Propofol Induced Procedural Excitation Rather Than Sedation in an Adolescent Patient

Introduction: Propofol is a common induction agent used for pediatric patients with myriad of pathology requiring procedural sedation. It is a sedative with quick onset of sleep, usually with 3-4 (1 mg/kg) boluses, with beneficial anti-convulsant and anti-emetic properties.

Case Description: 14-year-old healthy male was admitted for 1 week of worsening headache, diarrhea, myalgias, fever, seizure, back pain, unbalanced gait, body jerking, and patellar hyporeflexia. With the presentation concerning for Guillain Barre, transverse myelitis, acute demyelinating encephalomyelitis (ADEM), autoimmune encephalitis, and acute inflammatory demyelinating polyradiculoneuropathy (ADIP), immediate imaging and lumbar puncture was needed prior to either starting steroids or intravenous immunoglobulin (IVIG).

Vitals were in normal range. The patient was alert, awake, oriented and in no acute distress. Soft palate and base of uvula was visible (Mallampati III), neck was supple. Neurologic exam was positive for asymmetrical patellar reflexes 1+ on left and 2+ on right. Normal ankle reflex. Downward Babinski. Intermittent tremors noted. Normal speech, gait, strength, and sensation.

Patient required 8 mg of intranasal versed for MRI Brain and Spine. Deep procedural sedation for a lumbar puncture was started with 50 mcg of Fentanyl, 10 mg of lidocaine and 50 mg of propofol. Patient started with intermittent myoclonic jerks. There was a transient hypoxia of 89%, responsive to 2 liters of oxygen. The jerking movement started to worsen, peaking at 300 mg (6 mg/kg) of propofol infused in an attempt to sedate. The myoclonic jerks evolved into severe dyskinesia of upper extremity. No vital changes or apneas were noticed. The procedure was stopped. Ativan (4 mg) was given and successfully aborted the seizure-like activity. Keppra was started. Patient was stable in the post procedure course.

Discussion: Propofol is a GABA-mediated inhibitor of neuronal excitation, making the patient’s erratic body movement less likely to be a seizure. Adding 4 mg of Ativan to the 6 boluses of propofol was concerning for inducing apnea and subsequent respiratory failure. In the moment, administration of Ativan appeared to be a reasonable option to stop the mysterious movements.

In rare cases, myoclonic jerks can occur with propofol, although the neuroexcitation pathophysiology is poorly understood and even more so in demyelinating disease. Some mechanisms include dose-related effects, drug-induced decerebrate rigidity, and blockage of NMDA receptor in anti-NMDA encephalitis potentiating underlying dyskinesias.

Conclusion: Patient’s diagnosis was propofol induced myoclonus, a rare side effect with cases only reported in adults. Propofol induced myoclonus’s association in demyelinating disease is less understood and warrants further research to better understand the underlying mechanism for anticipating sedation complications and clinical management.