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The patient is a 58 y/o male who was driving in a stolen pickup when the police pulled him over.  Police noted that he had a bag of an unknown substance sitting on the seat next to him and he was quickly eating from a bag as they walked to the truck.  He was arrested and placed in the police car.  For the first 10 or 15 minutes with the police he appeared mildly agitated and was talking.  He then very quickly decompensated and became unresponsive, with multiple quick generalized tonic-clonic movements and “twitchiness” that he showed on arrival to the emergency department.  In my experience this appeared unlikely to represent true seizures, but made it very difficult to get vital signs, or appropriately evaluate him.  Staff was initially reluctant to obtain vital signs, worrying about possible personal injury.  He was foaming from the mouth, unresponsive, mouth clamped down and with a mediocre waveform appeared to have room air oxygen saturations about 90%. Past medical history: Unknown.  There is no history on file in epic. Allergies: Unknown Medications: Unknown Social and family history: Unknown   Physical examination: General: Obvious distress, mouth clamped down and moving moderate to poor air although with adequate respiratory rate, very agitated and unresponsive to painful and verbal stimuli Head: Atraumatic, normocephalic Eyes: Extraocular muscles appear to be intact with a difficult exam, pupils fully dilated bilaterally. ENT: No obvious nasal congestion.  Difficult exam initially. Neck:  Supple Lungs: Clear bilaterally with shallow breaths, noisy breath sounds from oral secretions Heart: Tachycardic and irregularly irregular Abdomen: Soft without obvious tenderness Extremities: No obvious trauma Neurologic: Awake and extremely agitated, unable to respond to verbal or painful stimuli.  Diffuse tonic-clonic movements and twitching that seemed unlikely represent true seizure, though of course status epilepticus remained possible.  He was…

Teaching Case: An Escalating Agitation Syndrome with Misleading Clues An 82-year-old woman with a history of chronic pain due to metastatic diffuse large B-cell lymphoma s/p radical neck and mouth dissection and G-tube placement presented to the ED with severe oral pain, nausea, worsening anxiety, and a profound sensation of “feeling toxic.” She lived alone and managed her medications independently. She reported taking multiple doses of hydrocodone/acetaminophen and diazepam over the preceding 24 hours. She was also maintained on a PRN Valium, hydrocodone and 125 mcg/hr fentanyl patch Q3 days, but instead of applying a new patch that morning, she had removed the old patch and moved it to a new location—a practice she used because she believed relocation to a location with more body fat was equivalent to replacement. She was a very low-body-weight patient, approximately 82 lbs, which heightened her sensitivity to rapid changes in opioid exposure. On arrival, her blood pressure was 179/67, with otherwise stable vitals. She remained alert and oriented but was increasingly restless and unable to remain still. Her laboratory studies—including CBC, CMP, magnesium, phosphorus, EKG CK, troponin, and TSH—were all within normal limits, and urinalysis was unremarkable. Her urine drug screen was negative for opiates and benzodiazepines, despite her reported intake of Valium and Hydrocodone. This tox panel did not test for fentanyl. Based on her symptoms and the interpretation that she may not have adequately taken her home medications, the initial working diagnosis was acute anxiety with poorly controlled pain. At 01:26 she received lorazepam 1 mg IV and morphine 2 mg IV. Shortly thereafter, she experienced a marked and abrupt deterioration: she became intensely agitated, thrashing in bed, gripping the rails, unable to sit still, and repeatedly describing the sensation of “jumping out of my skin.” Because this escalation occurred immediately…

Catatonia A 60 year old female with history of bipolar disorder with aggressive behavior, hypertension, and chronic kidney disease, was brought in by ambulance after her husband found her unresponsive on the floor. He reports that she was diagnosed with COVID two weeks ago. She had not had anything to eat or drink for two days. Her vital signs were: T 98.9, P 72, R 16, BP 148/88, SpO2 96% on RA. She was responsive to pain in the ED and would occasionally follow commands but was never alert or able to answer questions. WBC 18.7, Na 177, glu 145, BUN 135, crt 3.71, venous pH 7.36, lactic 1.8. CT head showed no acute findings. There were no beds available at larger facilities for transfer. She was started on D10 ¼ NS @ 160ml/hr. Her mental status waxed and waned but never returned to baseline. The following day she was finally transferred to Sacred Heart, where she remains weeks later. Her sodium and renal function were corrected. She was diagnosed with psychosis with catatonia and is now on a court-ordered hold for ECT on the psych service. Discussion: Catatonia is a behavioral syndrome marked by inability to move normally due to underlying psych or general medical disorder. The signs are heterogeneous but can include immobility, mutism, decreased alertness and responsiveness, negativism (resistance to attempts to move or to instructions), waxy flexibility, posturing, excessive purposeless motor activity, staring, robotic voice, and echolalia (senseless repetition of other person’s utterances) or echopraxia (senseless repetition of other person’s movements). These patients have frequent dehydration/malnutrition, DVT/Pes, contractures, pressure ulcers, and excitement/impulsivity, which all need to be managed. Antipsychotics and dopamine blocking agents should be avoided, as they can cause neuroleptic malignant syndrome. Treatment with benzodiazepines is the mainstay, usually lorazepam 1-2mg IV TID. If there…

Ketamine-induced Laryngospasm A 60 yo male presented for an angulated colles fracture. He was given IV dilaudid on arrival. A hematoma block was attempted, but the needle would not advance into the fracture site. Therefore, I decided to give a sub-anesthetic dose of ketamine to reduce pain during reduction. As soon as the ketamine was in, the patient’s upper body became stiff. He had a blank stare on his face and his chest stopped moving; I immediately reduced the fracture thinking the pain would initiate breathing. It did not. I let go of his arm and assisted the RN in bagging the patient. I made sure there was an excellent seal with the mask, and that the upper airway was open by performing head tilt, jaw thrust, and placing an oral airway. The pt could not be bagged; the epigastric area moved but the chest did not move with bagging. I realized that laryngospasm was preventing ventilation. O2 saturation dropped to the 77%. I ordered Ativan and the glidescope to the bedside. Then the larynx suddenly opened long enough to deliver two breaths to the lungs and the SaO2 improved. The larynx closed again for 30 seconds before reopening for a few seconds. This occurred a few times before the larynx opened and stayed open, at which time the patient breathed spontaneously and I augmented his breathing with the bag for a minute. The terrifying whole episode lasted about 6 minutes. I then placed a splint and the patient regained consciousness with complete recovery. For a few minutes, I felt like I could not continue working after the stress of this event. I went from being terrified to apprehensively hopeful that he would not be injured, to overwhelmingly grateful he was ok, all in the span of 10 minutes. I…