tag:blogger.com,1999:blog-4343514953505531932024-02-19T08:59:15.628-08:00icuroom.net May 2010 ArchiveUnknownnoreply@blogger.comBlogger30125tag:blogger.com,1999:blog-434351495350553193.post-47344874064205304512010-05-31T13:46:00.001-07:002010-05-31T13:46:57.630-07:00<strong><span style="color:#000066;">Monday May 31, 2010</span><br /><br /><span style="color:#990000;"></span></strong><br /><strong><span style="color:#990000;">Q;</span> <em><span style="color:#003333;">What is the five (5) "P" Philosophy before doing any Critical Care procedure?<br /></span></em><br /><span style="color:#660000;"><span style="color:#660000;">A</span>:</span> <span style="color:#000000;">Proper Preparation Prevents Poor Performance</span> </strong><br /><strong></strong>Unknownnoreply@blogger.com1tag:blogger.com,1999:blog-434351495350553193.post-57297686343243867742010-05-30T05:06:00.000-07:002010-05-30T05:09:00.532-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Sunday May 30, 2010</span><br /></span><span style="color:#990000;">5 Grades of SAH (Subarachnoid Hemorrhage)<br /></span></strong><br /><strong><span style="color:#000000;">Subarachnoid hemorrhage (SAH) implies the presence of blood within the subarachnoid space from some pathologic process (traumatic and nontraumatic hemorrhages).<br /></span></strong><br /><br /><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgphz8kaXBcgUUU4x7DymADbcbkdIuxTqLopsE9xztpDEBaYpMO719cdKjolUI5fxKc1D-YBSWqmViXcquzYaJWRNhwyxIhNL_nUJ41Wo0d5Ig8DX4Ctd6UtPNIEEz7RN5jYSvfJOMLpPFp/s1600/sah3.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 355px; DISPLAY: block; HEIGHT: 400px; CURSOR: hand" id="BLOGGER_PHOTO_ID_5477033470814379970" border="0" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgphz8kaXBcgUUU4x7DymADbcbkdIuxTqLopsE9xztpDEBaYpMO719cdKjolUI5fxKc1D-YBSWqmViXcquzYaJWRNhwyxIhNL_nUJ41Wo0d5Ig8DX4Ctd6UtPNIEEz7RN5jYSvfJOMLpPFp/s400/sah3.jpg" /></a><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">Grade I</span> - Mild headache with or without meningeal irritation<br /><br /><span style="color:#660000;">Grade II</span> - Severe headache but nonfocal examination, with or without mydriasis<br /><br /><span style="color:#660000;">Grade III</span> - Mild alteration in neurologic examination, including mental status<br /><br /><span style="color:#660000;">Grade IV</span> - Obviously depressed level of consciousness or focal deficit<br /><br /><span style="color:#660000;">Grade V</span> - Patient either posturing or comatose</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-51994548526946781412010-05-28T01:42:00.000-07:002010-05-28T04:32:16.943-07:00<strong><span style="color:#000066;">Friday May 28, 2010</span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Post-Dural Puncture Headache (PDPH) - </span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Part 2 (Blood Patch)</span><br /><br />If conservative measures are ineffective in ameliorating PDPH, another intervention is the epidural blood patch - in practice since last 50 years with success. The epidural blood patch consists of injecting 5-20 mLs of autologous blood into the epidural space, in the region of the suspected dural 'hole.' Once the epidural space is located, autologous blood is drawn from an intravenous (IV) line, and then injected as a bolus into the epidural space. In 90% of cases, the response is positive and immediate. And, long-term relief of PDPH occurs in the almost all cases.</span></strong><br /><br /><br /><img id="BLOGGER_PHOTO_ID_5475774823336164114" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 200px; CURSOR: hand; HEIGHT: 160px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhtwlU1zYJfawv2nhiajpe6_W0IVb1XfSVjbyZCAhod9rnRnQ3aLN-vS1_WQba4mjL2hQKGzVcqJUPCk8TA5hZkA4xDu3ZuBNnmP6fXB5trmWjIvZZtS3wO1UrRac2XQxxVtW-dBwLjmCIl/s400/Epiduralpatch2.jpg" border="0" /><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhHaB8oHJCIvxlgJd56TRdIzmQkrVHi1WvNxDXGSDbmSbkkL_fGlBdMv2rZXuA_dchK0Fh_DAC0z8oAzPuwWBuZPyFCA6uPBqHs2JthG1Kb-c7rcqv-IYQT3YRjL2B6a9-mBcl9IPLzRTm3/s1600/epiduralpatch.gif"><img id="BLOGGER_PHOTO_ID_5475774817533034946" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 400px; CURSOR: hand; HEIGHT: 248px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhHaB8oHJCIvxlgJd56TRdIzmQkrVHi1WvNxDXGSDbmSbkkL_fGlBdMv2rZXuA_dchK0Fh_DAC0z8oAzPuwWBuZPyFCA6uPBqHs2JthG1Kb-c7rcqv-IYQT3YRjL2B6a9-mBcl9IPLzRTm3/s400/epiduralpatch.gif" border="0" /></a>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-60484524288133828902010-05-27T00:17:00.000-07:002010-05-27T00:17:00.598-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Thursday May 27, 2010<br /></span></span><span style="color:#660000;">Post-Dural Puncture Headache (PDPH) - </span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Part 1 (conservative measures)</span><br /><br />After Lumbar Puncture (LP) larger hole in the dura are associated with a greater likelihood of CSF leakage and non-sealage. As CSF leaks out of the subarachnoid space, structures within the cranium(skull) gradually shift downwards. This mechanism stretches sensitive fascial and ligamentous structures, that are attached to cerebral tissue, and dilates cerebral vessels; thus, producing a typical postural headache. Termed "Post-Dural Puncture Headache," (PDPH) it is characterized by headache that dissipates while supine, but reoccurs when upright. Other symptoms