Dexmedetomidine/ketamine/lidocaine

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Various toxicities: case report A 28-year-old woman developed diplopia, dissociative feelings, nightmares and confusion during treatment with ketamine; she also developed anxiety and delirium during treatment with lidocaine, and low systolic BP during treatment with dexmedetomidine for cancer pain [durations of treatments to reactions onsets not stated; not all dosages stated]. The woman was admitted to hospice care after no treatment option left for triple negative left breast cancer. She had received chemotherapy followed by bilateral mastectomy, axillary lymph node dissection and radiotherapy to her left chest wall. She had also developed lymphoedema and metastases to the bone, left ribs and lung. Upon admission, her main complaint was severe throbbing, burning pain to her left chest wall (rating range of 8/10), which was radiating to the axilla and left upper extremity. She had been receiving a morphine patient-controlled analgesia (PCA) basal–bolus infusion, methadone, ketorolac on as needed basis and dexamethasone, without acceptable pain control. In the past she had failed topical lidocaine as well. She did not tolerate gabapentin due to unspecified side effects. Adjunctive therapy with antidepressants had also failed. Over the following 4 months, several interventions were tried to achieve acceptable pain control with multiple readmissions. The interventions included maximising methadone and dexamethasone doses, increase in PCA morphine settings, opioid rotation to a hydromorphone basal–bolus PCA, trials of ketamine infusions, and both rapid and continuous lidocaine infusions. However, all these interventions failed to achieve acceptable pain control owing to both intolerable side effects and ineffectiveness. She developed dissociative feelings, diplopia, confusion and nightmares, which were attributed to ketamine, and anxiety and delirium, which were attributed to lidocaine. Her lack of response to multiple pain control treatments was considered as a result of aggressive disease progression. Thereafter, the woman started receiving a trial of 48-hour infusion of dexmedetomidine. The initial dose of IV dexmedetomidine was 0.2 µg/kg/hour through subcutaneous port. At a dose of 0.2 µg/kg/hour, her pain score decreased to 0/10. The doses of methadone and hydromorphone were reduced without increase in the pain. The pain increased with activity but to a lower score of up to 6/10. On the following day, the dose of dexmedetomidine by 0.1 µg/kg/hour. Further increase was not possible due to drop of systolic BP to a low of 88mm Hg; however, she remained asymptomatic. During the infusion, she was fully alert, experienced no confusion or delirium, and did not require palliative sedation [not all outcomes stated]. Unfortunately, the improved pain control lasted only for

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