LITFL • Life in the Fast Lane Medical Blog https://lifeinthefastlane.com Emergency medicine and critical care medical education blog Thu, 19 Apr 2018 03:43:27 +0000 en-US hourly 1 https://wordpress.org/?v=4.9.5 https://i0.wp.com/lifeinthefastlane.com/wp-content/uploads/2017/03/LITFL_LOGO_Transparent_001.png?fit=32%2C32&ssl=1 LITFL • Life in the Fast Lane Medical Blog https://lifeinthefastlane.com 32 32 56961984 Eponymythology: Atraumatic Abdominal Ecchymosis https://lifeinthefastlane.com/eponymythology-atraumatic-abdominal-ecchymosis/ https://lifeinthefastlane.com/eponymythology-atraumatic-abdominal-ecchymosis/#comments Wed, 18 Apr 2018 07:37:52 +0000 https://lifeinthefastlane.com/?p=175827 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Review of the 5 commonly cited eponyms (n=6) associated with non-traumatic abdominal ecchymosis of the abdominal wall and flanks (Grey Turner, Cullen and Stabler); scrotum (Bryant) and upper thigh (Fox) as useful clues to consider potentially serious causes of abdominal pathology.

Eponymythology: Atraumatic Abdominal Ecchymosis Mike Cadogan

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Overview

We review the original descriptions of 5 eponymous signs (n=6) associated with non-traumatic abdominal ecchymosis.

These commonly cited eponyms involving the abdominal wall and flanks (Grey Turner, Cullen and Stabler); scrotum (Bryant) and upper thigh (Fox) may be useful clues directing the examiner to consider potentially serious causes of abdominal pathology.

Cullen sign

Thomas Stephen Cullen (1869–1953) was a Canadian gynecologist

Non-traumatic peri-umbilical ecchymoses associated with intra-abdominal haemorrhage, originally described in ectopic pregnancy – Cullen sign

Original publication: (n=1)

1918 – Cullen first described a bluish black discoloration of the periumbilical skin in a female patient with a ruptured extrauterine pregnancy with ‘no history of injury

Cullen originally described the finding at the 43rd annual meeting of the Transactions of the American gyecological society, Pennsylvania May 16-18 1918 [Am J Obstet Gynecol 1918;78:457]. He concluded that the umbilical appearance was due to intra-abdominal haemorrhage secondary to an ectopic pregnancy

cullen sign

Clinical context

  • Despite the original description, most literature relates Cullen sign of periumbilical ecchymosis to acute pancreatitis (being recorded in 1-3% cases) rather than secondary to an ectopic pregnancy.
  • In most described cases, it takes 3-5 days for Cullen sign to present and the sign been associated with a broad range of clinical conditions

CauseReference
Ruptured abdominal aortic aneurysmArmour et al 1978
Acute PancreatitisBosmann et al 2009
Percutaneous liver biopsyCapron et al 1977
Splenic ruptureChung et al 1992
Perforated duodenal ulcerEvans DM 1971
Rectus sheath hematomaGuthrie, Stanley 1996
Ischemic and gangrenous bowelKelley ML 1961
Hemorrhaging ascites from hepatic tumorMabin, Gelfand 1974
Bilateral acute salpingitis with IUPOrient JM, Sapira JD 2005
Cirrhosis with portal hypertensionOrient JM, Sapira JD 2005
Hepatocellular carcinomaOrient JM, Sapira JD 2005
Hypothyroid myopathyOrient JM, Sapira JD 2005
Ovarian cyst hemorrhageOrient JM, Sapira JD 2005
Renal sarcoma metastatic to the peritoneumOrient JM, Sapira JD 2005
Strangulation of ileum with hemorrhageOrient JM, Sapira JD 2005
Strangulated umbilical herniaOrient JM, Sapira JD 2005
Retroperitoneal necrotizing fasciitisPryor et al 2001

Epperla N et al. A Review of Clinical Signs Related to Ecchymosis. WMJ • APRIL 2015

Grey Turner sign

George Grey Turner (1877–1951) was an English surgeon

Non-traumatic abdominal ecchymosis, in particular – bruising of the flanks associated with retroperitoneal haemorrhage, originally described in acute pancreatitis – Grey Turner sign

Original publication: (n=1)

1919 – George Grey Turner submitted his article for publication as following a “…cursory examination of the voluminous literature on pancreatitis”, where he was unable to “…observe any mention of this sign”

1920 – George Grey Turner published ‘Local discoloration of the abdominal wall as a sign of acute pancreatitis‘ citing two cases of acute pancreatitis with fat necrosis and retroperitoneal haemorrhage [Br J Surg. 1920;7:394-395]

  • Case 1 [1912]: 54 year old female with three days of abdominal pain presenting with an area of discoloration (a bluish colour), about 6 inches in diameter involving the abdominal wall surrounding the umbilicus (see Cullen sign…).

“…the patient suffered from acute pancreatitis, with much effusion into the peritoneal cavity. She lived nine days after operation, and the post-mortem examination disclosed a sloughing pancreas with much fat necrosis

  • Case 2 [1917]: 53 year old male soldier with a history of recurrent bouts of self-limiting abdominal pain. He presented with unremitting abdominal pain and a rigid abdomen…looking ‘distinctly toxic’

The tenderness over the gall-bladder region was very marked, and I now noticed two large discoloured areas in the loins. They were about the size of the palm of the hand, slightly raised above the surface, and of a dirty-greenish colour.

Grey Turners Sign Original Photo 1919 COLOR
Grey Turners Sign: Original Photo: 1917. Colourised: 2017 Tor Ercleve

Clinical context

  • Incidence of 3-5% in patients with acute pancreatitis, associated with increased mortality (30-40%) and increased risk of pseudocyst formation. [Surg Gynecol Obstet. 1984 Oct;159(4):343-7.]
  • CT scanning has helped to define the anatomic pathway by which extravasated pancreatic enzymes and their effects lead to these cutaneous discolorations. [Pancreas. 1998 May;16(4):551-5.]. Extraperitoneal diffusion from the anterior pararenal space between the two leaves of the posterior renal fascia; to the lateral edge of the quadratus lumborum muscle and may then extend to the posterior pararenal space and the structures of the flank wall. The lumbar triangle, a site of anatomic weakness on the flank wall, provides an external window into the internal proteolytic events.
  • In most described cases, it takes 3-5 days for Grey Turner sign to present and the sign been associated with a broad range of clinical conditions

CauseReference
Acute PancreatitisBosmann et al 2009
Bilateral acute salpingitis with IUPOrient JM, Sapira JD 2005
Ischemic and gangrenous bowelKelley ML 1961
Retroperitoneal necrotizing fasciitisPryor et al 2001
Ruptured abdominal aortic aneurysmArmour et al 1978
Rectus sheath hematomaGuthrie, Stanley 1996
Sclerosing peritonitisPryor et al 2001
Cardiac catheterizationArmour et al 1978
Intra-aortic balloon pump insertionRob, Williams 1961

Epperla N et al. A Review of Clinical Signs Related to Ecchymosis. WMJ • APRIL 2015

Stabler sign

Francis Edward Stabler (1902–1967) was an English gynaecologist and surgeon

Non-traumatic abdominal skin ecchymosis in the inguinal-pubic area associated with intra-abdominal haemorrhage, originally described in ectopic pregnancy – Stabler sign

Original publication: (n=1)

1934 – Stabler published a paper titled ‘A case showing Cullen’s sign‘ concerning a patient presenting with an ectopic pregnancy: with left illiac fossa pain of fourteen days duration and ilioinguinal ‘bruising’, 7 weeks post last menstrual period

Clinical examination

C.S. Aged 34:One inch below and to the left of the umbilicus was a purple, almost black, clearly cut mark 3/4 in. by 1/4 in. shaped like a comma. Below it, about the junction of the upper third and lower two-thirds of the distance from the umbilicus to the pubes, was a ” bruise,” bluish in colour, about 1 in. in diameter, whilst abutting on the inguinal fold was a reddish-purple mark like a fresh bruise, shaped roughly like the ace of clubs, about 2 in. in diameter. The whole was within the triangle formed by the midline and a line drawn to the umbilicus from the middle of the left inguinal ligament. On bimanual examination a soft mass the size of a hen’s egg was evident in the left tubal region.”

Operative findings

At operation the distal half of the left Fallopian tube contained an ampullary pregnancy surrounded by blood clot. The tube was not ruptured, but a little dark blood was oozing from the abdominal ostium. In the peritoneal cavity there were not more than 3 or 4oz (88-118mL) of dark fluid blood…incision into the subcutaneous fatty tissue proved the stains to be true ecchymoses.

Hypotheses

It is an interesting speculation as to how the blood reaches the subcutaneous tissues. In the present reported case I forecast that there would be an intraligamentary rupture of the tube with a broad ligament haematoma from which blood had tracked up extraperitoneally as far as the umbilicus, possibly following the obliterated hypogastric artery by which the lateral spread of the discoloration was limited.

Clinical context

  • Initially described as an inguinal-pubic extension of the peri-umbilical ecchymosis of Cullen sign
  • Further cases of bruising to the inguinal-pubic area reported with AAA rupture and acute hemorrhagic pancreatitis
  • Although rare, this sign has most commonly been identified in neonates secondary to adrenal hemorrhage. This is associated with obstetric injury, perinatal hypoxia, and sepsis [Urology. 2002 Apr;59(4):601]. Rarely, it may be due to ruptured neuroblastoma.

Fox sign

John Adrian Fox English surgeon

Non-traumatic ecchymosis over the upper outer aspect of the thigh. Ecchymosis is parallel with, but distal to the inguinal ligament with a well demarcated upper border defined by attachment of the membranous layer of the superficial fascia (Scarpa’s fascia). Originally described with retroperitoneal haemorrhage. – Fox Sign

Original publication: (n=2)

1966 – JA Fox (London) detailed 2 fatal cases of non-traumatic ecchymosis determined as a diagnostic sign of retroperitoneal haemorrhage. In both cases, this sign was noticed late in the course and produced by tracking of the fluid extraperitoneally along the fascia of psoas and iliacus beneath the inguinal ligament until it became subcutaneous in the upper thigh.

