Archive for March, 2012


Clinical Case 046 Rash revealed

Filed Under: Clinical Cases, General Practice, Tropical disease by Jonathan — 2 Comments
March 30, 2012

Cutaneous Larva Migrans!

Once seen never forgotten..

The rash is characterised by the erythematous, serpiginous (snake like) and pruritic trail left by the microscopic larva as they burrow through the skin.

Erythematous, serpiginous and pruritic trail

(C) 2012 Image copyrighted to Jonathan Ramachenderan

It is a parasitic skin infection caused by hookworm larvae. Humans are accidental hosts with the larvae lacking the lytic collagenase enzymes needed to cross the epidermal basement membrane thus making this infection self limiting. Cats and dogs are the intended hosts with the larvae being able to cross into the blood and complete its life-cycle.

Infected animals pass the parasite eggs in their faeces into warm, moist sandy soil where the larvae hatch and make contact with human hosts. They penetrate hair follicles, cracked and intact skin to cause their creeping infection and produce a series of disorganised loops of irritated skin.

There are several treatment options and the non-interventional approach acknowledges Cutaneous Larva Migrans’s self limiting nature but requires adequate patient education and treatment of secondary infection.

Anti-helmintics are used to treat early and active cases. Topical thiabendazole can be used for localised and early lesions whereas oral treatment is used for widespread infection or when topical therapy has failed. Oral ivermectin 200mcg/kg can be used as a single dose, with caution in the elderly and young (<5years) and those with renal and hepatic impairment.

Education of the simple measures such as beach footwear and towels to prevent repeated contact with beach sand is important.

Our patient was promptly contacted soon after the diagnosis was made and received 21mg of ivermectin (7 x 3mg tablets) and on review reported that the rash had completely resolved 5days after treatment.

Thanks for playing guess that rash!

References

1) Dermnet NZ: http://dermnetnz.org/arthropods/larva-migrans.html

2) Medical Observer 2008: http://www.medicalobserver.com.au/news/cutaneous-larva-migrans

3) Reavis M, Jorgensen S. Acute Pruritic rash on the foot. Cutaneous larva migrans. American Family Physician 2010. 15;81 (2): 203

4) Sarasombath PA, Young PK. An unsual presentation of cutaneous larva migrans. Archives of Dermatology. 2007 143(7):955

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Clinical Case 046 Rash in the returned traveller

Filed Under: Clinical Cases, General Practice, Tropical disease by Jonathan — 6 Comments
March 29, 2012

Hi guys! GP land has been going really well with me slowly gaining a following of patients and some interesting cases. I wanted to share with you one which I sought help from and excellent service called Tele-Derm. It was set up by ACRRM and the Queensland Divisions of General Practice (QDGP) with Commonwealth funding in 2004 and it is run by one of the most hard working dermatologists dedicated to providing a reliable service for rural Australia, Dr Jim Muir.

If you are a rural doctor with a dermatology dazzler or puzzler, you can electronically submit cases for assessment and usually within 48hours or in my case 27minutes! Jim will give you a diagnosis or point you in the right direction. He also moderates a forum with great educational cases, links and discussions.

So…

45 year old man came to see me with the rash as depicted below.

It started  4 days after coming back from Thailand where he relaxed on the beach, went snorkelling and ate yummy thai food. He came in to see me 10 days after getting home.

The rash started spreading, beginning on his left flank and moving up toward his axilla with one lesion on his upper back and a few over his lower abdomen.

The main issue was itch and is pain at times (not unbearable). He described it as “catching your skin on a bit of metal”. He has put some over the counter creams to relieve the itch but nothing helped.

He didn’t report a fever or being unwell. He also concurrently did not have a productive cough, dysuria, diarrhoea, cachexia or anorexia.

On examination he was afebrile and other observations within normal limits. He did not have any inguinal or axillary lympadenopathy. He didnt have any other rashes or scaly and dry skin.

He assured me he wasnt bitten by any mosquitos nor was he bitten by any marine life.

