tag:blogger.com,1999:blog-76872830157267200122024-02-19T00:29:02.056-08:00July 2009 icuroom.net ArchiveUnknownnoreply@blogger.comBlogger30125tag:blogger.com,1999:blog-7687283015726720012.post-73568221102862683242009-07-31T04:36:00.000-07:002009-07-31T04:36:00.221-07:00<p><span style="color:#000000;"><span style="color:#000066;"><strong>Friday July 31, 2009</strong> <em>(pediatric pearl)</em><br /></span><strong><span style="color:#660000;">Uniqueness of Pediatric Lower Airway<br /></span><br /><br />The frequency of acute respiratory failure is higher in infants and young children than in adults for several reasons. This difference can be explained by defining anatomic compartments and their developmental differences in pediatric patients that influence susceptibility to acute respiratory failure.<br /><br />The respiratory pump includes the nervous system with central control (ie, cerebrum, brainstem, spinal cord, peripheral nerves), respiratory muscles, and chest wall. Features of note in pediatric patients include the following:<br /></strong></span></p><span style="color:#000000;"><strong><ul><li>The respiratory center is immature in infants and young children and leads to irregular respirations and an increased risk of apnea. </li><li>The ribs are horizontally oriented. During inspiration, a decreased volume is displaced, and the capacity to increase tidal volume is limited compared with that in older individuals. </li><li>The small surface area for the interaction between the diaphragm and thorax limits displacing volume in the vertical direction. </li><li>The musculature is not fully developed. The slow-twitch fatigue-resistant muscle fibers in the infant are underdeveloped. </li><li>The soft compliant chest wall provides little opposition to the deflating tendency of the lungs. This leads to a lower functional residual capacity in pediatric patients than in adults, a volume that approaches the pediatric alveolus critical closing volume.</strong></span></li></ul>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-77857194968087027812009-07-30T16:38:00.001-07:002009-07-30T16:40:53.652-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Thursday July 30, 2009</span>
<br /><span style="color:#660000;">Application of bundle does make difference!</span>
<br />
<br /><em><span style="color:#000066;">VAP bundle * impact in an intermediate respiratory care unit</span></em> </span></strong>
<br /><strong><span style="color:#000000;">
<br /><span style="color:#660000;">Introduction:</span> Ventilator-associated pneumonia (VAP) is the most frequent ICU-related infection in patients requiring mechanical ventilation, who have a mortality rate ranging from 20% to 50%, prolonging the duration of mechanical ventilation and the ICU length of stay, and increasing costs. We describe the impact of VAP bundle use in an intermediate respiratory care unit (IRCU) to prevent VAP in patients requiring prolonged ventilation.
<br />
<br /><span style="color:#660000;">Methods:</span> A prospective observational study enrolled all tracheotomized patients admitted to a seven-bed IRCU of a tertiary care hospital between March 2005 and October 2007. The daily VAP bundle checklist as described by the Institute for Healthcare Improvement was performed since March 2006 to evaluate compliance. VAP diagnosis was supported by the Clinical Pulmonary Index Score and microbiological quantitative criteria. The mean duration of mechanical ventilation and VAP rate per 1,000 ventilator-days pre and post the bundle period was evaluated and compared using the likelihood ratio for VAP from a Poisson distribution. P < 0.05 was considered significant.
<br />
<br /><span style="color:#660000;">Results:</span> Eighty-eight patients were studied, 40 females and 48 males. The mean age and APACHE II score were 76 ± 12 years and 14 ± 5, respectively. We analyzed 3,727 records during the study period. There were a total of 53 VAP episodes. The compliance rate was 97%. The mean duration of mechanical ventilation pre and post bundle was similar (17.8 and 17.78 days, respectively).
<br />
<br />The VAP rate decreased from 22 cases per 1,000 ventilator-days to 9.76 cases per 1,000 ventilator-days: a <em><span style="color:#003333;">55.78% reduction</span></em> at the end of 20 months of bundle use (P value less than 0.05).