Case 1: Fourteen hours after admission bruising was noted in both upper outer thighs. It had a sharp upper margin, was dark blue, and was quite distinct from the patchy mottling of her legs below [Post mortem: acute suppurative pancreatitis]

Fox's Sign 1966

Case 2: A man, of about 50…with severe abdominal pain and circulatory collapse. Resuscitatory measures were of no avail and he died within 24 hours of admission. Before death bruising was noticed in the upper outer aspect of one thigh. He had not been given injections in this region and no other cause for the bruising was apparent. [Post-mortem: dissecting and ruptured abdominal aortic aneurysm]

Hypotheses

..seems likely that the clinical sign seen in the above 2 cases is produced by tracking of the fluid extraperitoneally along the fascia of psoas and iliacus beneath the inguinal ligament until it becomes subcutaneous in the upper thigh.

Cadaver Experiment: This sign has been reproduced in two stages in the recent cadaver. A solution of methylene blue in normal saline was injected from a height of 10 feet into the loin for several hours. The blue dye was then traced by dissection until it was seen to pass beneath the inguinal ligament”

Clinical context

  • Initially recorded in acute pancreatitis and ruptured aortic aneurysm
  • Subsequently described with strangulated ileum, urethral instrumentation, reaction to subcutaneous injections, and pulmonary infarction.

Bryant sign

John Henry Bryant (1867–1906) was an English physician

Scrotal ecchymosis associated with ruptured abdominal aortic aneurysm (AAA) – Bryant sign

Original publication: (n=1)

1903 – Bryant described scrotal ecchymosis associated with ruptured AAA during two lectures in which he had evaluated 18,678 necropsies and the 325 deaths secondary to abdominal aortic aneurysm rupture. [Clin Jour. 1903;23:71-80].

In these two articles Bryant describes the diffuse nature of the atheromatous changes, the possible clinical presentation of AAA as apparent renal colic, and the scrotal and abdominal discolourations as diagnostic clues

In one case blood was effused into the right spermatic cord, and the corresponding half of the scrotum was much ecchymosed…When blood is extravasated into the anterior abdominal wall ecchymoses may appear…‘ [Clin Jour. 1903;23:79]

Bryant sign

1987 – RM Ratzan et al proposed eponymous historical attribution of lower abdominal/scrotal discolouration secondary to aortic aneurysmal disease to John Henry Bryant. [J Emerg Med. 1987 Jul-Aug;5(4):323-9]

Clinical context

  • Bryant sign is rare.
  • Blood must transverse the inguinal canal and spermatic cord down to the subcutaneous scrotal tissue.
  • It requires specific pathological circumstances such as a closed (retroperitoneal hematoma) or sealed (surrounding retroperitoneal and aortic tissue) rupture of abdominal aortic aneurysm. It requires a slow rate of aneurysmal leakage and a prolonged interval prior to final rupture.
  • Most recorded cases of Bryant sign occur three to six days after onset of abdominal symptoms – Pearlman (1940), Barratt-Boyes (1957) and Beebe (1958).

Summary

The original publications of the eponymised cases often include careful clinical descriptions and anatomopathophysiological hypotheses in an era devoid of adjunctive diagnostic aids. However, we now have the benefit of comparing the diagnostic validity of the signs in a vast array of published clinical cases illuminated by enhanced imaging techniques and a more in-depth understanding of pathophysiology.

The original n=1 published cases represent a springboard for us to review arcane terminology by first understanding the historical folksonomy and then to redefine in clinical context to reduce descriptive confusion and narrowing of our diagnostic differentials.

For example, in 1918 Cullen described a single case of umbilical ecchymoses in a patient with an ectopic pregnancy. Over the subsequent 100 years at least 17 alternate diagnoses have been ascribed to the external abdominal manifestation of his eponymous sign.

Of significant note, the topographic location of atraumatic abdominal ecchymosis does not point to the aetiology with any degree of certainty and these signs may be potentiated by anticoagulation therapy or qualitative/quantitative platelet abnormalities.

Of course there is a certain historical interest in relating these signs to pioneers in descriptive medicine. However, we may be better to describe ‘non-traumatic abdominal wall ecchymosis’ as a potential sign of intraperitoneal or retroperitoneal pathology which requires further evaluation…

[…unless you enjoy a ‘down and dirty‘ eponym spat with the inpatient specialists? Then read on, and prepare your semantygdala for the symphonic cacophony of ‘I told you so...’]

References

Eponymythology: Atraumatic Abdominal Ecchymosis Mike Cadogan

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Jellybean 93 with Naomi Diel https://lifeinthefastlane.com/jellybean-93-with-naomi-diel/ https://lifeinthefastlane.com/jellybean-93-with-naomi-diel/#respond Wed, 18 Apr 2018 03:22:07 +0000 https://lifeinthefastlane.com/?p=176884 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

The College of Intensive Care Annual Scientific Meeting is upon us. How do you make something like that happen? Lets ask Naomi Diel, part of last years organising committee.

Jellybean 93 with Naomi Diel Doug Lynch

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The College of Intensive Care Annual Scientific Meeting is upon us. How do you make something like that happen? Lets ask Naomi Diel, part of last years organising committee.

The CICM ASM is happening next month. It is in Hobart. That’s in Tasmania.

Last year it was in Sydney. There are probably more first year ICU trainees in one hospital in Sydney than there are Intensivists of any description in the state of Tasmania. This year will be different.

When I was a kid, many moons ago, Tasmania was a place I couldn’t ever possibly get to. It was very far away on the other side of the world. I could barely understand that it was real. It might as well have been another planet.

When I was in my first year as an intensive care medicine trainee, many moons ago, the College of Intensive Care Medicine ASM was a place I couldn’t possibly get to. I could get there physically but it was expensive. I could barely expect to understand what they were talking about. It was filled with the people that actually wrote the text books that I was supposed to have read and memorised but I hadn’t opened yet. It may as well have been another planet.

But I did go. I went to the ASM in Melbourne at the Sofitel in Melbourne and heard these men (and not enough women) speak about the brand new Sepsis Guidelines, the first ones. I remember listening to John Marshall and I remember listening to the non-believers. They questioned EGDT and whether Manny Rivers’ study could be applicable in New Zealand and Australia.. They questioned Activated Protein C and the interaction between Eli Lilly and the Surviving Sepsis Campaign. They were passionate and sometimes angry. This antipodean intensive care scene was a very different world to what I had seen in the US, the UK or in Spain. This was good. I did struggle to keep up as a fresh recruit from emergency medicine. I did want to mix it with these big brains, I did look at them in awe but I also saw that they were humans not gods. Tub Worthley won the medal. He’s human.

In the years that have gone by the Joint Faculty of Intensive Care Medicine has become the College, the ASM has become a significant event on the ICU world calendar. New Zealand and Australia are bloody good at this stuff and even though it’s expensive and difficult to get out here from Europe and the Americas people do come. However this is still a conference for New Zealand and Australia. We do things differently here and of this we should be proud. Indeed many of our international colleagues would be a little envious of the system we work in.

The ASM has evolved but it remains, unapologetically, an annual scientific meeting. It is not SMACC, it is not ESICM, it is the CICM ASM. It is higher end, senior level, single organ system focused and research driven. Nerdy, less fashion conscious, more old school, perhaps, but I love it. It is the only pure ICU conference I go to most years.

So now it comes full circle. I was wrong about Tasmania; it is not only real but it looks better than a  Dombrovskis Photograph.  You can go there. You should.

I was wrong 12 years ago about the speakers, they are not from Mars (or from Venus), they are from the same places that you and I are from. The ASM is not the reserve of the great and good of Kiwi and Australian intensive care. It is ours. It is for all of us, young and old, naïve and cynical. It is a much improved experience for the trainee and probably everyone. Credit must go to Stephanie Gershon and her team at CICM. As Paul Young said to me back in Jellybean 18 “the College have this running on rails”. That allows the organising committee to focus on new ideas, confident that they are building on solid foundations.

In 2017 the ASM was in Sydney and it was conspicuous for its efforts to bring more young trainees to the forum. Lewis Macken and company did a great job. Bringing youth and energy to the Sydney International Convention Centre. There were podcasts like this one, there were talks recorded and shared on IntensiveCareNetwork.com, there was humour, there was Fast Transit and there was a deliberate effort to get a better gender balance.

One of that team was Naomi Diel.; ebullient, brilliant, and brave. Naomi shook it up a bit with help from her friends, the same friends she constantly gives credit to. And it turns out that the ASM is as much about making friends as anything else.

Have a listen to her insights into running one of these things and then ask yourself: could you do that? I suspect you probably could, I also suspect that the College would like you to think about it.

Get involved, consider putting your hand up for your regional committee.

The ICU Update is already booked out but there are still places for the ASM itself and the trainee symposium ($330). Sara Yong is in the thick of the Trainee Symposium again. There are a bunch of excellent educators in there; Celia Bradford, David Pilcher, Priya Nair, David (Neo) Anderson, Peter Kruger, Ray Raper, Peta Alexander, Sara Allen and more. Sonia Langlais talks about rural ICU and there is a very interesting session on Fellowships years from people that know.

Personally I think we should be making the Trainee Symposium be cheaper, perhaps entirely free. We need a big sponsor that understands the big picture. The sort of trainee that turns up at this sort of thing will be the director of an ICU near you sometime soon. It would surely be a good value item to sponsor in an unobtrusive fashion.

Thanks to Naomi for talking to us.

Thanks to Low and The Dirty Three for two tiny grabs from their utterly brilliant “In The Fishtank 7” EP recorded in 1999 (Released in 2001) and produced by Zlaya Hadzic for the “In The Fishtank” series on Konkcurrent Records, available on iTunes and probably on vinyl but I have not found it.