Im sitting there scratching my head thinking, “its not cellulitis, its not fungal, its not dermatitis..what is it?”.

What do you think?  Its a once seen never forgotten clinical case!

       

(C) 2012 All images copyrighted to Jonathan Ramachenderan
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Clinical Case 045: Syncopal Salesman

Filed Under: Clinical Cases, Emergency, General Practice, Internal Medicine by Casey Parker — 23 Comments
March 26, 2012

37 yo man who works as a travelling sales rep.  He has a hectic lifestyle and is overweight.  Flies around the country a lot visiting hospitals selling medical equipment.  He presents via ambulance after having a syncopal episode in the local McD’s.

The event was witnessed by a client and staff at the restaurant – he was a bit sweaty, got up to go to the bathroom and fell, he narrowly avoided hitting his head on a chair as he collapsed to the ground. No seizure activity, incontinence or neurolgical deficit noted at the scene. He was unconscious for about a minute.  When the ambos arrived 5 minutes later he was GCS – 15, oriented, though seemed a ‘bit vague’.

Whilst in your small country town for a 3 day visit he notices that he has become increasingly “unwell” – he can’t really put a finger on it -he says he “has been hazy in the head”  and “feeling like nothing seems real”  for the last 48 hours.  No specific vertigo symptoms, headaches or pre-syncopal events have been noted.

Overweight BMI = 35

Hypertensive – was on ramipril, but stopped taking it as it interfered with his ‘performance’

Smoker – 10 -15 per day

1 episode of gout effecting MTP jt

Depression – currently on 40 mg paroxetine/day, good response to this and supportive therapy from GP

Dyslipidemia – trialing “diet and exercise”

He is a fat, slightly sweaty man, looks a good few years older than 37!

Obs: pulse = 85 reg, BP 145/90 no postural drop, SpO2 = 99% RA, RR 14/min, no clinical pallor, anaemia etc

Otherwise his heart, chest, neuro, abdo etc are all normal.

What specific negatives do you want to ensure on physical examination??  What can you exclude by looking and listening?

BSL is 6 mmol (~110 in the U.S.A)

ECG – normal, sinus rhythm, maybe borderline for LVH criteria, normal axis.

What specific features / conditions do you want exclude / or see on the resting ECG in a man with syncope?

Urninalysis is = SG 1.015, 1+protein, otherwise normal

Plum normal

pH 7.41, lactate 0.4 mmol He has a Hb of 156 g/l

Electric lights are all normal

Nothing to write home about… What were you hoping not to see ?

OK, that is it for now.  At this stage I will tell you that any further tests that you want to do are either negative or unavailable in our little ED scenario.

The diagnosis is out there…  first prize goes to the reader who asks the right questions to solve the puzzle.

Ready, set, go…. write your thoughts on the comments and I will respond

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Case 044: the answer

Filed Under: Clinical Cases, Useful Evidence by Casey Parker — 8 Comments
March 19, 2012

Ok, 24 hours in and we have a winner.  The most comprehensive and correct / first in (20 minutes) answer was from Egerton Yorrick Davis IV (I wonder what happened to the first 3 EYDs?)  His answer went right to the red heart of the problem and picked up the diagnostic pitfalls en route.  Here it is:

“Most 40y old women will have gallstones – it is easy to get entrapped by this diagnosis as a cause of epigastric pain.
Dyspepsia + anemia = upper GI bleed until proven otherwise – but penicious anemia or gastritis with parietal cell depletion and intrinsic factor deficiency leading to VitB12 is in the DDX.
Depression is also common – but can be a feature of anemia, or even B12 deficiency.
When she has her op she may have got nitrous oxide as part of her anesthetic – which could exacerbate B12 deficiency – and was probably fasted +/- eating a low B12 diet (meat, eggs, milk)
Neurological symptoms (including paraestheiae) are the other component of the triad for B12 deficiency.
EYD IV”

If you want to see more on Subacute Combined cord degeneration – check out this link(Neurology, Neurosurgery and Psychiarty 1998) which was sent in by Minh Le Cong as part of his answer (too slow sorry Minh).

