The pregnant patient is particularly susceptible to sepsis, owing to their borderline immune function. The typical pathogens of "puerpureal" or "childbed fever" were group A streptococci such as S.pyogenes. Toxic shock syndrome is not an uncommon feature. The college has examined this issue in Question 3.1 from the first paper of 2014 and the identical Question 14 from the second paper of 2009. Each time, the focus was on the difficulties in actually making a diagnosis of sepsis, the major causes of sepsis in pregnant patients, common bugs and antibiotics which are contrainidicated.
Probably the best article on this topic was by Barton et al (2012), but to be honest most of the college answers to the abovementioned SAQs was sourced directly from Oh's Manual, page 688 of the 7th edition. Beyond these brief notes any further reading will be at the cost of revising more important material, and should therefore be viewed as indulgently recreational.
Question 3.1 from the first paper of 2014 and Question 14 from the second paper of 2009 asked about "difficulties associated with the diagnosis of sepsis during late pregnancy and labour." Upon close inspection, one can discern that the majority of these problems are equaly applicable to non-pregnant patients, as they are problems of the obsolete definition of sepsis and SIRS.
The new Sepsis III definitions are somewhat better, as they call for organ dysfunction. Also, to make septic shock the recipe now calls for vasopressors and/or raised lactate, neither of which are features of normal pregnancy and labour. Which is good news: unlike SIRS and pregnancy, "Sepsis III" and pregnancy now appear to be distinct entities by criteria. One should never again be in a position where one is confused about which is which.
On a serious note, the LITFL entry on this topic brings up several additional points which this author is not above stealing:
If you like comprehensive lists and grey boxes, you're going to love Box 1 from Barton et al (2012)
It is more appealing by virtue of the fact that surgical neglect and the consequences of "conservative management" are included in the list of differentials.
Oh's Manual quotes the following bugs:
To this, the Sanford Guide adds a few:
(these are specific to chorioamnionitis and septic abortion)
Oh's Manual recommends ampicillin, gentamicin and clindamicin as an empiric therapy (with meropenem and vanc as a backup second tier). The Sanford guide agrees, replacing ampicillin with ceftriaxone, and suggesting that Tazocin could be used as a sole agent.
A full list of antibiotics which are contraindicated in pregnancy is also offered here for completeness (paraphrased from Mylonas, 2011 and Pilmis et al, 2015). It is not essential to memorise the entire list. Time-poor candidate should at least be able to recite the top five:
|Aminoglycosides in high doses||Increased uptake by neonatal kidney leads to increased nephrotoxicity (but apparently gentamicin is still relativey safe)|
|Streptomycin||8th cranial nerve damage|
|Sulfonamides||Kernicterus in the newborn due to displacement of bilirubin off albumin, particularly if used shortly before birth. The specific culprit is sulfamethoxazole. Trimpethoprim appears to be relatively safer.|
|Tetracyclines||Tetracyclines have nightmarish dental and bony effects. In fact, these drugs are contraindicated from 16th week of gestation all the way until the 7th year of extrauterine life.|
|Quinolones||Quinolones cause birth defects (though it seems fluoroquinolones are safe, and it was really mainly nalidixic acid that was the culprit).|
|Rifampicin||Seems to be somewhat teratogenic, mainly in animal studies (spina bifida and impaired osteogenesis seem to be the major consequences)- but in humans one may overlook this if rifampicin is strongly indicated (eg. treatment of lifethreatening tuberculosis)|
|Fusidic acid||Like sulfonamides, causes displacement of bilirubin by competing with it for albumin binding|
|Chloramphenicol||This "Grey baby syndrome" is the consequence of disrupted mitochondrial function, when chloramphenicol metabolites interfere with the electron transport chain. Foetal failure to properly metabolise chloraphenicol by glucourinidation seems to be to blame.|
|Azole antifungals||Teratigenic and embryotoxic. The specific dangerous ones are ketoconazole fluconazole and voriconazole, earning a D classification.|
|Echinocandins||Hard to discuss humans in the absence of real data, but in animals using normal treatment doses caspofungin and anidulafungin cause skeletal abnormalities, reduction of litter size, ossification and rib malformations.|
|Flucytosine||Embryotoxic and in fact abortificant in the first trimester, which is hardly surprising given that its main metabolite is 5-fluorouracil|
|Albendazole||Teratogenic and embryotoxic. If the pregnant lady has some sort of hideous helminthic parasitosis which cannot wait until after delivery, ivermectin is probably a safer alternative|
|Foscarnet||Seems to be teratogenic in animals, but if your CV infection is so severe and resistant that you've failed primary therapy, the chances are that your foetus is already significantly damaged by congenital CMV.|
The college answer for Question 3.1 from the first paper of 2014 also lists nitrofurantoin, isoniazid and macrolides as drugs which are relatively contraindicated. This in fact, is not true: