PICC vs central line: not that clear cut

From Patient Safety Solutions: http://www.patientsafetysolutions.com/docs/January_21_2014_The_PICC_Myth.htm

PICC lines (peripherally inserted central catheter)  are often seen as a lower risk alternative to central lines for patients with difficulty iv access, however this is a myth and piccs are not without risk including:

• Higher risk of upper extremity dvt (2.55 or and account for 35% of all ue dvt)
• Similar risk of infection!  Meta analysis and systematic reviews show no sig diff in clabsi! 
• Other complications include thrombophlebitis,and dysfx and malpositioning greater for PICC than central line 

These concerns prompted the ABIM choosing wisely campaign to include piccs on their list of treatments to question:

Don’t place, or leave in place, peripherally inserted central catheters for patient or provider convenience.

Peripherally inserted central catheters (or “PICCs”) are commonly used devices in contemporary medical practice that are associated with two costly and potentially lethal health care-acquired complications: central-line associated bloodstream infection (CLABSI) and venous thromboembolism (VTE). Given the clinical and economic consequences of these complications, placement of PICCs should be limited to acceptable indications (long-term intravenous antibiotics, total parenteral nutrition, chemotherapy and frequent blood draws). PICCs should be promptly removed when acceptable indications for their use ends.

So next time someone recommends a PICC over a central line, think about the indications and necessity! 

Technique: The Dominic Awake Fiberoptic

The Awake Fiberoptic Intubation – The DN Technique

Pre-Op

1. Educate patient what to expect and what they should do
2. This education gives you understanding of any language and/or comprehension barriers
3. D/W surgery team reason for awake fiberoptic (difficult airway, neuro, etc)

Intra-Op

1. Glycopyrrolate 0.2mg when patient enter room – essential to dry secretions and absorb topical local
2. 50 fentanyl prn for corporation up to 200mcg, slowly after patient demonstrates understanding
3. 4-5cc Xylocaine (2%) jelly swish and swallow (numbs oropharynx)
4. 5% Xylocaine spray (in atomizer), hold nose and have patient take deep breaths, on each inspiration spray oropharynx… confirm that “Xylocaine mist” is inhaled…. continue until mist comes out mouth at the end 0f inhalation.  Repeat for 3 breaths, then pause.
   1. note: if mist comes out too soon patient is breath holding -> reeducate
   2. repeat this process 5x
   3. Tip: put nasal airway in mouth and spray thru while inhaling
5. Optional Transtracheal Block:
   1. find cricothyroid membrane and topicalize with local
   2. fill a 5cc syringe with 5% xyolocaine, load onto a 20g needle with catheter
   3. insert needle into cricothyroid membrane aspirating continuously until you get air bubbles
   4. if blood, back off and reinsert, same goes for if you hit cartilage
   5. once air aspirated (bubbles), pull out needle (leaving catheter) and then inject 5cc
   6. Patient is expected to cough and this helps spread local (note if patient does not react strongly to this, and you had previously performed atomize technique per above, then likely adequate block!)
6. At this point, patient is adequately anesthetized and one can proceed with the awake fiberoptic, through use of a mouthpiece of choice.

A few further notes:

• If reason for awake fiberoptic is neurologic in nature (myelopathy), perform neuro exam with team before and after intubation
• Versed can interfere with patient cooperation
• Watch for local toxicity, if patient begins shaking, consider versed +/- propofol
• watch for hematomas in transtracheal blocks
• Consider having screen positioned for patient to watch intubation, can reduce trauma of experience.

Thoughts on awake fiberoptics? how do you do it?

 

Carcinoid Triad

Another kind of Triad: The Three Body Problem

Carcinoid Tumors and Anesthesia: Notes from TrueLearn

Carcinoid Tumors: Slow growing, benign, small intestine tumors that can metastasize

Hormonal secreting tumors -> cause cutaneous flushing of head neck and thorax, bronchoconstriction, hypotenion, diarrhea, heart disease

Carcinoid Crisis: triggered by physical/chemical such as histamin release, serotonin, bradykinin

Other triggers include: chemo, tumor necrosis, or succinycholine induced fasciculations!