Great answers though, thanks for the input.  Casey

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Clinical Case 044: Neuro Curio

Filed Under: Anaesthetics, Clinical Cases, General Practice, Internal Medicine by Casey Parker — 6 Comments
March 18, 2012

A  40 yo. woman presents for review to her GP a week after having a laparoscopic cholecystectomy.

She had been suffering with epigastric pain and and US showed gallstones, and a contracted GB.  So she elected to undergo cholecystectomy.She was discharged the morning after the surgery with oral oxycodone and paracetamol for pain.

PMHx:  anaemia, mild depression.  She takes an iron supplement and citalopram 20 mg daily

Today she has recovered well from the procedure, but has developed bilateral tingling of the hands since leaving hospital and it has not improved – in fact she now says after a week it has spread up her arms, and her toes feel ‘tingly’ over the last few days.

OK – that is it.  Usually when I put up these cases you smart docs work it out in a heartbeat – so I am giving you the minimum amount of info!  80% of diagnosis is on history - so go for it…

What is the diagnosis?  What investigation will make you look like a super-Sherlock?  and what intervention will fix her?

There just might be a real prize if you are first in!   Casey

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C-spine Trauma: in a town with no CT

Filed Under: Critical care / ICU, Emergency, Pearls and Pitfalls, Useful Evidence by Casey Parker — 3 Comments
March 12, 2012

I worked for 4 years in a town with no CT (but plenty of beer) – and it is fair to say that the protocols for managing C-spine trauma were often makeshift.  Logistics rather than clinical acumen often determined who got a CT rather than ‘just’ clinical exam and a set of plain films.  But…. why should my patient get less than gold-standard care – just because of geography?   I realize this is a bit idealistic, but when it comes to life-long disability – do we really want to take that risk?

Now in recent months there has been a lot of posting and banter about C-spine trauma on the popular medical blogs / podcasts.  So I thought I would trawl through the literature and come up with a pragmatic protocol for those of us who work in CT-isolation, or where it is not available 24/7.  Amusingly here is a hot debate about whether you need to MRI patients with pain and a normal CT – Yep, true!  We are not even close to that debate in regional Australia!

The logistics of distance mean that I break (‘scuse the pun) C-spine trauma into 3 main groups:

  1. The minor trauma – these are the patients whom you can clear with clinical history, exam and NO imaging is required.
  2. The fuzzy middle group: they cannot be cleared on clinical grounds for whatever reason, or they have failed the clinical clearance. Yet, they remain asymptomatic, have no high risk features –  your “gestalt” is that they are probably OK.
  3. The major trauma: these patients are high risk – based on the mechanism of injury, associated injuries or the presence of neurology suggestive of a cord injury

I will try and explain how I think each of these should be managed based on my reading of the recent evidence, the reality of rural practice and a measure of common-sense.  If you want to get some great background and refresher in anatomy I have a few suggestions for your valuable time:

