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Presentation Skills = August 21, 2018

Presentations are an integral part of a physician’s commitment to teaching. However, not all presentations are equal and not all presentations are effectively conveyed. There are different devices used to augment presentations (Slides, Whiteboard, models/manikins etc.). The choice is tailored according to the learner’s and presenter’s needs. The media for presentation also varies whether we are addressing a small group or large group. This article provides the basic principles of effective presentations that would hopefully, make you a better presenter.

The Basics
Know your audience – There’s nothing worse than presenting to people who don’t care about your topic or simply not pitched to their level.
Practice makes a great presentation – This is not a secret. Knowing your presentation inside-out accompanied by a good flow of information makes it a master class.
Feedback – The presentation will never be perfect. But, obtaining constructive feedback from expert presenters accompanied by self reflection brings you closer each time.
Set your objectives – Be committed to a few points you want your learners to take home. A few points supported by the best evidence goes a long way.
Know your setting – You can put more detail presenting in a small group whilst you can only put a few points in a large group. Being familiar with your lecture area gives you a better feel and imagery when you practice and perform your talk.
Learners would rather read than listen. Powerpoints/slides draw attention away from you. TED talks are powerful even without media as speakers know their talks by heart alleviating the need for a powerpoint. In contrast, unprepared speakers rely more on printed or projected notes. Use slides to augment your message, paint a picture or start a discussion. Remember its a TALK not a READ.
It’s ok to finish early but it is a bad form to finish late. So, cut the amount of slides you need to use and eliminate busy slides.
Purpose of presentation as a spectrum: To Inspire or to Inform
If we were to dichotomise the purpose of presentations, it will be to inspire in one end and to inform in the other. If we were to address these two ends purely, we should be theatrical in one end and factual in the other. We should not be heavy on both ends. Light theatrics catches your audience hearts and be engaged in your talk. The right amount of facts stimulates the audience to think and to listen. The fine line is somewhere between the two ends of the spectrum and should meet your learners expectations. Again, know who your learners are.

NOTE: There are different learners as there are presenters. Be flexible and adapt to your audience both in culture and education standard and norms.

4 Cs of a Presentation
CAPTIVATE – Learners decide early on if they want to listen or not. Be strong in your opening. The presentation is a means of communication in as much as it is a PERFORMANCE. Performance entails composure, poise and confidence. Your voice, tone and body language depicts your character and ignites the interest of your users.
CONNECT – Rather than set the objectives early, start by answering WHY are you doing the talk? Presentations are a way to communicate. Its a two-way street. Ask a question or allow your learners to interact early on. Share a story that is relevant to their practice and yours, from this you build on the talk. Connection entails allowing your audience to talk. When you ask a question, allow a 5 second pause to answer. Similarly, when you mention an important point, allow a few seconds for them to reflect on that salient information.
CONVINCE – Adult medical learners need evidence of good practice. The medical group is much more scientific. Providing facts to support your talk is essential. Presenting arguments and controversies stimulates the audience.
CONCLUDE strongly – This is your last chance to leave a lasting impression and summarise your key points. Always make a good summary. If it’s not yet obvious, you’ll need to start like champion and end like a winner!

Allowing questions at the end of your talk allows learners to bring home the points with clarity and conviction. Make it a habit.

The Enigmatic Dizzy Patient - January 13, 2018

Diagnosing Patients With Acute-Onset Persistent Dizziness

1. A link to the article by Jonathan A. Edlow, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, MA Published Online: November 24, 2017 PlumX Metrics

2. Also, a few points to make about the vertiginous patient (Not pre-syncope, lightheadedness or dizziness suggesting another differential diagnosis)
From the Journal of Emergency Medicine Dr. Edlow and Dr. Newman-Toker recommended asking five questions in the evaluation of vertigo with acute vestibular syndrome
Is the patient unable to sit or stand help?
Does the patient have a focal finding on neurological examination?
Does the patient have worrisome spontaneous or gaze-evoked nystagmus?
Does the patient have negative HIT?
Does the patient have skew deviation (vertical eye misalignment)?
If the answer is yes to any of the above, further evaluation for stroke is recommended.

We already know that CT Brain even with contrast has a poor sensitivity. Do you know what MRI- DWI sensitivity is? Even within 24 hours we can miss up to 20% of cases. The fact is, posterior circulation strokes occurs in less than 1% (in this article it was 0.7% in about 1300 cases) of the dizzy/vertiginous patients you see.

We don’t expect all vertiginous patients to have a neurology review or imaging for that matter. As the article suggest, posterior circulation stroke is one of those “needle in a haystack” diagnosis. This can lead to over- testing and over-referrals. In turn, over-referrals may lead to over-testing. A problem we see so often.

Bottom line, stick with the old good physical examination and ask the right questions. We could care less with other examination but, not on an acutely dizzy patient. Your neurologic exam and history is more impactful than imaging in making a safe disposition plan for your patient. If CT imaging or even a DWI-MRI is your first go to, its already the wrong foot forward.

Acute Heart Failure - July 29, 2017

Clinical Nugget: Acute (on Chronic) Heart Failure in the Emergency Department.
Harry Elizaga, EDSS

A 65 y/o man presents with shortness of breath. He has bilateral lung wheezes and bibasal crackles. He is known to have COPD and has been using his puffers more often for the past few days. He denies having fever or increased sputum production. He has PND and orthopnea with no peripheral oedema.
His medical history revealed admissions in hospital with both COPD exacerbations and Congestive heart failure.
Both respiratory and cardiology teams are refusing to take the patient. Does this sound familiar?

Shortness of breath diagnosis in ED can be complex and the primary diagnosis can co-exist with another illness. Acute heart failure may be the cause of the ED presentation or just the tip of the iceberg for an underlying issue waiting to be addressed or missed!
We need to think of the causes to address the problem appropriately. Here is a simple visual which runs through the causes in broad terms: 1. Preload(salt intake, missed diuretics, unrestricted intake) 2. After load (hypertension) 3. Arrhythmia (AF) 4. Muscle (AMI, myocarditis) and 5. Valvular (AS, Valve rupture)

BMDH ED Acute Heart image

Harry E | BMDH
Traditionally, heart failure has been dichotomised into systolic vs diastolic, low output vs high output, right vs left etc.
A pragmatic way of viewing this is related to the patient’s haemodynamic state: A normotensive patient, A hypertensive or A hypotensive patient with heart failure. This classification along with identifiable causes is what we care for in the emergency department as it allows us to tailor initial treatment accordingly.

