Thursday, 28 April 2016

The eyes have it

Prof Larry Mellick posts great medical vids on his Youtube channel. Here's his recent posts on opthalmological emergencies. 
Great tips include:
  • Grading and complications of hyphema
  • Pathophysiology of corneal ulcers
  • Distinction of periorbital and orbital cellulitis
This is modern learning at its finest and make a point to "like" and subscribe to his channel.

Thursday, 21 April 2016

Not another headache!

Here is another of our EM residents - Gayathi Nadarajan
She discusses 3 cases of non-traumatic headaches and their diagnoses with a focus on the evaluation of a patient with acute headache in the ED

Case 1:

A 19-year-old Chinese lady with a background of haemolytic anemia presented in the middle of the night with a 3-day history of the worst headache of her life with neck stiffness. On examination, besides profound neck stiffness, there were no other neurological findings.


CT scan: Acute subarachnoid hemorrhage in the left frontal lobe and acute subdural hemorrhage over the left frontal temporal convexity. Midline shift of 4mm to the right.

4 vessel angiogram : There were no aneurysm

Platelets: normal

All investigations were not completed as patient discharged against advice. Hence no cause was found for her non-traumatic bleed.


Case 2

33-year-old Malay lady with no medical problems as such, presented to the ED with a sudden onset, thunderclap headache, associated with vomiting, left ankle weakness and foot drop. She also noted bruising over her left ring finger tip a few days ago.

Examination revealed a left foot drop and weak ankle inversion with sensory deficit over the dorsum of the foot.

FullSizeRender IMG_0013

CT brain: Basal cisterns & pre-pontine SAH, small ICH, superior cerebellar arachnoid cyst & earl communicating hydrocephalus.

CT angiogram: 3mm aneurysm at epicenter of left PCA branch

4 vessel angiogram: Possible mycotic aneurysm of P4 segmental branch of left posterior cerebral artery likely septic emboli or seeding from IE.

Unsuccessful in coiling the aneurysm

She than had craniotomy and excision of the aneurysm.

Transthoracic echocardiogram: bileaflet MVP with severe MR and IE 1.4cmx1.0cm anterior leaflet and 0.5cm posterior leaflet vegetation

Hence a diagnosis of mycotic aneurysm from infective endocarditis was made.


Case 3

A 66-year-old independent and active Chinese gentleman presented to the emergency department as his blood pressure was noted to be high. He has hypertension and hyperlipidemia He routinely measures his blood pressure once a day and yesterday it was as high as 172/70 after measuring for about 3 times. His children than convinced him to come to the ED for a ‘check-up’ as they were worried about the high blood pressure.

He also had a headache for the past 3 days, which was resolving. It wasn’t the worse pain he ever felt but it was the first time he had such a headache. There were no associated or aggravating symptoms with the headache.

On examination, he was very well and had no neurological deficit. His blood pressure at triage was in fact 149/73.

In view of the new onset of headache in his age group, a CT head was ordered.


CT brain: Hyperdense enlargement of the left transverse and sigmoid venous sinuses suspicious for venous sinus thrombosis, complicated by an area of venous infarction & haemorrhage in left parietal lobe

MRI venous: Cerebral venous thrombosis involving the entire left transverse and sigmoid sinuses extending to the proximal internal jugular vein. There is involvement of the left superior and inferior petrosal sinuses and secondary left temporoparietal venous infarction with haemorrhage.

No identifiable cause on MRI.

Patient was diagnosd with cerebral venous thrombosis. He was investigated and started on anticoagulant.



Don’t worry… you are not alone….

While in the consult room, it is normal to have the sinking feeling at the bottom of our stomachs when you are faced with yet another patient with a headache. We know that the headache consult will be a long one indeed. A thorough history taking and examination is crucial to avoid missing an intracerebral bleed.

Headache red flags

For the first 2 cases, the severe, thunderclap headache was a red flag. However, for the 3rd case, it was not obvious as the triage complain was ‘high blood pressure’. But his pressure at triage was fine!

The red flag only came out from ‘digging out’ the history from him. He said “By the way doctor… I did have this headache for the pass 3 days… it actually is getting better. The severity was probably the worst when I measured my blood pressure yesterday. I don’t normally suffer from headaches, but neither would I say this is the worse pain I ever felt!” The red flag was the new onset of headache in a patient above the age of 40

Discussion and more algortithms!!!