include neck stiffness and pain across the upper back. Although the headache itself is harmless, it can be very severe and very debilitating. Most cases of PDPH are short-lived, resolving within 24 hours. However, when persisting for more than 24-36 hours, additional measures are needed. Conservative measures to reduce PDPH includes</span></strong><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">1. Bedrest</span> - Since the symptoms of PDPH are alleviated by assuming the horizontal position, keeping a patient horizontal for a period of time (eg. 24 hours) after an intervention is thought to enable spontaneous closure of the dural 'hole.' Unfortunately, it rarely works. </span></strong><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">2. Hydration</span> - Extra hydration is thought to facilitate increased CSF production. This, too, rarely works. </span></strong><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">3. Analgesics</span> - Narcotic analgesics and, in some instances, non-steroidal anti-inflammatory agents are often administered for symptomatic treatment of the headache. Other agents that have been used include; ACTH, theophylline, vasopressin, and sumatriptan.</span></strong><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">4. Caffeine</span> - Caffeine has been suggested as a mode of therapy to help constrict the vasodilated cerebral vessels. It is best administered early in the day so that the patient can sleep at night. The dose of caffeine sodium benzoate is 500 mg intravenously which can be repeated once; two hours later, if the first dose does not have the desired effect.</span></strong><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">5. Epidural saline injection</span> - Boluses or infusions of epidural normal saline can help to transiently increase the epidural pressure; thus, slowing the speed at which CSF leaks through the dural hole. This may facilitate spontaneous closure of the dural 'hole.' The bolus dose is 30-60 mls given every 6 hours for 4 doses. The rate of infusion is 1000 mls administered over a 24 hour period.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-80939854450245929092010-05-26T06:46:00.000-07:002010-05-26T06:46:00.490-07:00<strong><span style="color:#000066;">Wednesday May 26, 2010</span></strong><br /><br /><em><span style="color:#003333;">Following Pearl contributed by:<br /><br />Peggi Guenter, PhD, RN, CNSN<br />Director of Clinical Practice, Advocacy, and Research Affairs<br />American Society for Parenteral and Enteral Nutrition<br /></span></em><a href="mailto:peggig@aspen.nutr.org"><em><span style="color:#003333;">peggig@aspen.nutr.org</span></em></a><br /><em><span style="color:#003333;">(610) 649-7994<br /></span></em><a href="http://www.nutritioncare.org/"><em><span style="color:#003333;">www.nutritioncare.org</span></em></a><br /><br /><br /><strong><span style="color:#990000;">Nutrition Guidelines 2009<br /></span><span style="color:#000000;"><br />Would like to bring your attention to the following nutrition and critically ill guidelines developed by the American Society for Parenteral and Enteral Nutrition and the Society of Critical Care Medicine published in 2009. We also have a set of pediatric ICU and nutrition guidelines as well. These can be obtained by visiting this link for our guidelines and standards library:<br /></span></strong><br /><a href="http://www.nutritioncare.org/Library.aspx" target="_blank" rel="nofollow"><em><span style="color:#660000;"><strong>http://www.nutritioncare.org/Library.aspx</strong></span></em></a><br /><br /><strong><span style="color:#000000;">These are open access but one needs to create an account to download them.</span></strong><a href="javascript:EditItem("></a><br /><strong><span style="color:#000000;"><br /></span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-43759298069152666522010-05-25T06:22:00.000-07:002010-05-25T06:22:00.549-07:00<p><strong><span style="color:#000000;"><span style="color:#000066;">Tuesday May 25, 2010<br /></span><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">What is the modus operandi of Subdural Hematomas (SDH)?</span></em><br /><br /><span style="color:#660000;">Answer:</span> Contrary to popular belief that SDH happens due to direct trauma, Subdural hematomas actually are most often caused by rapidly changing velocities within the skull which may stretch and tear small bridging veins. In other words, subdural hematomas generally result from shearing injuries due to various rotational or linear forces.</span></strong></p><p><strong><span style="color:#000000;">Due to above modus operandi, SDH is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra- and pre-retinal hemorrhages. Cerebral atrophy - commonly seen in the elderly and in alcoholics - increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear.</span></strong> </p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-29347285890348311872010-05-24T09:53:00.000-07:002010-05-24T09:53:00.375-07:00<p><strong><span style="color:#000000;"><span style="color:#000066;">Monday May 24, 2010</span>
<br />
<br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">54 year old male with end stage liver disease may require large volume paracentesis. Patient is labeled as allergic to Albumin. What is your alternative to prevent circulatory dysfunction after large-volume paracentesis?
