[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:
- disseminated (think signs of sepsis, respiratory collapse, liver failure, disseminated intravascular coagulopathy, and pneumonitis.)
- 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)
- 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
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