The aim of these cases is to:
  • Re-emphasise the value of good history taking in order to avoid missing out a deadly diagnosis such as a intracerebral bleed
  • To revisit red flags that may suggest a bleed
  • Despite the triage complain, ALWAYS ask the patient why they turned up in the ED on that particular day and at that particular time
I will end off with some algorithms, to remind us of headache red flags.

The following from Up To Date is a flowchart on how to approach a patient with headache in the emergency department.




  • Perry, Jeffrey J., et al. "An international study of emergency physicians' practice for acute headache management and the need for a clinical decision rule." CJEM06 (2009): 516-522.
  • Perry, Jeffrey J., et al. "High risk clinical characteristics for subarachnoid haemorrhage in patients with acute headache: prospective cohort study." Bmj 341 (2010): c5204.
  • Perry, Jeffrey J., et al. "Clinical decision rules to rule out subarachnoid hemorrhage for acute headache." Jama12 (2013): 1248-1255.
  • Godwin SA, Villa J. “Acute headache in the ED: Evidence-Based Evaluation and Treatment Options.” Emerg Med Pract 2001; 3(6): 1-32.
  • Newman-Toker, David E., and Jonathan A. Edlow. "High-stakes diagnostic decision rules for serious disorders: the Ottawa subarachnoid hemorrhage rule." JAMA12 (2013): 1237-1239.

Thursday, 14 April 2016

So does it work?

Here is great article which may change the way you think about drug companies, evidence presentation, fads and the power of distraction. Credit to Prof Joe Lex for tweeting and of course the authors for daring...

BMJ Open 5:e007118 doi:10.1136/bmjopen-2014-007118
  • The effect of statins on average survival in randomised trials, an analysis of end point postponement


Objective To estimate the average postponement of death in statin trials.
Setting A systematic literature review of all statin trials that presented all-cause survival curves for treated and untreated.
Intervention Statin treatment compared to placebo.
Primary outcome measures The average postponement of death as represented by the area between the survival curves.
Results 6 studies for primary prevention and 5 for secondary prevention with a follow-up between 2.0 and 6.1 years were identified. Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively.
Conclusions Statin treatment results in a surprisingly small average gain in overall survival within the trials’ running time. For patients whose life expectancy is limited or who have adverse effects of treatment, withholding statin therapy should be considered.

Strengths and limitations of this study

  • This is the first study ever to systematically evaluate statin trials using average postponement of death as the primary outcome.
  • We have only estimated the survival gain achieved within the trials’ running time, whereas in real life, treatment is often continued much longer.
  • We have only focused on all-cause mortality. Other outcomes may also be relevant, for example, non-fatal cardiovascular end points.

Thursday, 7 April 2016

Yamahi technique for needle crics

Here's a technique for you might not have heard of or seen. Ventilating that needle cric site may be cumbersome but this quick solve is ingenious.
Here's hoping we never have to use it!

Thursday, 31 March 2016

K-wire removal

Prof Larry Mellick describes and assists in removal of this infected wire. Remember that source control is a pillar of sepsis treatment and this is one of those cases.

For more of his videos, go to his youtube site.

Friday, 25 March 2016

Webucation 25/3/16

This episode of webucation is brought to you by the disciplines of crit care and cardio as well as some imaging thrown in. Do visit/credit the content creators.
This last link is worth the read into current state of affairs. I you must take anything from it, take this pic. An all too forgotten philosophy that one must be complete and holistic, not just a paper reader/quoter.


Thursday, 17 March 2016

Rethinking Furosemide in Acute Pulmonary Edema

From Emergency Medicine News by Swaminathan, Anand @EMSwami.
Dr. Swaminathan is an assistant professor of emergency medicine and the assistant residency director of the NYU/Bellevue Emergency Medicine residency. He is the co-creator of the EM Lyceum blog ( and the editor and chief of the Core EM blog ( His interests are in resuscitation, residency education and knowledge translation.

