tag:blogger.com,1999:blog-45500067095334546312024-03-06T20:01:56.093+00:00Emergency Medicine IcelandAnonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.comBlogger10125tag:blogger.com,1999:blog-4550006709533454631.post-12490120625424072042014-11-16T00:16:00.000+00:002014-11-16T00:19:21.888+00:00Male with abdominal pain and a flabbergast passenger<div class="Intro">This case of a gentleman with lower abdominal pain is interesting not only clinically, but more so through the prism of basic cognitive science and how it applies to clinical judgement. We take a closer look at how we are prone to making mistakes due to heuristics and cognitive biases. Also included are some gems on the obvious usefulness of ultrasound at the bedside and a gentle reminder about interpreting an elevated D-dimer result. Sit back, grab a 'kókómjólk' and enjoy the case.</div>
<h1>Abdominal pain</h1>
<p>51 y/o B. F. with prior history of appendectomy in childhood presented to the ED with abdominal pain after referral from his GP.</p>
<p>The pain was localized to the left iliac fossa and had been intermittently increasing during the last week. It was coupled with increasing abdominal distension. No acute changes noted on the day of his visit. No fever or chills. Denies nausea and was not sick in the last week. He experienced runny stool earlier in the week and was constipated for 2 days but had a normal bowel movement yesterday without any blood or mucus. No bowel changes in the last months and no urinary tract symptoms. Noticed reduced appetite, did not eat since yesterday. B. F. also believed he had been losing weight over the last couple of weeks.</p>
<p>On physical examination the patient looked tired but in no acute distress. Vitals were all normal. Moderately distended abdomen, diffuse tympany. Bowel sounds present but faint and distant. Diffuse pain on pressure but no tenderness or guarding.</p>
<h1>Cue in bedside ultrasound</h1>
<p>Bedside ultrasound of the abdomen was performed. Visualizing was complicated by substantial amounts of air in the GI tract. Liver appeared normal without any suspicious growths on gross examination. Noted significant dilation of small bowel mostly in left flank with fluid contents and hyperperistalsis (like a "nest of worms").</p>
<p>At this point there was a strong consideration of ileus or at least subileus and since patient had distended abdomen a feeding tube was placed but which drained only 230 ml of GI fluids. Patient received 5 mg of Morphine.</p>
<div class="Iframer"><iframe width="480" height="320" src="//www.youtube.com/embed/5Dk-8N94qXM"></iframe></div>
<div class="qa1">What are the diagnostic criteria for small bowel obstruction on ultrasound examination?</div>
<div class="qa2">
<ul>
<li><img class="GrowMe" src="http://www.em.emory.edu/ultrasound/images/SBO.jpg" title="Source: http://www.em.emory.edu/ultrasound/ImageWeek/small_bowel_obstruction1.html">Dilated bowel loops > 25 mm</li>
<li>Increased intraluminal fluid</li>
<li>Characteristic alternating peristalsis</li>
<li>Keyboard sign (visible plicae circularis)</li>
<li>Tanga sign (circumscribed free fluid)</li>
</ul>
</div>
<p>The sensitivity and specificity of detecting a dilated bowel with bedside US after a merely 10-minute training session is 91 and 84 %, respectively. Compared to the 50-80 % diagnostic accuracy of a plain CXR, otherwise most commonly used at the ED for establishing the diagnosis. For further info see <a href="http://www.em.emory.edu/ultrasound/images/ED%20US%20SBO.pdf" target="_blank">Jang et al. - Bedside ultrasonography for detection of small bowel obstruction in the emergency department</a>.</p>
<p><img class="GrowMe" src="http://i.ytimg.com/vi/gREx33_FVzo/maxresdefault.jpg" width="521">A short but excellent introductory video tutorial on performing the examination can be found <a href="https://docs.google.com/file/d/0B1C7VchoNCmsVWlxREpPeFJTRWc/edit" target="_blank">here</a> and is presented by the legendary <a href="http://sonospot.wordpress.com/2012/05/20/sonofiler-profiling-dr-chris-fox/" target="_blank">Chris Fox</a>, emergency physician with a fellowship in ultrasound and book author - he is by far one of the best ultrasound teachers and all his lectures can be found online for free - FOAM at it's best! The small bowel exam starts at 13:30.</p>
<p>An informative and more academic post on SBO and the whole ultrasound vs other modalities, even a CT/MRI scan, can be found on <a href="http://www.aliem.com/small-bowel-obstruction-diagnosis-ultrasonography/" target="_blank">Academic Life in Emergency Medicine</a>, an incredibly useful site in general.</p>
<h1>Putting the pieces together</h1>
<p>Blood panel came back normal (WBC 5.000) aside from an elevation of CRP at 60 mg/L. Liver enzymes normal and urine dipstick test clean.</p>
<p>Because of suspected ileus/subileus patient was sent for an abdominal CT scan to look for underlying cause (remember, ultrasound is excellent for finding ileus but bad for finding the cause).</p>
<p>Radiologist's answer for the CT image was that there was no ileus, no free gas and no free fluid in abdomen. The clinical scenario was not on par with the radiologist's answer so the images were reviewed and discussed with the on-call surgeon. We agreed there were indeed partially dilated small bowel loops, "sentinel loops" and the surgeon was even concerned about some mesenterial veins being prominent, possibly suggest mesenteric venous thrombosis (MVT).</p>
<div class="qa1">What are sentinel loops?</div>
<div class="qa2">A sentinel loop is a focal area of adynamic ileus close to an intra-abdominal inflammatory process. The sentinel loop sign may aid in localizing the source of inflammation. For example, a sentinel loop in the upper abdomen may indicate pancreatitis, while one in the right lower quadrant may be due to appendicitis.<br>For more go to <a href="http://radiopaedia.org/articles/sentinel-loop" target="_blank">Radiopedia</a> or <a href="http://www.radiologymasterclass.co.uk/tutorials/abdo/abdomen_x-ray_abnormalities/pathology_small_bowel_obstruction.html" target="_blank">RadiologyMasterClass</a>.</div>
<div class="Iframer"><iframe src="https://drive.google.com/file/d/0B1C7VchoNCmsRlprVGR4VFBtUzA/preview" width="640" height="480"></iframe><br>CT abdomen; frontal, coronal and sagittal views</div>
<p>Incidentally the prostate is calcified.</p>
<div class="qa1">Are prostatic calcifications always pathologic?</div>
<div class="qa2">No. Prostatic calcification is most often an incidental, asymptomatic finding but it can cause symptoms such as dysuria, infection, haemautira, obstruction or pelvic/perineal pain. Occasionally calcifications can be passed via the urethra.
<ul>Prostatic calcification may be either primary (idiopathic) or secondary to:
<li>diabetes mellitus</li>
<li>infections - e.g. tuberculosis or bacterial prostatitis</li>
<li>benign prostatic hypertrophy - calcification occurs in 10%</li>
<li>prostate cancer</li>
<li>radiation therapy</li>
<li>iatrogenic - urethral stents or surgery</li>
</ul>
<a href="http://radiopaedia.org/articles/prostatic-calcification" target="_blank">Radiopedia has more information on prostatic calcification</a>.</div>
<p>A d-dimer was ordered which came back 2.890 ng/mL. A venous blood gas was also taken but came back within expected limits.</p>
<div class="qa1">What are the possible pathological and non-pathological causes of D-dimer elevation</div>
<div class="qa2">
<ul>Pathological possibilities are manyfold and can make life harder for us when we order it beyond its intended use:
<li>Acute coronary syndromes</li>
<li>Acute upper gastrointestinal haemorrhage</li>
<li>Aortic dissection</li>
<li>Arterial or venous thromboembolism</li>
<li>Atrial fibrillation</li>
<li>Consumptive coagulopathy – DIC, VICC</li>
<li>Infection</li>
<li>Malignancy</li>
<li>Pre-eclampsia</li>
<li>Sickle cell disease</li>
<li>Stroke</li>
<li>Superficial thrombophlebitis</li>
<li>Trauma</li>
On the not-too-pathological spectrum are the following standard conditions:
<li>Age</li>
<li>Cigarette smoking</li>
<li>Functional impairment</li>
<li>Post-operatively</li>
<li>Pregnancy</li>
<li>Race</li>
</ul>
</div>
<p>A D-dimer should be ordered when we have a low pre-test probability for venous thromboembolism (VTE). The latter can be assessed with any of the scores available, usually the Wells criteria for DVT, which can be found on <a href="http://www.mdcalc.com/wells-criteria-for-dvt/" target="_blank">MDCalc</a>. </p>
<h1>Gotcha ...</h1>
<p>As everybody's eyes were focused on the dilated bowels an important find was missed until the images were reviewed for the second time… a large fluid-filled urinary bladder measuring about 15x12x7 cm - even the radiologist made no mention of it!</p>
<p>B. F. was diagnosed with urinary retention and catheterised in the ED with 1.500ml of clear urine passing in a few hours.</p>
<p>It is interesting to note that B. F. passed urine about 2 hours before the CT study was performed and still had about 1000ml of fluid visible on the CT scan. His HPI also did not include any urinary tract symptoms but upon further inquiry he describes hematospermia but had not seen a doctor for this.</p>
<p>B. F. was admitted to general surgery for observation but as symptoms relieved the suspicion of MVT was aborted. Urology was consulted and patient diagnosed with <strong>overflow incontinence</strong>. Patient was sent home with a urinary catheter for 10 days and Tamsulosin 0.4 mg x 1.</p>
<p>At outpatient follow-up no cause was found for his retention - the prostate was described as normal on palpation and ultrasound and cystoscopy showed no pathology. Patient continued on Tamsulosin and had no further urinary events but noticed memory problems and was referred for further cognitive evaluation.</p>
<div class="qa1">What clinical entity could explain this?</div>
<div class="qa2">Non-pressure hydrocephalus - although unlikely since gait and memory problems normally present before incontinence.</div>
<div class="qa1">What causes overflow incontinence?</div>
<div class="qa2">Transient urinary incontinence is often seen in both elderly and hospitalized patients. The mnemonic <strong>DIAPPERS</strong> is a good way to remember most of the reversible causes of incontinence, as follows:
<ul>
<li>Delirium or acute confusion</li>
<li>Infection (symptomatic UTI)</li>
<li>Atrophic vaginitis or urethritis</li>
<li>Pharmaceutical agents</li>
<li>Psychological disorders (depression, behavioral disturbances)</li>
<li>Excess urine output (due to excess fluid intake, alcohol, caffeine, diuretics, peripheral edema, CHF, hyperglycemia or hypercalcemia)</li>
