This is a complex case. This 59 y/o woman had a long history of morbid obesity with OSA, OHV and all the other associated problems. About 1.5 years ago she underwent bariatric surgery and lost >100 lbs. One year ago she presented to an outside hospital with comma was treated in their ICU (I am deliberately making this previous episode vague) and eventually recovered.
She presented this time to one of the small outlying hospitals with fever, chills and cough with purulent sputum. A pulmonary infiltrate was identified. Despite adequate ABTx her overall status (particularly MS) continued to decline. She became comatose and on the day of her transfer had a tonic-clonic seizure. She was intubated and I was contacted as they don't have EEG and full time neuro back-up.
On arrival she was comatose, intubated on mech. vent., quite emaciated with mild anasarca. Ronchorous lungs, tachycardic, benign abdomen.
CxR confirmed a pneumonia. Blood Cxs had been negative with sputum + for MRSA. Blood work of note from the OSH: hyponatremia to 128, normal BUN/Creat, good oxygenation, negative cardiac enzymes, LFTs remarkable for albumin 1.9 and ammonia 300. Normal AST/ALT and coags.
Seizure activity was controlled after initial Ativan and Dilantin load. Any ideas?
Subscribe to:
Post Comments (Atom)
11 comments - CLICK HERE to read & add your own!:
Was she hypotensive?
What was her K+ and HCO3?
I guess it would be too obvious to say legionella with the low sodium and pneumonia, even though that would not grow in the sputum. Anyway, what was the legionella urinary Ag? I don't think the low albumnin would go with that though. Not sure what to make of the MRSA in someone not in the hospital for over a year and you didn't mention other risk fctors for her to be exposed to a nosocomial bug.
I think her general condition is obviously deteriorating ("dah"). It sounds like she is possibly becoming septic, although you did not give me a BP.
I would also be very concerned about her having meningitis. The seizure and worsening MS are a worrisom sign. Could she have Austrians triad? Negative blood cultures may support this diagnosis of meningitis (not Austrian's triad though).
Her Albumin being so low are not a good sign and will predispose her for complications, especially infections. The MRSA may be real!
She needs an LP.
In addition to Legionella and/or MRSA sepsis, which I'm sure is being covered appropriately, I'd think about endocrine disorders as a primary or contributing factor. Specifically, adrenal insufficiency can lead to this clinical picture in the setting of any infection. I'd consider myxedema coma, although her emaciated status makes this less likely. Of course, toxic ingestions/overdoses should be considered, including Lithium overdose, with the pneumonia due to aspiration.
In addition to broad spectrum antibiotics and a head CT, I'd check a tox screen and drug levels, as well as Cortrosyn stim and tyroid function tests.
Hi there,
Firstly, kudos on the excellent blog. It has great focus and is a regular stop for me.
On to the case.
The single most pertinent clinical fact about this woman is, to state the obvious, that she is in a coma. I say the following with the best of intentions, and with the greatest respect, but may I point out that in the entire discussion so far, not a single piece of information about any kind neurologic evaluation (history/ neuro exam) has been provided. It is often a bit unsettling to note that very little relevance seems to be attached to neurologic evaluation, even in patients with a neurologic disorder (you can’t get much more neurologically abnormal than become unresponsive), and with a condition so dangerous as a coma. Of course, it may be that everything was done but not reported here because nothing remarkable turned up, in which case I hope you will disregard the preceding, Baleeiro.
Nevertheless, one would like to get some basic data on the neuro exam. This is a coma, so by definition, something is either wrong singularly with her ARAS, or diffusely with her cerebral hemispheres, bilaterally. What are her pupils like? Eye position, eye movements? Corneal reflex? Oculocephalic reflexes/ vestibule-ocular reflexes? What is her neck like? Are there limb movements, and if so, what? Muscle stretch reflexes are crucial. Since I think she was not seen prior to being placed on mech vent, breathing patterns will not be reliably evaluable.
She had a seizure either before or soon after entering coma. Since this was in a hospital, did anyone observe and describe the seizure?
Did anything turn up on general exam? Rashes have obvious import. Dark discoloration in the folds? Does her breath smell funny? Presumably labs included the usual toxins. You say she had bariatric surgery, that she has lost a huge amount of weight, that she is emaciated, that there is some suggestion of anasarca, even. This is very interesting.
Anyway, we will assume that she has a metabolic disorder diffusely affecting her hemispheres, a not-unreasonable assumption given only the information you have provided. She has a known pulmonary infection, confirmed at two hospitals. However, despite being on “adequate ABTx” she declined. This is also very interesting. I am with the "Madhouse Madman" that what she needs immediately is an LP; I will be very nervous before this was gotten. When was the last blood culture done? Might it be useful to get this? Her syndrome, whatever it is, presented initially with pneumonia, so cerebral extension from this is clearly something to worry about.
