Critical Care

"High Quality CPR" and You!

CPR as we know it was “invented” by numerous resuscitation scientists working in competing labs during the 1950s.  Since then, CPR has gone through a number of changes, from compression-to-ventilation rates, training programs and even the manner in which it is delivered.  In the 1990s, pubic defibrillators became mainstream.  In the mid 2000s, external CPR devices became more common and in 2010 “hands-only” CPR was the predominant layperson resuscitation method.  The latest iteration of CPR and resuscitation science is the focus on “high quality” CPR, “team-focused” CPR and “cardiocerebral resuscitation” (CCR).

When discussing CPR and the holy grail of evidence-based practice, there are a number of caveats to acknowledge.  Firstly, there have been a very limited number of prospective, randomized and controlled trials on CPR and resuscitation due to many inherent barriers to performing such a study – cost, the infrequency of out-of-hospital cardiac arrest (OHCA), and the difficulty and ethical concerns inherent in studying something which is thought to be efficacious (CPR) against something else which may not be.  Fortunately, there have been a number of trials conducted that can inform our practice, and large, curated resuscitation outcomes databases exist for retrospective studies.  In this article, we’ll discuss CPR, Rhode Island State EMS protocols, and the evidence for and against them.

LifePACT.jpg

In March of 2017, the Rhode Island Department of Health instituted new protocols requiring EMS providers to stay on the scene of an atraumatic cardiac arrest for up to 30-minutes, or until return of spontaneous circulation (ROSC) is achieved[i].  Pre-hospital medicine policies and protocols vary according to the region, state, resources, distance from definitive care, and culture.  When treating trauma patients, for example, EMS providers are instructed to transport as quickly as possible to a hospital.  Traditionally, EMS providers have also been taught to transport OHCA patients to hospitals quickly as well, so asking them to remain on-scene for up to 30-minutes is controversial.  According to the American Heart Association (AHA), approximately 355,000 people each year suffer an OHCA event (110 events per 100,000 population).  Studies vary, but the overall survival rate for OHCA is anywhere from 6-12%[ii],[iii] nationally.  Extrapolating these statistics to Rhode Island’s population of 1 million, we can estimate that approximately 1100 Rhode Islanders are having OHCA each year, or 3 people every day.  Clearly, OHCA is an important topic and is worth exerting considerable effort to improve outcomes.

Historically, we know that certain factors in OHCA have prognostic importance and are associated with better outcomes, including witnessed arrest, time to CPR and defibrillation, initial shockable rhythm (VT/VF), AED use, and patient ageiii,[iv].  Although there are a myriad of factors that play into treating OHCA patients – airway use, mechanical or manual CPR, ACLS drugs, etc., the idea behind emphasizing on-scene CPR is that it gives EMS agencies the opportunity to defibrillate as soon as possible, perform great CPR and increase a patient’s chance of ROSC by re-establishing myocardial perfusion, instead of focusing on patient packaging and transport.  In other words, the theory is that you can run a code in the field, in the ER, or in the back of an ambulance, but the sooner you run it well, the better odds a patient has of a good outcome.  Below, we’ll review some of the key concepts of high-quality CPR.