<li>Restricted mobility (limits ability to reach a bathroom in time)</li>
<li>Stool impaction</li>
</ul>
</div>
<h1>To pee or not to pee</h1>
<p>Urinary incontinence is defined as the involuntary loss of urine that represents a hygienic or social problem to the individual. Urinary incontinence can be thought of as a symptom as reported by the patient, as a sign that is demonstrable on examination, and as a disorder. Urinary incontinence should not be thought of as a disease, because no specific etiology exists. The etiologies of urinary incontinence outlined above are diverse and incompletely understood.</p>
<p>Patients with urinary incontinence should undergo a basic evaluation including a history, physical exam and a quick urinalysis. </p>
<p>Here you can take a look at a nice drawing comparing different types of incontinence.</p>
<p><img src="http://sketchymedicine.com/wp-content/uploads/2012/02/20120215-231556.jpg" class="GrowMe"></p>
<p>It’s important to note the dynamics of urine loss with overflow incontinence since the bladder isn’t just filled to the brim and then it just empties at a certain point.</p>
<p>On the contrary, the bladder constantly remains full but just leaks small amounts of urine over time. Patients might not even notice any abnormalities, as was the case with B. F. The basic workup is aimed at identifying possible reversible causes. If no reversible cause is identified, then the incontinence is considered chronic. The next step is to determine the type of incontinence (urge, stress, overflow, mixed, or functional) and the urgency with which it should be treated. With slowly developing or chronic obstructions, patients typically are older, with multiple comorbid conditions, and they present with overflow incontinence and report little to no pain. But all that being taken into account, this is usually not a problem for the ED and should be handled by the patient’s GP.</p>
<h1>To err is human a.k.a. discussion</h1>
<p>Now, the reader that made it all the way through might come to ask the question: <em>“Why’d they chase the ileus diagnosis after doing an ultrasound, when they could’ve seen the bladder?”</em></p>
<p>This is a very valid question that opens up a further discussion of cognitive errors in clinical judgement. While doing bedside US the examiner might have gotten caught up in a possible diagnosis of ileus, focusing most of his attention on this eventuality. Once they noted a possible distended loop of bowel, they unknowingly paid less attention to the rest of the systems that might have been involved. This in turn led everyone to temporarily miss the overexpanded bladder that would have been clearly visible on US as well. This is called anchoring.</p>
<p>Anchoring occurs when we sink our teeth into a possible diagnosis and pursue it, while discarding other possibilities. It is a type of thinking much akin to the “horses and zebras” analogy.</p>
<p>It is the tendency to fixate on specific features of a presentation too early in the diagnostic process and to base the likelihood of a particular event on information available at the outset. This may often be an effective strategy. However, this initial impression exerts an overly powerful effect in some people and they fail to adjust it sufficiently in the light of later information. Anchoring can be particularly devastating when combined with confirmation bias.</p>
<p>Anchoring may lead to a premature closure of thinking. Patients may be labeled with an incorrect diagnosis very early on in their presentation. Diagnoses, once attached, are difficult to remove and may seal the patient’s fate. (Croskerry, 2002)</p>
<h1>Heuristics? Metacognition? Reflection ... Argh, where’s my Ritalin? Just tell me how I can fix it!</h1>
<p>Luckily some smart people have identified strategies to battle heuristics and cognitive biases.</p>
<p>First and foremost, as with all types of bias, we need to be aware at all times that we are prone to biased decision-making. This is called <strong>metacognition</strong> and it has been proven effective in the past.</p>
<p><img class="GrowMe" src="http://care2x.files.wordpress.com/2010/03/the_checklist_manifesto.jpg"></p>
<p><strong>Checklists</strong>. Checklists reduce cognitive load and can improve patient outcomes and safety. A properly structured and intelligently designed patient interview form that is thoroughly implemented in the work environment can help us avoid missing an important step. A very cool and accessible book on the subject by dr. Atul Gawande is <a href="http://www.amazon.com/The-Checklist-Manifesto-Things-Right/dp/0312430000" target="_blank">The Checklist Manifesto</a>.</p>
<p><strong>Morbidity and mortality conferences</strong> are helpful in highlighting cases where cognitive error was the source of raised morbidity.</p>
<p><strong>Clinical decision support</strong> (CDS) systems are emerging as a novel adjuvant to the classic approach to the clinical decision process. Modern solutions are integrated into the electronic health record (EHR) and can provide weighted suggestions to clinicians, based on multiparametric inputs. (Dinevski, 2011) One of the core objectives of the <a href="http://www.cms.gov/Regulations-and-Guidance/Legislation/EHRIncentivePrograms/Meaningful_Use.html" target="_blank">Meaningful Use</a> project in the United States, that aims to incentivize EHR adoption is implementation of at least one CDS system.</p>
<p><a href="http://www.bmj.com/content/349/bmj.g5702" target="_blank">Recent additions to the body of knowledge</a> on this subject however emphasize the importance of a wider change of culture that must take place in order to not only reduce errors but to also become aware of them in a healthy manner that does not promote defensive medicine.</p>
<h1>Four take home messages</h1>
<p><strong>1. D-dimer can tell you some things, but you wanna know which</strong>. In this case a follow-up measurement might be warranted to establish what the cause of the elevated D-dimer was, since ileus secondary to thrombosis was ruled out. Or was it ... (a CT venography was never done!)</p>
<p><strong>2. Ultrasound is cool for diagnosing ileus</strong>. High specificity and sensitivity compared to plain film. Can be performed at the bedside in the emergency setting. Fast, cheap, no radiation. Need we say more?</p>
<p><strong>3. We tend to make cognitive errors</strong>. Let’s not forget it. And with a bit of practice and vigilance we can avoid the most common pitfalls. We outlined some of the strategies above.</p>
<p><strong>4. Overflow incontinence presents as otherwise asymptomatic lower abdominal pain</strong>. This is attributed to the fact that there is no de facto retention since patients pass urine “normally”. The patient will present with discomfort in the abdomen. The thorough and systematic ultrasound examination is key to establishing the proper diagnosis in such cases. Plus it seems wise to keep urinary retention somewhere on the roster of differentials for lower abdominal pain with both genders.</p>
<p><strong>4. Overflow incontinence presents as otherwise asymptomatic lower abdominal pain</strong>. This is attributed to the fact that there is no de facto retention since patients pass urine “normally”. The patient will present with discomfort in the abdomen. The thorough and systematic ultrasound examination is key to establishing the proper diagnosis in such cases. Plus it seems wise to keep urinary retention somewhere on the roster of differentials for lower abdominal pain with both genders.</p>
<h1>Further suggested reading</h1>
<h2>D-dimer</h2>
<ul class="ItemList">
<li><a href="http://lifeinthefastlane.com/hematology-hoodwinker-001" rel="nofollow" target="_blank">Cool article on LITFL about the value, use and misuse of D-dimer in the clinical setting.</a></li>
</ul>
<h2>Ultrasound for SBO</h2>
<ul class="ItemList">
<li><a href="https://docs.google.com/file/d/0B1C7VchoNCmsVWlxREpPeFJTRWc/edit">The go-to instructable video by J. Christian Fox for learning how to perform an ultrasound exam when suspecting SBO</a></li>
<li><a href="http://www.em.emory.edu/ultrasound/images/ED%20US%20SBO.pdf">The article by Jang and collegues on the specificity and sensitivity of US versus plain film.</a></li>
<li><a href="http://www.aliem.com/small-bowel-obstruction-diagnosis-ultrasonography/">Blog post on Academic Life in Emergency Medicine about SBO + Ultrasound.</a></li>
</ul>
<h2>Overflow incontinence</h2>
<ul class="ItemList">
<li><a href="http://emedicine.medscape.com/article/452289-overview">A brief overview of urinary incontinence on Medscape</a></li>
<li><a href="http://www.ncbi.nlm.nih.gov/pubmed/23668444">Diagnosis of urinary incontinence</a></li>
</ul>
<h2>Clinical cognitive biases</h2>
<ul class="ItemList">
<li><a href="http://www.ncbi.nlm.nih.gov/pubmed/12414468">Great article with a nice chart of all the possible heuristics that influence our work</a> ("Achieving Quality in Clinical Decision Making: Cognitive Strategies and Detection of Bias")</li>
<li><a href="http://jabsom.hawaii.edu/jabsom/departments/CME/doc/Perkocha.pdf">Some nice quick lecture slides on clinical reasoning and the types of errors we tend to make</a></li>
<li><a href="http://www.intechopen.com/books/telemedicine-techniques-and-applications/clinical-decision-support-systems">A freely available chapter on clinical decision support. A good overview of the state of the art</a></li>
<li><a href="http://www.bmj.com/content/349/bmj.g5702">Intolerance of error and culture of blame drive medical excess, a recent article on the culture change that’s needed to improve healthcare in general</a></li>
<li><a href="http://www.nap.edu/openbook.php?record_id=9728&page=1">To Err Is Human: Building a Safer Health System (2000)</a></li>
<li><a href="http://www.ncbi.nlm.nih.gov/books/NBK2673">Very thoughtful review of efforts made since the publication of To Err Is Human and the advances in fairly attributing accountability in complex healthcare systems</a></li>
</ul>
<div class="Author"><u>Author</u>: <a href="https://twitter.com/jhanse90" rel="nofollow" target="_blank">Jan Hansel</a>, a 6th year med student from Slovenia, passionate about medical education, emergency medicine and music. A young FOAMer in training. [Editor's note: Jan visited our ED in August 2014 and not only practiced emergency medicine like a boss but also tried swimming in the cold Atlantic!]</div>