<br /></span></em>
<br /></span></strong></p><p><strong><span style="color:#000000;"><span style="color:#660000;">Answer:</span> </span><span style="color:#000000;">Use of terlipressin</span></strong></p><p><strong><span style="color:#000000;">The removal of 5 litres of fluid or more is considered large-volume paracentesis. The AASLD (American Association for the Study of Liver Diseases) suggests that postparacentesis albumin infusion may not be necessary for a single paracentesis of less than 5 litres; however, for large-volume paracenteses consider an albumin infusion of 8-10 g per liter of fluid removed.</span></strong></p><p><strong></a><span style="color:#000000;">Another alternative is to use terlipressin (1 mg every 4 hours for 48 hours) rather than albumin for prevention of circulatory dysfunction after large-volume paracentesis. Studies suggest that terlipressin is as effective as albumin.</span></strong>
<br />
<br /></p><p><span style="font-size:78%;color:#003300;">References: Click to get abstract</span></p><p><span style="font-size:78%;color:#003300;">1. </span><a href="http://www.ncbi.nlm.nih.gov/pubmed/18251131" target="_blank"><span style="font-size:78%;color:#003300;">The efficacy of terlipressin in comparison with albumin in the prevention of circulatory changes after the paracentesis of tense ascites</span></a><span style="font-size:78%;color:#003300;"> --a randomized multicentric study. Hepatogastroenterology. Oct-Nov 2007;54(79):1930-3. </span></p><p><span style="font-size:78%;color:#003300;">2. </span><a href="http://www.ncbi.nlm.nih.gov/pubmed/16460491" target="_blank"><span style="font-size:78%;color:#003300;">Terlipressin versus albumin in paracentesis-induced circulatory dysfunction in cirrhosis: a randomized study.</span></a><span style="font-size:78%;color:#003300;"> J Gastroenterol Hepatol. Jan 2006;21(1 pt 2):303-7.</span> </p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-21543648241320377092010-05-23T02:56:00.000-07:002010-05-23T02:56:00.237-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Sunday May 23, 2010
<br /></span></span><span style="color:#990000;">Relationship Between ICU Design and Mortality</span></strong>
<br /><strong><span style="color:#000000;">
<br />Architectural design of health-care facilities can influence patient safety; however, it is unknown whether patient outcomes are significantly affected by ICU design.
<br />
<br /><span style="font-size:85%;"><span style="color:#990000;">Methods:</span> Six hundred sixty-four patients admitted to the medical ICU (MICU) of Columbia University Medical Center during 2008 were included in this retrospective study. Patient outcome measures, which included hospital mortality, ICU mortality, ICU length of stay (LOS), and ventilator-free days, were compared based on random room assignment. Rooms that were not visible from the MICU central nursing station were designated as low-visible rooms (LVRs), whereas the remaining rooms were designated as high-visible rooms (HVRs).
<br /></span>
<br /><span style="color:#990000;">Results:</span>
<br /><ul><li>Overall hospital mortality did not differ among patients assigned to LVRs vs HVRs </li><li>Severely ill patients (those with APCHE II scores more than 30) had significantly higher hospital mortality when admitted to an LVR than did similarly ill patients admitted to an HVR (82.1% and 64.0%, n = 39 and 75, respectively; P = .046). ICU mortality showed a similar pattern. </li><li>ICU LOS and ventilator-free days did not differ significantly between groups. </li></ul>
<br /><span style="color:#990000;">Conclusions:</span> Severely ill patients may experience higher mortality rates when assigned to ICU rooms that are poorly visualized by nursing staff and physicians.</span></strong>
<br /></span></strong>
<br />
<br /><a href="http://chestjournal.chestpubs.org/content/137/5/1022.abstract" target="_blank"><span style="font-size:78%;color:#003333;">Relationship Between ICU Design and Mortality</span></a><span style="font-size:78%;color:#003333;"> - CHEST May 2010 vol. 137 no. 5 1022-1027</span>
<br />Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-23251848752901552372010-05-22T14:39:00.001-07:002010-05-22T14:39:48.270-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Saturday May 22, 2010</span><br /></span><span style="color:#990000;">Ice test - Poor man's test for Myasthenia Gravia</span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;">Most of the Myasthenia patients along with other symptoms of weakness usually exhibits ptosis. While at bedside place an ice cube over eye lids for 2 minutes. Cooling improves neuromuscular transmission. Resolution of ptosis with cooling is a positive test for Myasthenia Gravis and reported upto 80% reliable to diagnose ocular myasthenia.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-38183229842612533442010-05-21T19:56:00.000-07:002010-05-22T14:56:49.571-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Friday May 21, 2010</span><br /><br /><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">30 year old pregnant female admitted with Hyperemesis Gravidarum(HG). patient is hypotensive, dehydrated and hypoglycemic. Before writing IVF orders what would be your concern and which additional order you will consider?