I’m always looking for ways to improve myself. Lately, I’m looking at various clinical elements of my practice and select certain endpoints that will better my practice of medicine.
This time, I’ve focused on cutting back on opioids intraoperatively for pain. I’m looking specifically at ketamine, an old drug with multiple benefits (and some downsides). Not only does ketamine help with intraoperative pain, but it also helps with postoperative pain. I’d like to incorporate some type of ERAS model for all of my patients and surgeries.
Ketamine: (different doses I’ve seen in the literature below)
• Induction: 0.2-0.5 mg/kg
• Infusion: 0.1mg/kg/hr before incision
◦ 2mcg/kg/hr x 24hr (spine)
◦ 0.1-0.15mg/kg/hr x 24-72hrs (UW)
◦ 2mcg/kg/min
◦ 2-8mcg/kg/min
What I’m using nowadays:
Oct 2017:
Cardiac open hearts: induction bolus=0.5mg/kg + infusion=0.1mg/kg/hr and stopping when last stitch placed. Patients seem to require less postoperative narcotics. Looking at time to extubation to see if this is improved. Time to extubation seems the same as my prior non-ketamine patients because RT and RNs follow a weaning protocol. Patients are more comfortable and require less pain medication.
Dec 2018:
Cardiac open hearts: induction bolus = 0.5 mg/kg + another 0.5 mg/kg bolus when re-warming; infusion 0.2 mg/kg/hr stopping when last dressing placed.
July 2019:
Cardiac open hearts: induction bolus = 1 mg/kg + 0.5mg/kg bolus pre-CPB. No infusion. This formula is roughly in between the bolus (0.5mg/kg) + infusion (0.1mg/kg/hr and 0.2mg/kg/hr) for <5hr case. For hearts >5hr, add 0.25-0.5mg/kg bolus when re-warming (0.5mg/kg dosing roughly approximates a 7hr case).
Sept 2019:
Cardiac open hearts: No induction bolus. 1mg/kg bolus prior to incision. 0.5mg/kg bolus pre-CPB. 0.25-0.5mg/kg bolus rewarming on CPB based on length of case (see July 2019 notes).
Question 1: Which patients and acute pain conditions should be considered for ketamine treatment? Conclusion: For patients undergoing painful surgery, subanesthetic ketamine infusions should be considered. Ketamine also may be warranted for opioid-dependent or opioid-tolerant patients undergoing surgery, or with acute or chronic sickle cell pain. For patients with sleep apnea, ketamine may be appropriate as an adjunct to limit opioid use.
Question 2: What dose range is considered subanesthetic, and does the evidence support dosing in this range for acute pain? Conclusion: Ketamine bolus doses should not exceed 0.35 mg/kg, whereas infusions for acute pain generally should not exceed 1 mg/kg per hour in settings lacking intensive monitoring. However, dosing outside this range may be indicated because of an individual patient’s pharmacokinetic and pharmacodynamic factors and other considerations, such as prior ketamine exposure. However, ketamine’s adverse effects prevent some patients from tolerating higher doses for acute pain; therefore, unlike for chronic pain management, lower doses in the range of 0.1 to 0.5 mg/kg per hour may be necessary to achieve an acceptable balance between analgesia and adverse events.
Question 3: What is the evidence to support ketamine infusions as an adjunct to opioids and other analgesic therapies for perioperative analgesia? Conclusion: There is moderate evidence to support using subanesthetic IV ketamine bolus doses up to 0.35 mg/kg and infusions up to 1 mg/kg per hour as adjuncts to opioids for perioperative analgesia.
Question 4: What are the contraindications to ketamine infusions in the setting of acute pain management, and do they differ from chronic pain settings? Conclusion: Patients with poorly controlled cardiovascular disease or who are pregnant or have active psychosis should avoid ketamine. Similarly, for hepatic dysfunction, patients with severe disease, such as cirrhosis, should not take the medicine; however, ketamine can be given with caution for moderate disease by monitoring liver function tests before infusion and during infusions in surveillance of elevations. On the other hand, ketamine should not be given to patients with elevated intracranial pressure or elevated intraocular pressure.
Question 5: What is the evidence to support nonparenteral ketamine for acute pain management? Conclusion: Intranasal ketamine is beneficial for acute pain management by achieving effective analgesia and amnesia/procedural sedation. Patients for whom IV access is difficult and in children undergoing procedures are likely candidates. But for oral ketamine, the evidence is less convincing, although anecdotal reports suggest this route may provide short-term advantages in some patients with acute pain.
Question 6: Does any evidence support IV ketamine patient-controlled analgesia (PCA) for acute pain? Conclusion: The evidence is limited to support IV ketamine PCA as the sole analgesic for acute or periprocedural pain. There is moderate evidence, however, to support the addition of ketamine to an opioid-based IV PCA regimen for acute and perioperative pain therapy.
The guidelines were jointly developed by the American Society of Regional Anesthesia and Pain Medicine (ASRA), the American Academy of Pain Medicine and the American Society of Anesthesiologists.
Ketamine is an N-methyl-d-aspartate receptor antagonist that is commonly used as an adjunct for the treatment of acute postoperative or posttraumatic pain to improve pain scores and reduce opioid consumption by approximately 30-50%.[46] Certain patients seem to benefit more from the addition of ketamine, including those with chronic neuropathic pain, opioid dependence or tolerance and acute hyperalgesia.[47] 8% of administered ketamine is metabolized by the liver forming norketamine, which possess only 20-30% of the potency of ketamine. Norketamine is then hydroxylated into a water-soluble metabolite excreted by the kidney.[48] Most clinicians believe that dose modification for ketamine is not required for patients with decreased renal function.[48,49
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