Continuous Chest Compressions

Chest compressions.JPG

Many simulation, animal and observational studies have been performed on all manner of aspects of CPR, including compression depth, recoil, and speed.  Recently, focus has been drawn to cardiocerebral resuscitation (CCR), or minimally interrupted, continuous CPR.  The concept behind this mode of CPR delivery is that of coronary perfusion pressure – that it takes time giving compressions to reach the threshold at which the heart has enough coronary blood flow to possibly begin beating again, and each pause in CPR resets the pressure to 0. In the 3-phase model of VF arrest, the first 5 minutes are the “electrical phase”, in which defibrillation can result in ROSC. After this is the “hemodynamic phase”, during which restoration of “adequate arterial pressure” by CPR can increase odds of ROSC.  Importantly, it can take up to 45 seconds to establish adequate arterial pressure.  Lastly is the “metabolic phase”, during which outcomes are poor[v],[vi].  According to this theory, the sooner patients get defibrillation and CPR, and the better the CPR is, the higher odds they have of ROSC.  To date, several registry-based studies seem to agree with this idea, and have demonstrated improved outcomes among both VF and non-VF arrests with high chest compression fraction (i.e., less CPR interruptions)[vii].  Assuming that continuous CPR, or high chest compression fraction is beneficial, it also follows that any interruptions during CPR can result in worse outcomes – for example, pauses around defibrillation, intubation and transport, and research has borne this out[viii].  It’s worth noting, however, that although many of these concepts have become resuscitation truths, not all research agrees.  In one of the few RCTs on CPR, published in the New England Journal in 2015, Nichol et al. compared continuous to interrupted chest compressions, and found no statistically-significant difference in favorable neurologic function at discharge, although the protocol compliance was low, and many variables were similar between both groups[ix].  Both groups, for example, had CPR fractions higher than typical, so both study groups may not be representative of the real world.

Passive Oxygenation and Delayed Intubation

Bag Valve Mask.jpg

One of the key exposures in the NEJM study by Nichol et al., was the mode of ventilation.  In comparing continuous to interrupted chest compressions, the “interruption” was providing rescue breaths in the traditional 30:2 ratio.  If we subscribe to the idea that it takes up to 45 seconds to develop enough coronary perfusion pressure that defibrillation might be successful, stopping CPR every 30 compressions begins to seem like a bad idea.  We also know that a provider’s focus on airway management can detract from compression quality.  One observational study found that pre-hospital providers caring for OHCA patients paused CPR a median of 109 seconds for airway placement[x].  Coupling this finding with other studies showing that CPR pause duration is associated with increased mortality[xi] leads us to consider forgetting about the airway completely (at least initially).  Other literature seems to support this idea.  McMullan et al published a paper in 2013 on data from the Cardiac Arrest Registry to Enhance Survival (CARES), evaluating different airway management techniques and their association with neurologically intact survival.  The authors found that of 10,691 OHCA patients, survival was highest among those who received neither endotracheal intubation nor supraglottic airways (OR of 1.31)[xii].  Although this appears damning for any types of airway management at face value, it’s worth noting that patients with the best outcome often will have no opportunity for airway management – in other words, they are shocked out of VF, then wake up!  More information is coming soon, with an RCT due to be published in 2020 comparing airway management methods prospectively.

CPR During Transport

Another significant factor in deciding whether to work a code on scene or transport rapidly is the quality of CPR possible.  On scene, with a team of prepared EMS personnel, it seems a reasonable assumption that CPR metrics would be superior.  Prior literature seems to support this conclusion, with a number of simulation studies demonstrating worse or more variable CPR metrics in patients during transport, such as compression depth and rate[xiii].  In a small study published by Olasveengen et al., non-traumatic OHCA patients had increased time without compressions during transport compared with when on scene (27% vs. 19%).  However, in one 2017 registry-based study in Canada, the proportion of OHCA patients receiving “high-quality” CPR, defined as depth >5cm, rate >100/min, and chest compression fraction of >0.7 was similar between on-scene and transported groups[xiv].  Even if EMS providers are able to provide high-quality CPR in the back of a moving ambulance, consideration must be made of the danger to EMS personnel, who are then required to stand and perform a physically demanding task in a moving vehicle.  The science is not completely clear on which method is superior – on-scene or in transport, though clearly these studies have implications for proponents of running on-scene codes.