<br /></span></em><br /><br /><span style="color:#660000;">Answer</span>: Wernicke's Encephalopathy (WE)<br /><br /><br />There is a high risk of WE in HG after 3-4 weeks of persistent vomiting. Thiamine should be given prior to glucose and dextrose infusion.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-64253374738778182702010-05-20T08:24:00.000-07:002010-05-20T08:25:41.644-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Thursday May 20, 2010</span><br /></span><span style="color:#990000;">Insulin in TPN - a bad idea?</span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;">Adding insulin to the TPN bag itself - this is chemically compatible and has been done for years. The debate comes in when we start to discuss how much actually makes it to the patient. Study results have been variable. The amount of insulin adsorbed (i.e. stuck to) the glass bottle, plastic bag, or plastic IV tubing can be as high as 80%. Some factors affecting this adsorption include type of container, solution, administration set, previous exposure of tubing to insulin, etc. The binding appears to happen within the first 30-60 minutes. Some in vitro studies have been conducted to assess the effect of "priming" the line with a dilute insulin solution. Priming the tubing with a dilute solution or running through and wasting the first aliquot of the insulin-containing solution increases delivery of insulin from 38% to 85% at 2 hours. Once the priming is done, the amount of insulin delivered remains pretty constant.</span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;">Other options - although costly and controversial, adding albumin in small concentrations may help deliver higher amount of insulin by decreasing the amount of insulin available to bind to the container and/or tubing. Adding 0.3 gram/100ml seems to decrease adsorption. Flushing the tubing with the insulin-containing solution two hours before administration seems to saturate the binding sites and minimizes further adsorption. Giving the insulin as a separate IV infusion is another delivery option but adsorption should be considered in this setup as well.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-4802204710685008322010-05-19T02:41:00.000-07:002010-05-20T08:26:02.880-07:00<div align="left"><strong><span style="color:#000000;"><span style="color:#000066;">Wednesday May 19, 2010</span><br /><br /><span style="color:#660000;">Case:</span> <em><span style="color:#003333;">27 year old diabetic male is admitted to hospital and get diagnosed with osteomyelitis. After surgical intervention long term antibiotics are planned and PICC line is inserted. Following image is obtained after PICC insertion (arrows showing PICC path). What could be your concern?</span></em> </span></strong><br /><br /></div><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_TVJ3nzlUeXk2fJ-i9VXQSIDYWO6V9pGtqPUUe8GLWxbRjP8JvulJqAOma23wlvjdsj-BMSdHMhtlDjPwL98DF_3_Q9wzeCMrJL4QFAnGIsSyycyKP9qGu-HQhkVGeFIPka1C_BJETHES/s1600/leftsvc.jpg"><img id="BLOGGER_PHOTO_ID_5472728496559114962" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 320px; CURSOR: hand; HEIGHT: 260px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_TVJ3nzlUeXk2fJ-i9VXQSIDYWO6V9pGtqPUUe8GLWxbRjP8JvulJqAOma23wlvjdsj-BMSdHMhtlDjPwL98DF_3_Q9wzeCMrJL4QFAnGIsSyycyKP9qGu-HQhkVGeFIPka1C_BJETHES/s400/leftsvc.jpg" border="0" /></a><br /><br /><br /><br /><em><strong><span style="color:#003333;">Persistent Left Superior Vena Cava (SVC)</span></strong></em><br /><br /><strong><span style="color:#000000;">0.3% of normal population have Left Superior Vena Cava (SVC). In most cases, the right SVC is also present (i.e. double SVC). Left SVC courses lateral to the aortic arch, main pulmonary artery, anterior to the left hilum and typically enters the coronary sinus that drains into the right atrium. In some cases, left SVC enters the left atrium. The variation, in isolation, is considered benign but but may be very frequently associated with cardiac abnormalities. Left SVC draining into the left atrium is highly associated with commonly ASD.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-22424121173544269472010-05-18T02:49:00.000-07:002010-05-18T02:49:00.230-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Tuesday May 18, 2010</span>
<br /></span><span style="color:#990000;">Coagulopathy Does Not Protect Against Venous Thromboembolism in Hospitalized Patients With Chronic Liver Disease
<br /></span></strong>
<br /><strong><span style="color:#000000;"><span style="color:#660000;">Background</span>: It is uncertain whether pathologically prolonged international normalized ratio (INR) seen in chronic liver disease (CLD) protects against venous thromboembolism (VTE). Previous studies reported VTE incidence of 0.5% to 1.9% in patients with CLD. We sought to evaluate VTE incidence among hospitalized patients with CLD according to INR levels. </span></strong>
<br /><strong><span style="color:#000000;">
<br /><span style="font-size:85%;"><span style="color:#660000;">Methods:</span> </span><span style="color:#000000;"><span style="font-size:85%;">This was a retrospective cohort study performed at a tertiary university hospital. We included all adult patients admitted with a primary diagnosis of CLD over a 7-year period. The primary outcome was the development of VTE during hospital stay. Patients were divided into quartiles according to their highest admission INR. VTE events and prophylaxis rates were compared among INR quartiles.</span> </span>
