1/8 Recently, I was called to bedside to evaluate new tachycardia + hypertension (SBP >180) + AMS in a patient with MS. We were initially concerned for hypertensive encephalopathy, except he had no prior hx htn and BPs on previous admissions were always normal.

2/8 We didn’t have an immediate framework for acute tachy + HTN but we went back to physiology when approaching this combination of vital sign change: 𝘀𝘆𝗺𝗽𝗮𝘁𝗵𝗲𝘁𝗶𝗰 𝗵𝘆𝗽𝗲𝗿𝗮𝗰𝘁𝗶𝘃𝗮𝘁𝗶𝗼𝗻. When do you see this?

3/8𝗣𝗮𝗶𝗻: most common cause in the hospital.
𝗗𝗿𝘂𝗴 𝘁𝗼𝘅𝗶𝗰𝗶𝘁𝘆: meth,cocaine, caffeine,stimulants, serotonin syndrome, anticholinergics
𝗗𝗿𝘂𝗴 𝘄𝗶𝘁𝗵𝗱𝗿𝗮𝘄𝗮𝗹: ETOH,benzos, opiates
𝗘𝗻𝗱𝗼𝗰𝗿𝗶𝗻𝗼𝗽𝗮𝘁𝗵𝗶𝗲𝘀: Pheo, thyrotoxicosis, hypercortisolism

4/8 Our patient wasn’t in pain, and had negative tox screen. He was behaving exactly like he had delirium tremens, but was neither on benzos nor ETOH. What can mimic this?

6/8 Barbituate withdrawal! Barbituates have largely been replaced by benzodiazepines in modern medical practice, but mechanistically, have similar GABAergic effects. Withdrawal from barbituates looks very similar to DTs!

7/8 This patient had his longstanding barbiturate held on admission. Within 36 hours, he went into withdrawal which can happen when barbituates are stopped abruptly. After resuming his barbituate, his vital signs and mentation normalized.

8/8 Takeaways:
1. When you don’t have a set approach, go back to the physiology! @DxRxEdu
2. Barbituate withdrawal can happen within 48 hours of abrupt cessation and look just like DTs.
3. Work w/ your pharmacist to ensure safe med tapers and reconciliation. #MedTwitter #MedEd