Scott Helgeson

Normal carboxyhaemoglobin level in carbon monoxide poisoning treated with hyperbaric oxygen therapy

Throughout the world both intentional and inadvertent exposure to carbon monoxide (CO) remains an important public health issue. While CO poisoning can be lethal, the morbidity is predominantly due to nervous system injury. A previously healthy 22-year-old woman was found unconscious at home by her sister. Her parents were found dead in the house with a recent history of a dysfunctional furnace. She was presumed to have CO poisoning despite an initial carboxyhaemoglobin level of 2.5%. Patient had both clinical and radiological evidence of neurological damage. However, with multiple sessions of hyperbaric oxygen (HBO) therapy she recovered to a near normal functional status. There is no consensus that exists among treating physicians about the role of hyperbaric oxygen in management of neurological injury. The case described here has significant neurological damage related to CO exposure but improved after HBO therapy.

A 32-year-old man with hypoxemia and bilateral upper-lobe predominant ground-glass infiltrates on chest imaging

Abstract Diffuse alveolar hemorrhage (DAH) is a rare, but potentially fatal, complication of antiphospholipid syndrome, and may present with acute and fulminant symptoms. We report a case of DAH presenting as sudden onset dyspnea in a gentleman with known antiphospholipid syndrome. Chest computed tomography angiography with pulmonary embolism protocol showed right lower lobe segmental filling defects, upper-lobe predominant diffuse ground-glass opacities, and centrilobular nodules bilaterally. The presence of DAH can be confirmed by bronchoalveolar lavage with serial aliquots, but this procedure typically does not elucidate the specific etiology for the hemorrhage. The treatment for patients with severe disease typically consists of a combination of immunosuppressive medications in the form of high-dose intravenous glucocorticoids plus rituximab, cyclophosphamide or mycophenolate; and/or plasma exchange. This case both provides an example of high-quality diagnostic imaging of diffuse alveolar hemorrhage as well as demonstrates the clinical and image-based improvement after treatment.

Comparison of Brain Natriuretic Peptide Levels to Simultaneously Obtained Right Heart Hemodynamics in Stable Outpatients with Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH) is a progressive disease that requires validated biomarkers of disease severity. While PAH is defined hemodynamically by right heart catheterization (RHC), brain natriuretic peptide (BNP) is recommended by guidelines to assess disease status. Retrospectively collected data in 138 group 1 PAH patients were examined for the correlation of BNP levels to simultaneously obtained right heart catheterization (RHC). Patients were mostly Caucasian women, with functional class III symptoms, mean BNP of 406 ± 443 pg/mL, and an average right atrial pressure (RAP) of 9.9 ± 5.7 mm Hg and mean pulmonary artery pressure (mPAP) of 47.3 ± 14.7 mm Hg. Significant correlation was demonstrated between BNP and RAP (p = 0.021) and mPAP (p = 0.003). Additional correlation was seen with right heart size on echocardiography: right atrial (RAE; p = 0.04) and right ventricular enlargement (p = 0.03). An increased BNP level was an independent predictor of mortality (p < 0.0001), along with RAP (p = 0.039) and RAE (p = 0.018). Simultaneous collection of BNP at the time of RHC confirmed the correlation of BNP with right heart hemodynamics. The current results reinforce the use of BNP level as a continuous variable to assess disease severity in group 1 PAH.

1118: A 72-YEAR-OLD MAN WITH PERSISTENT RIGHT UPPER QUADRANT PAIN AFTER ABDOMINAL SURGERY

www.ccmjournal.org Critical Care Medicine • Volume 46 • Number 1 (Supplement) Learning Objectives: We present a very interesting case of postoperative complication that required critical care. Methods: A 72-year-old male underwent ileal enterotomy after developing gallstone ileus and post-operatively developed a perihepatic abscess and choledochal fistula. A percutaneous drain was inserted for treatment. Two weeks later, he developed right upper quadrant abdominal pain and returned to the hospital. On exam, vital signs were normal and laboratory testing revealed anemia, leukocytosis, and hypokalemia. C-reactive protein was markedly elevated and a chest x-ray showed opacities in the right lung. An abdominal MRI was performed to visualize the hepatobiliary tree and showed multi-loculated air-fluid collections along the subdiaphragmatic surface of the liver; a small right pleural effusion was also visualized. A Sinogram was performed through previously placed drain and showed contrast extravasation across the diaphragm and into the distal and bronchi of the right lower lobe. Cultures from the biliary drain grew Enterococcus, H. influenzae, and alpha-streptococci. Ertapenem and vancomycin were started. CT scan of the chest showed worsening right lower lobe consolidation and the drainage tube terminating in the pleural space. Subsequent bronchoscopy showed purulent secretions in the right middle and lower lobes. Repeat sinogram demonstrated a fistulous connection between subhepatic space and pulmonary bronchi with new intraparenchymal abscess. Ultimately, he underwent thoracotomy with right lower and middle lobectomy, takedown of subphrenic abscess fistula, and laparotomy with drainage of the abscess. Results: A few cases of broncho-pleuro-peritoneal fistula have been reported. Most described cases have been associated with subphrenic infections resulting in diaphragmatic ruptures and subsequent fistula formation. Therapy is primarily surgical, in addition to the supportive measures to keep the peak airway pressure low, such as differential ventilation or high-frequency oscillatory ventilation. Severe broncho-pleuro-peritoneal fistula requires debridement of bronchopulmonary tissue, repair of diaphragmatic perforations, drainage of subphrenic abscesses, and antibiotic therapy.