Further Listening

JellyBean Large

Jellybean 93 with Naomi Diel Doug Lynch

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TAPNA 2018: Its toxicology, Australian Style. https://lifeinthefastlane.com/tapna-2018-its-toxicology-australian-style/ https://lifeinthefastlane.com/tapna-2018-its-toxicology-australian-style/#respond Mon, 16 Apr 2018 20:52:43 +0000 https://lifeinthefastlane.com/?p=176873 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Get in quick for TAPNA 2018 from the 2nd to the 4th of May at Sydney. As always a stellar line up of toxicologist both from Australia and around the world.

TAPNA 2018: Its toxicology, Australian Style. Neil Long

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What is it?

TAPNA is the annual scientific meeting for the Toxicology and Poisons Network Australia. Join Australian and International toxicologists at Sydney to run through a plethora of topics including fomepizole (should we use it in Australia?), urine drug screens, what to do with an anion gap and the latest in OP poisoning.

TAPNA is hosting a stellar faculty including Dr Michael Eddleston from Edinburgh whose primary research is in pesticides and antidotes. He will be updating everyone on treatments in 2018 along with POC chemical analysis. Dr Sergej Zacharov from the Czech Republic with an interest in toxic alcohols will lead the charge on discussing fomepizole. Francois Oosthuizen will discuss how to detect illicit drugs followed by Dr Tom Robertson on toxicology sample analysis, rounded off with our own Dr Joe-Anthony Rotella discussing whether urine drug screen are ‘choosing wisely’. Dr Zeff Koutsogiannis will chair the anion gap, osomlar gap and all round VBG/ABG dilemmas to finish off the first day. Friday starts with an OP update, Dr Nick Buckley gives his cocktail for paraquat poisoning then Dr Thanjira Jiranantakan, will give her perspective on antidotes for pesticides in Thailand. Dr Katherine Isoardi will enlighten us in phenibut poisoning, Genevieve Adamao, Dr Michael Downe, Dr Jeffery Lai and Dr Peter Chai will keep us up to date with social medial and how this integrates with toxicology. And I haven’t even started on half the interesting cases or papers being presented.

Saturday includes the opportunity to attend a satellite Wiki Tox course ‘Tox issue in acute care’ covering 6 case-based sessions exploring key topics in toxicology.

How much is it?

Varied from $450 for a one day or $935 for the full conference ($1610 for the addition of the satelite session).
See the following link for all the prices and registration: TAPNA Registration

Where is it?

PARKROYAL Darling Harbour
150 Day Street, Sydney, NSW 2000

How do I apply?

Contact:
TAPNA Conference Secretariat
PO Box 180
Morisset NSW 2264
P: 02 4973 6573 F: 02 4973 6609 E:tapna@willorganise.com.auW: tapna 2018

Can I have more information?

TAPNA 2018: Its toxicology, Australian Style. Neil Long

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LITFL Review 327 https://lifeinthefastlane.com/litfl-review-327/ https://lifeinthefastlane.com/litfl-review-327/#respond Sun, 15 Apr 2018 22:13:35 +0000 https://lifeinthefastlane.com/?p=176861 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Welcome to the 327th LITFL Review! Your regular and reliable source for the highest highlights, sneakiest sneak peeks and loudest shout-outs from the web

LITFL Review 327 Marjorie Lazoff, MD

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LITFL review

Welcome to the 327th LITFL Review! Your regular and reliable source for the highest highlights, sneakiest sneak peeks and loudest shout-outs from the webbed world of emergency medicine and critical care. Each week the LITFL team casts the spotlight on the blogosphere’s best and brightest and deliver a bite-sized chunk of FOAM.

Readers can subscribe to LITFL review RSS or LITFL review EMAIL subscription

The Most Fair Dinkum Ripper Beauts of the Week

Nick CumminsRory Spiegel, in his typically eloquent manner, provides a rebuttal to the recent New York Times article on tPA in stroke. He suggests, “The question should not be, is tPA effective for the treatment of acute CVA but rather, why after 23 years do we still not know the answer?” [SR]

If you missed his talks at AAEM (or some other time), then definitely check out Bryan Hayes’s lecture handouts: [MMS]

The Best of #FOAMed Emergency Medicine

  • Rick Body explores the greys in between the oft-reported black and white of diagnostic tests. [AS, SR]. Another shade of grey: Josh Farkas, does it again…simplifying p values and what they actually mean.  The binary cutoff of <0.05 vs ≥0.05 is arbitrary and is used for simplicity > accuracy.  [SR]
  • Nice bread and butter review of DKA by Brit Long. Search for underlying etiology, intravenous fluids, electrolyte repletion, debate on bicarbonate, and insulin infusions. [SR
  • Steve Smith reminds us of the finding of inverted U waves in patients with chest pain. [SR]

The Best of #FOAMcc Critical Care and #FOAMres Resuscitation

The Best of #FOAMtox Toxicology

The Best of #FOAMus Ultrasound

  • In another collaborative project between The POCUS Atlas and DDxof.com, take a look at the ultrasound algorithm for the evaluation of suspected ectopic pregnancy. [MMS]
  • The Resuscitative TEE Project graciously shares open access to 3D printed TEE planes in their continued quest to spread the benefits of TEE. Print these models so learners can touch, hold and explore as much needed to understand the anatomy behind the different TEE planes. [MMS]
  • The SonoAUS team have released another great talk from their recent conference. Elissa Kennedy-Smith educates us on the enigma that is the Common Bile Duct [LP]
  • Let the right one in! The poor neglected right heart gets a polish and shine in the latest 5min Sono release. No reason to be afraid anymore. [LP]

The Best of #FOAMpeds Pediatrics

The Best of #MedEdFOAM and #FOAMsim

  • Reflection and continuous striving for improvement are two pillars of improving care of critically ill patients.  It is also important to have a construct to follow in the reflection process. Cliff Reid proposes using STEPS: Self, Team, Environment, Patient, and System in reflection of resuscitations. [SR]
  • Nice post by Clay Smith on the importance of metacognition, recognition of the Dunning-Krueger Effect, and how our egos are the real enemy. [SR]
  • How do you end a presentation? Don’t end it with ‘Any Questions’. For those who like this sort of thing, an INC article reminding us how to memorably end a presentation. [MMS]

Reference Sources and Reading List

Brought to you by:

LITFL Review 327 Marjorie Lazoff, MD

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The trouble with cognitive biases https://lifeinthefastlane.com/the-trouble-with-cognitive-biases/ https://lifeinthefastlane.com/the-trouble-with-cognitive-biases/#respond Sun, 15 Apr 2018 00:18:16 +0000 https://lifeinthefastlane.com/?p=176828 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

George Douros discusses the trouble with cognitive biases in terms of systems errors and a just culture.

The trouble with cognitive biases George Douros

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Don’t get me wrong, I am a big fan of Pat Croskerry and metacognition but I do wonder whether the rest of the medical profession has become a bit fixated on cognitive biases.

The fact that our errors now have names can lead to recrimination. Ever seen an M&M follow this cycle?

  • Name (the cognitive error)
  • Blame (usually the person isn’t named, but they feel it)
  • Shame (note that cognitive errors have been talked about before)
  • Train (having talked about it again, prescribed vigilance is the take-home point).

Even worse is when self-recrimination gets mixed up with self-reflection. Ever seen an M&M given by someone as penance with the take-home point a vow of vigilance, all for an error that if not for the grace of dumb-luck could have been you? They may have second-victim syndrome.

There’s actually two psychological schools of thought when it comes to error:

So…two somewhat opposing theories of error

  • Human error is the cause of everything
  • Systems faults cause human error

Professor of Psychology James Reason postulated that it’s more complicated than that as it’s a complex interplay of both – and he came up with surprisingly effective dairy-based analogy – the Swiss Cheese model of accident causation where each layer of cheese is a layer of defence and it’s only when the latent errors (holes) in multiple layers of defences fail to stop the hazard does an additional active error (not uncommon a cognitive bias error) by the provider result in patient harm. It’s more complex than that but let’s leave it at that for now.

James Reason’s Swiss Cheese Model (Click image for source: https://www.cmpa-acpm.ca/serve/docs/ela/goodpracticesguide/pages/patient_safety/Systems/systems_thinking_2-e.html)

Reason also proposed the concept of a ‘Just Culture’ as a response to what he saw as the ‘Unjust Culture’ of the emotionally satisfying and administratively convenient process of blaming the end provider. In a ‘Just Culture’, blame is appropriately allocated between person and system. If you are just doing your best by the patient, you invariably end up in ‘systems failure’.

NHS Incident Decision Tree for Patient Safety (Click image for source: https://www.ncbi.nlm.nih.gov/books/NBK20586/)

Of particular relevance to cognitive bias is the ‘substitution test’. By the very fact that errors due to cognitive biases occur so often and to so many that they have earnt themselves a name- means they pass the substitution test and thus should be treated as a systems failure, not a personal one if your goal is to prevent that error from happening again.

But it’s more than just that.

It’s about knowing when you should and should not berate yourself and to know when and how to defend yourself if you happen to find yourself in a particularly unjust culture.

Next week:

  • The trouble with mindfulness.

The trouble with cognitive biases George Douros

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James Hayes Fellowship Study Group 2018 https://lifeinthefastlane.com/james-hayes-fellowship-study-group-2018/ https://lifeinthefastlane.com/james-hayes-fellowship-study-group-2018/#respond Fri, 13 Apr 2018 15:50:10 +0000 https://lifeinthefastlane.com/?p=176820 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

The James Hayes Fellowship study group has started again at the college headquarters. See the current timetable here and also contact James if you would like to join the 2018 group.

James Hayes Fellowship Study Group 2018 Neil Long

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LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

The Victorian Registrar Study Group is held in at the Australasian College of Emergency Medicine Headquarters at West Melbourne on Saturday mornings, and has been a very great success since its inception.It was developed from Dr James Hayes’ Victorian Registrars Teaching program that ran from the Northern Hospital for just on 15 years. When this program was terminated in 2013, the current program at the College was created by a group of highly esteemed educators, (many of whom were students in James old study groups), dedicated to the finest principals of FOAMed.

