A common Kiwi presentation.

 I recently saw a patient for an off work certificate who was somewhat unusual for New Zealand.

He worked on a mine in Queensland and had been having a holiday before returning to NZ. Whilst wandering in the shallows he stood on something sharp and had severe pain in his foot. Lifting his foot he had four puncture marks and assumed he had stood on some coral.

He then describes ascending pain,  spreading erythema and severe oedema and pre-syncopal symptoms.

His mates loaded him into the Ute and rushed him to the local hospital.

On arrival he was mildly hypotensive BP 100/60 with a relative bradycardia of 50bpm for a patient in severe pain.

He was treated with a combination of oral, IV analgesia and hot water immersion (which he reports no effect from) and was kept for observation. Discharged with oral antibiotics and returned to NZ.

Discharge diagnosis of “Fish envenomation NOS”

He was kind enough to share his photos from the “holiday from hell”

 

foot 1

24 hours post injury.

foot 3

 Impressive oedema.

foot 4

 72 hours post injury.

When seen in clinic (2 weeks post injury) the patients oedema was resolving but he couldn’t get his boot on yet. The blistered areas had sloughed off and good granulation tissue in the bases. As he was working for a rich Aussie mining company I put him off for another week ;)

So I went looking for some info on fish envenomation’s. The Team at LITFL did a great review in 2009 so I chased about to see what the literature has come up with since then.

http://lifeinthefastlane.com/2009/04/scorpionfish-stonefish-lionfish/ (LITFL discussion of management)

Published at the exact same time as the LITFL review was a case series from Singapore hospital of 30 patients, showing most did very well and antivenom was not used very often.

http://www.ncbi.nlm.nih.gov/pubmed/19495521

 An article in French which discusses a case leading to cardiovascular collapse:

 http://www.ncbi.nlm.nih.gov/pubmed/20099677

My hand’s a bit munted.

Bloke arrived in ED holding  his “Munted hand!”

Patient was clearly in pain with a deformed hand:

image

Mechanism of injury was fall from BMX wedging hand between a large rock and tree.

image

Analgesia and off to x-ray:

metacarpal disolcation 3

 

Metacarpal dislocation 2

The films show Carpometacarpal dislocations of 3rd 4th and 5th (and possibly 2nd according to radiology) But no associated fractures on any views.

Titrated fentanyl was given for analgesia and midazolam was added for the reduction.
The reduction only required minor force applied to base of metacarpals and longitudinal traction.

Post reduction films showed:

metacarpal dislocation reduced

Patient was taken to theatre later that day for K-wire fixation.

The patient was planning to be back on the bike after removal but couldn’t help himself and was out riding 4 days post cast removal (day 11 post reduction)

So the Munter with the munted hand is doing well. K-wires removed at clinic increasing strength and not too much stiffness. (the benefit of early mobilisation?)

I was going to write more about Carpometacarpal Dislocations but Chris Partyka has covered it so well over at The blunt dissection I thought pointing you there would be better.

http://thebluntdissection.org/2013/04/quick-case-01/

I digress. Blister Beetles!

Recently had a patient pitch up after an afternoon in the garden, she had been gardening when a bug fell down her top and she squished it and carried on gardening. After an hour or so she noticed the area stinging and checked to find a red area. She had a shower and noticed that the stinging was  a little less but when the area blistered she came to the acute clinic.

Pt was happy to share her story but as she had squished the bug on her “Décolletage” she wasnt so keen to have photos taken and shared with the word. So here is a nice US Marine with a blistering injury from a bug:

blister beetle

So Blisters from Beetles:

There are a few types of bugs that cause blistering eruptions and/or dermatitis.

The most widely know are the Meloidae family from which comes the Spanish Fly. The Meloidae are known as blister beetles in many parts of the world. They are so named because they cause a painful blistering eruption within 2-3hours of exposure.

A few blister beetles:

 

Black_blister_beetleLytta-vesicatoria spanish fly

 

 

Paederus beetles also cause a dermatosis and blistering but this generally occurs 24-72 hours after exposure. These have been having a recent resurgence in research as they are common in Iraq and have caused outbreaks in a number of American Army camps there. These lead to the 2007 report attached.

Paederus_rove_beetles,_showing_size

Depending where you are in the world these beetles have a variety of illnesses named after them. If you are in Africa and squish one and wipe you face you may contract “Nairobi eye or Kenya fly dermatitis” In India Paederus beetles also cause seasonal outbreaks. 