<div style="text-align:center;"><img style="width:800px;" src="https://drive.google.com/uc?export=view&id=0B1C7VchoNCmsQ1BwdEpMNkNDbGM"></div>Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-5422599438870748002014-10-01T22:08:00.001+00:002014-12-01T11:22:50.082+00:00Elderly patient with persistent hypoxia<div class="Intro">We present an unusual case of hypoxemia that was difficult to diagnose. The clinical scenario contained several small clues which when added up could perhaps, in retrospect at least, have led to timely diagnosis if they had been identified earlier. As this is a condition often discrete yet important for the physician to recognize we have presented the case for others to learn from. It contains interesting learning points on how to approach the hypoxic patient. We have used the opportunity to review basic lung physiology relevant to the clinician.</div>
<p>A 75 year old female, smoker, presented to the emergency department in an ambulance after being found on the floor of her apartment. She was fully conscious but had left-side hemiparesis and dysarthria. She was dyspneic and complained about bilateral pain low in the chest, radiating to the back.</p>
<p>Previous history was of hypertension and “some kind of arrhythmia” and she was currently taking antihypertensive tablets, ASA and zopiclone. There was no history of lung disease.</p>
<h2>Examination and labs</h2>
<ul>General: Patient is awake,> Vitals on arrival:
<ul>
<li>BP 162/102, pulse 112/min</li>
<li>temp 37°C</li>
<li>RR 28/min, sat 84% with 6L O2 on a simple face-mask</li>
</ul>
<li>Cardiac auscultation: normal</li>
<li>Pulmonary auscultation: prolonged expiration, bronchial sounds with fine crackles at the base.</li>
<li>Chest: A fresh bruise at approximately 6-7th rib on the left side, laterally to midclavicular line.</li>
<li>Neurological examination: dysarthria, flaccid hemiparesis of left side.</li>
<li>Labs:</li>
<ul>
<li>WBC 8.6, CRP 29</li>
<li>Hemoglobin 170, platelets 115</li>
<li>Na 142 K 3.6 creatinine 73</li>
<li>D-dimer 8.47 (<0.25), CK 2.933</li>
</ul>
<li>ECG: atrial fibrillation 108/min, otherwise normal</li>
<li>CT head: Old infarcts at basal ganglia bilaterally, old infarct in left temporal lobe. No fresh infarcts, no intracranial bleeding.</li>
</ul>
<p>tPA was judged as not appropriate as time from onset of stroke was far too long. Admission to neurology was prepared but patient was stuck in ED as there were no beds available in hospital.</p>
<p>It was noted that she was persistently hypoxic and not responding to O2 despite general maneuvers (increased FiO2, sitting patient up).</p>
<div class="qa1">Why is the patient be better oxygenated by sitting up?</div>
<div class="qa2">V/Q and shunting physiology is complicated but it is quite clear that body position affects both ventilation and perfusion (eg. use of prone position for patients with ARDS in ICU). All in all, supine position tends to decrease patient's own breathing and collapse alveoli in posterior (dependent) part of the lung - this leads to increased 'physiological (right to left) shunting' which is otherwise discrete and nonsignificant in the healthy subject. Patient sitting up or with head elevated (20-30') will do more efficient breathing (ventilation) and open more alveoli and decrease V/Q mismatch.<br> <a class="SeeMore" href="http://physther.net/content/65/5/613.full.pdf">[Phys. Ther. 1985] Effect of Body Position on Pulmonary Function</a> </div>
<p>An ABG was drawn (with 10L of O2): </p>
<ul>
<li>pH = 7.46</li>
<li>pO2 = 52mmHg (80-100)</li>
<li>pCO2 = 31mmHg (34-46)</li>
<li>HCO3 = 24 (22-26)</li>
<li>(calculated) SaO2 = 87%</li>
</ul>
<div class="qa1">How do you interpret the ABG?</div>
<div class="qa2">Uncompensated, mild respiratory alkalosis and hypoxia. Patient is hyperventilating to compensate for hypoxic state. Notice that pCO2 is not elevated, an important clue in the underlying condition.</div>
<div class="qa1">Does the patient need to be intubated?</div>
<div class="qa2"><img src="http://upload.wikimedia.org/wikipedia/commons/thumb/a/a3/Hb.jpg/250px-Hb.jpg" class="GrowMe fr-fir">This patient does not have an immediate need of endotracheal intubation but certainly has a risk of decompensating fast due to exhaustion from hyperventilating, further decreasing SaO2 and starting a downward spiral of rising pCO2 and acidosis. We should keep in mind that having a SaO2 of 86%, this patient is at the rim of the steep slope of the oxygen–haemoglobin dissociation curve and there is no room for further desaturation.</div>
<h2>Hypoxia management - ABC first!</h2>
<p>Endotracheal ntubation is not risk free and there are still other options to help this patient. Emergency physicians are trained to always have a plan B and C, being mentally prepared for intubation is wise in this scenario and the patient should absolutely be placed in the critical care bay where the airway wagon is near. </p>
<ul>
<li>A - Airway: patient is awake and protects her airway, excluding need of nasopharyngeal (Guedel) airway</li>
<li>B - Breathing: patient breathes spontaneously and does not need BVM assisted ventilation. FiO2 is 100% but flow can be increased so we change from simple mask to 15L O2 on reservoir mask which theoretically can supply lungs with approximately 80% oxygen.</li>
<li>C - Circulation: is not a problem here, she has minor tachycardia but not so that it reduces carriage of O2 to tissues.</li>
</ul>
<p><br></p>
<p>This is a good time to review possible routes of oxygenation, although FiO2 from wall is 100% it can be difficult to provide the patient with air 100% saturated with O2 molecules.<a class="SeeMore" href="http://www.ccpnetwork.ca/GWG/resources/Oxygen_Devices.pdf">Oxygen therapy devices</a></p>
<h3>Plan B - high flow O2 in nasal cannula!</h3>
<p>Using the nasopharyngeal route for oxygenation has until recently been thought to provide only limited O2 to the lungs but airway guru Richard Levitan has proven otherwise and his work has led to game changers in approaching the desaturated patient. These two articles introduced the main publication in layman language; <a class="SeeMore" href="http://www.epmonthly.com/features/current-features/the-neglected-orifice-">[EpMonthly] The neglected orifice</a> <a class="SeeMore" href="http://www.epmonthly.com/archives/features/no-desat-">[EpMonthly] No desat!</a></p>
<p>In our case we’d throw on 15L of 100% FiO2 with a nasal cannula and ensure patient is sitting upright - this simple maneuver would most likely be enough to prevent an unnecessary RSI. BIPAP is not recommended if patient is tired or drowsy but a CPAP trial could easily be done.</p>
<div class="Info">The articles mentioned above have been widely accepted by front-line emergency physicians as breakthrough publications for airway management and considered a must-read for every physician practising airway management especially RSI. The authors, Richard Levitan and Scott Weingart, are both highly respected teachers of airway and high-intensive care management and one of todays most wanted speakers in emergency medicine conferences. Luckily they are also advocators of <a href="http://lifeinthefastlane.com/foam/">FOAM</a> and thus provide most of their material on the world wide web, free of charge!</div>
<h2>Hypoxia workup</h2>
<p>We now had time to focus on the cause of hypoxia. The patient had no fever thus pneumonia was considered unlikely. With the bruised left chest wall, pneumothorax was considered and bedside ultrasound done. The ultrasound found absence of lung sliding (not normal!) on left side so a chest x-ray was ordered to evaluate for suspected pneumothorax. Noticeably, there were no signs of pleural fluid and absence of B-lines, ruling out hemothorax and pulmonary edema.</p>
<div class="qa1">What is the DDX for lack of lung sliding on ultrasound</div>
<div class="qa2">
<ul>
<li>pneumothorax</li>
<li>pleural effusion</li>
<li>massive consolidation/atelactasis</li>
<li>pulmonary contusion</li>
<li>advanced COPD</li>
<li>pleural adhesion/pleurodesis</li>
<li>severe fibrosis</li>
<li>if intubated</li>
<ul>
<li>mainstem intubation</li>
<li>poor ventilation</li>
</ul>
<a class="SeeMore" href="https://www.youtube.com/watch?v=26RQyxk5vGc">[Sonosite] Lung sliding explained</a> </ul>
</div>
<p><img class="GrowMe fr-fir" src="https://drive.google.com/uc?export=view&id=0B1C7VchoNCmsU09hckxySS1vYWs">Bedside CXR showed no signs of pneumothorax but elevated left diaphragm and mediastinal shift to left side, indicating decreased left lung volume.</p>
<p>Formal radiologist review: “Decreased volume of left lung with shift of mediastinum and trachea to the left side. No evident infiltrates but suspected smaller peribronchial consolidations behind cardiac contour. No pulmonary stasis. “</p>
<p>Pneumonia could not be excluded even with lack of fever (remember elderly patients commonly have inappropriate vital signs) but ARDS was ruled out.</p>
<p>The meaning of mediastinal shift was not clear at this moment and the grossly elevated D-dimer value could not be explained so the next logical step was to have order a CT angiography of the lungs. Avid readers should by now be able to make a definite diagnosis as enough clues have stacked up!</p>
<div class="qa1">What is the DDX for mediastinal shift?</div>
<div class="qa2">
<ul>
<li>1. Pulled (loss of lung volume)</li>
<ul>
<li>atelectasis</li>
<li>fibrosis</li>
<li>agenesis</li>
<li>surgical resection</li>
<li>pleural fibrosis</li>
</ul>
<li>2. Pushed (space occupying lesions)</li>
<ul>
<li>pleural effusion</li>
<li>pneumothorax</li>
<li>large mass lesions</li>
</ul>
<li>3. Mediastinal masses and thyroid tumors</li>
<li>4. Kypho-scoliosis</li>
</ul>
</div>
<iframe class="Iframed" width="640" height="360" src="//www.youtube.com/embed/6ApRxtBURZs"></iframe>
<p>Radiologist's answer: "No sign of pulmonary embolism. Small consolidations posterobasally left side. No pathological lymph nodes. No pneumothorax."</p>
<h2>Progress</h2>
<p>IV antibiotics were initiated and we decided to consult the pulmonologist who then asked the radiologist to review the CT which on more thorough examination revealed a bronchial mucous plug (marked by red arrow at 0:28 in video). The patient went for bronchoscopy where the plug was drawn out and SaO2 rose.</p>
<p><em><img class="GrowMe fr-fir" src="http://library.med.utah.edu/WebPath/jpeg1/LUNG051.jpg" alt="Image of total bronchial cast (not from our patient">Final diagnosis</em>: obstruction atelectasis secondary to mucous plug. Not surprising for a patient - a smoker - who has been lying immobilised for a longer time with pain in thorax, restricting air movement and dehydration contributing to the mucus buildup. Not unlikely she also has an undiagnosed, underlying COPD.</p>