Anesthestic management: avoid histamine release (succ, atracurium, thiopental, morphine, vancomycin); Desflurane good for patients with liver metastasis as low hepatic metabolism (0.02%); Also the use of NE, epi, Dopamine and isoproternol a/w carcinoid crisis

Carcinoid Heart Disease seen in 60% of patients with carcinoid ->right side:  tricuspid and pulmonic valves (plaque like deposits on valves) with TR as most common finding; 50% of carcinoid deaths are from cardiac involvement

So Carcinoid Triad = flushing, diarrhea and cardiac involvement

Management I/O And Peri-Op:

Carcinoid tumors secrete variety of substances (serotonin, catecholamines, histamine)

Somatostatin therapy is standard of care

Be prepared for rapid BP changes
-alpha/beta blockers for HTN
-Vaso for hypotension, or neo

Avoid: Beta agonists -> increased release of from carinoid !

https://www.openanesthesia.org/carcinoid_crisis_treatment/

 

 

Levo vs. Neo: A Change of the Guards?

Vancomycin IV infiltration, yet we still give through PIV

From A&A May 2016: Should Norepinephrine, Rather than Phenylephrine, Be Considered the Primary Vasopressor in Anesthetic Practice?

http://www.ncbi.nlm.nih.gov/pubmed/27101504

GA = Sympathectomy, decreased NE and Epi concentrations

Phenylephrine (PE, trade name Neosynephrine aka Neo)
pure alpha 1 agonist
increase ABP, decrease HR
CO effect mixed +/- venous return, decreased HR

Norepinephrine (NE, trade name Levophed aka Levo)
alpha1 and beta1, some beta2
relaxation of venous resistance
NE enhances venous return +CO
+ionotropy, little chronotropy
+arterial vasoconstrict
+HR, +SV, +CO

Potency of NE:PE 20:1

NE levels increased in cardiac failure

PeriOp circulating Catecholamine levels

NE and Epi decreased by
-diazepam
-thiopental (even more in uremic)
-midazolam
-pancuronium
-spine surgery + prop or iso

NE and Epi increased by
-Ketamine
-1.5 mac Desflurane
-succinylcholine
-rapid increase in Isoflurane
-intubation
-abdominal surg + sevo/n2o
-emergence/extubation

little effect from roc/vec

Comparing NE to PE in specific studies and circumstances

Aortic stenosis
-PE resulted in higher MAP, no differencve in LV fx vs. Levo

CABG
-PE imparied LV function, unchanged with levo

Pulmonary HTN cardiac surgery pts
-CI maintained with NE, decreased with PE
-NE improved (reduvced) ratio of mean PA pressure to SBP

General Surgery, isoflurance
-NE increased LV performance
-PE decreased LV performance

General Surgery, prop+remi
-both PE/NE decreased CO and HR, increased MAP

C/S Spinal
-PE vs. NE infusion
-NE had same sbp, higher HR, higher CO c/w PE

If LV fx impaired, enhanced afterload from PE -> decreased CO and systemic perfusion

but what about infiltration? Largely overblown as, yes NE 7x more constrictive in radial ARTERY, yet only 76% more vasoconstrictive in veins and concentration of Levo is 20x less than PE

if infiltrate -> give phentolamine

 

Fluorite

Calcium Fluoride

http://www.apsf.org/newsletters/html/2007/fall/03_sevoflurane.htm

Sevoflurane: The Challenges of Safe Formulation

Do you know the water content of your sevo?

From the anesthesia patient safety foundation newsletter:

An incident of Lewis acid mediated sevoflurane degradation occurred in 1996.5,6 Several bottles of sevoflurane had cloudy drug, a pungent odor, marked acidity (pH <1), and high fluoride (863 ppm), all indicating substantial anesthetic degradation and formation of HF, in quantities far exceeding the safe limits of 3 ppm over an 8 hr average. Abbott subsequently determined that increasing the water content in sevoflurane formulations decreased Lewis acid-dependent sevoflurane degradation.7 They changed the sevoflurane formulation to contain at least 300 ppm water, in order to prevent Lewis acid degradation and formation of toxic degradants. The new “water-enhanced” sevoflurane formulation was approved later that year by the U.S. Food and Drug Administration (FDA), and awarded patent protection.

Why is all this important? Generic sevoflurane formulations do not contain Lewis acid inhibitors, nor can they contain water in concentrations higher than 130 ppm. As Dr. Baker concludes, “a potential remains for sevoflurane instability, . . . therefore some vigilance regarding product integrity remains prudent.”