<br />
<br /><span style="color:#660000;">Conclusion:</span> The application of the VAP bundle in chronic ventilated patients resulted in a significant reduction in the incidence of VAP.</span></strong>
<br />
<br />
<br /><em><span style="color:#003333;"><span style="color:#660000;">* Note</span>: The key components of the Ventilator Bundle are:
<br />
<br />Elevation of the Head of the Bed
<br />Daily "Sedation Vacations" and Assessment of Readiness to Extubate
<br />Peptic Ulcer Disease Prophylaxis
<br />Deep Venous Thrombosis Prophylaxis</span></em>
<br />
<br /></span></strong>
<br />
<br /><span style="font-size:78%;color:#003333;">Reference: Click to get abstract
<br />
<br /></span><a href="http://ccforum.com/content/12/S2/P433"><span style="font-size:78%;color:#003333;">Ventilator-associated pneumonia bundle impact in an intermediate respiratory care unit </span></a><span style="font-size:78%;color:#003333;">from 28th International Symposium on Intensive Care and Emergency Medicine, Brussels, Belgium. 18–21 March 2008, Critical Care 2008, 12(Suppl 2):P433</span>
<br />Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-32582397473613032112009-07-29T00:09:00.000-07:002009-07-29T00:09:00.517-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Wednesday July 29, 2009</span><br /><br /></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Case</span>: <em><span style="color:#003333;">34 year old female with history of recurrent DVT now on chronic Coumadin therapy, presented with black tarry stool and probable GI bleed. There was on change on her usual coumadin dose of 5 mg/day on which she had therapeutic INR of 2.8 since last 2 years. Today her INR is 7.8. One week ago, she has a bout of severe UTI (urinary tract infection) and started on antibiotics by her primary care physician?<br /></span></em><br /><br /><br /><br /><span style="color:#660000;">Answer</span>: </span><span style="color:#000000;">Quinolone (Ciprofloxacin/levofloxacin) - Coumadin interaction<br /><br />Coumadin-Quinolone are among top ten drug-drug interactions. The exact mechanism for the warfarin-quinolone drug interaction is unknown. Reduction of intestinal flora responsible for vitamin K production by antibiotics is probable as well as decreased metabolism and clearance of warfarin. It can notoriously increase effects of warfarin, with potential for life threatening bleeding.<br /><br />Best approach is to avoid quinolone in Coumadin dependent patient but if required, INR should be monitored daily during co-administration of warfarin with a quinolone.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-8239573953315537142009-07-28T02:13:00.000-07:002009-07-28T12:09:02.389-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Tuesday July 28, 2009</span><br /><span style="color:#660000;">Bedside tip<br /></span><br /><span style="color:#660000;">Case:</span> <em><span style="color:#003333;">After uneventful insertion of IABP (intra-aortic balloon pump) - you have been informed that, it will take a while before CXR can confirm proper location of tip of IABP. What is one easy method to determine that you have not 'over-shooted' the tip of IABP?</span></em><br /><br /><br /><span style="color:#660000;">Answer:</span> Check the left radial pulse<br /><br />Ideally, the tip of the balloon should be positioned 2–3 cm distal to the origin of the left subclavian artery (LSCA). This position results in maximum augmentation of coronary artery flow although minimizing the risk of embolization to the cerebral vessels and occlusion of the LSCA. If you have good left radial artery pulsation, probably your tip of IABP is distal to LSCA.<br /><br /><br /><span style="color:#003333;">Related previous pear</span>l: <a href="http://april08-icuroom.blogspot.com/2008_04_29_archive.html"><span style="color:#660000;">Carina as a Radiographic Landmark for Positioning the IABP</span></a></span></strong><br /><br /><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhgO2No-76jfpScRY9j4tnA2eIi-apUMpBwOPmToN1S_vQYpr233bhjJqTcsLofkdWNCk2oriRS_FIA7qB4y0XXH30fFQIPLEm996kBMrv5jK7q0bEnCN40YuiEs57uQeGRK5BW7z76Qw8/s1600-h/IABPtip.jpg"><img id="BLOGGER_PHOTO_ID_5363251467805137522" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 326px; CURSOR: hand; HEIGHT: 400px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhgO2No-76jfpScRY9j4tnA2eIi-apUMpBwOPmToN1S_vQYpr233bhjJqTcsLofkdWNCk2oriRS_FIA7qB4y0XXH30fFQIPLEm996kBMrv5jK7q0bEnCN40YuiEs57uQeGRK5BW7z76Qw8/s400/IABPtip.jpg" border="0" /></a>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-36334237410112752672009-07-27T06:14:00.000-07:002009-07-27T13:47:57.606-07:00<div align="center"><strong><span style="color:#000066;">Monday July 27, 2009<br /></span><span style="color:#990000;">Thoracic ultrasound for pneumothorax<br /></span></strong><br /><embed height="344" type="application/x-shockwave-flash" width="425" src="http://www.youtube.com/v/fntJ7GLjCSU&color1=" allowscriptaccess="always" allowfullscreen="true" feature="player_embedded&fs=" color2="0xcfcfcf&hl="></embed></div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-31761371863416131462009-07-26T08:23:00.000-07:002009-07-26T08:23:00.887-07:00<strong><span style="color:#000066;">Sunday July 26, 2009</span></strong><br /><strong></strong><br /><strong><span style="color:#660000;">Case:</span></strong> <em><strong><span style="color:#003333;">42 year old female presented with worst headache of her life. Following CT scan obtained. Your diagnosis (Hint: Watch Red marked area) ?