No single historical, examination or laboratory parameter can suggest the diagnosis. It is best interpreted as a whole. However, there are some features that are more predictive than others. I’ve included only the ones that are pertinent in terms of likelihood ratios as follows:

**(LR > 10 great predictor! LR> 5 good) _____________________+ve likelihood ratio_______________
Heart failure                                      5.8
Myocardial infarction                         3.1
Examination      s3 gallop                11 !
Hepato-Jugular Reflux                      6.4
Elevated JVP                                    5.1
Pulmonary Venous congestion       12 !
Interstitial oedema                          12 !
Alveolar oedema                              6
Pleural effusion                                3.2
Cardiomegaly                                  3.3
Atrial Fibrillation                               3.8
New T wave changes                      3.0

“Fortunately, our medical student was able to elicit a previous background of heart failure and AMI. On examination, he heard an S3 Gallop! JVP was < 3 cm so, he pressed on the patient’s RUQ which showed +ve hepato-jugular reflux. CXR showed signs consistent with heart failure and ECG showed atrial fibrillation with T wave changes.”
The cardiology registrar reviewed the patient and discovered the patient is being worked up for pulmonary fibrosis. Now what?
Luckily, the ED registrar thought of doing a lung ultrasound.”

Game changer
Bedside thoracic US for B-lines can be a useful test for diagnosing CHF. Predictive accuracy is greatly improved when studies are totally positive or totally negative. A two-zone protocol performs similarly to an eight-zone protocol

BMDH ED acute heart2.

When you see > 3 B-lines (like rays of the sun in a dark field) using the curvilinear probe. You’re golden! It’s worthwhile looking at the heart while you’re there.

“The cardiology registrar read about B lines in heart failure and accepted the patient’s care. But, then he also read that BNP can exclude a heart failure diagnosis and advised not to transfer the patient unless a BNP has been done.”

B-Type Natriuretic Peptide (BNP)
BNP is released when myocardial cells are stretched. This is true for heart failure. A BNP value <100 pg/mL essentially rules out heart failure as the cause of dyspnea, whereas values >400 pg/mL indicate a 95% likelihood of heart failure.

However, values between 100 and 400 pg/mL warrant further investigation. Unfortunately, the patients in the middle are the exact patients we want answers for. Before getting a result of >400 pg/mL, our patients are more likely already on NIV.

“The staff specialist knew that BNP wasn’t available in our local hospital and made the cardiology registrar aware of this fact. Besides, the constellation of symptoms suggests the diagnosis, why bother with a test that won’t change your impression or immediate management?”

Management questions (as Per ACEP policy 2007 for adult CCF patients
1. Is there a role for noninvasive positive-pressure ventilatory support in the ED management of patients with acute heart failure syndromes and respiratory distress?

Patients with acute heart failure syndrome who are dyspneic, but not necessarily in need of emergent intubation, may be candidates for noninvasive ventilatory assistance with either CPAP or BiPAP. CPAP provides a constant end-expiratory pressure, and BiPAP provides the same constant end-expiratory pressure, as well as added positive pressure at the onset of inspiration to assist ventilation.

CPAP and BiPAP have both been shown to improve differing respiratory, cardiac, and hemodynamic indices as well as specific outcomes among patients presenting with acute heart failure syndromes

Bottom Line:
Level B recommendation: Use 5-10 mm Hg CPAP by nasal or face mask as therapy for dyspneic patients with acute heart failure syndrome without hypotension or the need for emergent intubation to improve heart rate, respiratory rate, blood pressure, and reduce the need for intubation, and possibly reduce in-hospital mortality.

Level C recommendation: Consider using BiPAP as an alternative to CPAP for dyspneic patients with acute heart failure syndrome; however, data about the possible association between BiPAP and myocardial infarction remain unclear.

Should vasodilator therapy (e.g., nitrates, nesiritide, and ACE inhibitors) be prescribed in the ED management of patients with acute heart failure syndromes? Multiple studies suggest that nitroglycerin is effective in treating acute heart failure by its effective venodilation and preload reduction at low doses, and additional arteriodilation and afterload reduction at higher doses.

Nesiritide is a recombinant form of B-type (brain) natriuretic peptide that dilates veins, peripheral arteries, and coronary arteries with resulting reductions in preload and afterload similar to nitrates. However, nesiritide has failed to show superiority to nitrates in several studies of patients with acute heart failure syndromes. In addition, multiple meta-analyses have raised uncertainty regarding the safety of nesiritide and its possible association with worsening renal function and higher mortality.

Angiotensin-converting enzyme (ACE) inhibitors reduce both preload and afterload, improve renal hemodynamics, impair sodium retention, maintain or enhance left ventricular function, and attenuate sympathetic stimulation. However, no adequately powered, controlled, randomized clinical trials exist that evaluate the efficacy of ACE inhibitors in acute heart failure syndromes. In addition, several studies have reported first-dose hypotension in acute heart failure syndrome patients receiving oral ACE inhibitors.

Bottom line:
Level B recommendation: Administer intravenous nitrate therapy to patients with acute heart failure syndromes and associated dyspnea.

Level C: Angiotensin-converting enzyme (ACE) inhibitors may be used in the initial management of acute heart failure syndromes, although patients must be monitored for first-dose hypotension.

Should diuretic therapy be prescribed in the ED management of patients with acute heart failure syndromes? Although physicians have been reassured over the years by their bedside observations that loop diuretics (e.g., furosemide, bumetanide, and torsemide) appear to be effective in the treatment of patients with heart failure by increasing urine output and decreasing edema, currently there are no randomized clinical trials evaluating the clinical benefit of furosemide alone in patients with acute heart failure syndromes.

Studies have shown that aggressive diuretic monotherapy is unlikely to prevent the need for endotracheal intubation, as compared with aggressive nitrate monotherapy, and may also lead to worsening renal function. However, studies have shown there may be a role for diuretics in conjunction with nitrates, with a regimen of high-dose nitrates and low-dose diuretics providing more consistent clinical improvement than a regimen of high-dose diuretic and low-dose nitrates

Bottom Line
Level B recommendation: Treat patients with moderate-to-severe pulmonary edema resulting from acute heart failure with furosemide in combination with nitrate therapy.