The program is aimed as a “finishing school” for those about to sit their Fellowship exams.

It is – of course – not meant to replace any local programs – but rather supplement and compliment them.

It also allows for exposure to some of the best educators from across the state of Victoria as well as the promotion of future professional links and friendships between colleagues – breaking “silos” and the like – a good thing as you may not even get to meet half your colleagues otherwise!

We have some of the best teachers/ examiners / experts in their fields from across Melbourne and Geelong for these sessions

If interested in joining the group for this year – you can email James:  james.hayes@nh.org.au

2018 VIC FACEM STUDY GROUP PROGRAM
ACEM 34 Jeffcott St West Melbourne

  • Week 1, April 14: INTRODUCTION TO THE EXAM PROCESS
    • Victor Lee + Ruth Hew
  • Week 2, April 21: AIRWAY
    • George Douros + Lee Wong
  • Week 3, April 28: TRAUMA I
    • Joseph Mathew
  • Week 4, May 5: EMERGENCY DERMATOLOGY
    • Sean Arendse
  • Week 5, May 12: EMERGENCY RADIOLOGY
    • Andrew Dixon
  • Week 6, May 19: OPHTHALMOLOGY + ENT
    • Mani Rajee + Phil Visser
  • MONASH PRACTICE EXAM 23rd of May
  • Week 7, May 26: SURGICAL EMERGENCIES + ADMINISTRATION
    • Don Liew
  • Week 8, June 2: INFECTIOUS DISEASES
    • Alex Paspaliaris + Nicola Walsham
  • Week 9, June 9: TOXICOLOGY I
    • Shaun Greene
  • Week 10, June 16: CARDIOLOGY
    • Tom Reade
  • Week 11, June 23: TOXICOLOGY II
    • Shaun Greene
  • Week 12, June 30: EMERGENCY ULTRASOUND
    • Pourya Pouryahya
  • Week 13, July 7: PAEDIATRICS
    • Nadine Sharples + Sandy Hopper
  • Week 14, July 14: NEUROLOGY + PSYCHIATRY
    • Pascal Gelperowicz
  • Week 15, July 21: TRAUMA II
    • Amit Maini + Chris Groombridge
  • Week 16, July 28: ENVENOMATION
    • Zeff Koutsogiannis
  • EXAM 3rd AUGUST 2018

James Hayes Fellowship Study Group 2018 Neil Long

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Funtabulously Frivolous Friday Five 234 https://lifeinthefastlane.com/funtabulously-frivolous-friday-five-234/ https://lifeinthefastlane.com/funtabulously-frivolous-friday-five-234/#respond Thu, 12 Apr 2018 20:58:20 +0000 https://lifeinthefastlane.com/?p=176777 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Just when you thought your brain could unwind on a Friday, you realise that it would rather be challenged with some good old fashioned medical trivia FFFF...introducing Funtabulously Frivolous Friday Five 234.

Funtabulously Frivolous Friday Five 234 Neil Long

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LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Just when you thought your brain could unwind on a Friday, you realise that it would rather be challenged with some good old fashioned medical trivia FFFF…introducing Funtabulously Frivolous Friday Five 234.

Readers can subscribe to FFFF RSS or subscribe to the FFFF weekly EMAIL

Question 1:

What is Stabler sign?

  • Stabler sign: Non-traumatic abdominal skin ecchymosis in the inguinal-pubic area associated with intra-abdominal haemorrhage, originally described in ectopic pregnancy
  • Francis Edward Stabler published his paper in 1934, titled ‘A case showing Cullen’s sign‘ concerning a patient presenting with an ectopic pregnancy: with left illiac fossa pain of fourteen days duration and ilioinguinal ‘bruising’, 7 weeks post last menstrual period. This was 16 years after Thomas Stephen Cullen has published his works.
  • Initially described as an inguinal-pubic extension of the peri-umbilical ecchymosis of Cullen sign.
  • Further cases of bruising to the inguinal-pubic area reported with AAA rupture and acute hemorrhagic pancreatitis.
  • Although rare, this sign has most commonly been identified in neonates secondary to adrenal hemorrhage. This is associated with obstetric injury, perinatal hypoxia, and sepsis [Urology. 2002 Apr;59(4):601]. Rarely, it may be due to ruptured neuroblastoma.

Question 2

What infectious disease can been seen on an X-ray or ultrasound as a ‘water-lily’ sign?

  • Hydatid infection.
  • Caused from the larval stage of a small tapeworm of dogs (Echinococcus granulosus).
  • 20% of cysts develop in the lungs and most are asymptomatic, although if they rupture into a bronchus a patient can complain of tasting salty water.
  • A collapsed cyst’s membrane gives the appearance of a water lily on imaging. [Reference]
Hydatid cyst with water lily sign

Question 3

In acute appendicitis, palpation of the left lower quadrant may elicit pain in the right lower quadrant. If this occurs, it is said to be a positive Rovsing’s sign.
This is commonly taught to be attributable to eliciting peritoneal irritation, however, Rovsing’s original description and intention was quite different, what was his original idea?

  • Niels Thorkild Rovsing (1862-1927) was a Danish surgeon, he originally described the manoeuvre as an attempt to distend the caecum and appendix by applying pressure to the left colon, in an anti-peristaltic fashion.
  • Rovsing described the manoeuvre in his 1907 paper:

I press with my right hand onto the fingers of the left hand that is lying flat against the colon descendens and then let the hand glide up toward the splenic flexure…The entire method is based upon isolated rise of pressure within the colon.’ [Rovsing sign]

  • In doing this correctly, Rovsing suggests that if pain is elicited, then this isolates the source to the caecum or appendix, and rules out other structures in the right iliac fossa.
  • Rovsing T. Indirektes Hervorrufen des typischen Schmerzes an McBurney’s Punkt. Ein Beitrag zur Diagnostik der Appendicitis und Typhlitis [Indirect elicitation of the typical pain at McBurney’s point. A contribution to the diagnosis of appendicitis and typhlitis]. Zentralblatt für Chirurgie 1907;34:1257-1259

Question 4

What does a Trichotillomaniac need on his/her head?

  • A wig
  • Trichotillomania (TTM) is is obsessive hair pulling
  • Coined by the french dermatologist Francois Henri Hallopeau in 1889. [Reference]
  • He also coined the word ‘antibiotique‘ in 1871 to describe a substance opposed to the development of life long before Selman Waksman coined the term on the discovery of streptomycin. [Reference]

Question 5

What did eating white ants (a delicacy) in Kenya do to six people in 1979?

  • Gave them botulism. 5 of the 6 individuals died.
  • Actually termites and not ants, had been picked days before consumption in Nairobi. In fact the locals had eaten some of the termites fresh without any symptoms. 3 days later the rest of the termites were eaten but because they were stored in a polythene bag the anaerobic conditions were ideal for botulism growth and 5 patients developed flaccid paralysis while the 6th only had blurred vision.
  • Not able to test for botulism, two groups of mice were given the remaining termites, one group were pre-treated with anti-toxin and survived while all the other mice died. [Reference]

…and finally

Funtabulously Frivolous Friday Five 234 Neil Long

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Medmastery: Abdominal aorta https://lifeinthefastlane.com/medmastery-abdominal-aorta/ https://lifeinthefastlane.com/medmastery-abdominal-aorta/#respond Wed, 11 Apr 2018 00:01:54 +0000 https://lifeinthefastlane.com/?p=176476 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Exploring the Point of Care Ultrasound Essentials course with a video demonstrating the examination to identify abdominal aortic aneurysm.

Medmastery: Abdominal aorta Mike Cadogan

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LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

The team at Medmastery are providing LITFL readers with a series of FOAMed courses from across their website.

Exploring the Point of Care Ultrasound Essentials course with a video demonstrating the examination to identify abdominal aortic aneurysm.

Further reading:

Guest post: Viveta Lobo, MD (@vivetalobo). Attending Emergency Medicine Physician and Associate Director, Emergency Ultrasound Fellowship at Stanford University Medical Center in California, USA.

My fellowship training in point of care ultrasound (POCUS) fundamentally changed my clinical practice, and has made me a more confident and efficient physician. Having seen the benefits of using POCUS in my practice, I’m dedicated to teaching POCUS to all healthcare professionals.” – Viveta Lobo

Medmastery: Abdominal aorta Mike Cadogan

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LITFL Review 326 https://lifeinthefastlane.com/litfl-review-326/ https://lifeinthefastlane.com/litfl-review-326/#respond Sun, 08 Apr 2018 20:23:26 +0000 https://lifeinthefastlane.com/?p=176642 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Welcome to the 326th LITFL Review! Your regular and reliable source for the highest highlights, sneakiest sneak peeks and loudest shout-outs from the web

LITFL Review 326 Marjorie Lazoff, MD

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LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

LITFL review

Welcome to the 326th LITFL Review! Your regular and reliable source for the highest highlights, sneakiest sneak peeks and loudest shout-outs from the webbed world of emergency medicine and critical care. Each week the LITFL team casts the spotlight on the blogosphere’s best and brightest and deliver a bite-sized chunk of FOAM.

