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

Tasty Morsels of EM 039 BradyDysrhythmias

[Featured image via LITFL]

Approach to BradyDysrhythmias

EB Medicine Article [free via EMRA if you're a member. About 70 dollars a year. Well worth it.]

 

On a FOAMed note, it’s interesting that all the ECGs in the article are taken from LITFL. Another sign that FOAMed is not providing a marginal, niche resource, but a highly curated and high quality resource for all.

  • while usually thought benign, first degree block are more likely to develop AF and have a (moderately) increased rate of death [Cheng S, Keyes MJ, Larson MG, et al. Long-term outcomes in individuals with prolonged PR interval or first-degree atrioventricular block. JAMA. 2009;301(24):2571-2577. (Prospective analysis; 7575 patients)]
  • in sinus node dysfunction and in particular, tachy-brady syndrome most of the tachycardias will be AF (but not all)
  • sinus node dysfunction is seen in the oldies
  • pathological bradycardias in the context of ACS are typically associated with RCA occlusions. I have a vivid memory as a 1st year doc of seeing a bradycardic, diaphoretic guy with chest pain and the more senior doc coming down saying “what do you think? a nice big inferior?” with a grin on his face.
  • Some of the more interesting and esoteric causes of a pathological brady
    • hypothyroid
    • hyperkalemia
    • chagas disease (common world wide but not here)
    • Lyme disease
    • parvovirus or coxsackie (in the context of myocarditis)
    • syphillis (so it turns out that Amal Mattu might be wrong and it’s not just Hyperkalemia that is the syphilis of electrocardiography but syphilis itself is the syphilis of electrocardiography)
    • some chemo regimens (not in the article but I saw this last month…)
  • atropine is of course recommended but no surprise that it’s rarely effective. Given that most of the nasty bradys I see are third degree blocks then I find that it’s rarely helpful.
  • dopamine is also recommended but along with some other smart people I just use adrenaline for virtually all vasoactive situations as I actually know how to use it ;-)

Tasty morsels of EM 038 – Alcoholic Ketoacidosis

Click for source - Wikipedia

Click for source – Wikipedia

These little notes have become my way of documenting my text book reading. Mainly focused on the stuff I don’t already know about or don’t see very often.

  • Alcoholics become dependant on alcohol for caloric supply
  • The body can only utilise alcohol to make sugar or fatty acids. Therefore glycogen stores become depleted
  • Alcoholic Ketoacidosis (AKA) usually occurs during period of abstinence following binge (think of the alcohol withdrawal patient)
  • Lack of available glucose (low glycogen stores and previously abundant alcohol source now that patient is abstinent) leads to ketone body production
  • Increased anion gap present but pH may be normal.
    • due to mixed acid base probs like a metabolic alkalosis from vomiting. Hence the importance of doing the calculation using your favourite app.
  • Urine ketones are often low despite severe disease
    • this is a characteristic of the urine ketone test: it measures acetone or acetoacetate and doesn’t pick up beta hydroxybutyrate which is the big one here.
    • Of note urine ketones may actually rise as they get better due to a shift in the NADH/NAD+ ratio
  • Distinction from other ketoacidoses (?) is mainly on history.
  • Important to give glucose to these patients as it is the glucose which will stimulate insulin release and turn off ketogenesis
  • Remember at some point to give them some thiamine in your banana bag of choice. Thiamine is essential for glucose utilisation in the Krebs cycle.
  • Everywhere says correct magnesium and phosphate but often it seems like after a few hours of treatment and improvement in the acidosis these seem to improve either way. And where’s the benefit of treating asymptomatic low magnesium and phosphate (or am I missing something here? I may well be so let me know!!!)
  • They do not need insulin
  • They do not (almost no one does) need bicarb

Reference:

Hardwood-Nuss Clinical Practice of Emergency Medicine 5th Ed p1019

Tasty Morsels of EM 037 – Heart Transplants

I keep a little, ever-expanding note on my phone where I jot down little morsels of goodness that I pick up while listening to or reading one of the many excellent sites/podcasts in the useful resource section. They’re useful in a kind of “board review” way. I tend to skip the really basic stuff and try and focus on what I didn’t know.

I’ll try and transfer them here for your enlightenment.

  • 5 year survival about 75%
  • most common ED complaints are fever, SOB, GI probs, chest pain
  • baseline tachycardia is normal as no vagus innervation to the transplanted heart
  • patient has no pericardium but due to scarring clinical tamponade can still develop
  • chest pain is rarely related to ischaemia as heart is denervated (most anginal pain is probably sympathetically mediated and the sympathetic plexi around the heart would have been disconnected at transplant)
  • however ischaemia is common as atherosclerosis is accelerated in the graft. Often presents as CHF or arrhythmia.
  • CMV is a risk factor for accelerated atherosclerosis.
  • ECG Often demonstrates two p waves. One is from native sinus node (which is often left in place as it lies in the post RA) and the other is from the donor SA node. The donor p wave is the one that should conduct.
Via Wikipedia

Via Wikipedia

  • rarely a heterotropic transplant is done where the the native heart remains in entirety in the chest. The ECG in this scenario is understandably bizarre.

Reference:

Rosen 7th Edition p2369-70