You’re working the overnight shift, it’s 6:15 a.m., and you’re starting to dream of a breakfast sandwich and bed. But, no, it’s your lucky morning, and in rolls a 55-year-old man in acute respiratory distress. He is hypertensive, tachycardic, and tachypneic. A quick bedside ultrasound reveals bilateral B lines that convince you that the patient is in acute pulmonary edema (APE) or acute decompensated heart failure (ADHF). The 12-lead ECG reveals only sinus tachycardia, and your nurse asks you how much furosemide you want to give.
Congestive heart failure is a common problem in the United States with more than five million patients carrying the diagnosis and 500,000 new diagnoses each year. (Mt. Sinai J Med2006;73[2]:506.) APE occurs when blood backs up into the pulmonary vasculature, leading to increased oncotic pressure and leakage of fluid into the alveolar spaces. Put more simply: These patients are drowning.
APE patients suffer from increased afterload — making it more difficult for the left ventricle to function — and increased preload. As such, the goals of treatment must be directed at decreasing cardiac filling pressures (preload) and decreasing afterload. Neurohormonal activation also worsens cardiac performance and increases intravascular volume and vascular tone. The mainstay of APE treatment for decades has been loop diuretics, mainly furosemide. The central role these drugs continue to play highlights a lack of understanding of the underlying pathophysiology of the disease.

Pathophysiology of APE

The cardiorenal model was first put forward in the 1940s as the predominant explanation for APE. It was believed that decreased blood flow to the kidneys led to decreased renal function and fluid retention leading to volume overload. This was the basis for loop diuretics being recommended. It was clear, however, that this model was insufficient because it did not explain why the disease progressed or the finding of increased peripheral vasoconstriction from invasive monitoring studies.
The cardiocirculatory model was first put forth in the 1970s. This model argued that peripheral vasoconstriction led to decreased cardiac function, and that increased preload and afterload were at the center of the problem. This model explained much of what we see occurring in APE.
Finally, researchers in the 1990s established the neurohormonal model, in which neurohormones (norepinephrine, renin, angiotensin, aldosterone) are upregulated in APE. These compounds have vasoactive properties leading to vasoconstriction and increase intravascular volume. Current recommendations for APE treatment are based on the integration of the cardiovascular and the neurohormonal models.

The Myth of Volume Overload

Regardless of the pathophysiology, patients are still volume overloaded, right? The best evidence suggests it is not that simple. Zile, et al. demonstrated that most patients with APE have increased cardiac filling pressures, but most did not have a significant increase from their dry weight on presentation. (Circulation 2008;118[14]:1433.)
More than 50 percent of patients, in fact, gain less than two pounds. (Circulation2007;116[14]:1549.) If this is not fluid gain, where did the increased filling pressure originate? It turns out it is largely a result of changes in compliance in the splanchnic system that leads to fluid shifting from here to the cardiopulmonary circulation. (Circ Heart Fail2011;4[5]:669.)
Even in the face of this evidence, the loop diuretic supporters argue that some patients are overloaded, so why not give all of these patients the drug? This approach does not account for the potential downsides. Administration of furosemide activates the neurohormonal system, which leads to increased plasma renin and norepinephrine levels. This results in decreased LV function, increased LV filling pressure, increased MAP and SVR, and decreased GFR. (Ann Intern Med 1985;103[1]:1.) An ICU study from 1990 found that furosemide increased pulmonary capillary wedge pressure in the first 20 minutes of treatment. (Chest 1990;98[1]:124.) This is particularly worrisome because APE is a deadly disease, and what we do in the first 10 to 15 minutes of the patient’s presentation makes a huge difference.
So how should we treat patients with APE?
• Non-Invasive Positive Pressure Ventilation (NIPPV): NIPPV has multifactorial action in APE. It decreases work of breathing, stents-open alveoli during the entire respiratory cycle, leading to improved gas exchange, and, in the case of bilevel NIPPV, decreases afterload.
A number of papers have shown decreased intubation rates and decreased ICU utilization with the use of NIPPV. The most recent study showed a decreased ICU admission from 92 to 38 percent. (J Emerg Med 2014;46[1]:130.) A 2008 Cochrane review also found that NIPPV reduced hospital mortality (RR 0.6) and endotracheal intubation (RR 0.53). (Cochrane Database Syst Rev 2008 Jul 18;[3]:CD005351.)
The key for NIPPV is to start it immediately on presentation to the ED. It will likely help with preoxygenation even if it does not stave off intubation.
• Nitroglycerin: Many studies have looked at the use of nitroglycerin, comparing it with furosemide and evaluating at high-dose therapy. 
(Am J Cardiol 1978;41[5]:931; Lancet1998;351[9100]:389; Ann Emerg Med 2007;50[2]:144.) Nitroglycerin is recommended for all patients with APE. It reduces preload and at higher doses (> 100 mcg/min), and it decreases afterload, leading to increased cardiac output and decreased SVR. (Am J Cardiol1978;41[5]:931.) Despite widespread use, robust randomized studies enrolling the sickest APE patients are lacking.