Tasty Morsels of EM 044 – Thyrotoxicosis Factitia

As always, this is from the ever expanding google doc on bits and bobs I read and learn from and transfer here for all our learning pleasure.

This was something I wasn’t even aware existed but worth considering.

Classic symptoms of hyperthyroidism

  • tachycardia
    • usually sinus
    • a fib common too
  • sweating/feeling warm
  • poor sleep
  • weight loss
  • possible fine tremor
  • eye signs (Graves only)

Causes of these symptoms

  • usually Graves disease in the west
  • toxic multinodular goitre in areas of iodine deficiency
  • thyroiditis
  • the odd tumour here and there
  • the odd drug here and there (amiodarone and lithium being the big ones)
  • exogenous thyroid hormone use (rejoicing in the name thyrotoxicosis factitia)

The (very) basic physiology

  • Thyroid Stimulating Hormone (TSH) causes thyroid to produce more thyroid hormones
    • controlled by the axis of evil, hypothalamic-pituitary-thyroid axis
  • The hormones are:
    • T3 (triiodo- thyronine)
    • T4 (thyroxine)
  • Most T3 comes from conversion of T4 to T3 peripherally (liver and muscle mainly)
  • T3 is more biologically active
  • In most hospitals I’ve worked T3 isn’t measured routinely

Thyroid hormones can be taken surreptitiously in a few situations

  • reported outbreaks of hamburger thyrotoxicosis from ground beef from the neck of the animal
  • ingestion of various weight loss products that can contain either T3 or T4
    • note if it’s T3 causing the symptoms then T4 may be normal but the TSH should be suppressed. If your lab doesn’t normally measure T3 then it’s worth thinking about (a very smart biochemist had to explain all this to me)

The differentiating feature is probably the eye signs. Graves is the commonest cause of thyrotoxicosis in the west so if you see someone with classic hyperthyroidism and no eye signs then it’s always worth asking them about various supplements they may be taking.

References:

  • Rosens 8th Chap 128
  • UpToDate: Exogenous hyperthyroidism
    • An outbreak of thyrotoxicosis caused by the consumption of bovine thyroid gland in ground beef. Hedberg CW, N Engl J Med. 1987;316(16):993.

 

 

 

Tasty Morsels of EM 043 – Vibrio

As always, this is from the ever expanding google doc on bits and bobs I read and learn from and transfer here for all our learning pleasure.

At risk of this becoming an “Andy reviews EM:RAP” section here’s another one from the Dec 2014 program, again from the bounce back section. And once again it’s infectious disease.

As with the last one it falls into the category of pushing your diagnostic skills one step beyond. Most of us are happy to pick up the cellulitis that is sicker than normal but the step further is to track down the right bug and know why it matters.

Vibrio Vulnificans

If there was one take home point then it’s this:

  • Water born infections

Risk Factors

  • older male
  • liver problems (mainly alcohol, cirrhosis, haemochromatosis)
  • DM

Two types of Major Presentations

  1. Wound infections (stood on coral, cut getting off a boat, any cut sustained in the water). This can look like a necrotising infection but can be a simple cellulitis early
  2. Primary Septicaemia (classically from ingesting oysters). severe septic shock and usually with bullae formation on the skin

Treatment:

  • Doxycycline and Ceftazidime were suggested on EM:RAP
  • UpToDate suggested Doxy and Cefotaxime or Ceftriaxone
  • If you’ve got someone with a mild wound cellulitis and water exposure and you want to just treat with orals then you could add doxycycline to your usual meds.

References:

  • EM:RAP Dec 2014
  • UpToDate
  • Rosens 8th pg 1856 has a great table [137-2] for all the unusual skin infections and what to treat them with

Featured image from CDC public health image library via wikipedia

Tasty Morsels of EM 042 – MucorMycosis

As always, this is from the ever expanding google doc on bits and bobs I read and learn from and transfer here for all our learning pleasure.

