I’d love to incorporate my findings and use of lidocaine infusions and ketamine infusions on intraoperative and postoperative pain as a multimodal pain management pathway.
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
Infusion: 2-3mg/kg/hr after induction to end surgery
If cardiac on CPB: bolus 1.5mg/kg on induction; Infusion: 4 mg/min x 48 hrs or discharge from ICU; On CPB bolus 4 mg/kg.
July 2019
I am currently not using lidocaine infusions as my open heart patients are getting great relief with ketamine. I also came across some literature that said lidocaine infusions do not help postoperative cognitive decline. However, I may reassess this at a later time and reinstitute. We do not currently have an acute pain service. Look at the ASRA, May 2017 issue, I do like the dosing regimen used at UVA. See below.
In our institution, an infusion rate of 40 mcg/kg/min after 1–1.5 mg/kg bolus is used perioperatively as part of our ERAS protocols. The infusion rate is decreased to 5–10 mcg/kg/min at the end of the surgery and continues at the same rate until POD 2. Our acute pain management lidocaine infusion protocol uses a 0.5 mg/min starting dose with a maximum of 1 mg/min for adults, and doses between 15 to 25 mcg/kg/min for pediatric patients <40m kg.
I’ve been hearing more and more about PEC 2 block for mastectomy. What’s wonderful about this block is that it seems that the risk of pneumothorax is lower than for a paravertebral block.
U/S guidance: probe position similar to infraclavicular block. Find 3rd, 4th rib.
Pt position: Head away from side of block. Ipsilateral arm abducted.
PEC 2: Inject 20 ml 0.25% bupi between pec minor and serratus.
PEC 1: Inject 10 ml 0.25% bupi between pec major and pec minor.
Serratus: 5th rib, mid-axillary line. Inject 30 ml 0.125% bupi along top (superficial) and bottom (deep) of serratus muscle (which is just deep to the latissmus dorsi).
Today, we had a guest speaker Christian Spies from Queen’s Hospital in Hawaii who spoke on his experience with his TAVR team and conscious sedation vs. general anesthesia for these patients. More specifically, we are speaking of the transfemoral route.
Keypoints:
Patient selection is key (consider for COPD; bad for OSA)
Short surgical time for monitored anesthesia care (MAC)
Decrease invasive monitoring (no PA catheter,+/-CVP)
No difference in hospital LOS or 1 year mortality rate
Move from TEE to TTE if MAC
Be prepared to convert MAC to GA (can be difficult in already tenuous patient in a crowded space under the drapes)
MAC agents: dexmetetomidine, propofol, ofirimev
Decrease pressor use
Develop an algorithm for MAC vs. GA and patient selection
We at Scripps Memorial Hospital in La Jolla do most of our transfemoral TAVRs via conscious sedation assuming appropriate patient selection. These patients still tend to be the inoperable patients not cleared for open heart AVR (aortic valve replacement). My techniques and choices for setup have changed over time as I’ve had a chance to fine-tune my plan based on prior experiences with TAVR. Patients typically come to the hybrid room with a 20g PIV placed by the pre-op RN.
My Setup:
4 channel Alaris pump:
dexmedetomidine @ 0.7 mcg/kg/hr until incision –> 0.4 mcg/kg/hr until valve deployment –> off
norepinephrine @ 2 mcg/min (titrating on/off, up/down as vitals suggest)
Initially, I would have the interventional cardiologist setup a femoral venous line since they’re getting access to the groin. However, the cardiologist would use that femoral line for emergent ECMO cannulation and I would lose my venous access and have to depend on a measly 20g PIV. Nowadays, I try for a short 14g or 16g PIV. If I can’t get one, the patient gets an awake right IJ cordis for large venous access.
Hot line fluid warmer with blood-Y tubing: this is for hookup to a large PIV or cordis line
Right radial arterial line
I started only placing right radial arterial lines because there was a case of a dissection and I immediately lost my left radial arterial line and couldn’t do pressure monitoring. I insist on only using the RIGHT radial for my arterial monitoring. Do not let the cardiologist only give you arterial monitoring based on their femoral arterial access. It will only give you intermittent monitoring and there are critical points leading up to the deployment where you need CONTINUOUS arterial monitoring. Therefore, I’ve found the right RADIAL arterial line best for continuous monitoring.
Facemask for continuous oxygen at 10L/mim with ETCO2 monitoring
For trans-subclavian/axillary approach vs. transfemoral approach TAVR, I’ll put in a supraclavicular block right after Cordis/large-bore PIV venous access for patient comfort while still utilizing conscious sedation/MAC.
My Technique:
When the patient gets to the room, transfer patient to OR table. Start IV fluids @ 200ml/hr. Cases that go well are about 2 hours from start to end.
Facemask O2 at 10L/min.
Start sedation: precedex/dexmedetomidine @ 0.7 mcg/kg/hr. Some patients may receive 1-2mg midazolam x 1 and 25-50mcg fentanyl for radial art line placement.
Place right radial art line with lidocaine for skin numbing. Place PIV with lidocaine. If unable to get access for PIV, prep neck –> sterile gown/glove/drapes for U/S guided Cordis placement with lidocaine.
OR staff preps patient. Antibiotics prior to incision.
At incision –> precedex to 0.4 mcg/kg/hr. 25-50mcg fentanyl PRN discomfort. 10-20mg propofol push for discomfort if needed while large sheath placed for valve deployment.
Crossing valve –> BP changes. Manage with volume or levophed.
Valvuloplasty
Don’t treat over-drive pacing too aggressively when the valve is deployed. Typically, once the new valve is in, a little volume will help normalize the BP.
Once valve is deployed, turn precedex off. No other sedation or BP meds needed. Change IVF rate to 50ml/hr.
Patient heads to PACU awake, interactive, and comfortable.
What techniques do you like to do? Any suggestions on a different approach?
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