Thursday morning, Brian Coburn, one of amazing second year Med/Peds residents, presented an interesting case of a 35-year-old patient who presented with hypoactive delirium. The patient’s medical history was significant for epilepsy and opioid use disorder. We started our investigation of possible causes of the patient’s encephalopathy by going through the AEIOUTIPS mnemonic of common causes of altered mental status that can be investigated with basic history, exam, labs, and imaging. Our expert discussants from the Toxicology services provided us a comprehensive overview of the approach to hypoactive toxidromes and judicious interpretation of urine tox screening. After the initial work-up was unrevealing, the team pursued additional investigation with lumbar puncture, EEG, and MRI without contrast that were also negative. The team asked our friends from psychiatry to help elucidate whether the patient’s symptoms may be due to an underlying psychiatric disorder, but the determination was made that a primary medical disease was still the most likely cause.
The patient’s condition continued to progress, and an MRI with contrast ultimately revealed acute, diffuse white matter lesions. Per our radiology colleagues, the differential for these findings included infection/post-infectious causes (viral encephalitis, acute disseminated encephalomyelitis, acute hemorrhagic leukoencephalitis), autoimmune encephalitis, and toxic leukoencephalopathy. Following a repeat LP that was negative for a broad array of infectious, autoimmune, and malignant/paraneoplastic studies, we were left with a diagnosis of opiate-induced toxic leukoencephalopathy. The disease presentation is extremely variable, ranging from minor cognitive impairment, easily confused with psychiatric illnesses, to severe neurological dysfunction. Our toxicologist reminded us that some of these findings can also be seen with potential transient, out-of-hospital anoxic episodes. While there is no proven treatment for toxic leukoencephalopathy, antioxidant therapy with Coenzyme Q10, Vitamin E, and Vitamin C has been used to treat some patients with variable results in the past. The patient received this treatment and spontaneously improved after several days of therapy.
Thank you to Brian, our expert discussants, and our residents for working through the differential of hypoactive delirium and the sequential investigations we needed to get to the bottom of this fascinating case.
Who: Residents can take this course prior to obtaining their own DEA – your completion will be recorded for use later.
What: AAAP Buprenorphine Half and Half Course (½ online independently and ½ “in person” via Zoom)
Where: YOUR OWN HOME via Zoom! You MUST RSVP in advance, attendance will be taken
When: September 17th, 2020; 8 am -12:30 pm (you must attend the entire time for the waiver)
Why: To be qualified to get a DEA waiver to prescribe buprenorphine products (one common brand name is Suboxone) AND to feel confident managing this growing patient population
This course is designed to equip prescribers with the information necessary to understand and prescribe buprenorphine in a safe and effective manner. It also meets the 8-hour requirement (½ in person; ½ on line) for MD’s and DO’s to apply for the DEA waiver to prescribe buprenorphine.
This training is for ½ of the 8-hour requirement. The remaining 4 hours must be done online, and you must pass a self-study exam to apply for the waiver. Contact Carla Marienfeld (firstname.lastname@example.org) if you are interested in attending.
Today Dr. Tony Gao from toxicology joined us in a discussion of a young woman who presented to the ED with nausea, vomiting, and progressive somnolence after attempting suicide by ingesting an insecticide earlier that day. We discussed that this insecticide contains organophosphates, the result of which resulting in her clinical presentation. We then discussed several aspects of care for patients who have been poisoned with organophosphates. As these agents irreversibly inhibit acetylcholinesterase, they result in both diffuse and long-lasting effects in the poisoned patient. Our patient was intubated and spent several days in the ICU receiving both atropine and pralidoxime. She ultimately recovered and received further care from psychiatry before ultimately leaving the hospital.
Take Home Points:
Organophosphate poisoning causes a cholinergic toxidrome (SLUDGEBBB) via irreversible inhibition of AChE
Consider the typical ABCs of emergency management and have a low threshold for intubation due to the multifactorial respiratory failure
Atropine should be given first, followed by pralidoxime – continuous infusions may be necessary – and should be continued until respiratory symptoms have resolved
For those of you interested in obtaining a waiver for buprenorphine prescription prescribing, we wanted to list some options for you:
Sign up for one of the 1/2 and 1/2 in person training: 4 hr online training and a 4 hr in-person training. We have a session on November 5th (8:30 am -12:45 pm) on UCSD Medical School Campus, Basic Sciences Building, Garren Auditorium. Please email Dr. Charat (email@example.com).