Team-Focused CPR

Eager to implement these cutting-edge techniques, some EMS systems have published their results with high-quality, “pit-crew style” and “team-focused” CPR.  Stopyra published data from a prospectively collected pre and post-intervention cohort study in rural North Carolina.  Data was collected on OHCA from 1-year prior to the intervention and 1-year after the intervention implementation.  All OHCA of presumed cardiac etiology was included.  The intervention included training of all providers, including police and EMS.  They were instructed to fulfill a choreographed position based on the timing of their arrival to the code.  The first rescuer would begin CPR, the second would place defibrillation pads and insert a blind airway, the third would be the team leader.  After arrival of the third provider, parenteral access could be attempted.  Rescuers continued with resuscitation until ROSC or end tidal <10mm for 20 minutes.  They found that after protocol implementation, there was a significant increase in number of patients achieving ROSC (65.7% vs. 28.4%, p<0.001), though there was no statistically significant change in survival to discharge.  Some of the limitations of this study include the small n (105 total resuscitations), and the lack of ability to control for in-hospital care (with regards to the lack of difference in survival to discharge)[xv].

A second North Carolina was undertaken by Pearson et al, and published in Resuscitation, detailing OHCA outcomes before and after an intervention of “team-focused CPR”[xvi].  Researchers evaluated arrest characteristics of nearly 15,000 OHCA patients using CARES registry data.  EMS agencies self-reports compliance with “team-focused CPR”, which emphasized early defibrillation, high quality CPR, and airway management with BVM over advanced airways.  Authors used a logistic regression to control for arrest characteristics, such as CPR device used, witnessed or unwitnessed, race, comorbidities and hypothermia, and found that team-focused CPR had a better odds of good neurologic outcome as measured by cerebral performance category score (OR 1.5) compared with traditional CPR.

A similar effort was undertaken in Salt Lake City in 2011.  The results from SLC Fire Department’s “pit crew approach” were published in 2015 in the Journal of the American Heart Association.  This study had significantly larger numbers (737 attempted resuscitations), and was based in an urban department with 11 ALS units and 8 BLS units.   The intervention in SLC included use of defibrillator real-time feedback to rescuers, strong medical direction and QA of all OHCA calls, rhythm-filtering technology that allowed rescuers to see the rhythm during CPR prior to stopping for pulse-check, limited peri-shock pauses, and encouraged on-scene resuscitation (vs. early transport) to reduce interruptions inherent in transfer and transport.  Additionally, passive oxygen was applied via facemask for the first 6-8 minutes, and asynchronous BVM for all unwitnessed, pediatric and respiratory arrests. 

After the intervention, SLC Fire Department saw more field ROSC (44% vs. 30%, p<0.0001).  Among patients who survived to admission, there was more survival to discharge (50% vs. 37%, p=0.0005), and more patients with favorable neurologic function, defined as Cerebral Performance Category 1 or 2 (46% vs. 26%, p=0.0005), although there was no statistically significant change in survival to hospital admission.  Although these numbers are promising for high-quality CPR, several confounders are present, including improved medical control, and preferential triage of OHCA patients with ROSC to PCI-capable centers, which was not the practice in the pre-intervention period[xvii]

Rhode Island is among the first states to institute a protocol mandating 30-minutes of on-scene CPR. While some have demonstrated improved outcomes with the implementation of similar interventions, bundled together with CPR training, use of novel technology (such as real-time feedback, end-tidal CO2, and rhythm filtration programs), strong medical direction and QA, it remains to be seen whether a statewide intervention can lead to more ROSC in the field, and, more importantly, more neurologically intact survival to discharge.  Reviewing the resuscitation literature, we see the trend toward decreased initial advanced airway use, higher focus on continuous CPR and minimal interruptions, such as the peri-shock pause and, to delay transport of the patient until ROSC is achieved.  While local news reports have highlighted anecdotal success stories[xviii], the full impact of the Rhode Island intervention have yet to be described.

Faculty Reviewer: Nick Asselin, DO

References

[i] Rhode Island Statewide Emergency Medical Services Protocols.” Rhode Island Department of Health, p. 3.03a., health.ri.gov/publications/protocols/StatewideEmergencyMedicalServices.pdf.