<br />
<br /></span><span style="color:#000000;"><span style="color:#660000;">Results</span>: During the allotted 7-year period, we included 190 patients. </span>
<br /></span><ul><li><span style="color:#000000;">12 developed VTE events, yielding a VTE incidence of 6.3%. </span></li><li><span style="color:#000000;">There was no significant difference in the incidence of VTE between INR quartiles. </span></li><li><span style="color:#000000;">Hospital mortality rates were higher in the higher INR quartiles than in the lower ones, but hospital length of stay was not significantly different. </span></li><li><span style="color:#000000;">VTE prophylaxis was not used in 75% of patients. </span></li></ul><span style="color:#000000;"><span style="color:#660000;">Conclusions:</span> <span style="color:#000000;">An elevated INR in the setting of CLD does not appear to protect against the development of hospital-acquired VTE.</span> The notion that “auto-anticoagulation” protects against VTE is unfounded.</span><span style="color:#000000;"> Use of DVT prophylaxis was extremely low in this population.</span>
<br /></strong>
<br />
<br /><a href="http://chestjournal.chestpubs.org/content/137/5/1145.abstract" target="_blank"><span style="font-size:78%;color:#003333;">Coagulopathy Does Not Protect Against Venous Thromboembolism in Hospitalized Patients With Chronic Liver Disease</span></a><span style="font-size:78%;color:#003333;"> - CHEST May 2010 vol. 137 no. 5 1145-1149</span>
<br /></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-69163371226415275122010-05-17T03:17:00.000-07:002010-05-17T03:17:00.397-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Monday May 17, 2010</span><br /></span><span style="color:#990000;">Hypocapnia and the injured brain: More harm than benefit<br /></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Objectives:</span> <span style="color:#000000;">Hypocapnia is used in the management of acute brain injury and may be life-saving in specific circumstances, but it can produce neuronal ischemia and injury, potentially worsening outcome. This review re-examines the rationale for the use of hypocapnia in acute brain injury and evaluates the evidence for therapeutic and deleterious effects in this context</span>.<br /><br /><span style="font-size:85%;"><span style="color:#660000;">Data Sources and Study Selection:</span> <span style="color:#000000;">A MEDLINE/PubMed search from 1966 to August 1, 2009, was conducted using the search terms “hyperventilation,” “hypocapnia,” “alkalosis,” “carbon dioxide,” “brain,” “lung,” and “myocardium,” alone and in combination. Bibliographies of retrieved articles were also reviewed</span>.</span><br /><br /><span style="color:#660000;">Data Extraction and Synthesis</span>: </span><span style="color:#000000;">Hypocapnia—often for prolonged periods of time—remains prevalent in the management of severely brain-injured children and adults. Despite this, there is no proof beyond clinical experience with incipient herniation that hypocapnia improves neurologic outcome in any context. On the contrary, hypocapnia can cause or worsen cerebral ischemia. </span></strong><br /><ul><li><strong><span style="color:#000000;">The effect of sustained hypocapnia on cerebral blood flow decreases progressively because of buffering; </span></strong></li><li><strong><span style="color:#000000;">subsequent normocapnia can cause rebound cerebral hyperemia and increase intracranial pressure. </span></strong></li><li><strong><span style="color:#000000;">Hypocapnia may also injure other organs. </span></strong></li></ul><strong><span style="color:#000000;"><span style="color:#000000;">Accidental hypocapnia should always be avoided and prophylactic hypocapnia has no current role.<br /></span><br /><span style="color:#660000;">Conclusions:</span> </span><span style="color:#000000;">Hypocapnia can cause harm and should be strictly limited to the emergent management of life-threatening intracranial hypertension pending definitive measures or to facilitate intraoperative neurosurgery. When it is used, Paco2 should be normalized as soon as is feasible. Outside these settings hypocapnia is likely to produce more harm than benefit.</span></strong><span style="color:#000000;"><br /></span><br /><br /><br /><a href="http://journals.lww.com/ccmjournal/Abstract/2010/05000/Hypocapnia_and_the_injured_brain__More_harm_than.17.aspx"><span style="font-size:78%;color:#003333;">Hypocapnia and the injured brain: More harm than benefit</span></a><span style="font-size:78%;color:#003333;"> Critical Care Medicine: May 2010 - Volume 38 - Issue 5 - pp 1348-1359</span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-49790696447276852932010-05-16T09:40:00.000-07:002010-05-16T09:48:05.155-07:00<strong><span style="color:#000066;">Sunday May 16, 2010</span><br /><br /><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">What is the equivalent strength of PO vs IV of Lopressor (Metoprolol)?