<div class="qa1">Finally - why was the D-dimer increased in this patient?</div>
<div class="qa2">D-dimer is probably the single most incorrectly used lab test in the ED, commonly leading to unnecessary CTs. Remember, d-dimer was designed to RULE-OUT thrombosis in low-risk settings - the way we're using it today is no how it was supposed to be! <br>A study made 2007 demonstrated that immobility can elevate D-dimer titers by 50-60%. Other conditions and habits of the patient are also known to elevate D-dimer titres. Of the non-pathologic reasons include cigarette smoking and old age and pathological conditions including atrial fibrillation, stroke and infection. <a class="SeeMore" href="http://lifeinthefastlane.com/hematology-hoodwinker-001">[LITFL] Dealing with d-dimer debacles</a></div>
<h1>Atelectasis</h1>
<p>Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiology and leads to a deflated lung segment or even whole lung collapse causing hypoxia. There are several different types of atelectasis, depending on the cause, as exlained below.</p>
<iframe width="420" height="315" src="//www.youtube.com/embed/oKH7CtsEgHw"></iframe>
<p>The video above shows how recruitment (=PEEP + ventilation) re-expands a deflated lung and helps us understand the importance of atelectasis. <strong>Lung collapse</strong> is atelectasis of the whole lung.</p>
<p>Atelectasis is primarily <strong>obstructive</strong> or <strong>non-obstructive</strong>, seperated mainly by their pathophysiology. Common causes of obstruction are foreign bodies, tumors and mucus plugs and the size of atelectasis mostly depends on where the obstruction is located (main-, lobal- or segmental bronchi). Obstructive atelectasis (the more common type) is also called <strong>resorptive atelectasis</strong>, refering to gas absorption distal to the obstruction. In a few hours this leads to retraction of the affected lung and ventilation-perfusion (V/Q) mismatch and shunting as circulating blood is not oxygenated. Secondary infection may occur. If the area is large there will be significant volume loss of the affected lung and secondary hyperinflation of the healthy lung leading to the distinct x-ray features of elevated diaphragm and mediastinal shift towards affected area.</p>
<p>Chronic atelectasis will eventually lead to fibrosis and widening of the bronchi, better known as <strong>bronchiectasis</strong>.</p>
<p>Non-obstructive atelectasis is caused by loss of contact between parietal- and visceral pleura and shares the same final outcome or total lung collapse. There are different types of non-obstructive atelectasis as well. <strong>Relaxation/passive atelectasis</strong> is caused by pneumothorax or pleural effusion, <strong>compression atelectasis</strong> caused by any-space occupying lesion within the chest and <strong>adhesive atelectasis</strong> by any disruption in surfactant, classically ARDS.</p>
Atelectasis has many faces and the key to understanding its presentation, diagnosis and treatment is to know basic lung anatomy and the pathophysiologic mechanism. A detailed description of these can be found in the following excellent articles from eMedicine;<a class="SeeMore" href="http://emedicine.medscape.com/article/296468-overview">Atelectasis</a><a class="SeeMore" href="http://emedicine.medscape.com/article/1001160-overview">Pulmonary Atelectasis (pediatrics)</a>
<p>Atelectasis is a common concern in the ICU and post-operative ward. Decreased respiratory movements (eg. pain, diaphragma irritation), dehydration, O2 therapy and prolonged bed rest all contribute to atelectasis. The main methods to "recruit" alveoli are active adjustment of ventilator PEEP settings and the work of respiratory therapists encouraging patients to sit up and breathe properly with PEEP valves.</p>
<h3>Symptoms and signs</h3>
<p>They symptoms of atelectasis are subtle and non-specific; hacking, dry cough and sometimes mild fever. As atelectasis grows larger symptoms of hypoxia will dominate - cyanosis, dyspnea, tachycardia etc. On physical examination, dimishing breathing sounds may be the only clue.</p>
<h3>Radiology</h3>
<p>Plain chest X-ray (PA) is usually enough to diagnose the presence of an atelectasis but does neither define the type nor the exact cause.<br> </p>
<ul>
<li><u>Direct signs:</u>
<ul>
<li>displacement of interlobar fissueres (most reliable)</li>
<li>crowding of broncho-vascular markings</li>
<li>increased lung opacity (non specific)</li>
</ul>
</li>
<li><u>Indirect signs:</u>
<ul>
<li>hilar displacement</li>
<li>mediastinal shift</li>
<li>diaphragmatic elevation</li>
<li>Compensatory hyperinflation (if chronic)</li>
</ul>
</li>
</ul>
<p>In case of obstruction atelectasis air bronchograms are typically not present unlike the non obstructive types. The exact CXR signs to look for differ depending on which segment is involved. The signs are somewhat complicated, however, this short illustrated video gives an excellent explanation</p>
<iframe width="640" height="360" src="//www.youtube.com/embed/4oYBLkbDjhg"></iframe>
<p>A bedside chest X-ray (AP), as in our case has lower accuracy and will only reveal gross atelectasis and volume reduction of affected side. If there is a concurrent pleural effusion or large mass it can be difficult to define the cause of the atelectasis on CXR alone and CT is needed. CT scan will show the exact size, shape and location of the atelectasis. It can help in differentiating the obstructive type from the non-obstructive type, and serves as a guide for subsequent bronchoscopy. Although the obstructing lesion can be seen it may be difficult to define the exact cause, e.g. whether it is due to a tumor or a mucous plug. Such distinction will often require bronchoscopy and sampling of bronchial material by suction, endobronchial biopsy or transbronchial biopsy.<a class="SeeMore" href="http://radiopaedia.org/articles/lung-atelectasis">[Radiopedia] Lung atelectasis</a></p>
<h1>Systematic approach to hypoxia</h1>
<p>The patient´s data included the following important clues in the systematic approach to hypoxia: </p>
<ul>
<li>pCO2 was not increased and hypoxia therefore not caused by hypoventilation</li>
<li>A-a gradient was very high or 622mmHg (expected 21.5) excluding the cause to be low inspired O2 (see <a href="http://www.mdcalc.com/a-a-o2-gradient">http://www.mdcalc.com/a-a-o2-gradient</a>)</li>
<li>pO2 was not correctable by giving O2, suggesting shunt rather than V/Q mismatch and shunt is commonly caused by atelectasis, oedema, pneumonia or vascular shunt</li>
</ul>
Now wait a minute - what is the difference then between shunt and vascular shunt? Why doesn't pO2 increase with O2 when there's a shunt? It's time for a pulmonologist to explain some basic physiology! <u>TIP</u>: use Youtube's play faster feature for 1-2x playback speed (lower right corner)
<p><br></p>
<iframe width="640" height="360" src="//www.youtube.com/embed/wm1BA7EjYzU"></iframe><iframe width="640" height="360" src="//www.youtube.com/embed/pRIkwjlFRgo"></iframe>
<p>Recommended reading on hypoxia: <a class="SeeMore" href="http://medicalmediareview.com/2013/09/30/hypoxia">[The Medical Media Review] Hypoxia: Critical but Often Poorly Understood Concepts</a> <a class="SeeMore">[Sashidhar Reddy] Hypoxia</a></p>
<h1>Further reading</h1>
<p><strong><img src="http://empasite.com/wp-content/uploads/2013/04/Life-in-the-fast-lane-emergency-medicine-blog-FOAM.jpg" class="GrowMe fr-fir">Life in the Fast Lane</strong> is one of the giants in the emergency medicine blogosphere and contains vast amounts of free teaching material for emergency physicians. It is one of our favorite websites. The LITFL guys have summarised all kinds of vital information for both new and experienced EPs;</p>
<ul>
<li>Airway management from A to Z, text and videos, the best out there!<a href="http://lifeinthefastlane.com/own-the-airway/"><br>Own the airway</a></li>
<li>A case of atelectasis with even more learning points. Also reviews possible treatment options which we have not done here. <a href="http://lifeinthefastlane.com/pulmonary-puzzle-009"><br>Lung collapse, recruitment and bronchoscopy</a></li>
</ul>
<h1>Pulmonologist's comment</h1>
<p>Great case with many aspects and learning opportunities! In brief, if I had seen the patient I would have been immediately worried about the severe hypoxemia with respiratory alkalosis, commonly seen in pulmonary embolism. Therefore a lung CT angiogram would probably have been my first radiology test (I certainly hope so, but these things are so much easier in retrospect), after seeing the blood gas result. No CXR needed and I agree, definitely NO D-dimer! But the CT is difficult to read.<br>The case reminds us how easy it is to miss the unexpected on imaging studies, and that we should remember to thank our good colleagues in that field on a daily basis.<br>To view another aspect, this is a smoker with a mediastinal shift on CXR. This combination should make us think about lung cancer with endobronchial involvement. This was appropriately ruled out by bronchoscopy. Mucus plugs are common, especially in chronically ventilated patients, in those with asthma and in those with hypoventilation in general. Conservative treatment with mucolytics and respiratory therapy is often sufficient, however bronchoscopic suction with the help of saline may be required to remove plugs. In severe cases, mostly encountered in the ICU, different types of bronchoscopic instruments may be needed to pull out large, dry, and amazingly hard plugs, such as the one depicted above. Large or small, it is important to follow up on the removal of plugs with mucolytics, bronchodilators and physical therapy for several days to prevent the common problem of recurrence. /Ólafur Baldursson</p>
<h1>Summary</h1>
<p>So it turns out that the patient had a mucus plug leading to a large atelectasis resulting in hypoxia. The underlying mechanism is shunting where a large obstruction hinders blood flow from pulmonary arteries and redirects it to other areas already well oxygenated. Thus no increase in SaO2 is seen despite high flow FiO2 on a rebreather mask. As described, normal pCO2 is also typical for this type of hypoxia as ventilation itself is mostly unaffected.<br> </p>
<ul>
<li>A chest X ray can be used to diagnose atelectasis but CT and/or bronchoscopy may be required to find the cause</li>
<li>A-a gradient, pCO2 and pO2 response to oxygen are important to find the underlying cause of hypoxia</li>
<li>Elevated D-dimer is specific for thrombosis but there are many other causes that need to be considered as well</li>