[ii] Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., … Turner, M. B. (2015). Heart Disease and Stroke Statistics—2016 Update. Circulation, 133(4), e38–e360. https://doi.org/10.1161/cir.0000000000000350

[iii] Becker, L. B., Aufderheide, T. P., & Graham, R. (2015). Strategies to Improve Survival From Cardiac Arrest. JAMA, 314(3), 223. https://doi.org/10.1001/jama.2015.8454

[iv] Haukoos, J. S., Lewis, R. J., & Niemann, J. T. (2004). Prediction rules for estimating neurologic outcome following out-of-hospital cardiac arrest. Resuscitation, 63(2), 145–155. https://doi.org/10.1016/j.resuscitation.2004.04.014

[v] Weisfeldt, M. L., & Becker, L. B. (2002). Resuscitation After Cardiac Arrest. JAMA, 288(23), 3035. https://doi.org/10.1001/jama.288.23.3035

[vi] Berg, R. A., Sanders, A. B., Kern, K. B., Hilwig, R. W., Heidenreich, J. W., Porter, M. E., & Ewy, G. A. (2001). Adverse Hemodynamic Effects of Interrupting Chest Compressions for Rescue Breathing During Cardiopulmonary Resuscitation for Ventricular Fibrillation Cardiac Arrest. Circulation, 104(20), 2465–2470. https://doi.org/10.1161/hc4501.098926

[vii] Vaillancourt, C., Everson-Stewart, S., Christenson, J., Andrusiek, D., Powell, J., Nichol, G., … Stiell, I. G. (2011). The impact of increased chest compression fraction on return of spontaneous circulation for out-of-hospital cardiac arrest patients not in ventricular fibrillation. Resuscitation, 82(12), 1501–1507. https://doi.org/10.1016/j.resuscitation.2011.07.011

[viii] Cheskes, S., Schmicker, R. H., Christenson, J., Salcido, D. D., Rea, T., … Powell, J. (2011). Perishock Pause: An Independent Predictor of Survival From Out-of-Hospital Shockable Cardiac Arrest. Circulation, 124(1), 58–66. https://doi.org/10.1161/circulationaha.110.010736

[ix] Nichol, G., Leroux, B., Wang, H., Callaway, C. W., Sopko, G., Weisfeldt, M., … Ornato, J. P. (2015). Trial of Continuous or Interrupted Chest Compressions during CPR. New England Journal of Medicine, 373(23), 2203–2214. https://doi.org/10.1056/nejmoa1509139

[x] Wang, H. E., Simeone, S. J., Weaver, M. D., & Callaway, C. W. (2009). Interruptions in Cardiopulmonary Resuscitation From Paramedic Endotracheal Intubation. Annals of Emergency Medicine, 54(5), 645–652.e1. https://doi.org/10.1016/j.annemergmed.2009.05.024

[xi] Brouwer, T. F., Walker, R. G., Chapman, F. W., & Koster, R. W. (2015). Association Between Chest Compression Interruptions and Clinical Outcomes of Ventricular Fibrillation Out-of-Hospital Cardiac ArrestCLINICAL PERSPECTIVE. Circulation, 132(11), 1030–1037. https://doi.org/10.1161/circulationaha.115.014016

[xii] McMullan, J., Gerecht, R., Bonomo, J., Robb, R., McNally, B., Donnelly, J., & Wang, H. E. (2014). Airway management and out-of-hospital cardiac arrest outcome in the CARES registry. Resuscitation, 85(5), 617–622. https://doi.org/10.1016/j.resuscitation.2014.02.007

[xiii] Roosa, J. R., Vadeboncoeur, T. F., Dommer, P. B., Panchal, A. R., Venuti, M., Smith, G., … Bobrow, B. J. (2013). CPR variability during ground ambulance transport of patients in cardiac arrest. Resuscitation, 84(5), 592–595. https://doi.org/10.1016/j.resuscitation.2012.07.042

[xiv] Cheskes, S., Byers, A., Zhan, C., Verbeek, P. R., Ko, D., Drennan, I. R., … Morrison, L. J. (2017). CPR quality during out-of-hospital cardiac arrest transport. Resuscitation, 114, 34–39. https://doi.org/10.1016/j.resuscitation.2017.02.016