OK, without further waffling – lets analyse these 3 groups and try to cook up a rough protocol for each.
In some ways this should be the easiest group – but is also the one that causes the most frequent consternation!
Clearing a C-spine is one of those moments in medicine when you just have to trust your call. This is especially true in the bush – if you decide not to clear them – you are probably committing them to a long transfer strapped to a spinal board: uncomfortable and expensive!
So how do you clear a C-spine clinically? Here is how I do it – I use MDCalc’s Canadian C-spine tool – but be warned – you have to use it properly. These rules are derived and validated by following the protocol to the letter – if you do not follow the protocol as described you cannot achieve the same sensitivity. The Canadian C-spine seems to be better than the NEXUS rule (NEJM, 2003) – but you must have an alert, sober, orientated and cooperative patient – so a lot of our customers are self-excluded! Scot Weingart describes an interesting combination of the 2 rules.
As the receiving doctor in a CT+ town – I really want to know that the patient has had a proper attempt at C-spine rule clearance – otherwise we are squandering valuable flight resources and irradiating unnecessarily.
This group includes the people whom you cannot clear clinically as they are too drunk, disorientated, in pain, etc to qualify for a clear Canadian C-spine rule PLUS those who have failed the rule – ie. they have tenderness, pain on rotation, are too old etc.
So according to the rules they get “imaging”.  Easy: off for a set of plain films, right?  well maybe not such a great idea.
A good number will have sub-adequate views, and then you need to ask – what is the sensitivity OR the negative predictive value of plain films for C-spine injuries…?  Well they are not so great – in fact the term ‘suck’ has been used to describe them!
This series from the Journ. Trauma 2009 showed a sensitivity of plain films c/w CT for serious injury of less than 50% – that is worse than a coin toss!
However, some protocols continue to advocate plain films as a ‘screen’ for fracture in the lower-risk groups.  I guess this means the patient who so nearly passed the clinical clearance test (eg. were just 65 years old only, had transient pain…) But it is a small group – so the role of plain films is vanishing rapidly.
So in summary – there are not many patients we can reliably clear with plain films if you follow the evidence and guidelines as written.
Therefore if you are in a CT-less town, and have one of these patients – you probably should transfer for a CT.  If you think they are low-end risk, and have a good set of films then it is a judgement call on your part.  Traditionally we have cleared patients on this basis – but is it still the standard of care?
This is really the easiest group to decide upon. Sure, the toughest to manage, but the easiest to make a call on C-spine imaging.
If you have a patient with a high-energy mechanism, bony tenderness, neurological signs or major injury (esp head) then you need not bother with plain films. These patients need transfer – not imaging. This is the scenario where you want to get them to a trauma centre ASAP – probably for more than their neck injury. Taking them through the Xray Dept, moving them 3 or 4 times – for a series of images will add little to your management! Assume they have an unstable injury and manage them appropriately. If you are wrong – great, if you are right – then you have done the right thing!
Finally a quick note on C-Spine collars
  • Rigid C-Spine collars are omnipresent in ED trauma patients, they are almost like religious artifacts – there is a lot of belief in their powers, but is there the evidence to back them up??
    • The Journ Emerg Med 2012 published an article by Holla which looked at healthy people and the effect of collars – basically they did not actually immobilize any more than the padded boards / straps and decreased mouth opening.
    • There is no hard evidence to say they actually decrease neurological injury / improve outcomes.
    • We all know they are a pain, ill-fitting and your worst enemy when trying to intubate!
    • So here is my take – immobilisation is good, collars are window dressing.  If you really want to keep the neck still – provide good analgesia and anti-emesis, supervise the patient closely (esp. if they are drunk, head-injured etc), they will need a nurse / doc by the bedside constantly to do this right!
    • If you use a collar  and it is causing problems: pressure, pain, airway obstruction or really making the patient hostile – then take it off and keep a close eye on them.  Prima non nocere.
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Post op pain puzzler discussion

Filed Under: Anaesthetics, Clinical Cases, Critical care / ICU, Surgery, Useful Evidence by Jonathan — 2 Comments
March 9, 2012

Hope you guys enjoyed the case. Here is the discussion and hopefully some useful take home concepts.

This case illustrated a number of key acute and chronic pain concepts that all GP anaesthetists should consider when anaesthetising an opioid tolerant chronic pain patient, namely opioid induced hyperalgesia (OIH), central sensitization (wind up) and pre-emptive analgesia.

In this case, our patient did not receive adequate perioperative analgesia or pre-emptive analgesia based on his chronic pain and opioid dependent background. He was left in distress for a period of time in which his pain became unmanageable (wind up) and remained so for 16 hours. It seemingly became non-responsive (OIH) to opioids but rotation to a new opioid, a background infusion of a NMDA antagonist and the use of a regional technique helped immensely.