 In New Zealand Oedemeerida (the false blister beetles) are more common and famously caused an outbreak of blisters in soldiers near Auckland  in the 1980s. 74 Soldiers erupted with dermatitis after night exercises. An epidemiologists dream! Investigation lead them to the Thelyphassa lineata (Fabricius) after ruling out a number of other causes. Its ability to produce the reaction was tested on some willing participants (Medical Students)

So how do these little bugs cause such a wonderful bullous eruption and dermatitis. Both Melodiae and Oedemeerida produce Cantharidin which is a potent blistering agent. The male beetles produce all of the cantharidin and gift some to the females after mating. Male beetles secrete cantharidin from their joints so they dont need to be squashed to cause exposure and dermatitis. Wonderfully we dont know the exact biomechanical means of its production within the beetles. I also dont like to tell people where presents for my SO come from. Cantharidin is a very potent toxin with a LD50 of 0.5mg per Kg in humans. The most common animals poisoned by blister beetles are horses as the beetles commonly live in alfalfa and other green feed.

Paederus beetles have a more complex but better understood production of their toxin Pederin. The females in this case have  a symbiotic relationship with a Pseudomonas which produces the toxin. This is in turn deposited into the eggs and larvae. Further toxin is ingested when beetles eat the shell of their egg after hatching. Paederus dermatitis takes longer to reveal itself often 24 hours before discolouration which then goes on to blister.

Treatment: The best treatment is prevention, simple things such as removing beetles rather than squashing them. One prevention in Iraq was moving the night guards further from the light towers which attracted the beetles. With Cantharadin patient will usually have washed themselves as the burning is an early symptom. With Paederus they often only present well after the toxin has been spread and absorbed, these patients show classical Kissing signs where skin surfaces have touched eg: elbow flexures. Once the dermatitis is established the best treatment is topical steroids but if the case is severe oral antihistimines and even antibiotics have some benefit.

Blister beetles have been used for centuries and despite their toxicity people took them as an aphrodisiac. In roman times (wake up @eleytherius)  Livia Drusilla a great schemer of Rome attempted to poison visitors with cantharidin. Hoping they would act in a manner which they would later regret and allow her to blackmail them. (Its unclear if this was succesful) Cantarella which is the combination of Cantharidin and arsenic was reportedly the poison taken by Juliet to appear dead (We know how succesful that was)

References:

http://www.thefreelibrary.com/Outbreak+of+dermatitis+linearis+caused+by+Paederus+ilsae+and+Paederus…-a0242963583

http://www.ncbi.nlm.nih.gov/pubmed/2189910 Oedemerid blister beetle dermatosis: a review. Nicholls DS, Christmas TI, Greig DE.

Christmas TI, Nicholls D, Holloway BA, Greig D. Blister beetle dermatosis in New Zealand. N Z Med J. 1987;26:1515-1517 (paper copy)

When you think you see a dog but maybe it’s just spots.

Had this patient come in whilst on nights.

82 y/o female presented with chest pain.

Previously had CABG >15 years ago following presentation with “unstable angina”. which resolved her angina, nil since them.

Sudden onset chest and back pain and maybe between shoulders. not really a tearing quality but different to her pre CABG angina. pain wasn’t severe but enough to get her to come in. Felt her normal self otherwise.

Not on any medications.

Tachycardia 105. BP 108/64. (bilaterally)  Normal ECG sinus.

She looked pretty good TBH. sore but not “sick, sick”

Given GTN with no real change in pain. but settled with a push of morphine.

Istat troponin was negative.

Off for a CXR.

Was willing to say the mediastinum looked wide and the radiologist agreed that the aortic contour looked a bit funny.  We discussed presentation and decided that CT was indicated. I pushed for the scan as my gestalt was telling me there was something unusual about this patient.

Obviously there’s dissection from “top to bottom” as a colleague described it.

Formal report came back as extensive type A dissection extending from aortic root to abdominal aorta. There is no adjacent soft tissue reaction and no high density material on the unenhanced scan. These findings strongly suggest this is a chronic dissection.The false lumen is thrombosed in several locations and patent in others Major arch branches are patent.

Summary: extensive chronic aortic dissection with aneurysmal dilatation.

So my patient was now pain free, with an “old” dissection and lowish BP. Her tachycardia had settled after the CT. With discretion being the better part of valor I admitted her to the ward overnight. Repeat troponin in the morning was negative. She also had a D-Dimer added (no one confessed to this) which was negative. Discharged home.

I saw this patient recently in GP clinic and her BP remains low, no further episodes of pain. 

This was my first experience of when aortic dissection isn’t “aortic dissection” Anyone else had a similar case?

 Great discussion of Aortic dissection from LITFL: http://lifeinthefastlane.com/2010/09/die-like-a-king/

Leptospirosis in Aotearoa

 I recently had a patient a 42 yo dairy farmer who had not been right for a week. Flu like symptoms, headache and lethargy.