Readers can subscribe to LITFL review RSS or LITFL review EMAIL subscription

The Most Fair Dinkum Ripper Beauts of the Week

Nick CumminsRead this special collaboration between EMCrit RACC and Dr Smith : The OMI Manifesto. This well cited review is a detailed explanation of the false dichotomy between STEMI and NSTEMI, and suggests new terminology consistent with the latest evidence. [MG]

A powerful story from Ashley Liebig about the words we use in front of patients, expecting the unexpected, and the negative encounters that can and do happen in patient care. Our jobs are hard and stressful but don’t ever forget the importance of kindness and humanity in the patients you care for. [SR]

 

The Best of #FOAMed Emergency Medicine

The Best of #FOAMcc Critical Care and #FOAMres Resuscitation

The Best of #FOAMtox Toxicology

  • The latest installment of The Toxicologist Mindset from the ALiEM team describes a case of herbal induced delirium. There is an overview of autonomic toxidromes, physostigmine as an antidote, and the common causes and presentations of herbal medicine-induced anticholinergic toxicity. [TCN]

The Best of #FOAMus Ultrasound

The Best of #FOAMpeds Pediatrics

  • Hypertension in Children: White Coat or Wicked Curse? Tim Horeckzo helps simplify this topic in a whimsical Harry Potter-themed approach. Which hypertensive person is your patient? Hufflepuff? Gryffindor? Revenclaw? Slytherin? [MMS]

The Best of #FOAMim Internal Medicine

The Best of #MedEdFOAM and #FOAMsim

  • Fantastic talk from Sarah Gray at #dasSMACC about the voices in our heads. Compassion towards oneself is one of the hardest skills to learn in medicine. The good news is you can change this with 3 steps: Listen to your inner dialogue; Practice better self talk; and Have empathy towards others. [SR]
  • Stress growth and embracing it to build us to be better providers. The latest EM Over Easy episode tackles this idea with Anna Kalantari. [MMS]
  • Ego is the enemy, especially in academics. Learn how to fight the darkness of ego on many fronts on a daily basis. The tactics discussed in this post truly embodies the #FOAM movement. [MMS]

Reference Sources and Reading List

Brought to you by:

LITFL Review 326 Marjorie Lazoff, MD

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Mastering Intensive Care 029 with Simon Finfer https://lifeinthefastlane.com/mastering-intensive-care-029-with-simon-finfer/ https://lifeinthefastlane.com/mastering-intensive-care-029-with-simon-finfer/#respond Sun, 08 Apr 2018 03:33:42 +0000 https://lifeinthefastlane.com/?p=176631 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Andrew Davies talks with Simon Finfer about Mastering Intensive Care: patients, families, and an empowering ICU culture.

Mastering Intensive Care 029 with Simon Finfer Andrew Davies

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LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Does each bedside decision you make actually help your patient to feel, function or survive?

Have you considered how frightening and intimidating the Intensive Care Unit environment is to your patients and their families?

Do you feel empowered by the people you work with and the culture in your ICU?

Simon Finfer loves telling a tale. In this episode you’ll hear the story of the serendipitous and multi-national route Simon took to end up working for 25 years in one of Australia’s premiere Intensive Care Units. An Intensive Care Department where his colleagues and the culture they developed has fostered him to become one of Australia’s prominent intensive care researchers. You’ll also hear how he teaches his junior colleagues to question everything they do at the bedside to ensure their decisions truly help the patient.

Simon is a Professorial Fellow in the Critical Care and Trauma Division at The George Institute for Global Health, a Senior Intensivist at Royal North Shore Hospital and Director of Intensive Care at the Sydney Adventist Hospital in Sydney, Australia. He is an Adjunct Professor at the University of New South Wales, a Clinical Professor at the University of Sydney and is a past-Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Simon is a world leader in Sepsis and is an international expert in the design and conduct of large-scale randomised controlled trials in Intensive Care.

Simon has collaborated with me (and many others) through the ANZICS Clinical Trials Group, so we caught up at the Group’s recent 20th Annual Meeting on Clinical Trials in Intensive Care at Noosa Heads in Queensland. We had a fascinating conversation in which Simon talked about:

  • His early career in London where he was simply working too hard
  • The circuitous route he took to Royal North Shore Hospital in Sydney
  • The magnificent people-oriented culture inspired by Malcolm Fisher
  • His early collaboration with the George Institute for Global Health
  • How showing you care is what matters most in an end of life discussion
  • His thoughts on having family at the bedside for ward rounds
  • How the golf course is the only place he doesn’t think about patients
  • How moving to a property with animals has brought relaxation and peace
  • The rekindling of his passion for motorbike riding
  • Why he got a Twitter account and how social media is both a force for good and an echo chamber
  • How it’s almost “too easy” to write a paper in modern times
  • The unlikelihood of a magic bullet arriving anytime soon
  • His advice to look after our selves, to embrace uncertainty and to maintain our humanity

My genuine hope with this podcast is to inspire and empower you to bring your best self to work and to consider adopting some of the habits and behaviours my guests give their perspectives on, with the ultimate purpose of improving outcomes for all of our patients. Please help me to spread the message by simply emailing your colleagues, posting on social media or rating and reviewing the podcast.

Feel free to leave a comment on the Facebook “mastering intensive care” page, on the LITFL episode page, on Twitter using #masteringintensivecare, or by sending me an email at andrew@masteringintensivecare.com.

Thanks for listening on the journey towards mastering intensive care.

Andrew Davies

 

——————–

Show notes (people, organisations, resources or links mentioned in the episode)

5th SG-ANZICS Asia Pacific Intensive Care Forum: www.sg-anzics.com

ANZICS Clinical Trials Group: http://www.anzicsctg.org/

More information about Simon Finfer: https://www.georgeinstitute.org/people/simon-finfer

Twitter handle for Simon Finfer: @icuresearch

SAFE study: https://www.ncbi.nlm.nih.gov/pubmed/15163774

NICE-SUGAR study: https://www.ncbi.nlm.nih.gov/pubmed/19318384

SMACC: https://www.smacc.net.au/

Mastering Intensive Care podcast: http://masteringintensivecare.libsyn.com/

Mastering Intensive Care at Life In The Fast lane: https://lifeinthefastlane.com/litfl/mastering-intensive-care/

Email Andrew Davies: andrewATmasteringintensivecare.com

Twitter handle for Andrew Davies: @andrewdavies66

Mastering Intensive Care 029 with Simon Finfer Andrew Davies

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Funtabulously Frivolous Friday Five 233 https://lifeinthefastlane.com/funtabulously-frivolous-friday-five-233/ https://lifeinthefastlane.com/funtabulously-frivolous-friday-five-233/#respond Fri, 06 Apr 2018 19:46:50 +0000 https://lifeinthefastlane.com/?p=176608 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Just when you thought your brain could unwind on a Friday, you realise that it would rather be challenged with some good old fashioned medical trivia FFFF...introducing Funtabulously Frivolous Friday Five 233.

Funtabulously Frivolous Friday Five 233 Neil Long

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LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Just when you thought your brain could unwind on a Friday, you realise that it would rather be challenged with some good old fashioned medical trivia FFFF…introducing Funtabulously Frivolous Friday Five 233.

Readers can subscribe to FFFF RSS or subscribe to the FFFF weekly EMAIL

Question 1:

Who popularised museli?

  • Dr Maximilian Bircher-Benner (August 22, 1867 – January 24, 1939) was a Swiss physician with a keen interest in the benefits of nutrition to cure his patients. He came across a variation of muesli on a walking trip and later adopted the following recipe:
    • Apples, “[t]wo or three small apples or one large one.” The whole apple was to be used, including skin, core, and pips.
    • Nuts, either walnuts, almonds, or hazelnuts, one tablespoon.
    • Rolled oats, one tablespoon, “previously soaked in 3 tablespoons water for 12 hours”.
    • Lemon juice from half a lemon.
    • Either cream and honey or sweetened condensed milk, 1 tablespoon.
  • His idea met much criticism as “humans are not supposed to be herbivores” but a company called Somalon in 1959 after permission from the Bircher family manufactured a product called Birchermüesli, within a year was being exported to Germany, Austria, Great Britain, the Netherlands and the USA. [Reference]

Question 2

Which orthopaedic surgeon wrote the paper “Hazards of parachute jumping” in 1946 in the British Journal of Surgery?

  • Peter Essex Lopresti of the fracture fame.
  • An Essex Lopresti injury consists of a radial head fracture with dislocation of the distal radioulnar joint (DRUJ) and disruption of the interosseous membrane (IOM).
  • The paper has some brilliant quotes of soldiers sustaining concussion on landing “the period of unconsciousness varied from a few seconds to several days… results were satisfactory provided the patient’s activity was kept below headache threshold”. Also the image below shows “ringing the bell” which consists of hitting your head by not hyperextending it on exit. This results in “buying a round of drinks” and probably a pounding headache.
  • From the 20,777 jumps recorded by the Sixth British Airborne division he recommended:
    • Hyperextending the neck on exit and holding the static line correctly.
    • Landing with the body relaxed but the head well forward, shoulders round, elbows in and watch the ground.  Knees and ankles together, slightly flexed to take the initial impact. Feet parallel to the ground and then roll to the side. [Reference]
  • He unfortunately died at the age of 35 due to an MI. [Reference]

Question 3

What condition may sound appealing to a dairy farmer, but makes afflicted patients cough up blood and have ‘coca cola‘ urine?

  • Goodpasture disease. 
  • An Autoimmune disease characterized by hemorrhage of the lungs and glomerulonepheritis. This disease is caused by a type II hypersensitivity reaction to Goodpasture antigen on basement membrane of the glomerulus of the kidneys and the pulmonary alveolus. First signs of the disease are vague such as nausea and fatigue or pallor. Most patients seek medical attention with the development of hemoptysis or hematuria.
  • Dr Ernest William Goodpasture (1886-1960) performed autopsies on patients in a 1918 flu epidemic (note influenza was not isolated until 1933) and he was interested in what was killing these young men. He found two unusual patients who had “extensive hemorrhagic consolidation of the lungs associated with focal necrosis of alveolar walls and hyaline membranes as well as necrotising and proliferative glomerulonephritis“. The sections were discarded and Dr Goodpasture thought nothing more of his 1919 report until Drs Clare Stanton and Dr John Range reviewed his literature after having similar patients in their Melbourne Hospital in the 1950s.
  • They wrote an article in 1958 stating “… as the ethology of the condition is obscure, brevity and precedence are urged to justify the name ‘Goodpasture syndrome.” Dr Goodpasture wrote to the two communicating that his name should not be attached as he had not fully studied the disease. It is ironic that his name is attached to a disease he disclaimed knowing about but his other achievements were barely acknowledged:
    • 31 years as the first head of pathology at Vanderbilt University.
    • He discovered that viral inclusions in fowlpox contained active viral particles, that embryonate eggs could be used as a culture medium for viruses. Thus paving the way for vaccine development and to study the pathogenesis of viral and bacterial diseases.
    • He proved mumps was a viral infection. [Reference]

Question 4

What is Willis-Ekbom syndrome and Ekbom syndrome II?