Level C recommendations: 1) Aggressive diuretic monotherapy is unlikely to prevent the need for endotracheal intubation, compared with aggressive nitrate monotherapy. 2) Diuretics should be administered judiciously, given the potential association between diuretics, worsening renal function, and the known association between worsening renal function at index hospitalization and long-term mortality.

– Before commencing nitrates and overly diuresing the patient, ensure that they do not have severe aortic stenosis or a right ventricular MI as they are preload dependent.

Recommendation for high dose nitrates (>500mcg/min) as first line is prevalent. If the patient is critically ill and severely hypertensive, its a good thought. Remember, GTN 300-600 mcg SL is equivalent to a drip rate of 40-80mcg/min (Usual chest pain drip is at 10-20 mcg/min initially). Its a good marker that the patient will tolerate the same equivalent IV dose and titrate upwards 10-20 mcg every 10 minutes. There are other reasons why the patient is hypertensive during the initial few minutes in the resuscitation room. Apply NIV, give SL GTN, alleviate pain and determine appropriate initial dose once a blood pressure trend is established. – A patient with SOB with clear lungs- think of PE, high output states (thyrotoxicosis, anaemia), metabolic(acidosis/sepsis) and toxicologic causes

– Patients with End-stage renal disease- think of dialysis. If they are not anuric, they may respond to diuretic therapy in large doses >/=160mg IV

-Wang CS et al., JAMA, 2005
-Liteplo AS et al. Acad Emerg Med. 2009 Mar;16(3):201-10. doi: 10.1111/j.1553-2712.2008.00347.x. Epub 2009 Jan 29. ETUDES,
-Maisel A. B-type natriuretic peptide measurements in diagnosing congestive heart failure in the dyspneic emergency department patient. Rev Cardiovasc Med. 2002;3(suppl 4):S10-S17.

Influenza PCR and Tamiflu - August 21, 2017

As of this date, the flu risk is graded as HIGH across Australia. The flu risk stays lower during summer months and rises during the winter season. Our local hospital has recently been filled with influenza positive results. But, how reliable are the results of this test? Who are the patients at risk? Is tamiflu really beneficial?

The flu is a virus, and as such, is a self-limiting illness. However, severe illness and complications such as pneumonia, bronchitis, sepsis can develop. High risk groups include the elderly age group, pregnant women and Aboriginal and Torres strait islander people. Vaccination is recommended for these population.

It is also recommended that health workers have vaccination every year as influenza strains vary. Hence, the type of vaccine administered is also modified according to the prevalent strain. The evidence for this is not strong but, is fairly consistent in various studies: it reduces symptomatic influenza cases (NNT=33) and reduces morbidity and mortality in vulnerable patient populations.

Point of Care test (Requested as Rapid Respiratory Nucleic Acid Detection)
Our department utilises the GeneXpert flu assay- a PCR based influenza test. It has significantly higher sensitivity than Antigen detection tests. It only takes 60-80 minutes to process the results. Antigen-based studies showed decreased sensitivity in elderly patients and those with pneumonia. Xpert flu had sensitivity of 95.3% (95% CI). Some studies show a sensitivity as high as 97%-100%.

The increase in sensitivity of this test makes the flu season ever so prevalent in our emergency department. It is not safe to assume a false positive result in a season where the disease is prevalent. In other words, believe it!

Let’s remember that flu assays are intended as an aid in the diagnosis of influenza. A positive result can obviate the need for further testing. A negative result does not completely exclude the diagnosis. Furthermore, before leaning on this diagnosis, we need to discern high risk groups suffering from secondary complications of this viral infection.

Oseltamivir (Tamiflu)
CDC(Centre for Disease Control) recommends that antiviral treatment be started ASAP. Benefit is strongest if treatment is commenced within 48 hours. However, they aslo recommend this beyond 48 hours if a patient requires hospitalization.

The main study that showed benefit was Dobson’s meta-analysis of RCTs. This showed reduction of symptoms of one day, for a disease that normally lasts for a week. They also claimed reduction in hospitalisation. Two of the authors showed financial relationship with Roche(Tamiflu manufacturers).

The Jefferson’s study (Systematic review- Cochrane group) showed alleviation of viral symptoms by 16 hours. There was no significant effect on hospital admissions, pneumonia development, bronchitis or serious complications. They did show Oseltamivir had an increased risk of nausea and vomiting, headaches, renal events and appeared to have dose related psychiatric effects on two treatment trials.

Only 2 of 10 RCTs of oseltamivir have been published (Both funded by Roche and authored by Roche employees).

There is an ongoing fierce debate on Oseltamivir. Editors of the BMJ (Payne, Lenzer) and colleagues raised concerns about CDC’s recommendation of Tamiflu. They stated the recommendations may be substantially biasied by financial contributions CDC received from Gilead(Patent holder of Oseltamivir) and Roche. His analysis of the Dobson’s study showed only marginal benefit of Oseltamivir and criticized that the authors have understated the adverse outcomes of the drug.

When Cochrane attempted to update their review, ROCHE repeatedly refused to share unpublished data from the same study.

At the end of the day, institutional practice is followed and admitting teams decide on drugs to be prescribed for their patients.

But, what if this was your patient and yours only?

The stronger the level of evidence, the safer the practice.

In summary, get vaccinated, believe the PCR result, identify viral complications and consequent illness especially in high risk groups. Recommendations are only as good as the evidence behind them.

. References:

Aortic Dissection - June 22, 2017

Facts and Figures
  1. Bimodal distribution – A frail aorta in the young (connective tissue diseases) and the old (Peak 50-70 yrs old).
  2. Severe and abrupt pain are present in 90% of cases.
  3. Although pulse deficits are suggestive of dissection, these are present in only 15% of type A dissections.
  4. Advanced age and hypertension are the most common risk factors. Other risk factors include Marfan’s syndrome, giant cell arteritis, bicuspid aortic valve, coarctation of the aorta, trauma(deceleration injury), recent aortic valve surgery/ CABG, cocaine use and high intensity weight lifting!
    *70% of patients with dissections are hypertensive
  5. It’s a diagnostic challenge and the major cause of high mortality (68% in 48 hrs) is failure to recognise and treat in a timely manner.
  6. The most common site of dissection is the first few centimetres of the ascending aorta, 90% occurring within 10 cm of the aortic valve. The second most common is just distal to the left subclavian artery.
  7. The chances of survival are improved with early diagnosis, blood pressure and heart rate control and timely surgery if necessary.
  8. The mortality rate for Stanford Type A dissection (involving the ascending aorta) is 26% if managed surgically and 58% if medically managed.
  9. The mortality rate for Stanford Type B dissection (involving descending aorta, not ascending aorta) is 31.4% if surgically managed and 10.7% if medically managed.

