key: cord-0823465-83lzx6fs
authors: Lucchetta, Vittorio; Bonvicini, Daniele; Ballin, Andrea; Tiberio, Ivo
title: Propofol infusion syndrome in severe COVID-19
date: 2020-08-24
journal: Br J Anaesth
DOI: 10.1016/j.bja.2020.08.020
sha: 876808e3afc29edea4bfb15b7908dd34361efad1
doc_id: 823465
cord_uid: 83lzx6fs

nan

compliance for mechanical ventilation and satisfactory mean arterial pressure. On day two, clonic seizures were noticed on the patient's face, with progressive involvement of the right upper arm, which improved with boluses of midazolam i.v. Computed tomography showed no acute cerebral lesions, a cerebrospinal fluid examination gave no meaningful results and SARS-CoV-2 RT-PCR testing of cerebrospinal fluid was negative.

Multiple EEG recordings showed a general slowing with theta-delta dominance, disrupted by generalized slow-wave activity, that, together with the clinical persistence of clonus, led to inducing burst suppression through high-dose propofol infusion. The coexisting pulmonary compromise required deepening of sedation in order to resolve initial patient-ventilator desynchronisation, reaching on day 3 an infusion dose of propofol of 7.5 mg kg -1 h -1 and 0.2 mg kg - During the following days, ECG alterations, arterial pH and serum lactate levels rapidly corrected.

Serum CPK levels peaked ad 33000 U L -1 and myoglobin at 14000 µg L -1 , while aspartate and alanine amino-transferases reached 1059 and 197 U L -1 , respectively. A timeline of pharmacological and laboratory data is shown in table 1. The neurological status was monitored through a second cerebral scan and multiple EEG samplings. A slow tapering of sedation revealed no major neurological sequelae, cardiovascular support was suspended on the 7 th day and the patient was extubated on the 12 th day; continuous renal replacement therapy was continued until the Discharge to a sub-intensive care unit was organized after 22 days from referral.

The main risk factors 2 for PIS in this case were the high-dose propofol infusion maintained longer than 24 h and the need for vasopressor and inotropic therapy; the admission APACHE II Score was low, though, and the patient was not receiving corticosteroid treatment. As stressed by the recent review by Hemphill and colleagues 2 , the foremost therapeutic decision was the immediate change of sedation strategy from propofol to a combination of midazolam and dexmedetomidine; coexistence of acute kidney injury with rhabdomyolysis and severe alteration of serum ion concentrations induced us to initiate continuous renal replacement therapy, which helped with both clearing residual propofol concentration and restoring electrolyte homeostasis. Some authors 3, 4 suggest a dextrose infusion as part of PIS therapy, which was already part of our patient's parenteral nutrition strategy.

There is currently limited data on neurological involvement in COVID-19, and we cannot link with certainty the epileptic manifestations in our patient with the viral syndrome 5,6 . Such manifestations, which normally lead us to deepen the level of sedation, can coexist with an acute respiratory distress syndrome, that again often demands deep sedation and relaxation in order to optimise ventilation and reduce the risk of ventilator-induced lung injuries. In the context of COVID-19, the possibility of propofol-infusion syndrome should be considered, reinforcing the suggestion of Lönnqvist and colleagues to rethink our sedation strategies in COVID-19 patients.

The authors declare no conflicts of interest. 

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