Opioid induced Hyperalgesia

Opioid induced hyperalgesia is a paradoxical response to opioids in which patient receiving opioids have an enhanced response to painful stimuli resulting in hyperalgesia. This results from the upregulation of pronociceptive pathways in the central and peripheral nervous system.

Acute OIH occurs in various settings, most commonly post operatively in the opioid dependent patient but also in low dose and maintenance dose regimes. OIH is distinct from tolerance in that tolerance is reduced effectiveness of an opioid at a receptor over time.

NMDA receptor activation is important in the development of OIH. Antagonism of this receptor has been shown to reduce progression and improve post operative pain especially in opioid dependent patients (Wu + Macintyre + Huxtable et al).

Using an opioid PCA in opioid tolerant patients allows consumption and background requirements to be monitored. A basal infusion equivalent to the patient’s usual daily opioid use should be considered or given orally as tolerated.

Ketamine has been shown to reduce OIH in the post-operative setting (Vadivelu + Huxtable + Macintyre et al). There is evidence that subanaesthetic doses (0.1-0.2mg/kg) of ketamine provides excellent analgesia in opioid dependent patients and prevents opioid induced hyperalgesia in patients consuming high doses of opioid for postoperative relief. (Macintyre et al + Vadivelu et al).

Opioid rotation is the practice switching from one opioid to another to improve analgesia and reduce side effects (OIH in this case). This concept is based on the premise that individual opioids act differently on different opioid receptors and that tolerance between them is likely to be incomplete.

Practically this is preformed by using opioid equivalence charts and commencing with 50% of the equivalent dose and titrating up. (Huxtable)

Methadone together with its mu-receptor agonism has weak antagonistic properties on the NMDA receptor thereby playing a small role in OIH.

Wind up (central sensitization)

Post-operative pain results from peripheral nociception (primary hyperalgesia) from tissue injury and resultant central nociception (secondary hyperalgesia) in the spinal cord.

Any continuous barrage of activity to the spinal chord leads to central sensitization. Perioperatively this is related to periods of inadequate analgesia, extensive surgery or infection (Shipton).

As this central sensitization continues from the noxious stimuli, this maintains secondary hyperalgesia, amplifies post operative pain and contributes to chronic pain.  Central sensitization will manifest clinically as hyperalgesia (increased pain sensitivity) and allodynia (pain in response to a previously non-painful stimulus) (Macintyre et al).

 

NMDA receptor activation plays a key role in central sensitization. Medications such as Gabapentin, Pregabalin and Ketamine have been found to improve post operative pain and thought to reduce the progression to chronic pain.

Using Ketamine at subanaesthetic doses (0.1-0.2mg/kg) antagonizes the NMDA receptor and produces an antihyperalgesic, antiallodynic and anti-tolerance effect. It is useful in pain associated with central sensitization such as severe acute pain and opioid resistant pain.

Pregabalin is a safe and well tolerated and helps to reduce perioperative opioid consumption. It has been shown to decrease the incidence in the progression to chronic pain. Gabapentin similarly has been shown to prevent chronic post surgical pain syndromes (Shipton).

Pre-emptive & Preventative Analgesia

Pre-emptive analgesia is treatment that is initiated before the surgical procedure in order to reduce peripheral and central sensitization. This in effect helps to reduce post operative pain and prevent chronic pain development (Dahl)

Preventive analgesia is simply the well thought out provision of analgesia within the postoperative period and persistence of treatment beyond the expected duration and aims to minimize central sensitisation (Macintyre et al)

Ketamine modulates central sensitization caused by incision and tissue damage and can be used perioperatively to antagonize this (Vadivelu).

Preoperative pregabalin is opioid sparing and improves post operative pain scores. It is a useful adjuvant and anti-hyperalgesic agent used in a multimodal regime.

Prevention of Withdrawal

Inadequate opioid supplementations in the post operative period can lead to withdrawal characterized by excitatory autonomic symptoms. The onset will depend on the individual opioid’s duration of action (Macintyre et al).