He was a “good keen man” a deer hunter who brought home steaks with respectable frequency. His partner had bullied him to the clinic. He had been unwell enough to take to bed which his partner reported was most unusual. Usually fit and well with ono PmHx. Being summer and his symptoms he earned a leptospirosis serology test.

Which came back as positive with a significant titre.

Treatment for  symptomatic cases here is oral doxycycline and follow up to see if symptoms resolve.

#FOAMed and Leptospirosis

After looking around I found the Excellent talk from Dr Lane (ICU Queensland) http://www.intensivecarenetwork.com/index.php/icn-activities/icn-podcasts/393-39-lane-on-tropical-microbiology But his experience didnt fit with mine. Are kiwis just tougher than those weak australian soldiers he sees? or is there some other factors effecting the cases we see?

Also the Adventure doc blog had an article: http://adventuredoc.net/2008/12/29/leptospirosis/

Firstly what the hell is leptospirosis?

To quote professor wikipedia Leptospirosis (also known as Weil’s syndrome, canicola fever, canefield fever, nanukayami fever, 7-day fever, Rat Catcher’s Yellows, Fort Bragg fever, black jaundice, and Pretibial fever) is caused by infection with bacteria of the genus Leptospira

Have I heard of that?

Leptospirosis was in the news in 2010 when british olympic rower Andy Holmes passed away after contracting the disease.

How does it present?

“Lepto” can present like just about anything from a mild flu like illness to a severely sick patient with hepato-renal syndrome and meningitis.

Natural history of leptospirosis

Usually patients will have the initial phase with flu like symptoms For many this is all the patient will experience but for some this is resolves and they then have a second phase of illness. This is more severe and may include hepatic failure (Weil’s disease) and renal involvement.

So how common is it?

Worldwide it is one of if not the most common zoonotic disease.

Leptospirosis is a notifiable disease in NZ so we have good records of when lab tests come up positive.

New Zealand has between 80-140 confirmed cases a year, this is about three quarters of the positive lab serology results. (more on this later)

Making leptospirosis not common but not rare. So it falls into that BS category of “Maintain a high index of suspicion” Now im pretty sure there isnt a suspicion index but you will see it from time to time. (if you look)

Which leads to the question of who gets it? meatworksdeer

 

 

 

 

 

 

 

 

 

 

 

 

Meat workers, esp those who “pull kidneys” or work the offal line. Deer hunters and farm workers are other high risk groups.

Risk in NZ

Over the years there has been a number of vaccination campaigns in cattle, pigs and now they are trialing deer vaccines to reduce the carriage of leptospira in herds. Despite this amongst herds some animals remain positive/carriers. Around 70% of beef herds, 40% of sheep and 80% of deer herds have leptospira. This is highest amongst farms which graze both cattle and deer.

These figures lead to an estimated exposure of 8-25 leptospirosis carrying carcases per day for a meatworker.

Why is it not everywhere? Are we missing cases?

Waikato epidemiologists feel it is likely we have significant underreporting. The serological evidence that many people are infected and clear the leptospira without significant illness. Currently the ELISA has a low sensitivity and it is felt that serology is better for clinical diagnosis. The culture may take a number of weeks to become positive. To be eligible in NZ for Accident compensation corporation funding/payments you must have appropriate symptoms and a rise in your serology titer of 4 fold. It seems a safe bet that we are missing a number of cases.

Leptospirosis mortality:

In contrast to Dr Lanes Queensland experience deaths from leptospirosis are quite rare in New Zealand with one every few years.  New Zealand appears to have slightly different endemic strains of leptospira. Also the soldiers are likely exposed to rodent urine vs that of bovines. Rat urine is more commonly infected with the more virulent strains of leptospira. A final thought from me about deaths from Leptospirosis: As deaths are reduced by immunomodulation perhaps the soldiers who are often being exposed for the first time to these antigens vs the meat workers who have a chronic exposure simply do not have the same immune overreaction?

 So how did the patient do?

My patient improved over the following few days but took a couple of weeks to “come right” This was defined as  being able to spend a couple of days staking deer in rough terrain and delivering me some venison steaks!

vension steak

References:

Paul Lane, ICU (Queensland) http://www.intensivecarenetwork.com/index.php/icn-activities/icn-podcasts/393-39-lane-on-tropical-microbiology

A new dawn of leptospirosis in New Zealand“Turning prevalence to incidence”
C Heuer et al. http://epicentre.massey.ac.nz/acvsc/scwk_08/Heuer_050708.pdf

Professor Wikipedia et al. http://en.wikipedia.org/wiki/Leptospirosis