</span></em><br /><br /><span style="color:#660000;"></span></strong><br /><strong><span style="color:#660000;">Answer</span>: <span style="color:#000000;">Equivalent maximal beta-blocking effect of Lopressor is achieved with oral and intravenous doses in the ratio of approximately 2.5:1. But be aware - this is not the standard by any means. Literature shows coversion effect ranging anywhere from 2:1 to 5:1.<br /></span><br /><br /><em><span style="color:#003333;">Previous related pearls:<br /></span></em><br /><a href="http://january2008-icuroom.blogspot.com/2008_01_10_archive.html"><span style="color:#660000;">Labetolol and Hyperkalemia</span></a><span style="color:#660000;"><br /><br /></span><a href="http://icuroom-01-2010.blogspot.com/2010_01_16_archive.html"><span style="color:#660000;">Ratio of alpha and beta blockade in Labetalol<br /></span></a><br /><a href="http://icuroom-pearls.blogspot.com/2006/03/atenolol-and-renal-failure.html"><span style="color:#660000;">Atenolol & Renal Failure</span></a><span style="color:#660000;"><br /><br /></span><a href="http://icuroom-pearls.blogspot.com/2006/06/friday-june-16-2006-carvediol-coreg-q.html"><span style="color:#660000;">Carvediol (Coreg)</span></a><span style="color:#660000;"><br /><br /></span><a href="http://icuroom-pearls.blogspot.com/2006/06/labetolol-dose.html"><span style="color:#660000;">Guided dose of labetalol in hypertensive emergency</span></a></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-14514375916898251512010-05-15T05:35:00.000-07:002010-05-15T05:35:00.325-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Saturday May 15, 2010</span><br /><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">What is the conversion (or equivalent) of propranolol to Nadolol in portal hypertension?<br /></span></em><br /><br /><span style="color:#660000;">Answer:</span> </span><span style="color:#000000;">Decrease the dose to half and give once a day.<br /></span></strong><br /><strong><span style="color:#000000;">In portal hypertension treatment, Beta-blockers are noncardioselective and reduce portal and collateral blood flow by 2 methods<br /></span></strong><br /><ul><li><strong><span style="color:#000000;">Reduction in cardiac output (blockade of beta1-adrenoreceptors) occurs.</span></strong></li><li><strong><span style="color:#000000;">Splanchnic vasoconstriction (blockade of vasodilatory adrenoreceptors of the splanchnic circulation). </span></strong></li></ul><p><strong><span style="color:#000000;">Most commonly used noncardioselective B-blockers are propranolol and Nadolol.<br /><br /></span></p></strong><strong><span style="color:#000000;">Propranolol is usually started at a dose of 20 mg every 12 hours, and increased or decreased every 3-4 days until a 25% reduction in the resting heart rate occurs or the heart rate is down to 55 beats per minute (bpm). The average dose of propranolol usually is 40 mg bid.<br /><br />Nadolol dosing is half the daily dose of propranolol, administered once a day.</span><br /><br /></strong><strong></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-42825203298842771602010-05-14T09:40:00.000-07:002010-05-14T09:40:00.238-07:00<strong><span style="color:#000066;">Friday May 14, 2010<br /></span><br /><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">One dose of intravenous Vitamin K antagonize the effects of warfarin for how many days?<br /></span></em><br /><br /><br /><span style="color:#660000;">Answer</span>: <span style="color:#000000;">One week<br /><br />High dose of Vitamin K (= 10 mg) produce rapid reversal; however, overcorrection and warfarin resistance complicate therapy. The effects of warfarin on clotting factor synthesis are antagonize for 7 days by a 10-mg dose of vitamin K. Low doses (0.5-2.5 mg) reversed anticoagulation within 24 hours (taking little longer but) with less risk of overcorrection or resistance to reinstitution of therapy.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-40303346086657890712010-05-13T09:38:00.000-07:002010-05-13T09:38:00.110-07:00<span style="color:#000000;"><strong><span style="color:#000066;">Thursday May 13, 2010
<br /></span><span style="color:#990000;">On stroke
<br /></span>
<br /></strong></span>
<br /><span style="color:#000000;"><strong><span style="color:#660000;">Q</span>:<em><span style="color:#003333;">What is Balint syndrome?
<br /></span></em>
<br />
<br /><span style="color:#660000;">Answer</span>: Balint syndrome is a triad of </strong></span>
<br /><ul><li><span style="color:#000000;"><strong>visual simultanagnosia, </strong></span></li><li><span style="color:#000000;"><strong>optic ataxia, and </strong></span></li><li><span style="color:#000000;"><strong>apraxia of gaze </strong></span></li></ul><span style="color:#000000;"><strong>
<br /><span style="color:#660000;"><em>Visual simultanagnosia</em>:</span> implies an inability to examine a scene and integrate its parts into a cohesive interpretation. A patient can identify specific parts of a scene but cannot describe the entire picture.
<br />
<br /><span style="color:#660000;"><em>Optic ataxia</em></span>: implies a loss of hand-eye coordination such that reaching or performing a motor task under visual guidance is clumsy and uncoordinated.
<br />
<br /><span style="color:#660000;"><em>Apraxia of gaze</em></span>: is a misnomer describing a supranuclear deficit in the ability to initiate a saccade on command.
<br />
<br />This may occur with bilateral parieto-occipital infarction, most often in the watershed between the PCA and MCA territories.</strong> </span>
<br /></strong></span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-29632959942454480202010-05-12T05:57:00.000-07:002010-05-12T05:57:00.422-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Wednesday May 12, 2010<br /></span><span style="color:#990000;">On Haldol</span><br /><br /><span style="color:#993300;"></span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Q:</span><em><span style="color:#003333;">Give at least 5 un-conventional uses of Haloperidol at bedside?<br /></span></em><br /><span style="color:#660000;">Answer:</span> </span></strong><br /><ol><li><strong><span style="color:#000000;"> Adjunctive treatment of alcohol and opioid withdrawal </span></strong></li><li><strong><span style="color:#000000;">Treatment of disorders such as tic, Tourette syndrome, and chorea </span></strong></li><li><strong><span style="color:#000000;">Treatment of severe nausea/emesis (postoperative, chemotherapy etc.) </span></strong></li><li><strong><span style="color:#000000;">Adjunctive treatment of severe chronic pain, (with analgesics) </span></strong></li><li><strong><span style="color:#000000;">Also used in the treatment of intractable hiccups</span></strong></li></ol>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-45709943519932566712010-05-11T06:24:00.000-07:002010-05-11T17:57:24.269-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Tuesday May 11, 2010<br /></span><span style="color:#990000;">Steroid controversy?</span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#990000;"></span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#990000;">Corticosteroids in the Treatment of Severe Sepsis and Septic Shock in Adults - A Systematic Review</span><br /></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;"></span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Context:</span>The benefit of corticosteroids in severe sepsis and septic shock remains controversial.<br /><br /></span></strong><strong><span style="color:#000000;"></span></strong><strong><span style="color:#000000;"><span style="color:#660000;">Objective:</span> We examined the benefits and risks of corticosteroid treatment in severe sepsis and septic shock and the influence of dose and duration.<br /></span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;"><span style="font-size:85%;"><span style="color:#660000;">Design:</span> We searched the CENTRAL, MEDLINE, EMBASE, and LILACS (through March 2009) databases as well as reference lists of articles and proceedings of major meetings, and we contacted trial authors. All reviewers agreed on trial eligibility. One reviewer extracted data, which were checked by the other reviewers and by the trials' authors whenever possible. Some unpublished data were obtained from the trials' authors. The primary outcome for this review was 28-day mortality.</span> </span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><br /><strong><span style="color:#000000;"><span style="color:#660000;">Results:</span> We identified 17 randomized trials (n = 2138) and 3 quasi-randomized trials (n = 246) that had acceptable methodological quality to pool in a meta-analysis. </span></strong><br /><br /><strong><span style="color:#000000;"><ul><li>Twenty-eight-day mortality for treated vs control patients was 35.3% vs 38.5% in randomized trials and 23.1% vs 19.2% in quasi-randomized trials </li><li>In 12 trials investigating prolonged low-dose corticosteroid treatment, 28-day mortality for treated vs control patients was 37.5% vs 44% </li><li>This treatment increased 28-day shock reversal 66.9% vs 58.6%; and reduced intensive care unit length of stay by 4.49 days without increasing the risk of gastroduodenal bleeding [8.1% vs 7.3%, superinfection [18.4% vs 17.9%], or neuromuscular weakness [1% 1.7%]. </li><li>Corticosteroids increased the risk of hyperglycemia [51.6% vs 46%] and hypernatremia (31.4% vs 19.2%]</span></strong></li></ul><p><br /></p><strong><span style="color:#000000;"></span></strong><strong><span style="color:#000000;"><span style="color:#660000;">Conclusions:</span> Corticosteroid therapy has been used in varied doses for sepsis and related syndromes for more than 50 years, with no clear benefit on mortality. Since 1998, studies have consistently used prolonged low-dose corticosteroid therapy, and analysis of this subgroup suggests a beneficial drug effect on short-term mortality.</span></strong><br /><br /><br /><a href="http://jama.ama-assn.org/cgi/content/abstract/301/22/2362" target="_blank"><span style="font-size:78%;color:#003333;">Corticosteroids in the Treatment of Severe Sepsis and Septic Shock in Adults -</span></a><span style="font-size:78%;"><span style="color:#003333;"> A Systematic Review - Djillali Annane, MD; Eric Bellissant, MD; Pierre-Edouard Bollaert, MD; Josef Briegel, MD; Marco Confalonieri, MD; Raffaele De Gaudio, MD; Didier Keh, MD; Yizhak Kupfer, MD; Michael Oppert, MD; G. Umberto Meduri, MD - JAMA. 2009;301(22):2362-2375.</span> </span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-49962701467486212492010-05-10T14:40:00.000-07:002010-05-10T14:41:47.859-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Monday May 10, 2010<br /></span><br /></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Q:</span> <em><span style="color:#000066;">While starting treatment for DKA (Diabetes Ketoacidosis) how much time should be allowed between initiation of IVF (hydration) and Insulin infusion?<br /></span></em><br /><br /><br /><span style="color:#660000;">A:</span> About one hour<br /><br />Insulin should be started about an hour after intravenous fluid replacement is started to allow for checking potassium levels and because insulin may be more dangerous and less effective before some fluid replacement has been obtained. Danger of life-threatening hypokalemia due to aggressive insulin administration is possible, as well as there is no advantage in starting insulin prior to rehydration and evaluation of serum potassium levels</span>.</strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-48874434509166476822010-05-09T12:05:00.000-07:002010-05-09T12:06:11.437-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Sunday May 9, 2010</span><br /><br /><br /><span style="color:#660000;">Q</span>: </span><span style="color:#003333;"><em>Is Pregnancy contraindication (Exclusion criteria) for Hypothermia Protocol?