</span></strong></em><br /><br /><br /><p><img id="BLOGGER_PHOTO_ID_5362604387542802546" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 314px; CURSOR: hand; HEIGHT: 400px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiSdUl-ZYgJqvteDCMrCGqFMBRF_1P6aXnwXXAgWiTrx4sTaIQ98u_BA6lE9T1psy2mak24U6Q0QofABMA_8Tm7KiixbsPrDMisdsO8YgM1MWYtCxpkKJ99nasYtFdRCIPmMOZwtQiB79M/s400/sah4.JPG" border="0" /><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">Answer</span>: Subarachnoid hemorrhage (SAH)<br /><br />Subarachnoid hemorrhage (SAH) is the presence of blood within the subarachnoid space from some pathologic process, usually from rupture of a berry aneurysm or arteriovenous malformation (AVM).<br /></span></strong></p><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhO1k3iqgs7_q-dpzDeIYbX8tcmSDTBJIv8qFTRud6_Z7go4kdMXYcKcLT_m7qCi7pZh0G3QEu5VUWu9LqnjiJwA9Ca_-Ry7KmngDB8AMH9oJy3mbHzm0pYJUPHCJW8SbRID4dhPTuhYqw/s1600-h/sah3.gif"><img id="BLOGGER_PHOTO_ID_5362604386729446930" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 357px; CURSOR: hand; HEIGHT: 365px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhO1k3iqgs7_q-dpzDeIYbX8tcmSDTBJIv8qFTRud6_Z7go4kdMXYcKcLT_m7qCi7pZh0G3QEu5VUWu9LqnjiJwA9Ca_-Ry7KmngDB8AMH9oJy3mbHzm0pYJUPHCJW8SbRID4dhPTuhYqw/s400/sah3.gif" border="0" /></a><br /><br /><div></div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-6403909396522852532009-07-25T07:52:00.000-07:002009-07-25T19:45:12.638-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Saturday July 25, 2009<br /></span><br /><span style="color:#660000;">Q;</span> <em><span style="color:#003333;">What is the approximate half life of infusing epinephrine in septic shock patient?<br /></span></em><br /><br /><span style="color:#660000;">Answer</span>: <span style="color:#000000;">About 3.5 minutes<br /><br />Also, note that - Epinephrine pharmacokinetics is linear in septic shock patients, without any saturation at high doses. Basal neurohormonal status does not influence epinephrine pharmacokinetics</span>.</span></strong><br /><br /><br /><span style="font-size:78%;color:#003333;"><br />Reference: Click to get abstract<br /><br /></span><a href="http://ccforum.com/content/13/4/R120" target="_blank"><span style="font-size:78%;color:#003333;">Pharmacokinetics of epinephrine in patients with septic shock: modelization and interaction with endogenous neurohormonal status</span></a><span style="font-size:78%;color:#003333;"> - Published july 21, 2009 - Critical Care 2009, 13:R120</span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-37206503422946511022009-07-24T10:00:00.000-07:002009-07-24T10:01:16.142-07:00<span style="color:#000066;"><strong>Friday July 24, 2009</strong> </span><span style="color:#000066;"><em>(</em></span><em><span style="color:#000066;">pediatric pearl)<br /></span></em><strong><span style="color:#660000;">Kidney Blood Supply</span> <br /> <br /><span style="color:#000000;">Even though the kidney receives 25% of the cardiac output only 2% supplies the renal medulla. It is important so as to have sluggish flow and to be able to maintain high osmolarity in the interstitium for counter-current mechanism. However it predisposes the medulla to ischemia when there is arteriopathy (diabetes mellitus); abnormal blood cells (sickle cell disease); or with chronic use of analgesics (which impairs intra-renal auto-regulation and causes vasoconstriction). This can result in loss of concentrating capacity of the urine and causes the patient to have a fixed specific gravity (1.007 to 1.010).</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-38394079747862521132009-07-23T14:18:00.000-07:002009-07-23T14:19:53.808-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Thursday July 23, 2009<br /></span><span style="color:#990000;">Ambien Induced Delirium</span> </span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;">Relatively Zolpidem (Ambien) is a safe medicine and recently has been one of a drug of choice in critical care units to induce sleep. But it is important to be aware of reported cases of ambien related psychosis, delirium and mania. Atleast one case is reported with visual perception distortion after a single dose of zolpidem.One way to combat the problem is to decrease the prescribing dose particularly in elderly population and in hypoalbuminemia (5 mg instead of 10 mg). Also, female population has been reported to have more plasma level with same dose. Also note that Zolpidem metabolized through liver so it may be necessary to decrease the dose in liver insufficiency.</span></strong><br /><br /><br /><span style="font-size:78%;color:#003333;">References: click to get abstract/article</span><br /><span style="font-size:78%;color:#003333;"></span><br /><span style="font-size:78%;color:#003333;">1. </span><a href="http://www.theannals.com/cgi/content/abstract/35/12/1562" target="_blank"><span style="font-size:78%;color:#003333;">Delirium associated with zolpidem</span></a><span style="font-size:78%;color:#003333;"> - The Annals of Pharmacotherapy: Vol. 35, No. 12, pp. 1562-1564<br /><br />2. </span><a href="http://psy.psychiatryonline.org/cgi/content/full/45/1/88" target="_blank"><span style="font-size:78%;color:#003333;">Zolpidem-Induced Delirium With Mania in an Elderly Woman</span></a><span style="font-size:78%;color:#003333;"> - Psychosomatics 45:88-89, February 2004<br /><br />3. </span><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=8937915&dopt=Abstract" target="_blank"><span style="font-size:78%;color:#003333;">Zolpidem-induced agitation and disorganization</span></a><span style="font-size:78%;color:#003333;">. - Gen Hosp Psychiatry. 