Quick Hit: Myotonic Dystrophy

Myotonic Dystrophy
Quick hit notes from QBanks and Obstetric Anesthesia and Uncommon Disorders

-autosomal dominant CTG-trinucleotide repeat
-impaired muslce relaxation
-Succinycholine –> excessive fasciulations, difficult intubation
-restrictive lung disease -> P/O resp failure
-poor cough/pharyngeal muscle dysynch. -> aspiration/PNA
-imparied response to hypoxia and hypercarbia (senstive to opioids, benzos, barbs, inh)
-comorbidities include: cardiomypathy/dysrhythmias/av block, DM, adreneal insufficiency, thyroid dysfx
-OB pt with MD: increased heart failure risk and myotonic crisis, also increased is placenta accreta, failed labor
-Monitoring: Myotnoia can appear as sustainaed tetanus (even if there is actually sig blockade) -> too early extubations
-MYOTONIC CRISIS: marked contracture of skeletal muscles, 2-3+minutes, ventilation compromised, NOT relieved by nerve block/nmbd/GA
-Prevent Crisis: Warm patient, handle muscles gently, avoid succ and shivering
-Treat Crisis: Procainamide (100mg/min to 1g caution with conduction defects), dantrolene, phenytoin (if localized only, some suggest direct injection of local anesth into muscle)
Plan: avoid succ, easy on resp depressant meds, no superior regional vs. GA

Sufenta TIVA!

http://www.ncbi.nlm.nih.gov/pubmed/16750467

Clin Ther. 2006 Apr;28(4):560-8.

Anesthesia was induced with propofol and either remifentanil 1 microg/kg or sufentanil 0.25 microg/kg. Propofol was continued using a target-controlled infusion (TCI) system. Maintenance infusion rates for remifentanil and sufentanil were 0.25 and 0.0025 microg.kg-1.min-1 [or 0.15mcg/kg/hr for sufenta] respectively.

The median extubation time was similar in the remifentanil and sufentanil groups (10 minutes [interquartile range, 5-19 minutes] and 16 minutes [interquartile range, 10-30 minutes], respectively). Remifentanil was associated with the need for significantly fewer adjustments to maintain hemodynamic stability compared with sufentanil (0.8 vs 2.1; P=0.037), greater use of postoperative morphine (44.8% vs 22.6% of patients, P=0.01; mean IV morphine dose per patient: 4 vs 1.3 mg, P=0.016), and higher intraoperative opioid costs per patient euro vs euro P<0.001). The incidence of PONV did not differ significantly between groups.

Ketamine for Total Hip Arthroplasty

Bad Times in the K Hole

From: http://www.ncbi.nlm.nih.gov/pubmed/19923527
Anesth Analg. 2009 Dec;109(6):1963-71. doi: 10.1213/ANE.0b013e3181bdc8a0.

The early and delayed analgesic effects of ketamine after total hip arthroplasty: a prospective, randomized, controlled, double-blind study.

The gist: Ketamine can reduce post-op pain scores and is opioid sparing when given to patients undergoing General Anesthesia hip replacement (note this is NOT generalizable to spinal anesthesia)

Methods: Pts received IV ketamine before incision (0.5 mg/kg), and a 24-h infusion (2 microg x kg(-1) x min(-1)) or a similar blinded saline bolus and infusion. Postoperative analgesia included IV acetaminophen, ketoprofen, plus morphine/droperidol patient-controlled analgesia for 48 h

Results: Ketamine decreased morphine consumption at 24 h from 19 +/- 12 mg to 14 +/- 13 mg (P = 0.004). At Day 30, ketamine decreased the proportion of patients needing 2 crutches or a walking frame from 56% to 31% (P = 0.0035). From Day 30 to Day 180, ketamine decreased the proportion of patients with persistent pain at rest in the operated hip (P = 0.008).

Other evidence [apparently – I’m looking at you DP who never bothers to comment] shows the one time bolus 0.5mg/kg vs. infusion makes little difference in post-op pain scores… so go for the bolus!

 

 

Magnesium: a versatile drug for anesthesiologists

From: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726845/

MOA: multiple including blockade of nmda and Calcium channels 

Magnesium has multiple advantages including:

• Reduced opioid reqs post op
• Reduced Mac with tiva
• Tiva reduced remi use -> reduced hyperanalgesia post op
• Intrathecal MG prolongs labor analgesia, especially motor block and iv Mg prolongs muscle blockade when spinal wearing out 
• Potentiates Nondepolarizing blockade,  can improve incubating conditions while reducing hemodynamic response to intubation 
• Reduced post op shivering >70%

However caution:

• Reduced inh Mac questionable 
• Blunts release of NE / epi watch out in critically ill patients 
• Cardiovascular depression possible when given as bolus 

Dosing: 

loading dose of 30-50 mcg/kg followed by a maintenance dose of 6-20 mcg/kg/h (continuous infusion) until the end of surgery; alternatively 4mg bolus