  10. *Hence, type A dissections are managed surgically and type B dissections are managed medically. For Type B, there has been a current trend for endovascular repair (not surgery) for complicated cases. A complicated case is defined as having limb ischaemia, a severely collapsed true lumen, an impending rupture, intractable pain/HT despite optimal medical management. For uncomplicated cases, medical management is warranted.
    For dissections involving the arch, a hybrid surgical and endovascular approach is becoming popular.
    For both types of dissection an urgent transfer to a tertiary facility is required. However, pain and blood pressure control should be optimised for both.

Emergency Management
  • Immediate cardiothoracic/Vascular referral
  • Large bore IV access x2
  • If ruptured or impending rupture – activate massive transfusion protocol, crossmatch blood
  • Control heart rate (aim for PR 60-80) and BP (100-120 SBP) – use IV B-blocker (esmolol, labetalol, metoprolol) and if with difficult control use vasodilators. Beta blockers decrease the shear stress on the wall of the aorta, thus they should be initiated before vasodilators. Vasodilators when used alone can cause a reflex tachycardia. Labet­alol is used frequently as it has mixed vasodilatory and Beta-blocking effects. In some instances a combination of two drugs is more effective. Esmolol has a short half life and has the advantage of being easily titratable. Adding a vasodilator on top of this seem to be appropriate for better blood pressure control.
    * If there is a significant BP difference between the two arms use the higher number for treatment decisions.
  • Correct coagulopathy
  • Arterial line
  • Opiates or if need be PCA

Aortic dissection is part of AAS (Acute aortic syndrome). AAS is comprised of three diagnosis: aortic dissection, intramural haematoma and a perforated aortic ulcer. It is a general term used as it may be hard to discrimate between the three during an acute presentation.

Dissection presentation varies and like many ED cases they lie in a spectrum.

Most patients that reach the emergency department have stable vital signs. They can have an active dissection or a dissection that has stopped. Instability and death results from wall rupture, cardiac tamponade, myocardial infarction from RCA dissection or severe aortic insufficiency. Rupture has an 80% Mortality.

A patient can present overtly. That is, a patient in his 70’s with hypertension or a patient with Marfanoid features who presents with a ripping, sudden onset, severe chest pain radiating to the back with differential pulses and pain not responsive to Morphine.

Unfortunately, we see patients with non-classical presentations for which the “Chest pain plus” concept is important. The aorta has many branches. The dissection of the tunica media can involve the aorta solely or dissect through its branches causing occlusion. Hence, “chest pain plus” syndrome describes an aortic dissection (chest pain) and symptoms related to branch occlusion (plus).

Examples of plus symptoms are the following:

Stroke or TIA symptoms – when neck vessels are involved

Paralysis (leg weakness)- when spinal arteries are involved

Difference in radial pulse/femoral pulse, absent pulses or extremity paresthesias – when subclavian or femoral arteries are involved (most dissections will have normal pulses)

Flank pain, back pain, abdominal pain – Dissection of the descending aorta, renal arteries, coeliac artery (mesenteric ischaemia) or even rupture

Syncope – tamponade/concealed rupture, AMI from RCA involvement, severe pain

Why making this diagnosis is challenging ?
Pain is the most initial common symptom. However, in a study by Meszaros, pain was absent in 6 of 72 patients (8%)!

Chest pain is a common presentation and aortic dissection accounts for a small fraction of these. Our bias leads us to think about more common problems.

CT aortogram subjects patients to a high contrast load and ionizing radiation. We, rightly so, are selective with our approach.

An ECG may show ischaemic changes (dissection involving RCA territory) deviating the diagnosis to ACS.

Classical signs of widened mediastinum, obliteration of aortic knob on CXR are commonly not present.

The “plus” symptoms are more apparent than the chest pain.

Acceptable imaging modalities includes a CT aortogram, transthoracic echocardiography (TTE), transesophageal echocardiography (TEE), MRI. The choice of imaging depends on the availability and the experience of the emergency staff. Whilst we can perform bedside Transthoracic echo, this may only visualise the ascending aorta. This is 75% diagnostic for Type A, 40% for Type B while TOE has much higher values and is operator dependent.

Studies have shown a good sensitivity of d-dimer ( >98-99%) for aortic dissection but there is yet to be a validation study done. Furthermore, if clinician suspicion is high, it is hard to rest your decision on a d-dimer. It certainly should make you feel comfortable if it’s normal in a low risk patient with alternative diagnosis.

Aortic dissection is a life-threatening condition. As the symptoms of these are often nonspecific, physicians need to have a high index of suspicion. A sudden onset pain(chest, flank, abdomen, back) is still the most common presentation. But, it is worth knowing symptoms that suggest arterial branch dissection(plus symptoms) to clinch the diagnosis. A bedside echo can help establish the condition and exclude important differentials such a pulmonary embolism or cardiac tamponade. A negative d-dimer is reassuring but not definitive.

Tanabe. 2008 Aortic dissection in the elderly. Clinical Geriatrics: Vol 12, number 8

Meszaros et al. Epidemiology and clinicopathology of aortic dissection; Chest 2000 May;117(5)

IRAD ( International Registry of Acute Aortic Dissection

Michael DeBakey. Aortic Interlude- aortic dissection, and screening recommendations for abdominal aortic aneurysm; Issue: BCMJ, Vol. 53, No. 2, March 2011, page(s) 79-85 Articles


Ultrasound and Cholecystitis diagnosis in BMDH ED - April 4, 2017

Ultrasound and Cholecystitis diagnosis
source: MedRx

Biliary colic to cholecystitis is a diagnostic spectrum which can be difficult to diagnose clinically. Cholecystitis starts with gallbladder obstruction followed by irritation of bile salts and subsequent inflammation (note: not an infection at this stage!). Prolonged stasis can lead to subsequent bacterial infection.