</ul>
<div class="Author"><u>Authors</u>: Bergþóra Þorgeirsdóttir / David Thorisson</div>Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-76533074160970326022014-09-12T10:11:00.002+00:002014-12-01T11:22:57.367+00:00Young female with retrosternal pain and fever<div class="Intro">Following is a case of a disease not so commonly encountered but worth knowing because of a concerning presentation - chest pain.</div>
<p>A female presents to the emergency department with a two day history of epigastrial pain. The pain is located right under the xiphoid process, and described as a sharp pain radiating through her chest and to the back. The pain is constant and worsens while lying on her back, on deep inhalation and when she eats or drinks. Lying on her left side alleviates the pain somewhat.</p>
<p>Her previous medical history includes Darier's disease (time to freshen up on your dermatology) and gastritis. Medications include Hydroxyzine (Atarax), oral contraceptive pill and isotretinoin (Accutane).</p>
<p>On examination there are no major clues as to her condition. Normal examination of lung and heart. Abdomen is nondistended, soft without guarding but diffuse tenderness mostly in the upper region. Bedside ultrasound shows no pericardial effusion, contraction is seen as normal and no signs of hypo- or akinesia. Gallbladder is not distended and no calculi are found. ECG is evaluated as normal with sinus rhythm, minimal inferolateral ST depressions and T inversions - concluded as nonspecific in the current clinical scenario. In the tachycardic patient with dyspnea pulmonary embolism could have been suspected.</p>
<p>Blood tests reveal slightly elevated CRP at 54 but other tests normal, Troponin T and d-dimer included. Chest x-ray is normal.</p>
<p><img class="GrowMe" src="https://drive.google.com/uc?export=view&id=0B1C7VchoNCmsc3FfS3FwMVhkajQ" title="We couldn't make out the name of the original (chinese?) site but the url is http://tc.wangchao.net.cn/baike/detail_1090735.html">The morning after she develops fever 39°C. A trial of Gaviscon and Xylocain is unsuccessful. Augmentin 1,2g IV is administered empirically. On day three a gastroscopy is performed revealing <i>multiple small, white, indented lesions in the esophagus</i>. Candida infection is suspected and samples taken for PAD. CLO test is negative. She is suspected to have candida infection and admitted for treatment. The fever spikes occasionally up to 39.0°C but spontaneously resolves.</p>
<div class='qa'>
<p>What do you think is causing retrosternal pain and fever in this young female?</p>
<p>Results come back from PAD and virology, surprisingly revealing an active infection with <b>Herpes Simplex 1</b> (PCR positive). Other common causes of infectious esophagitis are candida and cytomegalovirus (CMV) and their presentation is similiar, requiring endoscopy for definite diagnosis.</p>
</div>
<p>A rare presentation for the above condition has been described where patient presented with intractable hiccups.</p>
<div class='qa'>
<p>How are persistent hiccups defined and what are other important ddx to consider?</p>
<p>Hiccups for >48h are true 'persistent hiccups'. Many etiologies have been described but scaring ED physicians the most is the patient with ACS presenting as hiccups, it's been documented with several cases - enough for the lawyers to recognize it and the media to write about it.
<a class="SeeMore" href="http://www.huffingtonpost.com/2012/01/27/hiccups-heart-attack-symptom_n_1236671.html">[Huffington Post 2012] Hiccups Were Patient's Only Heart Attack Symptom</a>
<a class="SeeMore" href="http://www.ncbi.nlm.nih.gov/pubmed/21277137">[Am J Emerg Med 2012] Hiccups as the only symptom of non-ST-segment elevation myocardial infarction</a>
</p>
</div>
<p>There are many treatment options and surely you should <a href="http://www.annemergmed.com/article/S0196-0644(88)80594-8/abstract">try rectal massage</a> before pushing in that chlorpromazine!</p>
<h1>Further reading</h1>
<p>eMedicine has an extensive and excellent review as always
<a class="SeeMore" href="http://emedicine.medscape.com/article/174223-overview#showall">[eMedicine] Esophagitis</a>
Amal Mattu as ever brilliant in his weekly ECG episodes, this time reviewing ECG findings in pulmonary embolism, do not start seeing patients in the ED until you have seen this!
<a class="SeeMore" href="http://ekgumem.tumblr.com/post/25873158451/ecg-findings-in-pulmonary-embolism-episode">[Amal Mattu] ECG findings in pulmonary embolism</a></p>
<p>Authors: JMÆ/DBT</p>Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-59150810984722124172014-01-26T02:27:00.002+00:002014-02-06T21:38:37.618+00:00A shocking blood gas!A healthy young man comes to the ED after having been chased by the police. They say he ran for his life at least 1km after which they found him lying down, presumably unconscious. With all systems intact and stable vitals he's presumed to be faking (pseudocoma).<br />
<br />
A quick glance in the ED reveals nothing new to refuse this theory - the patient has closed eyes and is totally resistant to pain stimulation but has all reflexes intact (eg. gag, cornea-) and with eyes forced open he's looking straight forwards (to contrast with eg. roving eye movements if true coma). ECG comes in normal.<br />
<br />
The police officers are informed that patient can return to police station as soon as
blood results have been seen. And here they come...
<br />
<br />
<div style="text-align: center;">
<img border="0" height="302" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi_sB7pe_rGMML2TkjXQ9saQtTxTP4t05Il_lW2VT-N6-LX93JvEet6xVlz1SiKG5ultnqJld74Kqq6BQUbpaexLYM93UgamtGc12mDM_ZMO4YdefH9nHOBZaLFu3xW8JN1ye-4RqoiYiw/s320/abg1.png" /></div>
<br />
With a hefty metabolic acidosis and lactate of 12,9 there's a minute of silence and doctors start thinking if there's a red herring in the room...<br />
<br />
Could the patient be intoxicated after all?<br />
<br />
Alcohols maybe?<br />
<br />
He doesn't smell - but do all alcohols smell?<br />
<br />
That's an anion gap of 18 - is it all explained by lactate?<br />
<br />
<br />
<br />
<br />
With a presumed intoxicated patient fluids are ordered and patient is prepared for admission. Just that 45mins later the policemen come to let know that the patient is now awake and feeling well and ready to leave the ED with the officers. So a new blood gas (venous of course, who's sticking arteries these days anyways!) is drawn and voila;<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiaDzuhmzg7mV7m3IJHpwnpe9NFjwdl7otljGnfaSphRBYQNy-HE0GrYTdTMurUswEUnknEvVlRUkABY280rSFAOTRWaIRBmwieOkQc5BQZu3iGkGGXGWaDQa6__5Zec95rzgwkPYp6uuI/s1600/abg2.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiaDzuhmzg7mV7m3IJHpwnpe9NFjwdl7otljGnfaSphRBYQNy-HE0GrYTdTMurUswEUnknEvVlRUkABY280rSFAOTRWaIRBmwieOkQc5BQZu3iGkGGXGWaDQa6__5Zec95rzgwkPYp6uuI/s1600/abg2.png" /></a></div>
<br />
<br />
All results normal... So the lactate acidosis turns out to be caused by strenuous physical exercise. Now howzaaat!<br />
<br />
<br />
<br />
<b>Learning points</b><br />
<ul>
<li>Lactate can be very high after exercise! I remember a study where alpine ski-ers had 6-7 after coming down a slope and I've heard experienced clinicians state it may temporarily reach 20 after seizure). But you can even get disturbing pH levels from it!</li>
<li>Ethylene-glycol and methanol are odorless!</li>
</ul>
<div>
<br /></div>
<div>
And my question to the audience: <i>can I somehow calculate presumed anion gap from lactate levels, so that I can exclude other agents?</i></div>Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-38488084608848914872014-01-26T01:31:00.001+00:002014-02-06T21:38:37.616+00:00Acute dyspnea and bedside ultrasoundElderly gentleman seeks the emergency department because of sudden dyspnea. He has no previous diagnosis of relevance such as COPD or heart failure. EMS notices crepitations on lung auscultation and treats patient with diuretics and CPAP with some relief. In the ED patient is still dyspneic and using accessory muscles for breathing but no clear crepitations are to be heard on auscultation and patient is not obviously obstructive. Stable vital signs, systolic blood pressure of 160mmHg.<br />
Bedside chest x-ray is ordered but image result is not expected for a while. The ultrasound machine is turned on and the cardiac probe put on patient's thorax, revealing...<br /><br />
<b>1. Heart, subxiphoid view</b><br />
<iframe allowfullscreen="allowfullscreen" frameborder="0" height="480" src="http://www.youtube.com/embed/7YS_R8tXw-g?rel=0" width="640"></iframe><br />
# Left > right ventricle => right strain and pulmonary embolism very unlikekly<br />
# No pericardial effusion anteriorly, 2-3mm black line seen and assumed to be physiologically normal fluid<br />
# Visually, decreased contractibility of left ventricle<br />
<br />
<b>2. Right pleura</b><br />
<iframe allowfullscreen="allowfullscreen" frameborder="0" height="480" src="http://www.youtube.com/embed/CuIK6rJRdM4?rel=0" width="640"></iframe><br />
Pleural effusion and several B-lines are clearly seen as the base of the lung reaches down, indicating right sided pulmonary edema<br />
<br />
<b>3. Left pleura</b><br />
<iframe allowfullscreen="allowfullscreen" frameborder="0" height="480" src="http://www.youtube.com/embed/jzPWnoBg4pU?rel=0" width="640"></iframe><br />
Great amounts of pleural effusion. No clots seen and thus no suspicion of blood. Multiple B-lines indicating left sided lung edema.<br />
<br />
<b>4. Right lung, apex</b><br />
<iframe allowfullscreen="allowfullscreen" frameborder="0" height="480" src="http://www.youtube.com/embed/2pIxbyo-984?rel=0" width="640"></iframe><br />
'Lung sliding' exludes pneumothorax. Multiple B-lines => edema reaches apex, suggesting massive pulmonary edema.<br />
<br />
<b>5. Left lung, apex</b><br />
<iframe allowfullscreen="allowfullscreen" frameborder="0" height="480" src="http://www.youtube.com/embed/d8P7fzT1vog?rel=0" width="640"></iframe><br />
Same as right side; thus patient has massive, bilateral pulmonary edema.<br />
<br />
The investigation was done in about 2 minutes.<br />
<br />
<b>The X-ray image arrives 45mins later</b><br />
<img class="GrowMe" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgB_YvO6OSrGmCGrhIyq7HEI4l-fH1u8CnTnFjf3o-Za0kwiNPMlEQ8E8VYk1BOn7-6Cd46mr2qqTMu92wWkTZWO_pCDKUXhO89Nwn8ccBm9_LIgV0Kf5-E7j1wEKH99ljkJ38eh091srk/" /><br />