This time it’s the somewhat obscure MucorMycosis.

This is of course from the just released Dec 2014 EMRAP [paid access but worth it] and I’m sure lots of you have heard it. This is going to be really rare and you may never see it, but it’s definitely a diagnosis you cannot afford to miss.

  • Invasive fungal infection can be disseminated but typically rhinosinusitis
  • being immunocompromised and DM (esp with ketosis) are the key risk factors
  • we all get exposed to the same fungi all the time and in immune competency its never a problem
  • it’s called “angioinvasive” meaning that you will see infarction and necrosis as vascular supply is interrupted
  • bizarrely the desferroxamine you use to treat iron poisoning increases your risk for this
  • presentation
    •  initially just think sinusitis, pain, fever, discharge
    • when they’re really sick you’ll probably think of orbital cellulitis (proptosis and eye movement or visual problems) and the danger is that you’ll stop looking – you’ll see a sick patient with probably orbital cellulitis and give antibiotics and refer
    • the key feature that gets mentioned is palatal eschars or eschars in the nasal cavity so the take home message is LOOK IN THE FREAKING MOUTH PEOPLE
  • there are great images on google images though they are pretty disturbing
  • as for treatment think of this the same way you think of necrotising fascitis
    • the most important thing is mobilising the surgeons (likely ENT)
    • Give Amphotericin B but they need debridement

References:

  • Dec 2014 EMRAP
  • Nice review paper in Clinical Infectious Diseases [FOAMed pdf, and it has pictures]
  • Rosen’s 8th Page 976

Tasty Morsels of EM 041 – Acute Urinary Retention

[Featured Image: Frivadossi, Wikimedia Commons]

As always, this is from the ever expanding google doc on bits and bobs I read and learn from.

This time:

ED Management of acute urinary retention. EB Medicine

  • Causes
    • Men – think prostate
    • Women – bladder masses, gynae surgery and prolapse
    • Drugs: calcium channel blockers (i didn’t know this), anticholergics (i did know this one)
    • Spinal cord compression is probably the real emergent cause we need to think of
    • In a similar manner to other neuropathies, diabetics can get a diabetic cystopathy resulting in AUR.
  • The big take home should be this: you need to bloody well examine them. There is a real (and justifiable) desire to just slip in the catheter (or worse get someone else to do it) and get disposal nice and quickly. But as simple as most AUR is, you will miss important things (say spinal cord compression, or a penile tumour, especially in the patient with dementia or non-verbal patients) if you don’t physically get involved with the gorey details.
  • there’s some ‘himming’ and ‘haaing’ over whether to put a finger in the rectum. The main concern seems to be in prostatitis and seeding the blood with a prostate exam. They’re right to say that there’s no evidence of this causing harm. But that works both ways – there’s no evidence either way. There’s not a great deal of diagnostic value here I don’t think. The bigger issue is whether to put a catheter through an infected prostate. I figure if they’re in retention then I do it, and they get a nice chaser of gentamicin and an admission.
  • there’s some interesting stuff on urine samples for prostatitis. You can collect wee at lots of different points of the wee cycle and then massage the prostate a bit and get another few mls. There’s even a study looking at semen cultures for prostatitis. I imagine if I had prostatitis the last thing I might be able to do is provide a semen sample…
  • getting the patient to exhale when the tip is at the prostate seems to be of some use in relaxing the relevant sphincters
  • an episode of hypotension following bladder decompression is common due to a reflex response in reduced vascular resistance. Doesn’t mean the you don’t have to think about whether that patient’s severe abdo pain was actually a AAA rather than AUR…
  • they (sensibly) state that if it’s a simple catheter and no reason to think infection then antibiotics are not indicated. Very different from the raging, septic prostatitis
  • they quote the common figure of 2 in 3 patients requiring repeat catheterisation if the catheter is immediately pulled. They also note that those with a spontaneous AUR (which is likely prostatic hypertrophy in origin) is more likely to need a second catheter than those with a precipitated cause (eg infection or constipation).
  • they suggest that the 2 in 3 rate of recurrence mandates that the catheter is left in whereas I think that “hey, I have a 1 in 3 chance of not needing this – i’ll take those odds and come back if I can’t pee again”
  • catheters that get stuck and can’t be removed are usually due a ridge forming on the balloon during deflation and can be dealt with very slow reinflation and deinflation. The inflation channel can also be cut. Interestingly they say that filling the balloon with 10mls of mineral oil will dissolve the balloon in about 15 mins and allow removal. I have no idea if this applies to all makes.