The above image findings on ultrasound plus sonographic Murphy’s suggests the diagnosis of cholecystitis. Gallstones causes about 90-95% of cases whilst acalculous cholecystitis accounts for 5-10%.

The sensitivity of sonography for gallstones exceeds 95% on various studies but much less for cholecystitis.

Some facts about diagnostic imaging in cholecystitis:

“Cholescintigraphy has the highest diagnostic accuracy of all imaging modalities in detecting acute cholecystitis, with a sensitivity of 96% at a specificity of 90%.

Summary estimates of sensitivity and specificity for Ultrasound are 82% and 81%, respectively.

Diagnostic accuracy of MR imaging is comparable to that of US.

Evidence on the diagnostic accuracy of CT, which is frequently used in clinical practice, for suspected cholecystitis is scarce.”.1

The US sensitivity is lower than what is commonly reported. However, this was a good systematic review which was adjusted for verification bias and was rigorously done. Most studies overstate ultrasound sensitivity to a value > 95%. This is concerning as this causes overdiagnosis and untimely surgeries. It is worthwhile mentioning that in this systematic review, the use of surgery and/or clinical follow-up as reference standard was assessed in evaluating eligibility. Details on the proportion of patients undergoing surgery and features used at surgery or at histopathologic analysis to diagnose acute cholecystitis were also recorded.
Now, how does this apply to ED bedside Ultrasound? A study done on ED trainees(2) showed ED bedside interpretation was 88% sensitive [95% CI, 84–91%] and 87% specific [82–91%]. It is important to note that the gold standard here was radiology US interpretation of the scan!

Does fasting and non-fasting scan matter? In Sinan’s study(3) they illustrated the fact that visibility of abdominal organs did not differ between fasting and non-fasting patients. It appears from this study that fasting before abdominal ultrasound examination is not necessary. I need to point out that these patients had light breakfast and not a heavy meal (which probably represents most of our sick patients who come to ED anyway).

Implications for Patient Care in our local hospital:

If we image a distended, inflamed gallbladder with pericholecystic fluid and gallstones, there is no argument regarding the need for a surgical review even if it were an ED performed US. I’ll go a bit further and state, if I perform a bedside US and see gallstones coupled with sonographic Murphy’s, the patient needs surgical review. If I don’t have an ultrasound machine but, do have a history and examination finding that suggests cholecystitis, the disposition is as above.

Ultrasound and pathology tests are nice to have tests that facilitates surgical referrals. They have definite value in evaluating differential diagnosis. But, having no tests or a negative finding does not exclude cholecystitis if our clinical judgment is strong.

Some of our sonographers adhere to mantras about fasting times and imaging. Whilst we have managed to overcome CT fasting time by an ED senior sign off, we are yet to apply this to upper abdominal sonography. This will be discussed in a consultant meeting.


1.Jordy et al, A Systematic Review and Meta-Analysis of Diagnostic Performance of Imaging in Acute Cholecystitis; RSNA Vol 264 Sept 2012

2. Scruggs et al, Accuracy of ED Bedside Ultrasound for Identification of gallstones: retrospective analysis of 575 studies; West J Emerg Med 2008 Jan
3. Sinan et al : Is fasting a necessary preparation for abdominal ultrasound? BMC medical Imaging 2003


ALS: Automated CPR device and the Resuscitation Team - January 25, 2017

By H.Elizaga EDSS

Guidelines and Team-based care

Population-based studies may fulfill the goal in public health.  However,  the application of this to our individual patient can sometimes be problematic. Cardiac arrest Guidelines and ALS recommendations addresses providers at a similar level despite having different expertise.  Experts can be conflicted by a prescriptive approach whilst less experienced operators feels discomfort deviating from guidelines.  Guidelines are important, it creates a common language and a platform from which teams can be trained on.  If we don’t speak the language and deviate from guidelines the rationale should be explicitly communicated to the team.  Otherwise, this becomes a common source of conflict.

The main challenge is being able to consolidate expert tasks, respecting guidelines and still maintaining patient-centred and team-based care.

Evidence-based interventions in Cardiac Arrest

In cardiac arrest, the patient’s course is influenced by the aetiology, demographics, health status, initial resuscitation (prehospital) as well as system level factors (paramedical and medical). To think that we can just extrapolate results from small changes in patient management is challenging, if not, simplistic.

Mechanical CPR

Will this be ever better than manual chest compressions?

Studies on mechanical CPR have continually looked at patient survival as their main primary outcome.  The LINC trial was published early 2014, comparing normal resuscitation with the LUCAS automated CPR device.  There were no difference in survival to hospital, or discharge from hospital found.  In the Ong et al study (Systematic review 2012) they found insufficient evidence to support or refute the use of mechanical CPR devices in settings of out-of-hospital cardiac arrest and during ambulance transport. They stated, there is some low quality evidence suggesting that mechanical CPR can improve consistency and reduce interruptions in chest compressions, but there is no evidence that mechanical CPR devices improve survival.

The study by Perkins (LANCET 2015) concluded that there was no evidence of improvement in 30 day survival with LUCAS-2 compared with manual compressions.   On the basis of this study and other recent randomised trials, adoption of mechanical CPR devices for routine use does not improve survival.

We may not be addressing the right questions in these studies. The benefit of automated CPR may not affect survival but may impact the resuscitation team(provider fatigue or stress) and the emergency department (provider availability, department safety) during a long resuscitation case.

Individual experience also tells us it’s a practical method when: 1. The patient needs to be transferred to a cath lab for PCI 2. There is a prolonged transport time to hospital 3. The arrest patient requires prolonged CPR (e.g. drug overdose, hypothermia).

So far, the CIRC trial tried to address the issue of equivalence.  That is, they compared integrated automated load distributing band CPR (iA-CPR) with high-quality manual CPR (M-CPR) to determine equivalence, superiority, or inferiority in survival to hospital discharge. Compared to high-quality chest compressions, automated CPR resulted in statistically equivalent survival to hospital discharge.

To answer the question in the heading, until a portable, miniature, easy access ECMO device is available,  I think we may never get better than efficient manual chest compressions.  We need to start researching the impact of automated CPR devices on ourselves and our department instead.

I’ll end by quoting our own ANZCOR statement “automated or mechanical chest compression devices are not recommended for routine use. However, they may be a reasonable alternative to high quality manual chest compressions in situations where sustained high quality manual chest compressions are impractical of compromises provider safety.”