1996 Nov;18(6):452-3. (pubmed)<br /><br />4. </span><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=8807033&dopt=Abstract" target="_blank"><span style="font-size:78%;color:#003333;">Zolpidem-induced psychosis</span></a><span style="font-size:78%;color:#003333;">. - Ann Clin Psychiatry.1996 Jun;8(2):89-91. (pubmed)<br /><br />5. Clinical pharmacokinetics of zolpidem in various physiological and pathological conditions, in Imidazopyridines in Sleep Disorders. Edited by Sauvanet JP, Langer SZ, Morselli PL. New York, Raven Press, 1988, pp 155–163<br /><br />6. </span><a href="http://www.theannals.com/cgi/content/abstract/37/5/683" target="_blank"><span style="font-size:78%;color:#003333;">Zolpidem-Induced Distortion in Visual Perception</span></a><span style="font-size:78%;"><span style="color:#003333;"> - The Annals of Pharmacotherapy: Vol. 37, No. 5, pp. 683-686</span> </span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-47081267728361538582009-07-22T19:53:00.000-07:002009-07-22T20:01:12.090-07:00<p><strong><span style="color:#000066;">Wednesday July 22, 2009</span></strong><br /><br /><strong><span style="color:#660000;">Scenario:</span></strong> <strong><em><span style="color:#003333;">You have a patient with acute exacerbation of asthma. Pharmacy informed you that only steroid available is hydrocortisone. What is the dose of hydrocortisone in acute exacerbation of asthma?<br /></span></em></strong><br /><br /><br /><strong><span style="color:#660000;">Answer:</span><span style="color:#000000;"> Hydrocortisone (Cortef) 100 to 250 mg IV q 6 hours<br /><br /><br />Following are different steroids can be use in exacerbation of asthma<br /><br />Betamethasone (Celestone) 0.5 to 0.9 mg IM/PO qd<br />Cortisone (Cortone) 25-300 mg PO qd<br />Dexamethasone (Decadron) 0.75-9 mg PO/IM/IV q q6h </span></strong></p><p><strong><span style="color:#000000;">Hydrocortisone (Cortef)<br />Parenteral: 100 to 150 mg IV/IM q2-6 hours prn<br />Oral: 20 to 240 mg/day PO in divided dosing<br /></span></strong></p><p><strong><span style="color:#000000;">Methylprednisolone<br />Parenteral (Solu-Medrol) 10 to 125 mg IV/IM q 6<br />Oral (Medrol) 4 to 48 mg PO qd</span></strong></p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-54840749192083034012009-07-21T13:45:00.000-07:002009-07-21T13:46:45.003-07:00<div align="center"><strong><span style="color:#000066;">Tuesday July 21, 2009<br /></span><br /><span style="color:#990000;">Interesting Echo<br />Cardiac Tamponade with clot after Trauma</span></strong></div><br /><br /><object width="425" height="344"><param name="movie" value="http://www.youtube.com/v/RfKL3Y94fi4&color1=0xb1b1b1&color2=0xcfcfcf&hl=en&feature=player_embedded&fs=1"></param><param name="allowFullScreen" value="true"></param><param name="allowScriptAccess" value="always"></param><embed src="http://www.youtube.com/v/RfKL3Y94fi4&color1=0xb1b1b1&color2=0xcfcfcf&hl=en&feature=player_embedded&fs=1" type="application/x-shockwave-flash" allowfullscreen="true" allowScriptAccess="always" width="425" height="344"></embed></object>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-10339987654870067812009-07-20T15:51:00.000-07:002009-07-20T16:02:57.962-07:00<p><span style="color:#000000;"><span style="color:#000066;"><strong>Monday July 20, 2009<br /></strong></span></span><span style="color:#660000;"><strong>Standardization of quality assurance for sleep technologist: a model<br /></strong><em>Salim Surani & Raymond Aguillar & Roy Aguillar & Shyam Subramanian</em></span></p><span style="color:#000000;"><p><br /><strong><span style="color:#660000;">Introduction</span>: Since the last decade, there has been a tremendous growth of sleep centers in the US to meet the increasing need of diagnosing and treating sleep disorders. However, this unregulated growth has resulted in tremendous variance in the quality of sleep centers across the nation. The American Academy of Sleep Medicine, in an attempt to provide a benchmark standard, has introduced a voluntary accreditation process, part of which involves assessment of technical quality parameters. However, measuring technical quality is not easy.</strong></p><p><strong><span style="color:#660000;">Hypothesis:</span> We undertook a study to determine if the implementation of point system and schematic feedback on technologist performance can result in improvement and tracking of their performance.</p><p><span style="color:#660000;">Materials and methods:</span> We randomly reviewed 100 charts from the preimplementation phase as control and 1,739 charts from the post implementation of the point system phase as study group.</p><p><span style="color:#660000;">Results:</span> There was a statistically significant difference in the score among technologist between the control and study groups with the average being 75±4.12 and 87.53±0.91, respectively, with a p value being 0.0001.</p><p><span style="color:#660000;">Conclusion:</span> Evaluating the performance of the sleep technologist can be a way to track and monitor their performance in a standardized way and to identify weakness at an earlier stage. We present a system, which we have developed and implemented at our sleep center, as a possible model of assessing and subsequently standardizing technical quality for polysomnography.