liver, adrenal glands, and bone marrow.
DISCUSSION:IVLBCL is a rare, aggressive and often fatal form of diffuse large B-cell lymphoma. It is characterized by malignant growth in small vessels of extranodal organs. Older patients are affected and present with skin lesions, non-specific neurologic complaints, anemia, or dyspnea. The vague presentation makes diagnosis difficult, and without a high index of suspicion, patients are often diagnosed post-mortem. The few published case series have reported a variety of neurological findings including dementia, tremor, seizures, paresis, sensory deficits and altered sensorium. Diagnosis can be made by biopsy of the affected organ. Anthracycline agents and rituximab have been used for the treatment of IVLBCL with improved survival; however, central nervous involvement portends a worse prognosis.
CONCLUSIONS:Unexplained neurologic symptoms should alert clinicians to consider IVLBCL as this is a rare but fatal illness, and recent treatment advances can improve survival.1) Shimada K, et.al. Presentation and management of intravascular large B-cell lymphoma. Lancet Oncol 2009; 10: 895-902.DISCLOSURE: The following authors have nothing to disclose: Patrick Meehan, Michael EzzieNo Product/Research Disclosure InformationThe Wexner Medical Center at The Ohio State University, Columbus, OH.
- Tracheal Epithelial Myoepithelial Carcinoma Ex Pleomorphic Adenoma Incidentally Discovered During Evaluation of Diffuse Lymphadenopathy in a Patient Presenting With Hypercalcemia. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):573A.
SESSION TYPE: Cancer Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:Epithelial myoepithelial carcinomas are rare tumors primarily of salivary gland origin. We report a case of a tracheal epithelial myoepithelial tumor incidentally discovered during bronchoscopy performed for suspected sarcoidosis. To our knowledge, this is the first reported case of sarcoidosis associated with epithelial myoepithelial carcinoma.
CASE PRESENTATION:A 61 year old Hispanic male presented with several weeks of altered mental status, weight loss, and malaise. Initial evaluation was notable for hypercalcemia (14.0 mg/dL), slightly elevated parathyroid hormone related protein (34 pg/mL), undetectable parathyroid hormone (<2.5 pg/dL), normal Vitamin D 1,25(OH)2 (27.5 ng/mL), and an elevated angiotensin converting enzyme level (108 U/L). Position emission tomography and computerized tomography revealed diffuse intrathoracic and intra-abdominal lymphadenopathy with mild to moderate (F-18) 2-Fluoro-2-deoxy-D-glucose uptake. His hypercalcemia was treated with normal saline, calcitonin and pamidronate with clinical improvement. On flexible fiberoptic bronchoscopy a 0.7 cm tracheal nodule was biopsied. Pathology demonstrated a tumor composed of glands with a double layer of lining cells. The inner layer was composed of eosinophilic cells. The outer layer was composed of clear cells. Immunohistochemistry demonstrated the inner cell layer was immunoreactive with CK7. The outer cell layer was immunoreactive with SMA and p63. Both cell layers were negative for CK20, TTF-1, PSA, and PSAP. The tumor was classified as an epithelial myoepithelial carcinoma. Bronchoscopy was otherwise non-diagnostic. Lymph nodes sampled by mediastinoscopy demonstrated noncaseating granulomas consistent with stage I sarcoidosis. There was no evidence of malignancy or infection. Three ring tracheal resection with primary reconstruction of the trachea was performed. The patient was clinically stable with a normal calcium level at his one month outpatient follow-up.
DISCUSSION:Sarcoidosis has been associated with a variety of malignancies including lung, breast, lymphoma, germ cell, and melanoma. It is unclear if there is a true relationship or if this is simply an incidental finding. Bronchial epithelial myoepithelial carcinoma is exceedingly rare with 28 reported cases in the literature. Treatment generally entails complete resection with lobectomy or pneumonectomy. In our case, three ring tracheal resection with primary tracheal reconstruction was performed.