</em></span></strong><br /><strong><span style="color:#000000;"></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;"></span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">A:</span> </span><span style="color:#000000;">Yes</span></strong><br /><strong><br /><span style="color:#000000;">Standard exclusions for Hypothermia protocol:</span><br /><ul><li><span style="color:#000000;">Another reason to be comatose (e.g. convulsive status epilepticus) </span></li><li><span style="color:#000000;">Pregnancy </span></li><li><span style="color:#000000;">A known terminal illness preceding the arrest </span></li><li><span style="color:#000000;">Known severe pre-existing coagulopathy or active bleeding (relative exclusion, esp for patients on warfarin) </span></li><li><span style="color:#000000;">No limit on duration of resuscitation effort; however “down time” of less than 1 hour most desirable </span></li><li><span style="color:#000000;">Pre-existing DO NOT INTUBATE code status and patient not intubated as part of resuscitation efforts</span></strong></li></ul>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-60767009164088295752010-05-08T19:16:00.001-07:002010-05-09T12:07:00.216-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Saturday May 8, 2010</span><br /><br /><span style="color:#660000;">Q:</span> <em><span style="color:#003333;">Ibutilide is a type III antiarrhythmic agent approved for the pharmacologic conversion of atrial fibrillation and atrial flutter. Conversion rates is described upto 80% of cases. What is the half-life of Ibutalide?</span></em><br /><br /><br /><br /><span style="color:#660000;">A:</span> </span><span style="color:#000000;">3-6 hours<br /><br />Ibutilide (Corvert) is a Class III antiarrhythmic agent that is indicated for acute cardioconversion of atrial fibrillation and atrial flutter of a recent onset to sinus rhythm. Due to unknown reason, It show better results in atrial flutter as compared to atrial fibrillation.<br /><br />Ibutalide should be use with caution as it may degenrate rhythm into sustained Torsade (polymorphic ventricular tachycardia) in 3% of cases. Also due to longer half life, its not recommended to repeat dose more than twice as it may take upto 90 minutes before normal sinus rhythm gets restored.<br /><br />Dose is usually 1 mg over 10 minutes (may repeat once) but in post-cardiac surgery patients, one or two infusions of 0.5 mg is usually effective in terminating atrial fibrillation or atrial flutter</span></strong><span style="color:#000000;">. </span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-69667439106445604662010-05-07T00:06:00.000-07:002010-05-07T00:06:00.228-07:00<strong><span style="color:#000000;"> <span style="color:#000066;">Friday May 7, 2010<br /></span><br /><br /><span style="color:#990000;">Case:</span> <em><span style="color:#003333;">25 year old male is admitted to ICU with severe ethylene glycol toxicity. Patient is intubated and in severe acidosis. Hemodialysis is initiated to enhance elimination of ethylene glycol. Pharmacy call you with info. that they have located Fomepizole and now its available for patient. What adjustment in dosing is required for Fomepizole in patients already on "HD"?</span></em><br /><br /><span style="color:#990000;"></span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#990000;"></span></span></strong><br /><strong><span style="color:#000000;"><span style="color:#990000;">Answer</span>: </span><span style="color:#000000;">Fomepizole is significantly (50-70%) removed through hemodialysis. Standard dose is loading dose of 15 mg/kg followed by 10 mg/kg every 12 hours for 4 doses and then 15 mg/kg every 12 hours until ethylene glycol levels fall below 20 mg/dl. In patient already on dialysis, reduction of the interval between doses to 4-6 hours is recommended or to just start drip with infusion rate of 1-1.5 mg/kg/hour.</span></strong><br /><br /><strong><span style="color:#000000;">The cost of Fomepizole per vial is around $1000, and therefore is not widely stocked in most hospital pharmacy. One vial contains 1500 mg of fomepizole.</span></strong>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-434351495350553193.post-31041746634152512562010-05-06T00:48:00.000-07:002010-05-06T00:48:00.166-07:00<strong><span style="color:#000000;"><span style="color:#000066;">Thursday May 6, 2010<br /></span></span><span style="color:#990000;">Intermittent intravenous urokinase for critical limb ischemia as a salvage therapy in diabetic foot ulceration<br /></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Background</span>: Patients with diabetic foot ulceration and critical limb ischemia have a high risk of major amputation, especially if limbs can not be revascularized. Urokinase is effective in improving microcirculation in critical limb ischemia and might improve outcomes.</span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;"><br />Method:</span> An open, prospective, non-controlled, multicenter phase II cohort study in 77 type-2 diabetic patients with critical limb ischemia and diabetic foot ulceration. Patients had no surgical or endovascular treatment option based on interdisciplinary consensus. Urokinase (1 Mio IU if plasma fibrinogen more than or=2.5 g/l, 0.5 Mio IU if fibrinogen less than 2.5 g/l) was administered for 21 days as an intravenous infusion over 30 minutes. Each patient was followed up for 12 months.<br /><br /></span></strong><strong><span style="color:#000000;"></span></strong><strong><span style="color:#000000;"><span style="color:#660000;">Results:</span> Treatment for a median of 21 days resulted in 33% of patients being alive, having no major amputation and completely healed ulcers after 12 months. Total survival rate was 84.6%, amputation-free survival 69.2% and rate of major amputation 21.1%. Eighty-two percent of patients experienced at least once a complete ulcer healing within the course of study. Three serious adverse events were urokinase-related.<br /></span></strong><br /><strong><span style="color:#000000;"><span style="color:#660000;">Conclusion:</span> Urokinase treatment in diabetic patients with critical limb ischemia appears to be effective, feasible and safe. Although this calls for a larger, randomized and controlled trial, the results are highly relevant for clinical practice to prevent these patients from receiving major amputation due to diabetic foot syndrome.</span></strong><br /><br /><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/18766265" target="_blank"><span style="font-size:78%;color:#003333;">Intermittent intravenous urokinase for critical limb ischemia in diabetic foot ulceration</span></a><span style="font-size:78%;color:#003333;"> - Thromb Haemost. 2008 Sep;100(3):475-82.</span>Unknownnoreply@blogger.com0