</strong></span></p><p><em><span style="color:#003333;"> - Dr. Surani is also co-editor of this website<br /></span></em><br /></p><p><span style="font-size:78%;color:#003333;">Reference: Click to get abstract</span></p><p><span style="font-size:78%;color:#003333;">Surani S, Aguillar R, Aguillar R, Subramanian S - </span><a href="http://www.unboundmedicine.com/medline/ebm/record/19565291/abstract/Standardization_of_quality_assurance_for_sleep_technologist:_a_model_" target="_blank"><span style="font-size:78%;color:#003333;">Standardization of quality assurance for sleep technologist: a model</span></a><span style="font-size:78%;color:#003333;">. - Sleep Breath 2009 Jun 30.</span></p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-2123050975665260082009-07-19T07:52:00.000-07:002009-07-19T07:52:00.477-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Sunday July 19, 2009</span>
<br /><span style="color:#990000;">ARDS - A Clinicopathological Confrontation</span>
<br /> </span></strong><a href="javascript:EditItem("></a>
<br /><strong><em><span style="color:#003333;">Very important read to understand why we get burn so much from ARDS!</span></em></strong>
<br /><span style="color:#000000;">
<br /><strong><span style="color:#660000;">Background:</span> The heterogeneity of populations meeting criteria for ARDS may explain in part why no specific treatment has yet been shown to decrease mortality. To define the pathologic alterations associated with the syndrome, particularly the typical pattern of diffuse alveolar damage (DAD), and to evaluate whether etiologies or precipitating factors were missed, we evaluated patients who died with a clinical diagnosis of ARDS and who had a postmortem examination. </strong>
<br />
<br /><strong><span style="color:#660000;">Methods:</span> We conducted a 3-year (2002 to 2004) review of all patients with ARDS (using the American-European Consensus Conference criteria) who died in our ICU and had a postmortem examination. Discrepancies between antemortem and postmortem diagnoses were classified as major and minor using the Goldman classification. </strong>
<br />
<br /><strong>Results: Of 9,184 hospital admissions, 376 patients had a clinical diagnosis of ARDS. Of these, 169 died; 69 had a postmortem examination, and 64 of these had complete data for analysis.</strong>
<br /><ul><li><strong> The main cause of death was multiple organ failure (27 of 64 patients). </strong></li><li><strong>Postmortem examination revealed DAD in 32 patients (50%), </strong></li><li><strong>pneumonia without DAD in 16 patients (25%), and invasive pulmonary aspergillosis in 8 patients (12.5%). </strong></li><li><strong>Major unexpected findings were found in 15 patients (23%): 7 Goldman class I (including 4 cases of invasive pulmonary aspergillosis and 1 of disseminated tuberculosis) and 8 Goldman class II.</strong></li></ul><strong>
<br /><span style="color:#660000;">Conclusions:</span> In this study, ARDS remains a heterogeneous syndrome because only half of patients with ARDS had typical DAD. Open lung biopsy, if performed, might have led to appropriate therapy and potentially better outcome in five of the patients. </strong>
<br />
<br /><strong>
<br /></strong><span style="font-size:78%;color:#003333;">Reference: Click to get abstract</span>
<br />
<br /></span><a href="http://www.chestjournal.org/content/135/4/944.abstract" target="_blank"><span style="font-size:78%;color:#003333;">ARDS- A Clinicopathological Confrontation</span></a><span style="font-size:78%;color:#003333;">- CHEST April 2009 vol. 135 no. 4 944-949</span>
<br /></span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-55747194013666910362009-07-18T03:47:00.000-07:002009-07-18T09:17:48.448-07:00<div align="center"><strong><span style="color:#000000;"><span style="color:#000066;">Saturday July 18, 2009</span> </span></strong></div><div align="center"><strong><span style="color:#990000;">Aortic Dissection</span></strong></div><strong><span style="color:#990000;"></span></strong><br /><strong><span style="color:#990000;"></span></strong><br /><img id="BLOGGER_PHOTO_ID_5359564762373405266" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 400px; CURSOR: hand; HEIGHT: 312px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjm5b_HU866Se1OB1KK80xLtlP-rRCLUZWs1WOwvHbWKTsOX28_bGfcGS5y9Rvwrwx647oISE_XgfeioWwd3wyRosKDDH1cWvupY03RYMRhnfgsjT15FL9HIXyg_y9WAl98fgrY2kqJfRU/s400/ad2.JPG" border="0" /><br /><div><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh-Uw2O5z_bI2qYtlzLXNugF65tKjI3eeCX7Gb7i0466mtwGfqIZVfLOzQROyGPEc6h9vKXZG_E19E4ntpj1dGlywRfGvc-vG4Tnyq3HFeRnyOKcc32i2VU_x-i6MmAJBGDxqMWOA8sf5w/s1600-h/ad1.JPG"><img id="BLOGGER_PHOTO_ID_5359564755281053218" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 400px; CURSOR: hand; HEIGHT: 339px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh-Uw2O5z_bI2qYtlzLXNugF65tKjI3eeCX7Gb7i0466mtwGfqIZVfLOzQROyGPEc6h9vKXZG_E19E4ntpj1dGlywRfGvc-vG4Tnyq3HFeRnyOKcc32i2VU_x-i6MmAJBGDxqMWOA8sf5w/s400/ad1.JPG" border="0" /></a><br /><br /><div><strong><span style="color:#990000;"></span></strong> </div></div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-65769741926404923032009-07-17T06:12:00.000-07:002009-07-17T06:12:00.348-07:00<span style="color:#000000;"><span style="color:#000066;"><strong>Friday July 17, 2009</strong> <em>(pediatric pearl)<br /></em></span><strong><span style="color:#990000;">Patent Ductus Arteriosus (PDA)</span><br /><br />Only 3% of PDA’s are patent by 3 days in TERM neonates (unlike pre-term neonates). Therefore if after this period the ductus arteriousus is still patient it is unlikely to close spontaneously.