CONCLUSIONS:To our knowledge, this is the first report of a pulmonary epithelial myoepithelial carcinoma associated with sarcoidosis. Surgical resection of the malignancy is considered curative for local disease and is generally recommended given its potential for metastatic disease.1) Chao TY, Lin AS, Lie CH, Chung YH, Lin JW, Lin MC. Bronchial epithelial-myoepithelial carcinoma. Ann Thorac Surg. 2007 Feb;83(2):689-91.DISCLOSURE: The following authors have nothing to disclose: George Girgis, Jaime Betancourt, Michael Lewis, Robert Cameron, Scott OhNo Product/Research Disclosure InformationCedars Sinai Medical Center, Los Angeles, CA.
- Pott's Puffy Tumor: A Case With Intracranial and Pulmonary Manifestation. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):167A.
SESSION TYPE: Infectious Disease Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION:The clinical entity of Pott's Puffy tumor is a subperiosteal abscess associated with osteomyelitis of the frontal bone. Here we describe a case of Pott's Puffy tumor involving the frontal sinus, spreading to subdura leading to intracranial abscess and septic emboli to the lungs.
CASE PRESENTATION:43 year old male with history of cocaine abuse and HIV was admitted with altered mental status. On exam he had large swelling of the right frontal bone with proptosis. He was diagnosed with sinusitis, multiple dural venous thromboses, subdural empyema and intra-cranial abscesses resulting in midline shift on head CT. Hypoxemic respiratory failure developed requiring intubation with associated finding of multiple bilateral cavitary lung abscesses in the bases. Subsequently he underwent drainage of the right frontal sub-periosteal abscess as well as left temporal craniotomy and evacuation of subdural empyema. Sepsis developed and he was treated for Streptococcus mitis which grew from sub-periosteal abscess. Despite initial ceftriaxone, metronidazole and ciprofloxacin therapy, fevers persisted leading to a 6 week course of meropenem. Oxygenation improved and patient made full neurologic recovery.
DISCUSSION:An increasingly rare disease in the era of antibiotics, Pott's Puffy tumor was first described by Sir Percival Pott in association with head trauma. Since its description, observations have been increasingly associated with frontal sinusitis. Pott's Puffy tumor is often an indicator of intracranial complications, however pulmonary manifestations are usually not associated with Pott's. It begins as an infection of the frontal sinuses which originally manifest as periorbital swelling, headache and fever. Complications arise through the spread of the infection via valveless diploic veins in the skull or direct extension to the subdural space. Both methods of spread are illustrated in this case and particularly unique is the pulmonary manifestation of septic emboli which led to a large abscess formation. The infection is usually caused by Streptococcus however Haemophilus influenza and anaerobes have been described. Treatment includes surgical drainage and intravenous antibiotics for 6-8 weeks.
CONCLUSIONS:In the antibiotic era, patients developing Pott's Puffy tumor has become less common. Knowledge of the sequelae including intracranial and pulmonary involvement of this disease can prove to be useful. This would allow for identification of the disease process and timely intervention. Prompt drainage of frontal and intracranial abscess and early antibiotic therapy, as illustrated in this case, are essential in the treatment of Pott's Puffy tumor.1) Kombogiorgas D, Solanki GA. The Pott puffy tumor revisited. J Neurosurg. 2006 Aug:143-9.DISCLOSURE: The following authors have nothing to disclose: Bryan Husta, Cristina ReichnerNo Product/Research Disclosure InformationGeorgetown University Hospital, Washington, DC.
- Validation of a Clinical Prediction Scale for Need for Mechanical Ventilation and Inpatient Mortality in Acute Exacerbation of Chronic Obstructive Pulmonary Diseases. [JOURNAL ARTICLE]
- Chest 2012 Oct 1; 142(4_MeetingAbstracts):677A.
SESSION TYPE: COPD: Severity and Risk PredictorsPRESENTED ON: Monday, October 22, 2012 at 11:15 AM - 12:30 PM