“Dad’s acting like a goldfish.”

55 year old man presents to ED in the presence of his son after becoming confused at the supermarket whilst doing his morning shopping.

No memory of why he was shopping, no memory of being in the supermarket or how he arrived there.

shopping trolley

Unable to remember drive to the hospital, unable to recall names of team.

repeated attempts to orientate to time and place. “whats going on bro?”

no other change in cognition. preservation of longer term memory.

denies drug use, no History of epilepsy, migraines, head injury.

 Normal neurological exam.

Throughout the time in the department the patient would catch the eye of staff who they knew before the episode wave and say “bro, whats going on?”

Bloods showed no abnormalities.

This constellation of symptoms is consistent with a diagnosis of:

 Pivot_Wave

 Transient global amnesia.

Diagnosis of exclusion.

Features:

Rapid lost of antegrade memory.

Repeated attempts to orientate themselves. often with a repetitive manner.

No change in level of consciousness.

lasting less than 24 hours.

Clinicians report perseveration as the predominant feature. Many can remember the specific mannerism of the TGA patients they have seen.

Rare condition: incidence in those over the age of 50 being: 20-30/100,000 per year

The cause of TGA is unknown but a number of hypotheses exist with migraines, epilepsy being initially linked but then more recently discounted. A vascular hypothesis is another disputed possible cause. With this number of possible causes being postulated it’s pretty clear we are unsure of the cause. This is likely due to TGA being a syndrome with multiple causes leading to hippocampal dysfunction.

The most comforting feature of TGA is that patients with “pure” TGA eg: only memory impairment which resolves they have a normal mortality and morbidity and a low chance of further events.

Follow-up:

Patient was admitted to the ward for observation, symptoms improved with return of normal memory within 8 hours at which time he stopped waving. No memory of events of the day.

 Ref: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600033/

http://www.uptodate.com/contents/transient-global-amnesia

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/