This statement is fair and flexible and allows us to incorporate automated CPR device in our department.

What really matters

  • 1. Early Defibrillation (decreased defibrillation time)

  • The chance of survival and live with minimal neurologic sequelae is increased if the initial arrest rhythm is shockable.
  • The chance of successful defibrillation decreases with time. Early defibrillation is a priority for shockable rhythms.

     2. Effective CPR (decreased hands off time)

  • The cornerstone of ALS
  • Maintains coronary and cerebral perfusion pressure
  • May enhance effectiveness of defibrillation
  • Longer periods of pauses are associated with decreased survival
  • Compressions over lower half of sternum
  • Depth of at least 5cm
  • Rate of 100-120/min
  • Minimise hands off time – COACHED mnemonic and pre-charging defibrillator. As we do a rhythm check:

“Continue chest compressions”

“Oxygen Away”

“All else clear”


“Hands off”

“Evaluate rhythm”

“Defibrillate or dump charge”

“Continue chest compressions”

Note: Ends and starts with Continue compressions

  • If you can remember this, great!  Otherwise, don’t stress this mnemonic is attached to every defibrillator in our ED for reference.

3. Effective Team (resuscitation and ED teams)

ALS studies have focused on patient centred-outcomes.  It rests heavily on the first two interventions aforementioned.  Whilst we’ve delivered these interventions well, we’ve fallen short determining ourselves and our team’s well being.  We talk about errors and mishaps but, don’t talk about our strengths and team effort.  Patients come and go but, the team needs to thrive to provide continued service.

Resuscitation creates a mix of emotions amongst providers. The more experienced the provider is the less anxiety it entails.  The more familiar everyone is with the team, their role and their equipment, the smoother the resuscitation goes. Preparation is key, training and practice are essential.

The effective team realises that errors occurs during time critical scenarios and high complexity situations. Good communication, clarity of priorities and goals of care amongst team members are essential. Everyone thinks of the next move and looks after each others back.

ALS requires highlighting key initial actions:

  • Team briefing and role allocation
  • LMA use during the early phase
  • Scribe as time keeper
  • 2 minutely rhythm check and 4-5 minutely adrenaline
  • Focus – Not on achievement of ROSC but discerning and acting on reversible causes

Key non technical tasks in an efficient TEAM:

  1. Leadership
  2. Team leaders(TL) should direct the team. To have a good grasp of the situation, if manpower allows, the TL should be hands-off and stands at the foot end of the bed.

First priority is a team briefing followed by task allocation.

The leader is the focal point of communication.

Status updates are important and this should be directed to the team leader to broadcast to the team.

  1. Shared Mental Model

One of the team leader’s main task is to update the team about priorities and objectives of the resuscitation.  Recapitulating or summarising events and the next steps required ensures everyone is in the same page.

Not all team leaders are equal. Experienced team members should encourage or remind team leaders to exemplify this model during a resuscitation.

  1. Closed loop communication

This is to be followed at all times. It starts by allocating a task clearly and ends by acknowledging the task is done.

e.g. “Mike, please give adrenaline 1:1000 dilution 0.5mg IM now.”

Mike replies “ok, 0.5mg IM adrenaline, that would be half a ml of 1:1000 IM?”

“Yes, correct”

Upon giving this Mike confirms the dose he is to give and state “given” once finished.

“Thanks Mike” to acknowledge you heard it and close the loop for the designated task.

Closing the loop of conversation is essential to avoid errors especially with critical drugs or interventions. It’s a bit prescriptive but it is good practice.

  1. Situational awareness and Task fixation

During an emotionally charged resuscitation, tunnel vision(too focused on a specific task or task fixation) can reduce awareness of patient’s condition, team hazards or even the departmental situation.

Being aware this happens is the first step. Recognising it when it counts and sharing it to the team is essential.  Individual team members should help each other be situationally aware by providing feedback to the team leader and vice versa when task fixation ensues.

  1. Timely escalation of care

Escalation of care is required if there are limitations with staff, equipment or resources.  The EDSS on call, ICU, MET team and anaesthetics teams should be involved in our escalation of care policy.

  1. Debriefing

Debriefing the team post resuscitation (hot debrief) may be essential to provide closure of the case and reset or address emotions for the remaining hours of the shift.  Asking what we did well and what we could have done better is a good start, if not the only questions you will ever need to ask.  Complex cases will benefit from a cold debrief (debriefing done later). However, staff organisation at a later date is more challenging.

If it wasn’t clear, after receiving an ALS call- talk before, talk during and talk after the resuscitation.


  1. ANZCOR guideline January 2016
  2. Mechanical CPR devices compared to manual CPR during out-of-hospital cardiac arrest and ambulance transport: a systematic review
  3. Ong et al, Scandinavian Journal of Trauma, resuscitation and emergency medicine 2012
  4. Mechanical Chest Compressions and Simultaneous Defibrillation vs Conventional Cardiopulmonary Resuscitation in Out-of-Hospital Cardiac ArrestThe LINC Randomized Trial   Sten Rubertsson, MD, PhD, JAMA. 2014;311(1):53-61. doi:10.1001/ JAMA,.2013.282538
  5. Manual vs. integrated automatic load-distributing band CPR with equal survival after out of hospital cardiac arrest. The randomized CIRC trial
  6. Lars Wik et al, RESUSCITATION journal  June 2014Volume 85, Issue 6, Pages 741–748.
  7. Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial 
  8. Prof Gavin D Perkins et al, The LANCET Volume 385, No. 9972, p947–955, 14 March 2015
  9. Greater Sydney HEMS website

Meningitis: Clinical Pearls and Pitfalls - May 4, 2017

This is a link to good read from emdocs. Click on the title

Meningitis: Clinical Pearls and Pitfalls

Thanks for picking our Website Logo - October 1, 2016

It is essential to have our own website identity.  However, due to trade mark infringement limitations we’re limited with the designs we can use.

We strive to uphold the mission and vision of BMDH by adhering to the core values

  1. Professionalism
  2. Teamwork and collaboration
  3. Competency
  4. Innovation

The four core values impacting on emergency care is represented in the logo.  Thanks for voting.  We have officially chosen the the logo for our website.