It shows enlarged heart with widened pulmonary veins and interstitial fluid bilaterally. Bilateral pleural effusion, more on left side. ProBNP arrives at 2500 with minimal Troponin elevation. Patient is treated as acute left sided heart failure and treated with CPAP and nitro infusion (SCAPE).<br />
<br />
<b>Discussion</b><br />
Previously, ultrasound has been said to be impossible to use for evaluating lungs, after all <i>"air is ultrasound's greatest enemy"</i>. Experimenting with this has shown that indirect signs can be seen such as A- and B- lines and as air is replaced with consolidations and edema, ultrasound will immediately pick this up. For pneumothorax and pleural effusion, pulmonary edema and consolidations (pneumonia or ARDS), ultrasound is becoming a first choice for quick bedside evaluation. Increasing amount of data is supporting this and in some emergency departments, bedside chest x-ray has been replaced by ultrasound as only CT has better sensitivity for most conditions of relevance in the ED.<br />
<br />
<u>Pneumothorax:</u><br />
<a href="http://www.ncbi.nlm.nih.gov/pubmed/16141018">Acad Emerg Med. 2005 Sep;12(9):844-9</a><br />
“The sensitivity for chest radiography was 75.5% (95% CI = 61.7% to 86.2%) and the specificity was 100% (95% CI = 97.1% to 100%). The sensitivity for US was 98.1% (95% CI = 89.9% to 99.9%) and the specificity was 99.2% (95% CI = 95.6% to 99.9%)”<br /><br />
<u>Pleural effusion, pulmonary edema, consolidation:</u><br />
<a href="http://www.ncbi.nlm.nih.gov/pubmed/14695718">Anesthesiology. 2004 Jan;100(1):9-15</a><br />
“Auscultation had a diagnostic accuracy of 61% for pleural effusion, 36% for alveolar consolidation, and 55% for alveolar-interstitial syndrome. Bedside chest radiography had a diagnostic accuracy of 47% for pleural effusion, 75% for alveolar consolidation, and 72% for alveolar-interstitial syndrome. Lung ultrasonography had a diagnostic accuracy of 93% for pleural effusion, 97% for alveolar consolidation, and 95% for alveolar-interstitial syndrome. “<br />
<br />
Let's summarize the data above:<br />
<table class="Easy" cellpadding="0" cellspacing="0">
<tbody>
<tr><td></td><td>Auscultation</td><td>Chest X-ray</td><td>Ultrasound</td></tr>
<tr><td>Pleural effusion</td><td>61%</td><td>47%</td><td>93%</td></tr>
<tr><td>Consolidation</td><td>36%</td><td>75%</td><td>97%</td></tr>
<tr><td>Pulmonary edema</td><td>55%</td><td>72%</td><td>95%</td></tr>
</tbody></table>
<br />
<u>Pulmonary embolism</u><br />
The story of ultrasound becomes only better and better. Here, ultrasound is compared with CT for diagnosis of pulmonary embolism - the condition every physician fears to miss.<br />
<a href="http://www.ncbi.nlm.nih.gov/pubmed/11742931">Chest. 2001 Dec;120(6):1977-83</a>:<br />
“The sensitivity of TS [transthoracic sonography] for detecting PEs was 80% (sensitivity of CT scanning, 82%), and the specificity of TS for detecting pulmonary lesions was 92%”<br />
<br />
<br />
<u>Volume status and heart - ultrasound for evaluation for shock</u><br />
With ultrasound, a rough estimate of cardiac function and volume status (~vena cava status) can be done in instant. Together with above mentioned evaluation of thorax, ultrasound can in only 2-3 minutes give the physician a reliable diagnosis of acute dyspnea or shock. Add to this testing for free abdominal fluid, evaluating aorta and DVT diagnosis of lower extremities and then we have a full RUSH protocol (also known as FATE):<br />
<a href="http://emcrit.org/rush-exam/">RUSH: Rapid ultrasound for Shock and Hypotension</a><br />
<br />
Yes folks, the ultrasound is certainly here to stay!Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-48119666573752448772013-12-31T11:33:00.000+00:002014-06-12T11:48:06.051+00:00Iceland to the foreignerIceland is a country of 320.000 inhabitants known for welcoming visitors wholeheartedly. The landscape is rough yet soothing and has fostered inspiring artists such as Björk and Sigurrós and lately been attracting Hollywood’s film-makers. The wild highlands, mountains and clean water provide the world’s best raw-materials such as salmon and lamb-meat and Reykjavik is renowned for it’s high quality restaurants. The atmosphere in Iceland is unique and if you at anytime need peace from all the ongoing events you never far a way from a natural hot spring to soak in. Iceland is definitely the place to visit for the adventurer seeking something different!
<h1>More about Iceland</h1>
<a href="http://www.guidetoiceland.is/about-iceland/article/the-5-best-hot-springs-in-iceland">The 5 best hot springs in Iceland</a>
<h1>A few selected videos from Iceland...</h1>
<iframe allowfullscreen="" frameborder="0" height="320" mozallowfullscreen="" src="//player.vimeo.com/video/10022953" webkitallowfullscreen="" width="640"></iframe>
<iframe allowfullscreen="" frameborder="0" height="320" mozallowfullscreen="" src="//player.vimeo.com/video/75736121" webkitallowfullscreen="" width="640"></iframe>
<iframe allowfullscreen="" frameborder="0" height="320" mozallowfullscreen="" src="//player.vimeo.com/video/40558553" webkitallowfullscreen="" width="640"></iframe>
<iframe allowfullscreen="" frameborder="0" height="320" mozallowfullscreen="" src="//player.vimeo.com/video/30581015" webkitallowfullscreen="" width="640"></iframe>Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-89496037866817934272013-12-07T05:48:00.001+00:002014-11-15T00:08:41.662+00:00Chest pain with subtle yet serious ECG changes<div class="Intro">Following is a classic case underlining the importance of "STEMI equivalents" or ECG patterns requiring prompt attendance and cath lab activation as if it were a true STEMI.</div>
A 74 year-old previously healthy woman presented to the emergency department by ambulance with chest tightness and left arm numbness following exercise. She was stable on arrival, BP was 140/65 and pulse regular 65/min and pain free after receiving nitroglycerin.
<img class="GrowMe" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgDoXuWwoKvXPDWisFLE7GP7nQcP6X5YlaziEDXF6h7ItwZwkmw8fP2_iBf-HwC2G8dfGfNbKKLPdTRoDk6XUafgtJGJsE_n7Rc-zGeGw-l5qh6xkKF5qdfJmjrjzjQD0RKyyYseE84sXdh/s1600/Wellens.jpg" />
<div class='qa1'>Describe the T waves shown on the ECG</div>
<div class="qa2">This ECG mainly shows prominent inverted T waves in V2-5.</div>
<div class='qa1'>What are they indicative of?</div>
<div class="qa2">Biphasic or inverted T waves in precordial leads strongly suggest critical left anterior descending coronary artery stenosis. This pattern is referred to as <b>Wellens syndrome</b> or "LAD coronary T-wave syndrome". Generally, there is a history of angina and troponin levels are either normal or mildly elevated. ST elevations are rarely present. The majority of patients with this ECG pattern will develop extensive anterior myocardial infarction within weeks if no intervention is taken. Therefore, recognizing this pattern is of critical importance and cardiac catheterization should be performed promptly, despite a pain free patient.</div>
<div class='qa1'>Which test could be lethal for this patient?</div>
<div class='qa2'>This patient is likely to have very limited circulation to the anterior myocardium. A stress test could easily induce arrhythmias or in worst case cardiac arrest.</div>
<div class='qa1'>What are STEMI equivalents?</div>
<div class="qa2">Patients with <b>STEMI equivalents</b> have acute coronary artery occlusion without the classic ST elevation patterns we have all been taught not to miss.</div>
A paper by Rokos et al published in the American Heart Journal in 2010* reviewed STEMI equivalents requiring cath lab activation:<br/>
1) Posterior (V1-3) ST depressions<br/>
2) ST elevation >1mm in aVR along with depression of anterior leads<br/>
3) de Winter ST/T wave complexes anteriorly<br/>
<br/>
This article is free to view in link below but our great colleague and emergency physician Andy Neill in Ireland <a href='http://emergencymedicineireland.com/2011/08/advanced-ecg-findings-in-stemi/'>has reviewed the article nicely on his blog</a>.<br/><br/>
Wellens syndrome is a chronic coronary artery occlusion and therefore not a STEMI equivalent. It is nonetheless a serious and unstable condition that requires prompt intervention and every physician should be able to recognize it.<br/><br/>
Our patient was admitted to the cardilogy ward and was scheduled for cardiac catheterization the following day. She was stable and pain free on admission. A few hours later she developed a circulatory collapse and underwent acute catheterization which revealed critical stenosis of the left main coronary artery, LAD, circumflex artery and right coronary artery.<br/><br/>
* IC Rokos, WJ French, A Mattu, G Nichol, ME Farkouh, J Reiffel, GW Stone. <a href='http://download.journals.elsevierhealth.com/pdfs/journals/0002-8703/PIIS0002870310007581.pdf'>Appropriate Cardiac Cath Lab activation: Optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction</a>. Am Heart J, 160 (2010), pp. 995–1003.<br/><br/>
Read more about Wellens at LITFL
<a href='http://lifeinthefastlane.com/what-is-wellens-syndrome'>What is Wellens syndrome?</a><br/><br/>
<div class="Author">Maria Reynisdottir (stud. med.)</div>Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-29218457627435902882013-11-01T15:21:00.001+00:002014-11-15T00:39:54.210+00:00A case of extreme heart failure<div class="Intro">
This is a case of a complex heart failure patient I encountered in my residency. It contained many learning points which I'd now like to share, especially relating to clinical examination and approach to the patient with dyspnea and heart failure.</div>
60 y/o female comes with an ambulance to the ED because of increasing dyspnea for the last week. No chestpain, no fever, no coughing. She had initially sought her GP who noted low systolic blood pressure of 80mmHg and called an ambulance to send her directly to the hospital. Because of hypotension, paramedics decided not to give diuretics.<br/><br/>
In the emergency department, the patient is awake but tired and has resting dyspnea. Cheyne-Stokes breathing pattern is noted (frequency of 30 respirations/minute with few seconds of apnea intermittently). She has central and peripheral cyanosis and is peripherally cold, her skin is not marmorized or clammy. Vital signs show varying blood pressure, initial measurement 128/70, pulse 90/min. Intermittently her systolic pressure is as low as 75mmHg. Pulsoximeter shows show saturation of 74% with 3L O2, it has been placed on both hands and even earlobes and always has same values. She is afebrile.<br/><br/>
Patient has a previous history of 3-vessel coronary disease and end-stage heart failure, EF has previously been evaluated as 15-20%.
<div class='qa1'>What is Cheyne-Stokes breathing and what does it imply in this case?</div>
<div class='qa2'>It is the pattern of alternating periods of hyperventilation and apnea and is often frightening to those who see it for the first time. CS is generally coupled to neurological diseases and palliative care but has a strong correlation (30-50%) with congestive heart failure. The pathophysiology is not fully understood but is thought to derive from an imbalance between central respiratory drive and pCO2 in blood.
<a href="http://www.ncbi.nlm.nih.gov/pubmed/16138241">[Clinics (Sao Paulo). 2005] Cheyne-Stokes respiration in patients with congestive heart failure: causes and consequences</a></div>
<div class='qa1'>What is the difference between central and peripheral cyanosis?</div>
<div class='qa2'>Central cyanosis is a sign of desaturated blood because of poor ventilation or low cardiac output while peripheral cyanosis is because of poor perfusion. Not so important to distinguish clinically but central cyanosis is generally more serious.</div>
<div class='qa1'>Is the saturation of 74% in this case a reliable value?</div>
<div class='qa2'>No. A standard ED pulsoximeter estimates O2 saturation by using infrared light to calculate the difference between bound and unbound hemoglobin. It therefor depends on several factors such as pulsation of blood and thus adequate circulation. Which is not true in this case (previously documented decreased EF and clinical signs such as cold, cyanotic hands).
Other factors known to interrupt the pulsoximeter are carboxyhemoglobin and methemoglobin (false normal values).
<a href='http://lifeinthefastlane.com/education/ccc/pulse-oximeter'>LITFL has more details on the clockwork of a pulsoximeter</a></div>
<div class='qa1'>How can we obtain a more correct value?</div>
<div class='qa2'>Obviously, whatever we do with this kind of pulsoximeter, we will always get a false saturation value. Some ICUs use a more advanced pulsoximeter e.g. Masimo which doesn’t rely on peripheral circulation. In the ED, we need an arterial blood gas.
<a href='http://www.masimo.com/rad-57'>Masimo pulsoximeter</a></div>
<p>Patient was evaluated as critically ill but did not show clincal signs of immediate threatening circulation or organ failure; she was awake and alert so we decided we had some time to work her up and wanted to start with blood samples, first of all blood gas. The patient was cachetic and we had a hard time finding proper, pulsating arteries; the radial pulses could not be found and the inguinal ones were very vague.</p>
<div class='qa1'>Would it be safe to draw an ABG from the femoral artery?</div>
<div class='qa2'><img class="GrowMe" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiQRauUUF1uRNyDzIktZaaSG45sU0EVRTUR7HzAy5zwXBzbAygXfPzNuZ4QHJwwiorfOtgY4Dah7RjxiXpiwO9PhJAY3BWoQ09t-OasdmKJjc2lSx6vnIpe9IcU0rwzwZC5-uGqrJLInYhg/s1600/VAN+at+3cm+depth.jpg" alt="The VAN bundle is only 2-3cm deep! Image source: http://www.emergencyultrasoundteaching.com" />The risks involved in punctuating an artery are infection, bleeding and hitting other structures such as the accompanying femoralis nerve.<br/>
Using sterile techniques the infection risk can be minimized and the fact that we are only punctuating, not inserting a catheter, makes the risk even lower. Bleeding risk with a small needle such as the one mounted to the blood gas syringe is minimal. The risk of hitting the femoral nerve is overestimated, especially if ultrasound is used where the needle can be seen to hit the artery and nothing else. Even in the case of touching or even penetrating the thick sheath of the femoralis nerve, the risk of permanent damage is astronomical with needle so small. This has been thoroughly documented in the literature from research of femoral nerve blocks where complications are extremely rare. Expect the femoral artery at 1,5cm depth in the normal-sized patient and expect problems in obese patients where it may lay as deep as 5-7cm, far beyond reach for the short ABG needle.<br/>
Despite very low risk of injury, punctuating the femoralis artery (or vein even) is in my opinion rarely seen unless in extremis such as cardiac arrest and should be considered as a valid option when other sites are not possible.</div>
<div class='qa1'>What other punctuation sites would be feasible for an ABG?</div>
<div class='qa2'><img class="GrowMe" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhJrAQs-egQ6kk81EymL6evAO6a7Oy5Fysh8x57XzPwEEbDPUMF1aeilX-nikvmPvNTGG2TJdPRxKcOfNs7FPktq0MKwa-mCAmB8djs-8-jZVcVLH59r_jraybK-my9Q0bQ3pvctTp5YfRa/s1600/brachial+artery.jpg" alt="The brachial artery. Image source: http://www.medicine.mcgill.ca/physio/vlab/cardio/back.htm" />
<p>An alternative for those not so intrigued would be to find the brachialis artery which in most patients is easily palpated in the antecubital fossa, between the medial epicondyle and biceps brachii tendon.</p>
<p>The brachialis artery lies much deeper and will commonly move away from needle and thus harder to get to. It is though though commonly used in pediatrics where it is easier to maneuver.</p>
</div>
<div class='qa1'>We have been taught that volume status can be estimated from hemoglobin levels, what in the ABG tells us that Hb=153 is likely false?</div>
<div class='qa2'>Estimating volume status from Hb is known practice but should not be done from the sole value but rather the clinical picture. This patient is a heavy smoker and it shows in the CO-Hb value of 6.9% (normal: less than 1%). The patient has developed secondary polycythemia and the Hb values should be considered as falsely elevated.</div>
<p>A decent brachialis vein was seen and a venous blood gas (VBG) was drawn, revealing the following values:</p>
<div class="Info">
<ul>
<li>pH 7.280</li>
<li>pCO2 6.42 kPa</li>
<li>pO2 2.74 kPa</li>
<li>Na 128</li>
<li>K 4.8</li>
<li>Crea 86 umol/L</li>
<li>Ca 1.13 mmol/L</li>
<li>Cl 95 mmol/L</li>
<li>Glu 6.1 mmol/L</li>
<li>Lactate 7.0</li>
<li>Hb 153 g/L</li>
<li>CO-Hb 6.9%</li>
<li>MetHb 0.8%</li>
<li>calcluated SatO2 27.6%</li>
<li>HCO3 19.0mmol/L</li>
<li>BE -3.8mmol/L</li>
</ul>
</div>
<p>A lactate of 1.0 was found only a week ago. This VBG shows a state of mixed respiratory (uncompensated) and metabolic acidosis with normal anion gap (14) - most likely explained by lactic acidosis. As expected, the patient is sick! Increased lactate tells us that tissues are not being perfused adequately and most likely this is because of the heart failure and impending respiratory failure - the patient was getting tired of prolonged hyperventilation and needs help.</p>
<div class='qa1'>Lactate from VBG... that's not possible?!</div>
<div class='qa2'>So untrue, it's perfectly doable as long as it's correctly done; put on ice, take it to the analyzer within 10 mins!
<a href="http://emcrit.org/wp-content/uploads/lactate-faq.pdf">Scott Weingart's Lactate FAQ</a></div>
<div class='qa1'>A pO2 value of 2.74kPa is low, even for a VBG. Is the patient severely hypoxic?</div>
<div class='qa2'>There are two important learning points here and we should spend some time discussing this. The pO2 is very low and reflected in the SatO2 of 28% which is *calculated* from PO2. But that's where the fallacy begins.<br/>
A VBG has been show to correlate very well with ABG except for very high pCO2 states, uncommonly encountered and mostly irrelevant (have you heard of the patient who was incredibly hypercapnic? Would you run faster than if he was "just" hypercapnic?). For obvious reasons, VBG cannot measure PO2 since it is always presumed to be arterial and more commonly denoted as PaO2 (note that extra "a") to indicate it's arterial origin. Thus the calculated SaO2 value will always be wrong from a VBG - something I learned by error in this case!<br/>
But more important is the distinction between PaO2 and SaO2, mistakenly believed to correlate pretty well. After all they both measure the amount of oxygen in the blood. But PaO2 does not measure effective oxygen, ready for use by the tissues. It's just free O2 molecules and they need to be bound to hemoglobin to be of any use peripherally in tissues. Indeed, too high PaO2 (eg FiO2 100% for longer periods) sets ground for harmful free radicals - Amal Mattu recently had a great post on this on EmRap, reminding us to use O2 sparingly in the post-resuscitative phase after cardiac arrest.<br/>
Nontheless - PaO2 clearly indicates how much O2 the patient is taking in through the alveoli and low values suggest you should increase FiO2 and/or assist ventilation and even intubate if everything else fails. What PaO2 does not indicate is if the tissues are *receiving* O2 - the intubated patient on 100% FiO2 can die from hypoxia if hemoglobin is not working (eg. CO poisoning, severe anemia) or perfusion decreased (heart failure, severe bleeding). <i>Indeed, that's the definition of shock</i>, whatever it's cause.