Today, we discussed a case of TCA overdose in a young man who presented with confusion, dry mouth, and tachycardia. He developed a wide QRS, hypotension, and somnolence that improved with sodium bicarbonate treatment. Remember that TCA toxicity often features profound anticholinergic effects, and the QRS duration predicts prognosis. Don’t forget to check acetaminophen and salicylate levels as these are common co-ingestions!
On Monday Kim Chau and Robert Thomas presented a case of scombroid poisoning. This acute histamine intoxication results from ingestion of poorly refrigerated fish. Neither infectious gastroenteritis nor a food allergy, this is the most common ichythyotoxicosis. Ultimately, the case comes down to the exposure history. When more than one person gets sick at once, look for the food they all ingested.
Today, Dr. Holton-Burke presented a case of a young man who presented with weakness and falls. History revealed a 2-3 week progressive worsening of his symptoms. The VA teams then split up to perform the neuro exam, which showed problems with proprioception, vibration, and hip flexor weakness (think L2 &L3). Quick tips from our expert neurologist, Dr. Kevin Mcgehrin, included keeping commands as short as possible, “miming” to help the patient understand each command, and a review of grading reflexes (0 is no reflex, 1 is muscle twitch, 2 is normal, 3 is when the reflex spreads to another joint, and 4 is clonus). Based on the exam, we reviewed how to localize the lesion. Our patient had the dorsal column (proprioception, vibration) and corticospinal tract (strength) affected, which is a syndrome called Subacute Combined Degeneration. What causes this? B12! But what would cause B12 deficiency in a young man? We discussed the differential, which included pernicious anemia, veganism, chronic
This morning, Dr. Megan O’Brien, Assistant Professor of Medicine at UCSF and the regional director of the California Bridge Project, presenting a highly informative morning report on a (fictional) young man with HIV/AIDS and IV heroin abuse presenting with signs and symptoms of opiate withdrawal. I highly recommend you check out her Powerpoint because there’s an immense number of clinical pearls and resources packed in there. If you’re interested in an executive summary, well, here you go! Opiate use disorder is incredibly prevalent and leads to a lot of morbidity and mortality (particularly w/ IVDU) Morbidity: serious infections (endocarditis, cellulitis, epidural abscess; respiratory depression) Mortality: 285 overdose deaths in San Diego (2017) These patients are HIGH RISK for leaving AMA (largely because we don’t do a great job of treating their condition… and that has disastrous consequences Assess your patient’s withdrawal symptoms with the COWS score (moo) Buprenorphine (or Buprenorphine/Naloxone AKA Suboxone) is a relatively safe and effective treatment that
We had the pleasure of welcoming our toxicology colleagues at our morning report today! Dr. Adrian Lai presented a case of a patient who presented with tremors and confusion in the setting of initiating lithium 3 weeks prior and lisinopril 2 weeks prior to presentation, who was found to have chronic lithium toxicity. Drs. Matthew Riddle and Binh Ly were our expert discussants. Dr. Riddle reviewed the pharmacokinetics of lithium – basically, think of lithium the same way that you think of sodium. Our bodies handle it the same way. It is absorbed quickly in the GI tract, reaching peak levels 1-2 hours after ingestion (4-6 hours if a sustained release formulation is ingested). It is freely filtered by the kidney and reabsorbed in the proximal tubule. Anything that causes volume depletion or renal impairment can cause increased lithium levels – this includes: GI volume losses (vomiting/diarrhea), acute heart failure exacerbations, decompensated cirrhosis, NSAID use, diuretics, or ACEi. The most likely
Today at the VA Dr. Schokrpur presented a case he saw last year. The presentation started with just how he met this patient; as a holdover on wards. The patient initially presented with muffled voice and painful/difficult swallowing. In the ER he had been evaluated by ENT and given his findings on their exam was diagnosed with supraglottitis. He was admitted to medicine for antibiotics and followed by ENT though his airway was “widely patent.” We discussed what we would want in addition to what was listed on the H&P to confirm/refute the diagnosis as we always do with holdovers. On exam that day the patient said he also had some arm weakness and diplopia leading to a full Neuro exam! We thought hard about what could be causing all of these symptoms with the help of Nelly the Nervous system and determined that due to the localization to motor pathways that are diffuse and involve bulbar system we put