BMDH ICross Icon

2. BMDH cross

PE and thrombolysis…when it really matters - November 25, 2016

By Harry Elizaga, ED Staff Specialist


A 72 y/o lady presented to St. Team hospital via ambulance service with ongoing lightheadedness, clamminess and diaphoresis.  She had a pre-syncopal episode at home about 2-3 hours ago.  She had no chest pain but, states she had a sudden onset shortness of breath when she woke up in the morning that has mildly persisted.

BP 100/60  HR 70 regular  RR 20  T36.5  02 sats 95% on room air.  She had chemotherapy 2 weeks ago for a recent diagnosis of ****** lymphoma.  She has hypertension and is on atenolol.  No gross cardiac murmurs, no wheezes, mild bibasal crackles on chest auscultation. ECG showed a sinus rhythm with a rate of 75, T wave inversions over the anteroseptal leads with no axis deviation.  CXR and blood tests are not yet available.

A bedside echo showed a dilated right ventricle with no evidence of hypertrophy.  No pericardial effusion or regional wall motion abnormalities. Aorta looked normal. No B-lines on lung US and lung sliding was positive..

The patient was transferred to our resus bay.  CVC and arterial lines were not successful! The patient’s blood pressure dropped to 60 systolic and HR of 40-50(despite 2 Litres of fluid) with alteration in mental state.  A decision was made to thrombolyse the patient with tenecteplase.  A good 15-20 minutes after thrombolysis she was conversing with her relatives.  Peripheral inotropic support and heparin infusion was commenced and was transferred out with an eventual CT showing bilateral distal left and right pulmonary emboli with extensive clot burden within the segmental branches.  She was weaned off the peripheral pressor whilst in the ED of the admitting hospital.

It is important to note that deterioration was anticipated and, prior to thrombolysis, a discussion with our patient, relatives and attending physician regarding her care plans were established.

She was discharged from hospital after 10 days.

Must Know definitions (AHA, circulation 2011)

Massive PE: Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).

Submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis.

  • RV dysfunction means the presence of at least 1 of the following:
    • —RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography
    • —RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT
    • —Elevation of BNP (>90 pg/mL)
    • —Elevation of N-terminal pro-BNP (>500 pg/mL); or
    • —Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)
  • Myocardial necrosis is defined as either of the following:
    • —Elevation of troponin I (>0.4 ng/mL) or
    • —Elevation of troponin T (>0.1 ng/mL)

Let’s have a look at some conclusions of notable studies about this topic:

  1. Thrombolysis in hemodynamically stable patients with acute pulmonary embolism: a meta-analysis.

Riera-Mestre A1, Becattini C, Giustozzi M, Agnelli G.

Conclusion: Due to increased risk for MB and ICH with no evidence of reduction in mortality, thrombolysis should not be used for most normotensive PE patients.

  1.  Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis.

Chatterjee S1

Among patients with pulmonary embolism, including those who were hemodynamically stable with right ventricular dysfunction, thrombolytic therapy was associated with lower rates of all-cause mortality and increased risks of major bleeding and ICH. However, findings may not apply to patients with pulmonary embolism who are hemodynamically stable without right ventricular dysfunction.

  1. Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial).

Sharifi M1

The role of low-dose thrombolysis in the reduction of pulmonary artery pressure in moderate pulmonary embolism (PE) has not been investigated at that time. They postulated the lungs are very sensitive to thrombolysis, and that effective and safe thrombolysis might be achieved by a lower dose of tissue plasminogen activator.  The “safe” dose was based on patient weight:

  • For patients weighing ≥50 kg, the dose was 10 mg tPA in 1 minute followed by 40 mg in 2 hours
  • For patients weighing <50 kg, the dose was 0.5 mg/kg for a total dose of 10 mg in 1 minute followed by the remaining dose in 2 hours

In conclusion, the results from the present prospective randomized trial suggests that “safe dose” thrombolysis is safe and effective in the treatment of moderate PE, with a significant immediate reduction in the pulmonary artery pressure that was maintained at 28 months.

Recommendations for Fibrinolysis for Acute PE (AHA, circulation 2011)

  1. Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).
  2. Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).
  3. Fibrinolysis is not recommended for patients with low-risk PE (Class III; Level of Evidence B) or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence B).
  4. Fibrinolysis is not recommended for undifferentiated cardiac arrest (Class III; Level of Evidence B).

 Percutaneous techniques to recanalize complete and partial occlusions in the pulmonary trunk or major pulmonary arteries are potentially life-saving in selected patients with massive or submassive PE.

 Emergency surgical embolectomy with cardiopulmonary bypass has reemerged as an effective strategy for managing patients with massive PE or submassive PE with RV dysfunction when contraindications preclude thrombolysis.  Surgical embolectomy can also rescue patients  whose condition is refractory to thrombolysis.

My take on thrombolysis in general

Thrombolysis has a role in select patients with AMI and Pulmonary embolism.  These are patients with STEMI and Massive PE(hypotensive PE) respectively.  It makes sense to give thrombolysis, with varied reported bleed rate from 1-7 %, to patients who have a higher mortality rate.  Both untreated STEMI and massive PE have a mortality rate of >25-30%.  Despite not being a 100% effective, the benefits of lytics outweighs the risks in these instances.  In a shocked patient, lytics does not get rid of the whole thrombus but reduces clot burden that will hopefully buy us some time to dispose our patient for definitive interventions.  Submassive PE is a more controversial topic and it would be best to consult our specialty teams for such group.  A half dose TPA or safe dose TPA sounds reasonable.  So as percutaneous approaches depending on local and logistical considerations.  Currently, our tertiary referral centre offers endovascular thrombolysis.

Thrombolysis for CVA or ischaemic stroke is a subject of debate up to this date. The evidence is not clear as to who are the select patient group likely to benefit from this therapy. There was a time when we followed a NIH score of 4-22 to determine consideration for lytic therapy.  A score of less than 4 is said to have minimal symptoms to even consider lytics whilst a score of >22(severe deficit) suggest a massive infarct that is prone to adverse bleeding or haemorrhagic transformation.  This criteria seem to have undergone more flexibility and even a deficit of <4 is considered for lytic therapy nowadays.  It doesn’t make much sense withholding therapy for those who, I would think, will benefit most-those who have severe disabilities.  If we are to look at STEMI and PE patients, the worst group is where the benefit is.

