What would be in the differential?
The radiologist made me order that (unnecessary) test! I’ve heard this excuse many, many times. Do these phrases look familiar?
- … recommend clinical correlation
- … correlation with CT may be of value
- … recommend delayed CT imaging through the area
- … may represent thymus vs thoracic aortic injury (in a 2 year old who fell down stairs)
- Those that are afraid of being sued if they don’t do everything suggested, because they’ve done everything and shouldn’t miss the diagnosis
- Those that don’t completely understand what is known about trauma mechanisms and injury and think the radiologist does
Reference: Pitfalls of the vague radiology report. AJR 174(6):1511-1518, 2000.
Ask the family what the patient was like when they found him. Patients with syncope have a normal mental status after waking up. Patients with seizures are dazed (post-ictal) after waking up. Tongue biting, incontinence, etc are not as sensitive or specific. It doesn’t give you the answer all the time, but it’s an easy way to make the diagnosis sometimes.
While in the ED, the patient has a generalized tonic-clonic seizure while being interviewed by a resident. What should we do while the patient is having the seizure? (Yes, this is a “guess what I’m thinking” question).
The ddx of intractable retching is fairly limited. The most-likely dx has changed over the years based on where I work and when I work (1990s v 2010s). When I was a med student in the suburbs, the common dx is gastroparesis. Now, as an EM doc in a city, the common dx is cannabis hyperemesis. As marijuana use becomes decriminalized, we see more and more patients in the ED with this problem.
There are numerous causes of vomiting (e.g. brain lesion with increased icp), but they don’t generally result in the type of agitated intractable vomiting that you see in cannabis hyperemesis. Patients often say that a hot shower makes them feel better. Some patients with intractable vomiting are withdrawing from opioids.
Reglan, zofran, and the common anti-emetics don’t seem to be as effective in cannabis hyperemesis. Haldol (or droperidol) and ativan (or other benzos) seem to work better for some reason. This is based on my anecdotal experience and not on any studies.
Patients with cannabis hyperemesis typically do not have anion-gap metabolic acidosis, as is seen in this patient. This patient was also an alcohol user, so alcoholic ketoacidosis is a likely candidate; but the patient can easily have both problems (aka and cannabis hyperemesis). Patients with cannabis hyperemesis usually do not have ketoacidosis because they’re not sick for that long. Most people don’t become ketotic from being npo for a few hours.
It takes two tubes of blood to work up an unexplained / unexpected anion gap – a chem and a lactate. An urine sample is very helpful sometimes. If you’re not worried about a poison, the ddx is uremia, ketones, and lactate. If you’re worried about an ingestion, send serum osm, asa level, lactate, and look in the urine for crystals.
Our patient received haldol, ativan, ivf, iv glucose, and it calmed her down. She felt better after a few hours and went home. We didn’t repeat the labs.