Third Nerve Palsy and ESBL Sepsis

Today's case centred around an elderly man with a number of comorbidities including coronary artery disease, congestive heart failure, diabetes mellitus, atrial fibrillation, peripheral vascular disease, and chronic kidney disease. He had a

history of infection with Extended Spectrum Beta-Lactamases (ESBL).  He was admitted with fever and altered mental status, which is a common reason for admission at our hospital.

We talked about a few different learning points:

-Cranial Nerve III palsies are a favourite question for internal medicine residents.  CN III controls all of the extraocular muscles except for the lateral rectus (CN VI) and the superior oblique muscle (CN IV).  A CN III palsy results in the affected eye being “down and out” due to the unopposed actions of the aforementioned two muscles.  The nerve also controls the levator palpebrae muscle (which keeps the eye open) and the parasympathetic pupillary fibres (which constrict the pupil).  The organization of the nerve is important: the parasympathetic fibres are around the outside, while the motor fibres run in the centre of the nerve.  Why is this important?  It gets to the two etiologies of CN III damage.  The more worrisome type is from compressive lesions (berry aneurysms, raised intracranial pressure, mass effect, tumours, hemorrhage, uncal herniation, etc).  Since these lesions mechanically compress CN III, they impair its pupillary and motor fibres resulting in a fixed, dilated pupil (“blown pupil”).  The other type of CN III palsy typically happens to diabetic patients, and is a microvascular infarction of part of the nerve (sort of like a stroke).  These lesions spare the pupil because the blood supply to the core of the nerve is more sensitive to vascular events.  The reason this is important, is treatment of a pupil-sparing CN III palsy is supportive (gets better in months) while treatment of a compressive CN III palsy involves emergent calling of a neurosurgeon!

-We talked about Extended Spectrum Beta-Lactamase organisms (ESBL).  I think it’s important to remember that in the early 20^th century, penicillin was our only antibiotic and killed virtually all bacteria.  Now it is used rarely due to resistance patterns, mostly from overuse.  ESBL organisms produce beta-lactamases that are capable of neutralizing most penicillins and cephalosporins.  They come in two varieties: those that constitutively express ESBL’s and those that are inducible.  The reason inducible resistance is a problem, is that in vitro testing will make the organism appear susceptible.  The mnemonic people use for organisms with inducible resistance is SPICE (Serratia, Providencia, Indole-positive proteus (i.e. not mirabillis), Citrobacter, and Enterobacter).  Some people add Acinetobacter to this list, and some people use the P to remember Pseudomonas even though its resistance mechanism isn’t the same.  ESBLs are treated with carbopenems (meropenem, imipenem, and ertapenem) and sometimes ciprofloxacin or aminoglycosides (gentamicin, amikacin).  You may want to consider avoiding some antibiotics in SPICE organisms once you’ve identified them.

 

-We talked about an approach to altered mental status or delirium.  I can’t emphasize enough that the “DIMS” framework should be considered, if only briefly, in everyone.  This includes drug causes (withdrawal or adverse effect), infectious causes, metabolic causes, or structural causes (CNS lesions, bleeds, etc.).  In the patient discussed today, pyelonephritis or an ascending urinary tract infection was the most likely culprit of his delirium.

-We talk a lot about asymptomatic bactiuria.  We have all heard of patients put on antibiotics “just in case” who have suffered complications like C. difficile infection and even death.  In general, bactiuria should only be treated if it produces symptoms like dysuria, frequency, urgency, etc.  Fever is a sore point from a lot of ID physicians because it should be thoroughly investigated before being attributed to a cystitis.  The example from today’s Morning Report was turning the patient over to find a deep sacral ulcer.  The final point I’ll make here is that Foley catheterization and urinary bleeding can all alter the urine dipstick findings to the point that it’s uninterpretable.

Further Reading:

Paterson, D. L., & Bonomo, R. A. (2005). Extended-spectrum β-lactamases: a clinical update. Clinical microbiology reviews, 18(4), 657-686.

Nadeau, S. E., & Trobe, J. D. (1983). Pupil sparing in oculomotor palsy: a brief review. Annals of neurology, 13(2), 143-148.