</strong></span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-60374535550768227222009-07-15T08:26:00.000-07:002009-07-15T08:27:00.804-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Wednesday July 15, 2009</span><br /><br /><span style="color:#660000;">Case:</span> <em><span style="color:#003333;">You are performing 'code blue' on a patient. You do not have an arterial line. What would be the best way to determine the efficacy of resuscitation?</span></em><br /><br /><br /><span style="color:#660000;">Answer:</span> </span><span style="color:#000000;">Venous Blood Gas (VBG)</span></strong><br /><br /><strong><span style="color:#000000;"> Arterial blood gas (ABG) analysis is useful in evaluation of the clinical condition of critically ill patients; however, arterial puncture or insertion of an arterial catheter may not be feasible or available in many situations. The VBG is easier, quicker, and safer to obtain and is associated with significantly less pain for the patient. It would be convenient for physician and patient to be able to replace the ABG with the VBG for analysis of base excess(acidosis). Actually, in code situation VBG would be a better indicator of overall acidosis. If VBG results are normal, ABG analysis should not be necessary. Conversely, abnormal venous levels predicted abnormal arterial values. A venous pH of 7 or lower, for example, predicted an arterial pH of 7.2 or lower.<br /><br />In cardiac arrest victims, the disparity between arterial and venous values is even greater. During cardiac arrest, tissue hypoxia is all but a certainty and is reflected by the lower pH and higher PCO2 on the venous side.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-90145116726710476072009-07-14T15:12:00.001-07:002009-07-14T15:12:45.926-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Tuesday July 14, 2009</span><br /><span style="color:#990000;">Milrinone for coronary vasospasm?<br /></span><br /></span><span style="color:#000000;">A 42-year-old male presented to the emergency department with acute chest pain. The electrocardiogram revealed inferior wall myocardial infarction. Emergency coronary angiography revealed total occlusion of the distal right coronary artery with thrombus. Patient was taken up for primary percutaneous coronary angioplasty with stenting of distal right coronary artery. Six hours following the procedure, the patient developed re-elevation of ST-segment in inferior leads of electrocardiogram and subsequent haemodynamic instability. Repeat coronary angiography revealed patent stent and coronary artery spasm in proximal part, which was relieved by intracoronary injection of nitroglycerine. After an hour, the patient re-developed symptoms of chest pain along with bradycardia, hypotension and ST segment elevation. Intravenous infusion of nitroglycerine did not improve the condition but produced persistent hypotension. Infusion of milrinone was then started. Over time, normalisation of electrocardiogram occurred. The patient was discharged in stable condition. This case suggests that milrinone may be effective in alleviating coronary artery spasm when the use of other agents fails.</span></strong><br /><strong></strong><br /><span style="font-size:78%;"><br /><br /><span style="color:#003333;">Reference: click to get abstract<br /><br /></span></span><a href="http://www.annals.in/article.asp?issn=0971-9784;year=2009;volume=12;issue=1;spage=67;epage=70;aulast=Singh" target="_self"><span style="font-size:78%;color:#003333;">Milrinone infusion: A therapeutic option in coronary vasospasm after primary percutaneous transluminal coronary angioplasty</span></a><span style="font-size:78%;color:#003333;"> - Case Report Year : 2009 Volume : 12 Issue : 1 Page : 67-70</span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-51610794635395825822009-07-13T09:33:00.000-07:002009-07-13T09:35:24.820-07:00<strong><span style="color:#000066;">Monday July 13, 2009<br /></span><br /><span style="color:#660000;">Case:</span> <em><span style="color:#003333;">32 year old female presented with acute left sided shoulder pain and swelling. Hint: see picture below?</span></em><br /></strong><br /><br /><img id="BLOGGER_PHOTO_ID_5357983865123342034" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 310px; CURSOR: hand; HEIGHT: 307px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhIBrf6e_8fBVd6KL0C67gLptQgF_IAdjarZEPANX-9FRSyX5HLspDJFBFWg7WqJ8ZbM0C2UTDprkAvtHSjCoef9cX0RyKXbRBBsrMnqpXKQphGEqbQPGlvswH_s7ao8IK5I0XRMtLMgrQ/s400/tos.jpg" border="0" /><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Answer:</span> Thoracic Outlet Syndrome (TOS)<br /><br />In general, TOS occurs in young people. There are 3 kinds of TOS<br /><br /><em><span style="color:#003333;">Neurogenic TOS (80%):</span></em> an injury probably causes tearing and spasm in the scalene muscles, which become inflamed and scarred, irritating the adjacent nerves.<br /><br /><em><span style="color:#003333;">Arterial TOS (5%):</span></em> the patient has developed an aneurysm of the subclavian artery in the neck; clots may break off and travel to the hand, which turns painful and numb.<br /><span style="color:#003333;"><em><br />Venous TOS (15%)</em></span> — sometimes called “effort thrombosis” — begins when the subclavian vein is pinched between the rib and collarbone, which leads to a vein injury. With repeated injuries, a cuff of scar tissue forms, narrowing the vein; pressure builds up behind it, and the body forms collateral vessels to handle the blood flow. But the obstructed vein still has some stagnant blood flow, prone to forming a clot; if this clot propagates, blocking the collaterals, the arm suddenly swells.<br /><br />Surgery is mostly required.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-68997275319797518012009-07-12T18:10:00.001-07:002009-07-13T09:33:16.234-07:00<div align="left"><strong><span style="color:#000000;"><span style="color:#000066;">Sunday July 12, 2009<br /></span></span><span style="color:#990000;">Picture Diagnosis - What is your diagnosis?</span></strong><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg_6jQMOtBrjxcaq0vqIakvI36KdOMQvFB1Jj_CtKyX1ipC48VOnryo45vakir2LW9UE9uz8X_86t74JDDK00ptDSGQ68ekJkmojKaeX_bQzHuhfYzebsKL9MeV48nMwDOZQ2XsAydc2EQ/s1600-h/ge2.jpg"> </a></div><div align="left"><br /> </div><div align="left"></div><div align="left"></div><img id="BLOGGER_PHOTO_ID_5357745886781077874" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 201px; CURSOR: hand; HEIGHT: 175px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg_6jQMOtBrjxcaq0vqIakvI36KdOMQvFB1Jj_CtKyX1ipC48VOnryo45vakir2LW9UE9uz8X_86t74JDDK00ptDSGQ68ekJkmojKaeX_bQzHuhfYzebsKL9MeV48nMwDOZQ2XsAydc2EQ/s400/ge2.jpg" border="0" /><br /><a href="javascript:EditItem("></a><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">Answer:</span> Giant Bullous Emphysema<br /><br />Above chest x-ray showing a giant bulla occupying more than two thirds of the right hemithorax and compressing the underlying lung upward and towards the mediastinum. This can be misdiagnosed as pneumothorax.<br /></span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-50935020659836133732009-07-11T10:41:00.000-07:002009-07-11T10:43:00.445-07:00<strong><span style="color:#000066;">Saturday July 11, 2009</span><br /><br /><span style="color:#660000;"></span></strong><br /><strong><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">Does Phenytoin (Dilantin) get cleared by hemodialysis or hemoperfusion?</span></em><br /><br /><span style="color:#660000;"></span></strong><br /><strong><span style="color:#660000;">A;</span> No (clinically insignificant removal)</strong><br /><strong></strong><br /><strong><em><span style="color:#003333;">Clinical significance:</span></em></strong><br /><strong></strong><br /><strong>1. In Phenytoin toxicity, Hemodialysis or hemoperfusion are ineffective for enhancing elimination.</strong><br /><strong></strong><br /><strong>2. Hemodialysis patients do not require extra dosing post dialysis though require frequent monitoring due to lower albumin level.</strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-38467035430349547542009-07-10T11:20:00.001-07:002009-07-10T11:20:49.786-07:00<strong><span style="color:#000066;">Friday July 10, 2009</span><br /><br /><span style="color:#660000;">Q:</span><em><span style="color:#003333;"> In which of the following conditions mixed venous oxygen saturation (SvO2) could be more than 80%? </span></em></strong><br /><ul><li><strong><em><span style="color:#003333;">Sepsis </span></em></strong></li><li><strong><em><span style="color:#003333;">Cirrhosis</span></em></strong></li><li><strong><em><span style="color:#003333;">VSD (Ventricular septal defect)</span></em></strong></li><li><strong><em><span style="color:#003333;">Cyanide poisoning</span></em></strong></li><li><strong><em><span style="color:#003333;">All of the above</span></em><br /><br /></strong></li></ul><p><strong><span style="color:#660000;">Answer:</span> All of the above conditions may give higher than normal value for mixed venous oxygen saturation (SVO2).</strong></p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-87072576394382903542009-07-09T12:22:00.000-07:002009-07-09T12:24:08.264-07:00<p><strong><span style="color:#000066;">Thursday July 9, 2009</span></strong></p><p><span style="color:#000000;"><strong><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">Tachyphylaxis to IV nitroglycerin drip develop in how many hours?</span><br /></em><br /><span style="color:#660000;">Answer:</span> Tachyphylaxis to IV nitroglycerin develop approx. in about 16-24 hours.</strong></span><br /><br /><br /><span style="font-size:78%;"><br /><span style="color:#003333;">References: Click to get abstract</span></span></p><p><span style="font-size:78%;color:#003333;">1. </span><a href="http://pt.wkhealth.com/pt/re/amhj/abstract.00000406-199709000-00015.htm;jsessionid=KV8dkknRRGvJpPQbxKyv0y5vHwNNV9Ysztbh0W1r1p1mZpPjXxTd!1109661354!181195629!8091!-1" target="_blank"><span style="font-size:78%;color:#003333;">Comparison of the degree of hemodynamic tolerance during intravenous infusion of nitroglycerin versus nicorandil in patients with congestive heart failure </span></a><span style="font-size:78%;color:#003333;">- Clinical Investigations - American Heart Journal. 134(3):435-441, September 1997.</span></p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-17527142328705557372009-07-08T17:32:00.001-07:002009-07-09T12:22:18.846-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Wednesday July 8, 2009</span>
<br />
<br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">Which very commonly use resuscitation fluid in ICU may cause pesudo-hyperamylasemia?
