Tasty Morsels of EM 046 – Reactive vs Gonococcal Arthritis

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.

REACTIVE ARTHRITIS

  • You probably used to know this as Reiter’s Syndrome (at least it was when I went to medical school) but it has gone the way of Wegener’s and had its name changed due to the Nazi associations.
  • usually 2-6 weeks following infection
  • GU or enteric infections
    • GU: chlamidiya (remember chlamidiya less likely to have urethritis symptoms than gonococcal)
    • Enteric: Salmonella, Shigella, Yersinia, or Campylobacter
  • both have asymmetric arthritis, knees, ankles feet and heels most often involved.
  • can also have conjunctivitis and even uveitis
  • up to 10% can have painless ulcers of mouth and tongue which can later become painful shallow ulcers, penis can also be involved.
  • look for dactylitis (remember this also occurs in psoriatic arthritis)
  • NSAIDS work well for both
  • antibiotics work for chlamidiya associated cases but not enteric ones

GONOCOCCAL ARTHRITIS

  • gonocoocal arthritis the most common cause of septic arthritis in sexually active population
  • more females than males
  • does not present the same as classic septic arthritis and much less chance of joint destruction
  • can be split into two syndromes that overlap
    • oligoarthritis (usually a couple of joints rather than just one).
    • disseminated gonococcal infection syndrome (migratory polyarthalgias, skin lesions, tenosynovitis)
  • very difficult to grow GC from a joint, but other cultures may well be +ve (e.g. pharyngeal or genital)
  • admission for treatment (ceftriaxone IV/IM daily) recommended

References:

  • Rosen’s 8th Chapter 116

[Featured Image: Wikimedia Commons]

Tasty Morsels of EM 045 – Parvovirus B19

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.

Everyone knows the slapped cheek syndrome that runs in epidemics in kids. Hopefully you’ll be aware of the risk to pregant mothers with this infection.

There are however other complications that you need to know about that just might appear in your ED or in your FCEM

Arthralgia/arthritis

  • keep parvovirus in your differential for someone presenting with an acute poly arthritis, especially if there’s a recent flu like illness in the back ground
  • usually symmetric and in the small joints (something that might make you think rheumatoid but you probably shouldn’t head that direction until symptoms have been present for more than 6 weeks)
  • most will have a rash but in adults don’t expect the classic slapped cheek
  • should resolve within 3 weeks and there shouldn’t be any joint destruction

Transient Aplastic crisis

  • typically someone with some kind of haematologic problems eg sickle or iron def anaemia
  • the scenario you should think of this is when you get the FBC back and there an unexpected anaemia
  • usually it’s only red cells involved. If checked reticulocytes should be low

References:

  • UpToDate
  • Rosen’s 8th Chapter 116

[Featured image CC license, via Wikipedia]

 

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