[xv] Stopyra, J. P., Courage, C., Davis, C. A., Hiestand, B. C., Nelson, R. D., & Winslow, J. E. (2016). Impact of a “Team-focused CPR” Protocol on Out-of-hospital Cardiac Arrest Survival in a Rural EMS System. Critical Pathways in Cardiology, 15(3), 98–102. https://doi.org/10.1097/hpc.0000000000000080

[xvi] Pearson, D. A., Darrell Nelson, R., Monk, L., Tyson, C., Jollis, J. G., Granger, C. B., … Runyon, M. S. (2016). Comparison of team-focused CPR vs standard CPR in resuscitation from out-of-hospital cardiac arrest: Results from a statewide quality improvement initiative. Resuscitation, 105, 165–172. https://doi.org/10.1016/j.resuscitation.2016.04.008

[xvii] Hopkins, C. L., Burk, C., Moser, S., Meersman, J., Baldwin, C., & Youngquist, S. T. (2016). Implementation of Pit Crew Approach and Cardiopulmonary Resuscitation Metrics for Out‐of‐Hospital Cardiac Arrest Improves Patient Survival and Neurological Outcome. Journal of the American Heart Association, 5(1), e002892. https://doi.org/10.1161/jaha.115.002892

[xviii] http://wpri.com/2017/02/16/new-rule-cpr-for-30-minutes-before-taking-cardiac-arrest-victims-to-hospital/

AEM Early Access 05: The Role of Prehospital ACLS for Potential E-CPR Candidates

Welcome to the fifth episode of AEM Early Access, a FOAMed podcast collaboration between the Academic Emergency Medicine Journal and Brown Emergency Medicine. Each month, we'll give you digital open access to an AEM Article in Press, with an author interview podcast and links to curated FOAMed supportive educational materials for EM learners.

Find previous podcasts and subscribe to this series on I tunes here.

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  Dr. Alexis Cournoyer, MD   Universite de Montreal, Montreal, Quebec, Canada Hospital du Sacre-Coeur de Montreal, Montreal, Quebec, Canada Institut de Cardiologie de Montreal, Montreal, Quebec, Canada

Dr. Alexis Cournoyer, MD

Universite de Montreal, Montreal, Quebec, Canada
Hospital du Sacre-Coeur de Montreal, Montreal, Quebec, Canada
Institut de Cardiologie de Montreal, Montreal, Quebec, Canada

 

 

 

Listen now: Interview with Dr. Alexis Cournoyer, lead author, interviewed by Dr. Thomas Ross

Open Access Through September 30th. Click below:

Prehospital Advanced Cardiac Life Support for Out-of-Hospital Cardiac Arrest: A Cohort Study. Cournoyer A, et. al

Article Summary:

Objectives: Out-of-hospital advanced cardiac life support (ACLS) has not consistently shown a positive impact on survival. Extracorporeal cardiopulmonary resuscitation (E-CPR) could render prolonged on-site resuscitation (ACLS or basic cardiac life support [BCLS]) undesirable in selected cases. The objectives of this study were to evaluate, in patients suffering from out-of-hospital cardiac arrest (OHCA) and in a subgroup of potential E-CPR candidates, the association between the addition of prehospital ACLS to BCLS and survival to hospital discharge, prehospital return of spontaneous circulation (ROSC) and delay from call to hospital arrival. 

Methods: This cohort study targets adult patients treated for OHCA between April 1010 and December 2015 in the city of Montreal, Canada. We defined potential E-CPR candidates using clinical criteria previously described in the literature (65 years of age or younger, initial shockable rhythm, absence of return of spontaneous circulation after 15 minutes of prehospital resuscitation and emergency medical services witnessed collapse or witnessed collapse with bystander cardiopulmonary resuscitation). Associations were evaluated using multivariate regression models.