<br /></span></em>
<br />
<br /><span style="color:#660000;">Answer:</span> </span><span style="color:#000000;">Hetastarch
<br />
<br />The infusion of hydroxyethyl-starch leads to hyperamylasemia due to the complex structural interrelation of the amylase molecules in the serum and the hydroxyethyl-starch molecules. The amylase clearance is reduced because glomerular filtration of the macromolecules thus formed is not possible. It takes about a week for a level to return to normal after hetastarch infusion.
<br />
<br />Workup for presumed pancreatitis may be expensive and futile.</span></strong><span style="color:#000000;">
<br /></span>
<br />
<br />
<br /><span style="font-size:78%;color:#003333;">References: Click to get abstract </span>
<br /><span style="font-size:78%;">
<br /><span style="color:#003333;">1. Gofferje H, Kozlik V. </span></span><a href="http://www.ncbi.nlm.nih.gov/pubmed/70402" target="_blank"><span style="font-size:78%;color:#003333;">[Hyperamylasemia following infusion of hydroxyethyl starch with different molecular weight distributions</span></a><span style="font-size:78%;color:#003333;"> - Infusionsther Klin Ernahr. 1977 Jun;4(3):141-4 </span>
<br /></span><span style="font-size:78%;">
<br /><span style="color:#003333;">2. Treib J, Baron JF, Grauer-MT, </span></span><a href="http://www.ncbi.nlm.nih.gov/pubmed/10229159" target="_blank"><span style="font-size:78%;color:#003333;">Strauss-RG. An international view of hydroxyethyl starches</span></a><span style="font-size:78%;color:#003333;">. Intensive Care Med 1999;25:258–68.</span>
<br />Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-42616596485046584762009-07-07T04:50:00.000-07:002009-07-07T06:39:18.721-07:00<span style="color:#000000;"><strong><span style="color:#000066;">Tuesday July 7, 2009
<br /></span><span style="color:#990000;">Assessment of Left Ventricular Function by Intensivists Using Hand-Held Echocardiography
<br /></span>
<br /><span style="color:#660000;">Background:</span> Bedside transthoracic echocardiography (TTE) provides rapid and noninvasive hemodynamic assessment of critically ill patients but is limited by the immediate availability of experienced sonographers and cardiologists. </strong></span>
<br /><span style="color:#000000;">
<br /><strong><span style="color:#660000;">Methods:</span> Forty-four patients in the medical ICU underwent near-simultaneous limited TTE performed by intensivists with minimal training in echocardiography, and a formal TTE that was performed by certified sonographers and was interpreted by experienced echocardiographers. Intensivists, blinded to the patient's diagnosis and the results of the formal TTE, were asked to determine whether left ventricular (LV) function was grossly normal or abnormal and to place LV function into one of the following three categories: </strong>
<br /><ul><li><strong>normal</strong></li><li><strong>mildly to moderately decreased; and </strong></li><li><strong>severely decreased
<br /></strong></li></ul><strong><span style="color:#660000;">Results:</span> </strong>
<br /><ul><li><strong>Using the formal TTE as the “gold standard,” intensivists correctly identified normal LV function in 22 of 24 cases (92%) and abnormal LV function in 16 of 20 cases (80%). </strong></li><li><strong>Intensivists correctly placed LV function into one of three categories in 36 of 44 cases (82%); in 6 of the 8 cases that were misclassified, the error involved an overestimation of LV function. </strong></li></ul>
<br /><strong><span style="color:#660000;">Conclusions:</span> Intensivists were able to estimate LV function with reasonable accuracy using a hand-held unit in the ICU, despite having undergone minimal training in image acquisition and interpretation.
<br />
<br /><em><span style="color:#003333;">icuroom editors' note:</span></em> <em>All intensivists should be encouraged to seek minimal training in bedside echocardiography.</em></strong>
<br />
<br /><span style="color:#003333;">
<br /></span>
<br /><span style="font-size:78%;color:#003333;">Reference: Click to get abstract</span>
<br />
<br /></span><a href="http://www.chestjournal.org/content/135/6/1416.abstract" target="_blank"><span style="font-size:78%;color:#003333;">Assessment of Left Ventricular Function by Intensivists Using Hand-Held Echocardiography</span></a><span style="font-size:78%;color:#003333;"> - CHEST June 2009 vol. 135 no. 6 1416-1420</span>
<br /></span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-7687283015726720012.post-4094528207023244512009-07-06T08:45:00.000-07:002009-07-06T16:35:10.931-07:00<strong><span style="color:#000066;">Monday July 6, 2009<br /></span><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">Rewarming after therapeutic hypothermia should begun 24 hours after the<br /><br />A) time of initiation of cooling or<br />B) from the time the target temperature (32-34 C) is achieved.<br /><br />(Choose one)</span></em><br /><br /><br /><br /><span style="color:#660000;">Answer:</span> <span style="color:#000000;">Countdown for rewarming after therapeutic hypothermia should begun 24 hours after the time of initiation of cooling. The patient should be actively cooled by using an induced hypothermia protocol for 24 hours to a goal temperature of 32-34ºC. The goal is to achieve the target temperature as quickly as possible. In most cases, this can be achieved within 3-4 hours of initiating cooling.<br /><br />See very good review article on </span></strong><a href="http://emedicine.medscape.com/article/812407-overview" target="_blank"><strong><span style="color:#660000;">Therapeutic Hypothermia</span></strong></a><strong><span style="color:#000000;"> (emedicine.com)</span></strong>Unknownnoreply@blogger.com0