39-Year-Old Woman With Dyspnea and Chest Pain.

Resident in Internal Medicine, Mayo School of Graduate Medical Education, Jacksonville, FL (S.A.H.); Resident in Internal Medicine, Mayo School of Graduate Medical Education, Rochester, MN (A.U.N.); Advisor to residents and Consultant in Cardiovascular Diseases, Mayo Clinic, Jacksonville, FL (J.L.B.). A 39-year-old woman was admitted to the hospital with a 7-month history of dyspnea that had worsened over the preceding 2 days, along with several months of pleuritic chest pain that radiated from the left side of the chest to the back. Her medical history was notable for atrial fibrillation (AF) treated with catheter ablation 10 months earlier and nonischemic congestive heart failure diagnosed at age 30 years at an outside institution. The patient did not have orthopnea, edema, cough, or weight gain. She had been treated previously with warfarin prophylaxis for AF, but this treatment was discontinued 2 months before presentation. Her family history was notable for pulmonary embolism in her father at age 40 years. The patient had been hospitalized twice at other facilities in the preceding 2 months, the first hospitalization for hypoxemic respiratory failure. Work-up included chest radiography and computed tomography (CT), which revealed patchy areas of ground-glass opacities and bilateral consolidations. Echocardiography documented an ejection fraction of 63%, normal diastolic function, and an estimated mean pulmonary artery pressure of 24 mm Hg. A videoassisted thorascopic lung biopsy identified nonspecific interstitial pneumonitis. The patient received a 7-day course of meropenem and linezolid. During the second hospitalization, pulmonary infiltrates were treated with cefepime and levofloxacin. On presentation to our facility, the patient’s vital signs were normal, and physical examination findings were remarkable for an increased pulmonic second heart sound on cardiac auscultation and diffuse chest wall tenderness. No jugular venous distention was noted, nor were cardiac murmurs, right ventricular lift, peripheral edema, or stigmata of chronic liver disease or venous congestion. Electrocardiography revealed sinus tachycardia (heart rate, 106 beats/min) with no other

1942: AN UNUSUAL CASE OF ANGIOEDEMA

Learning Objectives: Both the etiology and pathogenesis of angioedema (AE) is broadly categorized to either mast-cell or bradykinin mediated, with reports of unclear mechanisms. We report a case of a man who required intubation for airway protection for AE, and the etiology was made retrospectively. Methods: A 53-year-old African-American male with history of hypertension presented to the ED with progressively worsening tongue swelling and increasing difficulty speaking and swallowing of 4-hours duration. He denied any history of allergies, asthma, recent ingestions of sea or exotic food, new medications, or herbal products. He never had similar problems in the past and his family history was negative for AE. Examination showed a swollen tongue protruding out of his mouth, swollen lips, inspiratory stridor, and drooling saliva. He was hypertensive and his oxygen saturation was normal while breathing room air. A CBC, BMP, and LFTs were normal. He was intubated and transferred to the ICU. He received an intravenous H2 blocker, epinephrine, and steroids prior to transfer. Diffuse edema of the uvula, arytenoids, and larynx were observed during intubation. Further workup showed a normal ESR, CRP, and C4 level. After 48-hours of supportive care, he improved and was extubated to room air. On revisiting the patient’s history, he reported to have smoked crack cocaine about 8-hours prior to presentation. Results: There has been an increasing array of substances and diseases associated with angioedema, either alone or in combination with anaphylactic reactions. Angioedema associated with cocaine use has been sparsely reported. Recently, a case of isolated angioedema of the uvula, called Quincke’s disease, was reported in association with cocaine inhalation. Our case is the first reported case in which the involvement is more diffuse with life-threatening airway edema and an uncomplicated outcome. Given the potential association of angioedema and anaphylaxis, and the different treatments, physicians should be aware of varied etiologies to diagnose and manage patients properly.