Results: A total of 7134 patients with OHCA were included, 761 (10.7%) of whom survived to discharge. No independent association between survival to hospital discharge and the addition of prehospital ACLS to BCLS was found in either the entire cohort [adjusted odds ratio (AOR) 1.05 (95% confidence interval 0.84-1.32), p=0.68] or amongst the 246 potential E-CPR candidates [AOR 0.82 (95% confidence interval 0.36-1.84), p=0.63]. The addition of prehospital ACLS to BCLS was associated with a significant increase in the rate of prehospital ROSC in all patients experiencing OHCA (AOR 3.92 [95% CI 3.38-4.55], p<0.001) and in potential E-CPR candidates (AOR 3.48 [95% CI 1.76-6.88], p<0.001) as compared to isolated prehospital BCLS. Delay from call to hospital arrival was longer in the ACLS group than in the BCLS group (difference=16 min [95% CI 15-16], p<0.001). 

Conclusions:  In a tiered-response  urban emergency medical service setting, prehospital ACLS is not associated with an improvement in survival to hospital discharge in patients suffering from OHCA and in potential E-CPR candidates, but with an improvement in prehospital ROSC and with longer delay to hospital arrival. 

Suggestions for Further Reading: 

Open Access:

RAGE Podcast: E-CPR by Vincent Pellegrino

EM Docs: ECMO in the ED

Subscriptions/Abstracts:

Sanghavi P, Jena AB, Newhouse JP, Zaslavsky AM. Outcomes after out-of-hospital cardiac arrest treated by basic vs advanced life support. JAMA Intern Med 2015;175:196-204. 

Ma MH, Chiang WC, Ko PC, et al. Outcomes from out-of-hospital cardiac arrest in Metropolitan Taipei: does an advanced life support service make a difference? Resuscitation 2007;74:461-9.

Bakalos G, Mamali M, Komninos C, et. al. Advanced life support versus basic life support in the pre-hospital setting: a meta analysis. Resuscitation 2011;82:1130-7.

Stub D, Bernard S, Pellegrino V, et. al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation 2014. 

Siao FY, Chiu CC, Chiu CW, et al. Managing cardiac arrest with refractory ventricular fibrillation in the emergency department: Conventional cardiopulmonary resuscitation versus extracorporeal cardiopulmonary resuscitation. Resuscitation 2015;92:70-6. 

Faculty Editors/Reviewers: Dr. Gita Pensa and Dr. Kristy McAteer 

Podcast credits: Used under creative commons license: intro music by freemusicarchive.org , sound effect from freesound.org, exit music by bensound.com

The Obtunded Patient

The Case

52 y/o male with HTN, hyperlipidemia, chronic back pain, and recent depression came back from a walk and per family was ataxic, dysarthric and confused, so his family drove him to the ED. On the way, he began vomiting repeatedly and became increasing obtunded.  As he entered the ED went into apparent cardiovascular and respiratory collapse. Given 2mg of Naloxone without response and intubated by RSI for further evaluation.

Examination

Vitals on arrival in the ED:  Temp: 36, RR:-no spontaneous breaths noted after entering the ED O2: 88% on bag valve mask, HR: 68 BP: 88/64. Glucose 104.  GCS 3 (non verbal, no motor movement, pupils 2mm and fixed). No corneal or occulacephalic reflexes noted, no cough or gag elicited. All extremities were flaccid and areflexic. EKG show sinus rhythm, no obvious conduction abnormalities.

Medication hx: Simvastatin 40 mg daily, amlodipine 10 mg daily, Baclofen 20 mg TID, Vicodin 5-300 1 tablet q6 hrs

Labs: ETOH: 150. CBC, lactic acid, chemistry, venous blood gas (on ventilator), CPK, LFT’s, troponin asa, acetaminophen, UA, UDS all WNL

Imaging: CTA pan scan negative except for mild aspiration in the R lung base.

 

So what happened…..?

Baclofen Toxicity

What is it?

Baclofen is a synthetic derivative of the naturally occurring inhibitory neurotransmitter GABA.

Acts principally on the GABA-B receptor at the spinal level and reduce the post-synaptic potentials along motor neurons, thus relaxing the skeletal muscles.