Tasty Morsels of EM 040 HSV in Kiddies

[Featured Image: Ben Tillman, Wikimedia Commons]

Another review from the EB Medicine series of publications. Remember this comes free with EMRA membership if you’re a trainee. Along with EM:RAP, Emergency Medical Abstracts and lots of other good stuff. This time it’s Paeds:

Pediatric Herpes Simplex Virus Infections: An Evidence-Based Approach To Treatment. Paediatric Emergency Medicine Practice. 2013 Dec 24;:1–20.

Sorry it’s a bit longer than usual but I found a lot of important stuff in here, a lot of new to me.

  • CytoMegalo Virus, Varicella and Epstein Barr are all types of herpes virus
  • HSV can be transmitted even without visible lesions
  • HSV-11 tends to reside within the trigeminal ganglion, while HSV2 commonly resides in the sacral ganglia which makes sense with the clinical distribution of oral HSV-1 and genital HSV-2
  • Lifelong latency and periodic recurrences are hallmarks of HSV infections. As Mark Crislip might say, Herpes is for life not just for Christmas…
  • in herpes encephalitis 1/3 is primary, 2/3 are reactivation. Just because they don’t have a cold sore doesn’t mean it’s not HSV encephalitis
  • HSV-1 prevalence is 90% by old age
  • HSV encephalitis has 2 peaks: <20 and >50. Virtually all are HSV-1
  • most neonatal HSV (non-encephalitis) is HSV-2
  • peripartum HSV in 3 categories:
    1. disseminated (think signs of sepsis, respiratory collapse, liver failure, disseminated intravascular coagulopathy, and pneumonitis.)
    2. CNS disease (with or without lesions. think seizures, irritability, a bulging fontanel, and temperatures either high or low. Most of these will have skin lesions at some point)
    3. disease limited to skin eyes and mouth
  • mortality for untreated disseminated disease is 85% and even if treated it remains high
  • common differentials for the rash include
    • erythema toxicum or pustular melanosis
    • It is important to note that both of these present in the first few days after birth, unlike disseminated HSV which typically presents after at least 10 days or so. I remember seeing pustular melanosis as a paeds doc doing baby checks and being almost as freaked out as the parents were. Reassurance from the boss was all both of us needed.
  • in CNS HSV 5-10% of LPs can be normal initially. How on earth do you even make the diagnosis in these kids then?
  • they note that LFTs might be useful as they are typically quite abnormal in babies with disseminated disease. I’m not sure this is fit as a rule out but in the crashing infant with crappy LFTs it might prompt you to consider it in addition to the usual bacterial sepsis.
  • if you’re looking for CNS disease with imaging then the temporal lobes are where the money is and MRI is the test to see it. However you will sometimes see it on CT, and i’ve seen it missed on CT by those who sit in dark rooms for a living.
  • the first drug for this was something called vidarabine. When aciclovir came out they did a randomised trial between the two and found no difference. And aciclovir rules the day due to its apparent favourable side effect profile (ring a bell for amiodarone v lidocaine or verapmail v adenosine anyone?)
  • Kaposi-Juliusberg Varicelliform Eruption – you’ve all heard of that right? It’s important and potentially life threatening so get on it!
  • Some others
    • herpes gladiotorum – typically athletes getting HSV-1 through abraded skin
    • herpetic whitlow – the one on the finger that looks like a paronychia but isn’t