Opioid tolerant patients should firstly be identified preoperatively and continue their preadmission opioid regimes with appropriate route substitutions as clinically directed.

Heavily weighted non-opioid regimes should be used with caution as opioid tolerant patient due their risk of withdrawal (e.g.: pure non opioid regime or tramadol as a sole opioid).

If withdrawal is suspected, Clondine can be used orally and intravenously to aid in the symptomatic management.

 

Key Messages

Preoperatively identify opioid tolerant and chronic pain patients and make a peri/post operative analgesia plan

 Always replace a patient’s preoperative opioid use in the post-surgical period

Consider preventative analgesics such as Ketamine, Pregabalin and Gabapentin to prevent central sensitization and subsequently wind up pain.

Consider an opioid rotation in patients who respond poorly to an opioid regime or with escalating requirements

Reverse analgesic ladder on recovery with background opiate titration

 

Hope this helps. Let me know what you think.

Jonathan

 

Baron R (2006) Mechanisms of Disease: neuropathic pain – a clinical perspective. Nature Clinical Practice Neurology 2: 95-106 http://www.nature.com/nrneurol/journal/v2/n2/full/ncpneuro0113.html

Dahl JB, Moinche S (2004) Pre-emptive analgesia. British Medical Bulletin 71(1) 13-27 http://bmb.oxfordjournals.org/content/71/1/13.long

Huxtable CA et al (2011) Acute pain management in opioid-tolerant patients: a growing challenge. Anaesthesia & Intensive Care 39: 804-823 http://www.aaic.net.au/document/?D=20110262

Macintyre PE et al (2010) Acute Pain Management: Scientific Evidence 3rd Edition. Australian & New Zealand College of Anaesthetists & Faculty of Pain Medicine http://www.anzca.edu.au/resources/college-publications/Acute%20Pain%20Management/books-and-publications/acutepain.pdf

Mitra S et al (2004) Perioperative Management of Acute in the Opioid dependent Patient. Anesthesiology 101: 212-27 http://journals.lww.com/anesthesiology/Fulltext/2004/07000/Perioperative_Management_of_Acute_Pain_in_the.32.aspx

Patanwala A et al (2007) Opioid Conversion in Acute Care. Annals of Pharmacotherapy 41: 255-67 http://www.theannals.com/content/41/2/255

Shipton E.A (2011) The transition from acute to chronic post surgical pain. Anaesthesia & Intensive Care 39: 824-836 http://www.aaic.net.au/document/?D=20110056

Vadivelu N et al (2010) Recent Advances in Postoperative Pain Management. Yale Journal of Biology and Medicine 83: 11-25 http://www.ncbi.nlm.nih.gov/pubmed/20351978

Wu CL et al (2011) Treatment of acute postoperative pain. Lancet 377: 2215-25 http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60245-6/abstract

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RSI: made stupidly simple

Filed Under: Anaesthetics, Emergency, Pearls and Pitfalls, Useful Evidence by Casey Parker — 6 Comments
March 8, 2012

The Rapid Sequence Intubation is one of those “gotta have” skills for clinicians who work in frontline medicine. Fair to say there are a lot of sequences out there, but they all follow the same basic plan – prepare, inject the juice, and get the airway secured ASAP.  In recent years there have been a few changes to the long-held anaesthetic dogma, based on good evidence.  So I thought I would take a look at a few, see what is new in RSI.

 Pre-oxygenation strategy:

In case you have been living under a rock and missed the Weingart & Levitan paper on Pre-oxygenation and Avoiding Desaturation in Emergency Airway Management here it is.  The practice of throwing on a Hudson mask at 6 litres/min for 5 minutes is no longer the standard of pre-ox we should be aiming for.   Weingart and Levitan have broken down the evidence and created a 3 tier risk-stratification of sick patients with incredibly practical strategies to optimise the pre-ox and decrease the rate of desaturation that inevitably occurs in the sick patients.