Baclofen is primarily used for the treatment of spastic movement disorders and now more ubiquitously for the treatment of chronic back pain.

 

How is it given?

Oral: Until the past 10 years, the primary method of administration of Baclofen was oral.

  • Peak concentration in 2 hours and half life of 3.5hours
  • Dosage 40-80mg daily dosed q8 hrs
  • Centrally acting but crosses the blood brain barrier ineffectively, limiting its bioavailability
  • Very low toxic range with severe toxicity from oral baclofen, necessitating ICU level care occurring fairly consistently with baclofen overdoses of over 200mg (a 3 day supply for most people)
 Figure 2: Baclofen pump concept

Figure 2: Baclofen pump concept

Intrathecal: Intrathecal baclofen is administered through the implantation of a pump subcutaneously with a catheter from the pump inserted directly into the CSF fluid.

  • Dosage: 90 mcg to 800 mcg daily
  • Intrathecal baclofen allows for 4x the amount of baclofen to be delivered to the spinal cord with just 1% of the oral dose.

Intrathecal Baclofen Pumps: The pump is surgically implanted under the skin in the abdomen and the catheter is tunneled under the skin and inserted into the intrathecal space usually between the 1st and 2nd lumbar vertebrae.

Currently SynchroMed is the only pump currently being used in the US for intrathecal baclofen, hydromorphone and morphine

  • The catheter holds 3-4ml
  • The reservoir holds 20-40ml
  • Pump battery lasts for 5-7 years
 Figure 3: Synchromed Baclofen pump

Figure 3: Synchromed Baclofen pump

Toxicities 

Baclofen has the potential for both overdose and withdrawal, which can both present with a wide array of symptoms.

Overdose Symptoms

Most commonly include CNS depression, lethargy, somnolence, hallucinations, agitation, mydriasis/miosis, nausea and vomiting

Severe toxicity is associated with bradycardia, hypotension (more common) or hypertension, respiratory failure, hypothermia, seizures, coma and death.

Rarely, rhabdomyolysis and conduction disturbances may occur

Causes

Oral Baclofen overdoses:

  • Usually intentional overdoses-either for recreational or self harm

Intrathecal baclofen overdoses:

  • Wrong dose is manually programmed into the pump
  • Wrong concentration is placed in the pump
  • Wrong bolus is given when starting the pump
  • Wrong port is accessed or wrong port filled

Treatment

Patients are usually treated by supportive methods only.

In severe overdoses, this often means supporting blood pressure with fluids and pressors and often-mechanical ventilation for respiratory failure until drug toxicity subsides.

Generally overdose symptoms will resolve in approximately 24-48 hours

For Intrathecal baclofen overdoses:

Most are correctable by emptying the pump reservoir:

  • Turn off pump-programmer (need external device programmer to do this)
  • Empty reservoir: Use a 22 gauge needle to stick the middle of the pump and pull out all the drug
 Figure 4: Emptying the reservoir

Figure 4: Emptying the reservoir

Remove the CSF- Use a 24-25 gauge needle to stick the side port and aspirate 30-100 ml of CSF

In severe cases performing a lumbar puncture to reduce circulating baclofen in the CSF while performing all normal supportive strategies (small case reports- this involves replacing entire circulating volume of CSF with saline and has been used successfully in a few cases of massive overdose)

Withdrawal Symptoms

Similar to withdrawal from alcohol or benzodiazepines, with the loss of gaba-mediated inhibition: hyper metabolic states, spasticity/rigidity, hallucinations/seizures, tachycardia, hyperthermia, and hypertension are more commonly observed.

Mild: pruritus, agitation, diaphoresis and increased tone

Moderate: fever, tachycardia, spontaneous clonus and painful muscle spasm

Severe: worsening of above along with seizures, delirium, hallucinations, rhabdomyolysis and death.

Remember the mnemonic, "ITCHY, TWITCHY, BITCHY."