  • Willis-Ekbom syndrome is restless legs syndrome. Named after Karl Axel Ekbom (1907-1977) and Thomas Willis.
  • Wherefore to some, when being abed they betake themselves to sleep, presently in the arms and legs, leapings and contractions of the tendons, and so great a restlessness and tossing of their members ensue, that the diseased are no more able to sleep, than if they were in a place of the greatest torture’ – The London Practice of Physick: Or the Whole Practical Part of Physick Contained in the Works of Dr. Willis. [Of the Watching Evil, p404]
  • Ekbom syndrome II is a delusional parasitosis. [Reference]

Question 5

How did Jack Barnes determine that the thumbnail-sized jellyfish now known as Carukia barnesi was the cause of Irukandji Syndrome?

  • In 1964, John (Jack) Handyside Barnes (1922-1985), after managing to catch the tiny jellyfish decided to sting himself, his 9 year-old son and a local surf-lifesaver.
  • They all developed Irukandji syndrome and needed treatment at Cairns Base Hospital.
  • Irukandji syndrome is named after the Irukandji people who live along the coastal strip of North Queensland. Wise enough to know not to go into the water during certain times of the year. Hugo Flecker in 1952 first documented the syndrome but no one had identified the culprit. [Reference]

    The lad reported mild abdominal pain twelve minutes after being stung…

    As systemic effects became manifest, subjects were seized with a remarkable restlessness, and were in constant movement, stamping about aimlessly winging their arms, flexing and extending their bodies, and generally twisting and writhing…

    … muscle groups in tonic contraction, little short of spasm… and the volunteers adopted a stance which I can best liken to that of an infant with a full nappy…

    All had abdominal and back pain, pain in the anterior chest wall with some difficulty in breathing, and diffuse aches in muscles and joints……it was agreed that movement did not relieve symptoms, nor did pressure and rubbing…

    Forty minutes after the stinging, the abdominal musculature of the three subjects was in unrelenting spasm, so rigid as to warrant fully the term “board-like”.

    Vomiting… was not troublesome for some forty minutes.

    The adults obtained complete relief two minutes after the injection of 50 mg pethidine… Symptoms began to return 20 minutes after…

    As the effect of the second injection wore off, all subjects complained of neuralgic pains… and intermittent administration of aspirin was necessary for approximately 24 hours. Thereafter no ill-effects were apparent.

    – Barnes, 1964.

…and finally

Funtabulously Frivolous Friday Five 233 Neil Long

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Tropical Travel Trouble 007 Mega Malaria Extravaganza https://lifeinthefastlane.com/tropical-travel-trouble-006-malaria-extravaganza/ https://lifeinthefastlane.com/tropical-travel-trouble-006-malaria-extravaganza/#respond Thu, 05 Apr 2018 19:48:56 +0000 https://lifeinthefastlane.com/?p=175890 LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

Part 1 of 3 of our mega tropical series covering Malaria, TB and HIV. It is key to understand these common tropical diseases because some patients will adopt the Hickams dictum, 'I can have as many diseases as I damn well please', it's not always going to be a unifying diagnosis.

Tropical Travel Trouble 007 Mega Malaria Extravaganza Neil Long

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LITFL • Life in the Fast Lane Medical Blog LITFL • Life in the Fast Lane Medical Blog - Emergency medicine and critical care medical education blog

aka Tropical Travel Trouble 007

When you think tropical medicine, malaria has to be near the top. It can be fairly complex and fortunately treatment has become a lot simpler. This post is designed to walk you through the basic principals with links to more in depth teaching if your niche is travel medicine, laboratory diagnostics or management of severe or cerebral malaria. If you stubbled on this post while drinking a cup of tea or sitting on the throne and want a few basic facts then skip to the end for a brief summary of the salient teaching points. As always do not hesitate to contact a specialist but hopefully armed with a little bit more knowledge.

Questions:

Q1. What is malaria and can you name the five types that infect humans?

  • Malaria is a protozoan parasite transmitted by the female anopheles mosquito. Like many vectors in tropical medicine it is the female who is responsible, they require blood meals in order to produce their eggs. Males feed exclusively on fruit. 
  • There are 5 types known to infect humans:
    • Plasmodium falciparum (most dangerous form and associated with death).
    • Plasmodium viva (causes relapsing fevers due to hypnozoites that hide in the liver).
    • Plasmodium ovale (causes relapsing fevers due to hypnozoites that hide in the liver).
    • Plasmodium malariae and Plasmodium knowlesi appear identical under microscopy and require PCR to differentiate them.


Q2. What is the life cycle of malaria?


Look at the above diagram and watch the video below for an excellent visual summary.

Q3. Where are the different types of malaria, and why is this important to know for my patient?

  • Falciparum: throughout tropics, sub-Saharan Africa, SE Asia and S.America.
  • Vivax: Central/S America, African horn, India/Pakistan, SE Asia.
  • Ovale: Only in West Africa.
  • Malariae: Worldwide.
  • Knowlesi: Borneo and peninsular Malaysia.
  • It is important to know whether your patient is at risk of P.Falciparum, which is the most significant for causing cerebral malaria and mortality. Or, is your patient having relapsing fevers a year after being in West Africa or India, then you’ll need to consider hypnozoites in the liver from P. ovale or P. vivax.

Spatial distribution of P. Knowlesi 2016

Q4. What are the signs and symptoms of malaria?

  • Uncomplicated:
    • Fever in 90%. 
    • Classically described as a regular periodic fever, with tertian fever (P.falciparum, P.vivax and P.ovale) causing fevers every third day (every 48 hours) and quartan malaria (P.malariae) with fever every 4th day (every 72 hours). This periodicity only occurs if patients present late; it is unreliable in most instances. 
    • Non-specific flu-like symptoms: Headache, rigors, myalgia, malaise, minor gastrointestinal symptoms and jaundice from haemolysis. Splenomegaly and signs of anaemia may be seen clinically. 
    • Requires a high index of suspicion with some cases of patients returning to the UK having been diagnosed a year after returning from an endemic country.
    • In endemic areas it has become common to say ‘I have malaria‘ when you have a fever.
  • Severe:
    • Mortality of severe malaria approaches 100% and can occur within hours. With prompt treatment and supportive care this falls to 10-20% overall.
    • Often thought of in P. falciparum although there have been cases in P. vivax and P. knowlesi. P. falciparum is particularly troublesome because the infected RBCs are prevented from entering the spleen by ‘sequestration’ – deformities in the red cell membrane which results in adhesions to capillary walls resulting in hypoxia to downstream tissues and potentially the relapse of increased cytokines.
    • Severe P. falciparum is defined as:
        • GCS <11 in adults or a Blantyre coma score <3 in children.

      • Cerebral malaria is mis-diagnosed 25% of the time based on autopsies in Malawi. A good clue is to perform a fundoscopy looking for malarial retinopathy (white centred haemorrhages, vessel changes and whitening).
      Malarial retinopathy
      • Generalised weakness, the person can not walk without assistance.
      • More than 2 convulsions in 24 hours.
      • Acidosis: base deficit >8 mEq/L of bicarbonate <15 mmol/L or lactate >5 mmol/L.
      • Hypoglycaemia <2.2 mmol/L (<40 mg/dL).
      • Severe malarial anaemia: haemoglobin concentration <5 g/dL or a haematocrit of <15% in children <12 years of age (<7 g/dL and <20% , respectively , in adults) with a parasite count >10,000/uL.
      • Raised creatinine >265 umol/L (3 mg/dL) or urea >20 mmol/L.
      • Raised bilirubin >50 umol/L (3 mg/dL) with a parasite count >100,000/uL.
      • Pulmonary oedema either radiographically confirmed or saturations <92% on room air with a respiratory rate >30/min.
      • Significant bleeding.
      • Shock: capillary refill >3 seconds. Evidence of poor perfusion to their peripheries or s systolic blood pressure <70 mmHg in children or <80 mmHg in adults.
      • Hyperparasitaemia: >2%.
    • Severe Vivax
      • Same as falciparum but no parasite density threshold.
    • Severe Knowlesi
      • Parasite density >100,000/uL.
      • Jaundice and parasite density > 20,000/uL.

Q5. What is the mechanism of “immunity” to malaria?

  • Innate immunity:
    • Haemoglobinopathies (Thalessaemia).
    • RBC enzyme deficiencies (G6PD).
    • RBC surface components (Duffy blood group).
    • Sickle cell haemoglobin.
  • Incomplete immunity from prior repeated exposure:
    • In populations who are continually exposed to malaria (inoculation rate >10/year) a partial immunity to clinical disease and a reduced risk of developing severe malaria can occur. Clinically you will see disease in young children but adolescents and adults seldom suffer clinical disease. This immunity is lost if the person moves out of an endemic area.
    • In pregnancy the placental tissue has a preference from PfEMP1. Once antibodies are developed they are usually protected from malaria in pregnancy but until this stage there is higher morbidity and mortality for both the mother and foetus.

Q6. Why does pregnancy increase susceptibility to malaria?

  • Physiological changes – increased ‘host signature’ helps mosquitoes to detect the host (increased production of oestrogen and cortisol)
  • Behaviour changes – leave protection of bed nets during the night twice as frequently to urinate.
  • Pregnancy causes a generalised immuno-suppression (reduced type 1 helper cells)
  • Acquisition of protective immunity against placental malaria is only acquired over successive pregnancies.
  • Parasites accumulate and replicate in the placenta, higher densities and mature stages. Interferes with oxygen and nutrient transfer. As the parasite sequesters in the placenta the sensitivity of our diagnostic methods falls dramatically. A high index of suspicion and multiple blood films are required.
  • Malaria is more severe in pregnancy and requires prompt treatment. Awaiting WHO policy update but current evidence states risk-benefit balance favours ACTs in all 3 trimesters for proven malaria. When compared to quinine, artemisinin is not associated with an increased risk of spontaneous abortions, or still births or congenital malformations.
  • Intermittent Preventative Treatment in pregnancy (IPTp or SP-ITPp) if offered to all women in endemic areas of Africa in the first and second pregnancy. The reason ‘screen and treat’ is not adopted is due to the reduced sensitivity of our diagnostic tests, sometimes down to 50% in certain populations.
    • Sulfadoxine-pyrimathamine (SP), monthly from the second trimester.
    • HIV+ve women receive daily cotrimoxazole instead of IPTp.
    • IPTp reduces maternal malaria by 10%, placental malaria by 52%, LBW by 29% and increases mean birth weight by up to 79g.
    • Given every scheduled visit in the 2nd and 3rd trimester.
    • Folic acid reduced to 0.4mg/day when using SP.
  • It has also been proposed to use a similar strategy for infants <12 months to receive SP in conjunction with their vaccinations of DTP and measles in moderate to high transmission areas. This is called Intermittent Preventative Treatment for infants (SP-IPTi). Do not give to infants who are already on co-trimoxazole.
  • Some children under the age of 6 years in seasonal malaria will receive seasonal malaria chemoprevention (SMC) with monthly amodiaqunie + SP during the transmission season. Do not give to infants who are already on co-trimoxazole.

Q7. What is Blackwater Fever?

  • Blackwater fever (BWF) is a severe clinical syndrome, characterised by intravascular hemolysis, hemoglobinuria, and acute renal failure. Haemoglobin is eliminated via the kidneys causing a black urine – the Blackwater Fever.
  • It was a particular problem in European expatriates chronically exposed to Plasmodium falciparum and drinking tonic water which contained quinine. Once given treatment dose of quinine for malaria a number of expatriate developed BWF and several theories were hypothesised. BWF virtually disappeared after 1950, when chloroquine superseded quinine.

Q8. How do you diagnose malaria?

  • There are two methods routinely used, light microscopy (thick film and thin films) and immunochromatographic rapid diagnostic tests (RDTs). The latter detects parasite-specific antigens or enzymes that are either genus or species specific.
  • Thick and thin is the gold standard and any competent microscopist should see malaria parasites.
  • RDT target antigens:
    • Some will detect Histidine-rich-protein-2 (HRP-2) which is only expressed by plasmodium falciparum.
    • Parasite lactate dehydrogenase (pLDH) can be P.falciparum specific (Pf-pLDH) or P.vivax specific pLDH (Pv-pLDH)
    • Pan-specific pLDH will detect all malaria species.
Malaria RDTs
  • RDTs are useful when you don’t have a microscopist, a malaria parasite is seen but you are unsure of the species or if a patient has had incomplete antimalarial treatment. With incomplete treatment the thick and thin films may be negative and repeat films should be performed if suspicion is high (every 6-12 hours) or an RDT that can detect LDH is the first to turn negative, indicating potential early treatment benefit. PfHRP2 will be positive for a couple of weeks after treatment, but again could indicate treatment success if negative after this time period.
  • If both a slide examination and an RDT is negative it is extremely unlikely the patient has malaria and other causes should be sought. Be aware the traditional teaching was for 3 thick and thin films 12 hours apart and your institution may still practise this strategy.
  • PCR is available but is largely used in research or looking at drug resistance.
  • If you are out in the field and need some microscopy tips see the WHO learners guide and also test yourself with their malaria quiz.

W0042190 Plasmodium falciparum
Credit: Wellcome Images.[/caption]

Q9. How do you treat malaria?

  • Uncomplicated:
    • If you want to only remember one drug – oral Artesunate combination therapy (ACT) on day 1,2,3 for children and adults except women in the first trimester (simple, although reports of resistance in SE Asia to artesunate are emerging and longer courses are required or new ACT regimens that are not yet licensed – see your local guidelines).
      • Artemether + lumefantrine.
      • Artesunate + amodiaquine.
      • Artesunate + mefloquine.
      • Dihydroartemisinin + piperaquine (in children <25kg this should be dosed as 2.5mg/kg of dihydroartemisinin and 20mg/kg of piperaquine). Can prolong the QT interval.
      • Artesunate + sulfadoxine-pyrimathamine (SP). Women taking 5mg of folic acid greatly reduce the efficacy of SP and this combination should be avoided. 0.4mg of folic acid is okay.
      • These five ACT regimens are used because artemisinin rapidly clears the blood of parasites by a factor of 10,000 each 48hr asexual cycle. It is also active against the sexual stages of the parasite that meditate onward transmission to mosquitoes. The longer-acting partner drug clears the remaining parasites and provides protection against artemisinin resistance.
    • In low transmission countries give a single dose of Primaquine 0.25mg/kg in addition to ACT for anti-gametocyte effect as part of malaria elimination programme for P.falciparum. (G6PD testing is not required but currently not approved for pregnant and breast feeding women and children <6 months).
    • Chloroquine can be used to treat P. vivax, P. ovale, P. malariae and P. knowlesi if sensitive but to keep things simple you can just use ACT (except women in the first trimester). Chloroquine is dosed at 10mg/kg on day 1, day 2 and 5mg/kg on day 3.
    • To prevent a relapse of P. vivax or P. ovale use a 14 day course of primaquine 0.25-0.5mg/kg unless G6PD is a possibility (i.e. infants, pregnant women, women breast feeding and those with confirmed G6PD). If G6PD is a possibility or confirmed treat with primaquine but at 0.75mg/kg once a week for 8 weeks with close medical supervision. It has dose related complications.
    • Anyone with P. falciparum should be admitted for 24 hours due to the risk of sudden deterioration at the beginning of treatment.
  • Special Populations:
    • Pregnancy and breast feeding:
      • In the 1st trimester of pregnancy give quinine +/- clindamycin 10mg/kg BD (P.falciparum) for 7 days (guidelines may change later in 2018 to ACT as new safety data is about to emerge).
      • To eradicate P. ovale and P. vivax in pregnant or breast feeding women, consider weekly chemoprophylaxis with chloroquine until delivery and breastfeeding is complete, on the basis of G6PD status treat with primaquine to prevent a future relapse.
    • Children < 5kg get dosed at 5kg for ACT.
    • HIV patients, avoid artesunate + SP if on co-trimoxazole. Or artesunate + amodiaquine if they are also on efavirenz or zidovudine. HIV patient drug interactions.

  • Artemether + lumefantrine

  • Artesunate + amodiaquine

  • Artesunate + mefloquine

  • Dihydroartemisinin + piperaquine (in children <25kg this should be dosed as 2.5mg/kg of dihydroartemisinin and 20mg/kg of piperaquine).

  • Artesunate + sulfadoxine-pyrimathamine (SP).

  • Severe Malaria:
    • Intravenous or intramuscular artesunate for at least 24 hours until oral medication can be tolerated (usually a complete 3 day course of ACT on top of the parenteral treatment and add primaquine in areas of low transmission).
      • Artesunate slow IV injection (3 to 5 minutes) or, if not possible, slow IM injection, into the anterior thigh.
      • Children less than 20 kg: 3 mg/kg/dose.
      • Children 20 kg and over and adults: 2.4 mg/kg/dose.
        • One dose on admission (H0).
        • One dose 12 hours after admission (H12).
        • One dose 24 hours after admission (H24).
        • Then one dose once daily.
      • Administer at least 3 doses, then, if the patient can tolerate oral route, change to an ACT.
    • If artesunate is not available use artemether over quinine. All of these drugs can be given intramuscular if you are in a remote area (IM is not appropriate in shock).
      • Artemether is 3.2 mg/kg intramuscular loading and then 1.6 mg/kg intramuscular daily thereafter. Once the patient can tolerate oral medications change to ACT.
    • If in the community and IM artesunate or artemether is not available, children under the age of 6 years can have a single rectal dose at 10mg/kg of artesunate while awaiting transfer (reduced mortality by 25%). In older children and adults it was associated with more deaths.
      • Children 3 to 6 kg = 1 suppository of 50mg.
      • Children 6 to 11 kg = 2 suppositories 50mg.
      • Children 11 to 20 kg = 1 suppository 200mg.
    • Other options include the cinchona alkaloids (quinine and quinidine) but the largest clinical trials have shown substantial reduction in mortality with artesunate when compared with quinine.
      • Quinine loading dose is 20 mg salt/kg BD (do not load if the patient has received oral quinine or mefloquine in the previous 24 hours), followed by 10 mg salt/kg Q8hrly as maintenance, starting 8 hours from the first dose. If there is no improvement in the patient’s condition within 48 hours the dose should be reduced by one third e.g. 10mg salt/kg Q12 hours.
      • Rapid infusion of quinine is toxic (hypotension, blindness and deafness) and is usually administered in 5% dextrose over 4 hours making sure the rate does not exceed 5 mg salt/kg per hour. Hence the intramuscular route can be quite attractive in resource-limited settings.
      • Quinine also causes hypoglycaemia and should be monitored. MSF recommends alternating an infusion of 5% glucose over 4 hours after the quinine and also in adults giving the quinine in 250 ml of 5% dextrose and 10ml/kg in children.
    • Special populations:
      • Only quinine needs to be dose reduced by one third if there is an acute kidney injury. Those on dialysis do not need a dose adjustment and artemisinin derivatives do not require any dose adjustments.
      • Pregnant women have a higher mortality and should receive the parenteral treatment available. Ideally artesunate, then artemether and then quinine. Hypoglycaemia is also more common.
      • HIV patient drug interactions: https://www.hiv-druginteractions.org.
    • Switching to oral:
      • If the duration of parenteral treatment was less than 7 days: treat 3 days with an ACT or seven days with quinine.
      • If quinine IV has been used and AS-MQ is to be used, an interval of 12 hours should elapse between the last dose of quinine and the administration of MQ.
      • If the patient initially presented with impaired consciousness then mefloquine should ideally be avoided due to the increased neuropsychiatric complications.
      • When ACT is not available consider artesunate+clindamycin, artesunate + doxycycline, quinine + clindamycin or quinine + doxycycline. Clindamycin is preferred in children (<8 years) and pregnant women.
      • Check haemoglobin 14 days after the start of IV treatment to check the extent of potential haemolysis both due to the destruction of infected RBCs and also secondary to the treatment given.
  • Other Treatments:
  • Antipyretics: paracetamol is still recommend by WHO.
  • Blood: transfuse as required:
    • Hb <7g/dL in areas of low transmission.
    • Hb <4g/dL in high transmission areas unless there are signs of decompensation prior to this.
    • If <36/40 weeks pregnant transfuse Hb <7 g/dL.
    • If >36/40 weeks pregnant transfuse Hb <8 g/dL.
    • If the patient is bleeding then use fresh whole blood or cryoprecipitate, fresh frozen plasma and platelets. Vitamin K can also be administered.
  • Glucose:  these patients require regular monitoring.
  • Anticonvulsants: if two or more seizures occur within 24 hours. This is because seizures from P. falciparum are more common in children but there is also an overlap with febrile convulsions. Therefore 2 seizures within 24 hours constitutes severe malaria and should be treated as such. There is no specific recommendation for one anticonvulsant other another except to say when using anything that can cause respiratory depression, respiratory support/equipment needs to be available as one study showed increased mortality when using phenobarbitone for this very reason.
  • Renal failure: may require renal supportive care (haemodialysis, haemofiltration or peritoneal dialysis).
  • Broad spectrum antibiotics: by definition of severe malaria it will be impossible to differentiate severe malaria +/- meningitis or septicaemia especially in children. Therefore it is recommended to cover for severe infection and where possible perform a lumbar puncture.
  • Fluids: there is no particular recommendations for fluid management in malaria and do whatever is your current practise, as no doubt as long as there are doctors there will be a fluid argument. Importantly if a child has concurrent malnutrition resulting in oedema (kwashiorkor) then there is a very high mortality and risk that fluids will cause heart failure.