Jeff has suggested the important things to check where labs are concerned. May I add blood transketolase? I recall a small literature describing Wernicke’s encephalopathy in patients who have had bariatric surgery and become quite malnourished as a result. Her albumin is low, she is emaciated. She has had a coma in the very recent past, and your intentional exclusion of this history suggests that it was the same condition, or one that would clue one in to the diagnosis – it is thus not incompatible with Wernicke’s, whose sufferers can be repeat offenders. The pneumonia might be a result of the frequent, sometimes intractable, vomiting in these patients, and will be the source both of her respiratory tract infection as well as a contributory factor to her malnutrition.
Thanks once more for your great cases.
ACR, MD
may I suggest feedback on our suggestions as to where this case went/or is going.
it will make it interesting
Great comments and questions! I did leave out some details from the neuro exam/work-up but not to mislead the case. She had been non-focal on initial presentation to the OSH just encephalopathic with asterixis. An unenhanced CT scan of the brain was quite unremarkable and LP showed no evidence of CNS infection. On exam, she had minimal withdrawal to pain and was quite symmetric. Pupils were sluggish but responsive. She still had preserved brainstem reflexes. No hyperspasticity, more just deep encephalopathic-like coma. The seizure was witnessed in the OSH, from their description it was a true generalized (as opposed to partial with generalization) tonic-clonic seizure.
She was not septic on arrival but her condition deteriorated briskly within the first 36 hours and she went into septic shock. Legionella Ag was negative and MRSA was the only isolate throughout (as she got sicker we recovered it from a blood Cx as well).
The suggestion on the Transketolase was excellent. I did leave some info out but the previous coma suggest an underlying process triggered or unmasked by the gastric bypass.
Any ideas on the high ammonia?
Hmm...Maybe you are steering us towards fatty liver/cirrhosis (from obesity), and her MS is thus consistent with a hepatic encephalopathy (hence the low albumin). WHat happens to her level of consciousness when you give her lactulose?
The low albumin - could that also be related to absorption problem after the surgery (in which case you would want to check B12).
Not sure how to explain the sz, unless she has cirrhosis and failure of hepatic clearance of some toxin..
She had normal coag's, normal AST, ALT, Alk Phos and Bilirubin.
Normally, a high ammonia level is very non-specific and really can't be trusted unless done correctly and ahvign a previous baseline. (Arterial and on ice until lab). I will presume that in this case it was.
Still, she has normal liver function thus far presumably because coags are the first thing to be prolonged in severe liver failure.
Could the surgery have anything to do with the high ammonia?
As ar as I am aware (I am not a surgeon)Bariatric surgery is somewhat comparable to a Roux on Y procedure, where, in addition to minimizing gastric size the outlet of the stomach is relocated to the jejunum. This would thus impair absorbtion of many proteins but would not have a smaller effect on coags as the fat soluble proteins needed to maintain normal coag measurements are absorbed in the ileum. This may explain the low albumin in the absense of other liver disfunction.
I would second the choice of checking a B12 level at this juncture as the bypass may have lowered her ability to synthesize intrinsic factor.
I would put a minimal impolrtance to the ammonia level (aLthough lactuose is warrneted) and would turn my attention elsewhere. did she have a megaloblastic anemia?
Excellent comments and ideas on the surgery unmasking or leading to a metabolic disorder.
The patient had developed a similar episode after surgery. Prior to surgery she had the standard high-fat, high-starch obesity-related diet. After the surgery she was asked to follow a relatively higher-protein, low-cal and certainly low starch, diet. This unmasked an Ornithine Transcarbamylase deficiency (she had already been tested by the time of this presentation). This leads to high ammonia (hers was real and remained >200-300 prior to transfer to us) levels that worsen in catabolic states (her pneumonia) and with high protein intake (like her post surgery diet).
Treatment includes a steady intake of calories/carbs to prevent further muscle breakdown, lactulose is only partially effective since this is truly endogenous and not from translocation, and aceptors of nitrogen / urea compounds.
We did manage to bring down the ammonia with these measures and she actually had an improvement in MS with eye opening to verbal stimuli and more vigorous withdrawal to stimuli.
Unfortunately, with her very poor performance status and malnutrition, she became septic, eventually developed renal failure, ALI and MOSF and expired.
Hello, I realize this all took place 2 years ago, but my father has slipped into a comma at Waynesboro hospital with something very similar. Hi amonia levels throughout his bloodstream and amonia toxins in his brain.
Have you learned any new tricks since then that could perhaps help his doctors who are currently stumped with what the next move should be? -- Michael Hogan mseanh@gmail.com
Post a Commenttest post a comment