<br/>The "perfusing O2" in blood is called 'oxygen content', CaO2 and it's value is calculated by the following formula:<br/>
CaO2 = SaO2 * 1.34 * Hb + 0.003 * PaO2<br/>
Which underscores the above; perfusing oxygen is literally independent on PaO2. To actually measure tissue perfusion (or hyperperfusion to be accurate), we need... lactate (there are more advanced tools in the ICU eg. Picco)! It's not the most important clinical knowledge but one of the cornerstones of understanding O2 in clinical medicine and reminder to the physician to not only look at the PaO2 value but the whole clinical picture.
<a href="http://dwb4.unl.edu/Chem/CHEM869V/CHEM869VLinks/www.mtsinai.org/pulmonary/ABG/PO2.htm">Excellent in-depth explanation of difference between pO2 and SatO2</a>
<a href="http://www.emrap.org/episode/2012/april/cardiology">Amal Mattu on EmRap: Post Cardiac Arrest Syndrome</a></div>
<p>Because of hypotension the nurse was getting impatient and wanted to start fluids. A more thorough examination is done:</p>
<div class="Info">
<ul>
<li>Skin: no turgor but general, diffuse pitting edema of whole body, hands, feet, sacrum and even up to flanks.</li>
<li>Cardiac: distant heart sounds, possibly S3 and a pansystolic murmur. Neck vein distension.</li>
<li>Lungs: normal respiratory sounds, no crackles, no wheezing heard.</li>
<li>Bedside ultrasound: a large liver but IVC was hard to visualize properly (this was in my first months of doing ultrasound, no pleural windows were done!). A rough "ECHO" shows all four chambers diffusely dilated and severe global hypokinesia of left ventricle, EF estimated 5-10%.</li>
</ul>
</div>
<p>A chest x-ray is done revealing considerable amounts of pleural fluid on right side, none on left. Slightly dilated central veins, no edema, no infiltrates.</p>
<div class='qa1'>Should this patient have fluids or diuretics?</div>
<div class='qa2'><img class="GrowMe" alt="The Forrester classification of AHF" src="http://www.uspharmacist.com/CMSImagesContent/2010/2/USP1002-ADHF-F1.gif" />This is a topic of great debate and a very interesting one as myths have been debunked and treatment protocols changed in only recent years (eg. Morphine is now out of AHF treatment unless palliative). All in all - recent studies have taught us that we have been doing it wrong for a long time and there is no single approach to the acute heart failure patient. The Forrester classification is an excellent categorization into four general categories of warm/cold (degree of perfusion where cold is hypoperfused as in this case) and wet/dry (with regard to pulmonary edema - our patient is dry). The different types of AHF need different treatment modalities and the patient above is a cold/dry one (with regards to pulmonary edema - chronic heart failure has collected edema peripherally with pitting edema, neck vein- and liver stasis). <br/>
Diuretics may be causing more harm than good as admitted patients get electrolyte imbalances and kidney failure. Their immediate circulatory effects are minimal and very short living and thus doubtful if they fit in AHF treatment at all. Inotropic medicines such as dopamine or simdax are much more relevant in this scenario, even vasopressors to induce better perfusion to tissues.<br/>
As Amal Mattu has so excellently pointed out, what seems “most correct” is to use diuretics to treat volume overload, not AHF by itself. If the lungs are full of edema because the whole body is and that fluid puts even more strain on the decompensated heart - whole body fluid needs to be removed. But these patients most commonly will present with acute onset of symptoms and with high blood pressure and need nitro and CPAP, not diuretics. These are the <b>SCAPE</b> patients, standing for “Sympathetic Crashing Acute Pulmonary Edema”. <a href='http://emcrit.org/podcasts/scape/'>Scott Weingart’s podcast about SCAPE</a> is a must listen as you will encounter these patients often in the ED and with no time to prepare yourself. They will be terrified when you see them because their adrenaline levels are sky high - thus the hypertension.
<a href="http://eurheartj.oxfordjournals.org/content/26/4/384.full">European Heart 2005 guidelines on acute heart failure</a></div>
<div class='qa1'>What is the medical jargon for massive pitting edema?</div>
<div class='qa2'>Anasarca.</div>
<div class='qa1'>Could unilateral, right sided pleural fluid originate from heart failure?</div>
<div class='qa2'>The most common cause of pleural effusion is heart failure. Frequently the effusions are bilateral (approximately 75%) but may occur alone on either side with the right side being more common.</div>
<p>Cardiology was consulted and was a little puzzled on the diuretics question but decided it was worth trying small dose lasix on the assumption that some inotropy (contractility) might be gained by shifting the Frank-Sterling curve. Patient was not obviously dehydrated and hypotension is most likely because of low cardiac output. In the cardiology unit Simdax and vasopressors (noradrenaline) were infused to treat a previous diagnosed 'dilated cardiomyopathy' on ischemic basis. The patient had previously stated she didn't want to be operated and only wanted medicines for symptomatic relief.</p>
<h1>Major learning points from case</h1>
<div class="Suffix">
<ul>
<li>Standard pulsoximeters in the ED cannot be relied on for SaO2 in heart failure or any form of decreased circulation.</li>
<li>VBG can be drawn from femoral vein, as long as sterile technique is used and navigated by ultrasound.</li>
<li>VBG correlates excellently with ABG values except for PO2, in low perfusion states an ABG must be used since the pulsoximeter gives false values.</li>
<li>Hypotension does not equal hypovolemia!</li>
<li>Diuretics should not be pushed thoughtlessly in acute heart failure and are seldomly first line treatment anymore - not even in acute, pulmonary edema or congestive heart failure!</li>
</ul>
<div class="Author">David</div>
/David
</div>Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-33828819392888057752013-09-11T17:06:00.001+00:002014-12-29T19:50:13.134+00:00The state of emergency medicine in Iceland in 2013<div class="Intro">This article originally appeared in issue 11 of Emergency Physicians International, as the original text was slightly modified it is published here in it's original state.</div>
<img class="GrowMe" src="http://www.ruv.is/files/imagecache/frmynd-stor-624x351/myndir/malinbrand_20120623_14_53_34.jpg" />
Emergency medicine (EM) in Iceland has has grown beyond all expectations in recent years. Currently nearly 20 consultants are working in the Emergency Department (ED) at the University Hospital in the capital, Reykjavik. With approximately 90.000 visits per year it is by far the busiest ED in Iceland. The hospital has all major specialties and most subspecialties represented and is thus able to provide a good back-up for it’s ED.<br />
<br />
Some resistance was met when the specialty was established about 20 years ago. The need was obvious and other specialties had minimal interest in working on the floor additionally to working daytime but some specialties had vested interests to keep a presumed position of power at the front line.<br />
<br />
Jón Baldursson (board certified 1992) came back from US in 1991, having himself experienced the practice of modern emergency medicine in Cincinnati, where the first EM training program in USA was established in 1970. With patience and excellent personal skills and formal training in emergency medicine he was able to convince the hospital management and political bodies that EM was the only right way to go and of paramount importance as the speciality was unheard of in Iceland at the time.<br />
<br />
A formal 2-year training program in EM was launched in 2002. It’s scope was and still is to provide physicians with the first half of the required training in the field. With an increasing interest worldwide and excellent conditions to practise emergency medicine in an academic hospital, a large group of ambitious and eager residents was recruited, many of whom are now returning having completed specialty training in the USA, UK, Australia, New Zealand and Sweden.<br />
<br />
Now that more consultants have returned with expertise from abroad the group has taken over nearly all lines of acutely sick patients but not wholly psychiatry, pediatrics (we do ped. trauma) and gynaecology. Airway management and procedural sedation is mostly in our hands by now. Being located far up in the Atlantic we are far away from bigger and more specialised centers and thus are mostly on our own - a utopia for the emergency physician!<br />
<br />
Our island is nearly half the size of the UK (103.000km2) but only populated with 320.000 inhabitants in a wild landscape of mountains and fjords. Thus, backup and medical consulting to rural clinics, EMS and HEMS (also serving surrounding Atlantic ocean for up to 250 miles off shore) is closely tied to our ED activity. Many rotating residents have thus had their first knowledge of emergency medicine through prehospital work which has helped to attract them to our program.<br />
<br />
Being a nation of few inhabitants creates short communicative distances and working in the ED you are most likely to somehow know your colleagues working in other departments of the hospital. There is only one medical school in Iceland. Thus, collegiality is respected, interhospital communications are softer and problems are usually solved without conflicts. This friendly climate made the introduction of emergency medicine easier.<br />
<br />
The relative isolation of the country increases need for communications with colleagues abroad and thus social media is greatly welcomed for emergency medicine in Iceland. We have 10 days per year set off for CME and strive to attend conferences overseas to stay up-to-date and establish relations with colleagues in the field.<br />
<br />
We see a bright future for emergency medicine in Iceland. We are a large group of young and enthusiastic physicians building up an academic emergency department with ever growing number of patients in a country having just ducked a financial crisis. With a tight budget and a growing need of resources, management welcomes new ideas and solutions to old problems creating a flourishing environment for young and creative physicians whether they want to do academic research or improve flow and statistics.<br />
<br />
It is worth noticing that all Icelanders learn English at school and speak the language fluently. Thus we have been able to invite colleagues from abroad who are interested in working in our department and thus become acquainted with the way we practice EM in our country and even see our country, from outside the ED.Anonymoushttp://www.blogger.com/profile/14025209991541600819noreply@blogger.com0tag:blogger.com,1999:blog-4550006709533454631.post-63200720125391984772013-08-02T19:30:00.001+00:002014-01-26T00:48:51.790+00:00Hold your horses...<img class="GrowMe" src="http://upload.wikimedia.org/wikipedia/commons/c/ce/Flag_of_Iceland.svg" />
This is a recently opened blog, created by emergency physicians in Iceland. Stay tuned as we expect to start activity in autumn 2013.Anonymoushttp://www.blogger.com/profile/13352773777783633683noreply@blogger.com0