  • NIV as pre-oxygenation device – minimise the shunt, maximise the alveolar recruitment
  • Use of a viva-bag with a cheap PEEP vlave as a poor mans CPAP device
  • USe of high flow (15l/min) nasla cannula oxygen to keep the flow of oxygen throughout the procedure and make your apnoeic time much safer for longer.
  • Check out the tables on the last page of the above paper – it is pretty simple and self-explanatory

 

 

The role of cricoid pressure in emergency airway management has come under a lot of scrutiny in recent years.  As is often the case when we look back at the original data – it seemed like a good idea, had some experimental data to support it – but there was no good large-scale evidence that it made a difference to the outcome which we and patients care about!

There was a good review published last month taht asked the hard questions – in Trends in Anaesthesia and Critical Care 2012, Priebe looked at the data in a systematic manner and tried to separate facts from fiction.

In summary: 

  • Cricoid pressure does not have the evidence to make it a mandatory manouvre
  • Clinicians should use individual judgement to guide its use
  • It may be applied, and may help prevent gastric insufflation during BM ventilation
  • If your glottic view is obscured / inadequate – remove it ASAP, then consider BURP instead
  • There is a paucity of good, reliable evidence to support or deny the use of cricoid pressure!

 

There have been a few recent debates on the use of muscle relaxants.

  1. Should they be used at all in critical care settings?  For me this was a surprise, as I was trained by anaesthesia docs who always used them, but there is a tendency to avoid them in some ICUs.  If you want to hear the low-down on the debate in a very enertaining deabte go to Emcrit and listen to the Paralytics debate. Fair to say it has yet to be decided – but I think for the average GP-intubation it remains the standard to use a muscle relaxant.
  2. Which muscle relaxant?  Roc vs. Sux?   well there have been a few posts and opinions out there – check out my post from last year and links to other resources.
    • In summary – Roc seems to prolong the time to desaturation
    • Give it in a big dose ~ 1.2mg/kg and its onset is comparable to Sux
    • The “back out” plan that Sux ‘allows’ usually is not an option in true critical / emergency RSI
    • You don’y have to worry about the patient fighting the vent anytime soon if you use Roc!

 Last point – The PPPPPPP rule [proper planning and preparation prevents piss poor performance]

Having a well thought-out team-orientated approach to emergency airways is the most important thing to do to make your RSIs go well.  This should be done as part of your departments training / drills and education programme.

Dr Tim (KI Docs) has sent me this nifty little aide-memoir to help get your preparation right and to jog one’s thoughts with asimple checklist included.  I will put it in the Resources section at the bottom of the blog, but click here to have a look at the RSI DUMP kit mat.  Print it out in A# or bigger and put it on your resus room trolley.  Thanks Tim

Let me know if this helps – or if you have other new pearls for the old RSI setup.

Casey

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Clinical Case 044: vesicles down under

Filed Under: Clinical Cases, Emergency, General Practice, Paediatrics by Casey Parker — 4 Comments
March 6, 2012

Todays case is bread and butter GP / Paeds.

13/12 old boy presents with a 2 day history of mild fever, irritable and loose stools.

This rash – yep those are vesicles

What is your differential diagnosis?

OK all you Paeds sleuths – hit me on the comments – the prize (love and respect – as always) goes to the first in / best answer.

Casey

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Happy birthday to Us

Filed Under: Uncategorized by Casey Parker — 3 Comments
March 5, 2012

Broome Docs clocked up one year on the net this week!

The stats:  118 posts, about 350,000 views and about a comment a day.

Gotta say that at this time last year I did not expect this site to be much more than a repository of my teaching for my local trainees and colleagues. So I am really happy to get such great reader feedback from all over the globe.  The input from  you guys makes it all worthwhile and fun.

What is ahead this year?

  • More of the same – clinical cases, evidence at your mouse click, some profoundly smart guest contributors
  • I hope to get it accredited for some type of CME –  watch this space
  • A few new regular editors

Thanks to you all, keep reading and sending in comments and feedback.

From the remote NW of Oz.  Casey

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