Despite a paucity of data, the role of intravenous lidocaine (IVLI) as adjunctive analgesia in the intensive care unit (ICU) seems promising due to a low potential to contribute to respiratory depression. A retrospective chart review was conducted to evaluate the safety and effectiveness of IVLI for the treatment of pain in ICU patient with varying degrees of organ dysfunction from March 2014 to March 2016. The primary outcomes included the time to a ≥ 20 % reduction in pain scores after the initiation of IVLI and the difference in opioid requirements as well as pain scores prior to and during IVLI therapy. Other variables included the presence of IVLI-related adverse events and the dosage and duration of IVLI. A total of 21 ICU patients were included from two different hospitals. The mean time to a ≥ 20 % reduction in pain scores from the start of IVLI was 3.3 hours (SD = 2.2). The median morphine dose equivalents required during 6, 12, and 24 hours pre-IVLI were significantly higher compared to the same time periods after IVLI (18.3 vs. 10 mg, p=0.002; 41.8 vs. 18.3 mg, p=0.002; 93.5 vs. 30.5 mg, p=0.037). Neurological adverse effects of lidocaine were noted in 3 patients, but the effects were reversed upon IVLI discontinuation. This report suggested that IVLI as an adjunctive agent in the treatment of acute pain may be a potential option in ICU patients who are refractory to opioids or those in whom opioid-induced respiratory depression is a concern.

Rhabdomyolysis is characterised by muscle breakdown with release of damaging proteins that can have devastating consequences. Acute influenza infection is being increasingly recognised as an underlying aetiology. We report an unusual case of severe rhabdomyolysis with acute renal failure due to influenza A infection that improved with high-dose oseltamivir and intravenous fluids. In our case, we also noticed a temporal relation between fever spikes and subsequent increase in serum creatine kinase. The precise mechanism between the rise in temperature and creatine kinase is unclear but it could be due to direct viral invasion of myocytes or due to release of new viral progeny following replication in the myocyte.

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