Causes of Withdrawal

Oral Baclofen Withdrawal:

  • Oral Baclofen withdrawal can occur when a person is abruptly stops taking baclofen or weans off to fast.
  • Of note oral baclofen diffuses through the blood brain barrier deep into the brain whereas- intrathecal baclofen stays almost exclusively in the CSF with a penetration of only approximately 1-2 inches into the brain. Therefore, a person who is being switched to intrathecal baclofen must still be tapered off their oral baclofen or they will withdraw.

Intrathecal Baclofen Withdrawal:

  • Intrathecal Pump Malfunction
    • Intrinsic pump malfunction is exceedingly rare.
  • Pocket Refill
    • Rather than an overdose this results in acute withdrawal as intrathecal dosing is 1/100th of oral dosing/subcutaneous dosing.
  • Battery failure
    • Expected to die at 84 months.
    • Will alarm 3 months prior. 

Medication Changes or interactions:

  • SSRI’s especially known for decreasing effect

Catheter malfunctions: (kink, micro/macroleaks, scarring, migration)

  • Most common cause of pump failure
  • KUB and AP/lateral spine first step to look for catheter fracture or migration
 Figure 6: KUB demonstrating Baclofen pump

Figure 6: KUB demonstrating Baclofen pump

Treatment

Oral Baclofen withdrawal is usually easily treatable by restarting baclofen and introducing a slow tapered wean if discontinuation is desired.

Intrathecal Baclofen Withdrawal presents more of a challenge in both recognition and treatment.  It can be tricky to recognize baclofen withdrawal as it often masquerades as sepsis (ex-tachycardia, hyperthermia, altered mental status). It is important to recognize that many of these patients have severe spasticity and may have limited verbalization skills. Often they come from long term care facilities without much information, along with the fact that many times the baclofen will not be listed on their daily facility medication list, making it extremely important to look for a pump every time.

Recognizing that a patient’s symptoms may be secondary to intrathecal baclofen and interrogating the pump and obtaining pump series imaging to evaluate for catheter related malfunctions is a key first step

Essentially intrathecal baclofen withdrawal requires intrathecal baclofen. The key is finding the reason for the withdrawal and fixing the primary cause. Everything else is a temporizing measure.

To help with symptoms while attempting to fix the primary cause of pump failure treatment can include:

  • High Dose Oral Baclofen
    • Treating intrathecal baclofen withdrawal with oral baclofen is often unsuccessful as the vast difference in bioavailability of oral doses and intrathecal doses.
  • Benzodiazepine treatment
  • Propofol low dose
  • Experimentation with Dexamedetomidine and cyproheptadine
  • CSF infusion of Baclofen

So what happened to our patient?

After approximately 18 hours intubated, our patient began waking up, became agitated and self-extubated himself. He admitted to taking approximately 900 mg of baclofen in a suicide attempt the day of admission. He was discharged to inpatient psychiatry without any further medical sequela on hospital day 3. 

Take Home Points

  • Overdose: variable presentation, CNS depression is often involved, good supportive care is key.
  • Withdrawal: variable presentation, Itchy/twitchy/bitchy. Will have increased muscle tone from baseline.
  • Always remember the pump is there.
  • Overdose: For intrathecal overdose-2 ports from which you can draw drug and CSF back out.
  • Withdrawal: Look for the cause and treat supportively with oral baclofen, benzos, and propofol.

Faculty Reviewer: Dr. Kristina McAteer

References

Image 1: “Spasticity2” by Bill Connelly- Own Work

https://commons.wikimedia.org/wiki/File:Spasticity2.svg

Image 2: http://www.gablofen.com/patients/intrathecal-baclofen-therapy

Image 3: http://www.ajnr.org/content/32/7/1158

Image 4: http://www.rch.org.au/kidsinfo/fact_sheets/Intrathecal_baclofen_3_the_ITB_pump/

Image 5: http://www.cliparthut.com/clip-arts/175/people-clip-art-175256.gif

Image 6: https://emcow.files.wordpress.com/2014/01/baclofen-3.jpg