To place the PV catheter at the T4-5 level, the authors used an in-plane transverse technique under ultrasound guidance, with the probe in a transverse orientation. After identifying the anatomic landmarks on ultrasound, a 17-gauge Tuohy needle was advanced in a lateral to medial direction, until the tip was beneath the transverse process. For all recipients in the study, the authors further confirmed correct PV catheter placement with real-time infusion of a local anesthetic (1-3 mL of 1.5% lidocaine with epinephrine 1:200,000); they were able to visualize on ultrasound the spread from the tip of the catheter.
Once it was confirmed that the tip remained in position, the PV catheter was secured with skin glue (Dermabond®, Ethicon, Inc.; Somerville, NJ). Next, at the PV catheter insertion site, the authors placed an occlusive dressing on a chlorhexidine-impregnated sponge (BioPatch®, Johnson & Johnson Wound Management, a division of Ethicon, Inc.; Somerville, NJ). The PV catheter was connected to an elastomeric pump (ON-Q®, Halyard Health, Alpharetta, GA), an infusion of 0.2% ropivacaine was started at a rate of 0.2 to 0.25 mL/kg/h; the maximum dose was 7 mL/h per side in bilateral lung transplant recipients and 14 mL/h in unilateral single-lung transplant recipients.
Under sterile conditions and while patients still were in the lateral position with the diseased side up, a linear ultrasound transducer (10-12 MHz) was placed in a sagittal plane over the midclavicular region of the thoracic cage. Then the ribs were counted down until the fifth rib was identified in the midaxillary line (Fig 1).18 The following muscles were identified overlying the fifth rib: the latissimus dorsi (superficial and posterior), teres major (superior), and serratus muscles (deep and inferior). The needle (a 22-gauge, 50-mm Touhy needle) was introduced in plane with respect to the ultrasound probe, targeting the plane superficial to the serratus anterior muscle (Fig 2). Under continuous ultrasound guidance, 30 mL of 0.25% levobupivacaine was injected, and then a catheter was threaded. A continuous infusion of 5 mL/hour of 0.125% levobupivacaine then was started through the catheter.
For my single shot blocks, I’m always looking for ways to prolong my regional anesthetic effect. For awhile, Exparel was the most talked about drug to have a 72 hour blockade. We don’t have this medication available to us at the hospital. Therefore, it’s time to get creative and hit the literature to see what has worked for prolonging our blocks.
Sensory block duration was prolonged by 150 min [95% confidence interval (CI): 96, 205, P,0.00001] with intrathecal dexmedetomidine. Perineural dexmedetomidine used in brachial plexus (BP) block may prolong the mean duration of sensory block by 284 min (95% CI: 1, 566, P¼0.05), but this difference did not reach statistical significance. Motor block duration and time to first analgesic request were prolonged for both intrathecal and BP block. Dexmedetomidine produced reversible bradycardia in 7% of BP block patients, but no effect on the incidence of hypotension. No patients experienced respiratory depression.
Considerable differences existed in the doses of perineural dexmedetomidine; doses varied between 3, 5, 10, or 15 mcg for the intrathecal route, and 30, 100, 0.75, 1 mcg/kg for the peripheral route.
Intravenous DEX at a dose of 2.0 μg/kg significantly increased the duration of ISBPB analgesia without prolonging motor blockade and reduced the cumulative opioid consumption at the first 24 hours in patients undergoing arthroscopic shoulder surgery.
Below knee surgery under combined femoral-sciatic nerve block were randomly allocated into two groups to have their block performed using bupivacaine 0.5% alone (group B) or bupivacaine 0.5% combined with 100 μg bupivacaine-dexmedetomidine
Randomized to receive ISB using 15 ml ropivacaine, 0.5%, with 0.5 μg/kg dexmedetomidine administered perineurally (DexP group), intravenously (DexIV group), or none (control group). DexIV was noninferior to DexP for these outcomes. Both dexmedetomidine routes reduced the pain and opioid consumption up to 8 h postoperatively and did not prolong the duration of motor blockade.
I have been utilizing ERAS in general surgery, OB, and ortho cases. Diving into one of my more tricky populations, I opted to see what ERAS practices are out there for cardiac surgery. Careful what you look for my friends. There’s actually a good amount of information out there!
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)
What I’m using nowadays:
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.
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.
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).
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.
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%. Certain patients seem to benefit more from the addition of ketamine, including those with chronic neuropathic pain, opioid dependence or tolerance and acute hyperalgesia. 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. 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.
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.