Q10. I’m going to a malaria endemic country, how do I protect myself?

  • Awareness: – see NaTHNac for up to date information specific country malarial risk and resistance if taking prophylaxis.
    • For an in-depth walk through for travellers download the UK guidelines.
  • Bites by mosquitoes:
    • Knock down insecticides (probably not something you will personally have).
    • Pyrethroid impregnated nets.
    • Permithrin impregnated clothing.
    • Air conditioning (the life cycle is slower in colder conditions and mosquitoes will avoid these environments).
    • Pyrethroid vaporisers.
    • Repellents (DEET 20-50% lasts up to 12 hours. Citronella effective for 30mins, Lemon Eucalyptus oil 10-30% – mosiguard natural – is the only proven “natural” repellent lasts 2-5 hours.
    • Chloroquine / proguanil:
      • Now only used in Central America north of the Panama Canal and the Island of Hispaniola (Haiti & the Dominican Republic). It remains effective against most P. vivax, all P. ovale, P. knowlesi, and virtually all P. malariae.
      • Contra-indicated in epilepsy and amiodarone use.
      • Can exacerbate psoriasis, myasthenia gratis and hypoglycaemia (more commonly in diabetics).
      • Other drug interactions include cyclosporin, digoxin, mefloquine and moxifloxacin. It also supresses the antibody response to intradermal rabies vaccine (intramuscular is unaffected).
      • Proguanil in pregnancy requires the addition of 5mg of folic acid in the first trimester.
      • Dosage: 200mg of proguanil daily and chloroquine 500mg once a week. Start one week before travel and continue for 4 weeks post. See more drug information here and dosing in paediatrics, pregnancy and breast feeding.
    • Mefloquine:
      • Mefloquine, once weekly. Concern over neuropsychiatric side effects but these are typically low and are present by about the third dose. Therefore there is some advantage in those who have poor compliance. A test dosing could be done prior to a trip away.
      • Avoid in epilepsy, neuropsychiatric problems or a FH in a first degree relative.
      • Contraindicated in quinine or quinidine allergy, blackwater fever history, liver impairment.
      • Adult dose is 250mg weekly, starting 2-3 weeks before departure and continue 4 weeks afterwards. See more drug information here and dosing in paediatrics, pregnancy and breast feeding.
    • Doxycycline:
      • Effective for P. falciparum, less effective against P. vivax.
      • Limited use in children (UK recommend over the age of 12 whereas the USA state 8) and pregnancy (can be given if the whole course will be completed before the 15th week of gestation). Prone to giving vaginal candidiasis, heartburn and concerns about photosensitivity. Contraindicated with tetracycline allergies. Caution in patients with hepatic and renal impairment, myasthenia gravis and SLE.
      • Daily dosing of 100mg one week before and 4 weeks post travel. Need to give BD if the patient is taking phenytoin or carbamazepine. See more drug information here.
    • Atovaquone/proguanil (Malarone):
      • Prevents the development of parasites in the liver. Take 24-48 hours prior to arriving and 7 days after.
      • Daily doses of 100mg proguanil and 250mg atovaquone. Can start 1 to 2 days before travel and continue for 7 days after.
      • Contraindicated if allergic to the drugs, eGFR <30 mL/minute. General advice is to avoid during pregnancy and breast feeding.
      • See more drug information here and dosing in paediatrics.
    • Primaquine:
      • Unlicensed second line option. Prevents hypnozoite development therefore useful against P. vivax and P. ovale. Can be used in children. G6PD testing is necessary.
    • Special Populations:
      • Renal failure
        • Chloroquine for mild/moderate renal failure.
        • Atovaquone/proguanil if creatinine clearance >30ml/min.
        • Mefloquine or doxycycline in severe renal failure i.e. low creatine <10ml/min.
      • Smoking cessation
        • If on bupropion avoid chloroquine or mefloquine as this can decrease the seizure threshold.
      • Hepatic failure
        • Moderate: Atovaquone/proguanil, mefloquine or doxycycline.
        • Severe: limited data but consider Atovaquone/proguanil.
      • Epilepsy
        • Atovaquone/proguanil.
        • Doxycycline but at an increased dose of 100mg BD if on phenytoin or carbamazepine.
      • HIV (ART interactions)
        • All prophylactic regimens are probably safe.
        • Doxycycline has the least chance of drug interaction.
      • Children are at increased risk of severe malaria and fatal outcomes therefore parents should be counselled appropriately. Your drug options are:
        • Chloroquine/proguanil from aged 1 year.
        • Mefloquine from 5kg.
        • Atovaquone/proguanil licensed above 11kg but ACMP state half a paediatric dose between 5-8kg can be used.
        • Doxycycline contraindicated under 12 years (UK) or 8 years (USA).
        • No suitable regimen for a child under 5 kg.
      • Conception:
        • Mefloquine wait 3 months.
        • Doxycycline wait 1 week.
        • Atovaquone/proguanil (Malarone) wait 2 weeks.
      • Pregnancy
        • Women are generally requested not to travel to malaria areas, due to an increased risk of developing severe malaria and increased mortality. However, if travel is not avoidable:
        • Chloroquine/proguanil safe with extra folate (5mg daily) in the first trimester.
        • Doxycycline is contraindicated unless the full course can be completed before 15 weeks gestation.
        • Mefloquine – caution in 1st trimester due to limited association with foetal loss, although this was not statistically above the background rate. However, this has led to the general recommendation of use in the 2nd and 3rd trimester unless it is the only option in the first trimester.
        • May consider atovaquone/proguanil in 2nd and 3rd trimester in the absence of alternatives. There is just very limited data on its use and therefore any comments on its safety are sparse.
      • Breast Feeding
        • Mefloquine safe.
        • Debatable that doxycycline is contra-indicated, UK say no but the USA state very low levels are secreted in the breast milk and that it is safe.
      • Long-term travellers
          • Chloroquine is safe for long-term use but requires 6-12 monthly ophthalmic examination once 6 years of cumulative usage has been reached.
          • Mefloquine licensed for 1 year but can be used up to 3 years.
          • Atovaquone/proguanil – can be used up to 1 year and longer if there is still ongoing risk.
          • Doxycycline, can be used up to 2 years and longer if there is still ongoing risk.

  • Diagnose malaria promptly
    • Some travellers are doing self rapid tests and only screening once they get a fever and taking treatment for malaria at this point. Highest sensitivity for P. falciparum. (P. vivax 66-88%, P. ovale 5.5-87%, P. malariae 21-45%).
  • Presumptive anti-relapse therapy (PART):
    • 14 days course of primaquine to eliminate potential hypnozoites after return.
    • Only appropriate after very high risk exposure in vivax/ovale area.
    • Should overlap with final week of standard prophylactic drug.
    • See expert opinion/help if doing this.
  • Summary:

    • 5 types of malaria infect humans. P. falciparium causes the most morbidity and mortality and is associated with cerebral malaria. Hence one not to miss.
    • P. vivax and P. ovale can be dormant in the liver (hypnozoites) and hence months later cause another bout of malaria. You need treat with primaquine to eradicate the hypnozoites.
    • Fever in the returned traveller, think malaria and order a thick and thin and rapid diagnostic test (RDT), if negative you are done, think of other causes (unless highly suspicious – repeat).
    • Malaria is hard to diagnose in pregnancy as the parasite likes the placenta and reduces test sensitivity. Repeat thick and thin in this scenario and speak to an expert.
    • To treat malaria, pretty much everyone (except 1st trimester pregnancy – guidelines likely to change shortly) can be on a 3 day course of ACT – artesunate combination therapy.
    • If severe treat everyone with IV artesunate.
    • Protect yourself by taking chemoprophylaxis, sleeping under a impregnated bed net (the mosquito bites at dusk and night time), use air conditioning where possible, use mosquito repellant.
    • The following are useful websites for the traveller and treatment in adults and paediatrics:

    References

    LITFL Resources

    Tropical Travel Trouble 007 Mega Malaria Extravaganza Neil Long

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