Whilst I don’t question thrombolysis for STEMI and massive PEs, ischaemic CVA still has grey areas.  Despite this, we need to be aware of our institutional policies and protocols.  At the end of the day, the improved outcomes from thrombolysis may not be from thrombolysis alone but, the result of robust care brought forward by our stroke team and post thrombolysis ICU care.

Subarachnoid haemorrhage
 - 29 September 2016

By: Harry Elizaga, FACEM EDSS

Clinical question

  • What is your approach to SAH diagnosis within 6 hours of symptom onset?

Key facts

  1. Headaches accounts for 1-2% of ED visits
  2. About 5% of confirmed SAH are missed diagnosed
  3. One third to half of patients will experience a sentinel headache that precedes a catastrophic subarachnoid hemorrhage
  4. About 80% of SAH are secondary to an aneurysm (85% are in the anterior circulation)
  5. The most common specific locations of intracranial aneurysms are at the middle cerebral artery bifurcation and along the anterior communicating artery. These 2 locations account for approximately 60% of all intracranial aneurysms.
  6. CT/LP is considered standard if onset of headache is > 6 hours from a CT head scan.

  • CT scan is very sensitive(100%) soon after the onset(< 6 hrs) of SAH (Perry BMJ 2011). Is it?
  1. This study has been validated and results failed to replicate this CT sensitivity. The issue of a qualified radiologist/neuroradiologist has been a point of contention as  non-academic centres have staff radiologist or trainees interpreting scans.   There were 3 missed SAH by the initial provider reading the scans in the study.  Hence, sensitivity is just around the 97% mark if this is taken into account.   It is important to note that only 50%  of the patients in the study had an LP done making it  impossible to really know how many CTs are True negatives. There also have been deaths from the study(they have not been autopsied) and attributed to other causes.
  2. Blok et al investigated whether staff radiologists working in nonacademic hospitals can adequately rule out subarachnoid hemorrhage (SAH) on head CT <6 hours after headache onset.  Independent review of these patients’ CTs identified one patient (1/52; 2%) with a perimesencephalic nonaneurysmal SAH. Negative predictive value of 100%.
  3. Also, a retrospective study by Mark et al concluded:  “We found the sensitivity of early cranial CT for SAH to be 95.5% among patients presenting to non-academic EDs in an integrated healthcare system. Application of a SAH clinical decision rule in addition to early cranial CT improved sensitivity to 100% (95% CI [97.6–100.0]). Prospective decision rule refinement and validation of this approach is warranted.’
  4. The clinical decision rule added here was the Ottawa SAH rule from a Perry  2013 as follows:

           SAH: OTTAWA Rule
For alert patients older than 15 y with new severe nontraumatic headache reaching maximum intensity within 1 h

Not for patients with new neurologic deficits, previous aneurysms, SAH, brain tumors, or history of recurrent headaches (≥3 episodes over the course of ≥6 mo)

Investigate if ≥1 high-risk variables present:
Age ≥40 y
Neck pain or stiffness
Witnessed loss of consciousness
Onset during exertion
Thunderclap headache (instantly peaking pain)
Limited neck flexion on examination

Unfortunately, this rule does not significantly reduce the number of LPs in the U.S., more so, in Australasia

Why not just do LPs?

Lumbar puncture is cumbersome, invasive and painful.  It is associated with complications.  Post LP headache is common and can be mitigated by using a smaller gauge LP needle with an atraumatic tip (e.g. Pencil type). Diminishing RBC count in each tube are not reliable enough to exclude SAH.  Xantochromia via visual diagnosis and spectrophotometry are being used to identify SAH amongst patients with non diagnostic CTs despite LP(gold standard) not being a sensitive and specific test. 


   By no means a CT is a perfect test to diagnose SAH during the 6 hours of symptom onset. Like the infamous stroke thrombolysis studies, where most studies have negative outcomes, the three studies presented here may appear acceptable.  However, let’s not disregard the other good studies, beyond our scope,  that makes nondiagnostic CT a cause for concern due to its  miss rate. Besides, is 3 mls of blood in the CSF enough to be picked-up by modern scanners?  How much bleed is a sentinel bleed? Is it 1,2, 3 mls or perhaps more?  At the end of the day, the sentinel bleed is the time-critical diagnosis as prognosis is better when diagnosed and treated early.  In contrast, large SAH has a terrible prognosis. So, correct or incorrect diagnosis doesn’t alter the outcomes.

 A thunderclap headache “defined as a headache maximal at onset (1 minute)” is suggestive of SAH. If it’s not a thunderclap headache, how would you feel if the patient has a family history of SAH or aneurysm, or a history of polycystic kidneys? Whether we like it or not, gestalt plays a role in our decision making process.  Atypical presentations, like our chest pain patients, is a possibility. And, as long as atypical presentations come, a scoring system will have loop holes.

 Like anything that we do in ED, If our pre-test probability is high, we should be advocating for definitive testing (LP or even CTA).  If the patient is low risk with a normal CT, a shared decision making process with the patient is necessary.  Knowledge translation of available data should guide us into making this decision.

    Potential Fellowship questions to reflect on:

   What are the pros and cons of doing an LP?
   What are the most common complications of LP?
   How do we reduce the incidence of post LP headache?
   If LP is negative, do we do a CTA?
   When do you request a CTA?  Why can’t we just do CTAs?
   What is the value of MRA in SAH diagnosis?


Vermeulen MJ, Schull MJ. Missed diagnosis of subarachnoid hemorrhage in the emergency department. Stroke. 2007;38(4):1216-1221.

Perry JJ, Stiell IG, Sivilotti ML, etal. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343:d4277.

Jeffrey J. Perry, MD, MSc; Ian G. Stiell Clinical Decision Rules to Rule Out Subarachnoid Hemorrhage for Acute Headache, JAMA 2013 Editorial Vol 210

Mark et al, Sensitivity of a Clinical Decision Rule and Early Computed Tomography in Aneurysmal Subarachnoid Hemorrhage, West Emerg Med 2015

Blok et al, CT within 6 hours of headache onset to rule out subarachnoid hemorrhage in nonacademic hospitals. Neurology 2015

Congratulations - September 30, 2016

Congratulations to Dr Rasel Ahmed for passing the fellowship written exam and to Dr Ahmed Kalamchi for passing the primary exam

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