REMI 1968. Predicción de recuperación sin secuelas tras la parada cardiaca intrahospitalaria

Artículo originalDevelopment and validation of the Good Outcome Following Attempted Resuscitation (GO-FAR) score to predict neurologically intact survival after in-hospital cardiopulmonary resuscitation. Ebell MHJang WShen YGeocadin RGGet With the Guidelines–Resuscitation InvestigatorsJAMA Intern Med 2013; 173(20): 1872-1878. [Resumen] [Artículos relacionados]
     
Introducción: En pacientes que presentan una parada cardiorrespiratoria (PCR) en el hospital se plantea a menudo la recuperabilidad del paciente y la conveniencia o no de iniciar y/o continuar las maniobras de resucitación cardiopulmonar (RCP), por tratarse a menudo de pacientes con múltiples comorbilidades. En estudios previos se han identificado distintos factores asociados a mal pronóstico [1]. Hay situaciones en que obviamente sí hay que realizar la RCP y otras en que es evidente que estamos ante un “fallecimiento” más que ante una PCR, pero en otras situaciones menos claras disponer de una puntuación pronóstica previa a la parada podría ser de gran ayuda para discutir y aplicar órdenes de no reanimar.
     
Resumen: Los autores analizan el registro norteamericano de PCR intrahospitalaria en un periodo de 3 años, con un total de 51.240 pacientes, analizando multitud de variables de los enfermos y en base a ellas calculan una puntuación "GO-FAR"("Good Outcome Following Attempted Resuscitation"), para intentar predecir la probabilidad de recuperación con variables obtenibles antes de la parada. Es su estudio multivariable, tabulan 13 variables predictoras del pronóstico de estos pacientes (Tabla I), y en base a esta puntuación estiman la probabilidad de sobrevivir o no a la RCP y si sobreviven, si es con buena o mala situación neurológica (tabla II). El modelo que ellos desarrollan tiene un buen área bajo la curva ROC (ABC 0,78 en la fase de validación del modelo). Con este modelo se identificaría a más de una cuarta parte de los pacientes que sufren PCR y a los que probablemente no merecería la pena realizar RCP en base a su baja/muy baja probabilidad de recuperación sin secuelas graves.
      
Comentario: Los sistemas de puntuación pronósticos genéricos (APACHE, SOFA) en pacientes críticos ayudan a clasificar a los pacientes en grupos de riesgo de fallecimiento, pero su aplicación pronóstica a pacientes individuales es más problemática. Con este sistema predictivo para la PCR intrahospitalaria podría pasar algo similar, pero puede servir de apoyo en la toma de decisiones. Para ello sería conveniente una validación externa en otro registro o estudio prospectivo más cercano a nuestro ámbito. Los mismos autores presentan en un trabajo adicional unos árboles de decisión basados en los datos derivados del presente análisis [2].
   
Antonio García Jiménez
Hospital Arquitecto Marcide, Ferrol, A Coruña.
© REMI, http://medicina-intensiva.com. Junio 2014.

Tabla I. Puntuación de diferentes variables del modelo predictivo GO-FAR

Variable
Puntuación GO-FAR
Neurológicamente normal o cuasi-normal a su ingreso
-15
Trauma grave
10
Accidente cerebrovacular
8
Metástasis o paciente oncohematológico
7
Sepsis
7
Diagnóstico médico no-cardiaco
7
Insuficiencia hepática
6
Ingresado en residencia con alto apoyo
6
Hipotensión o hipoperfusión
5
Insuficiencia renal
4
Insuficiencia respiratoria
4
Neumonía
1
Edad      70-74
2
             75-79
5
             80-84
6
              ≥ 85
11

Tabla II. Puntuación GO-FAR y probabilidad de sobrevivir con buena situación neurológica (función cerebral normal o discapacidad leve)
Probabilidad de recuperación
Puntuación
GO-FAR
% supervivientes con buena situación neurológica
% de pacientes en esta categoría
Muy baja (< 1%)
> 23
0,8%
9,4%
Baja (1-3%)
14 a 23
2%
19%
Intermedia (3-15%)
-5 a 13
9,2%
53,6%
"Alta" (> 15%)
-15 a -6
27,8%
18,1%


Enlaces:
  1. Pre-arrest predictors of failure to survive after in-hospital cardiopulmonary resuscitation: a meta-analysis. Ebell MH, Afonso AM. Fam Pract 2011; 28: 505-515. [PubMed]
  2. Prediction of survival to discharge following cardiopulmonary resuscitation using classification and regression trees. Ebell MH, Afonso AM, Geocadin RG; American Heart Association’s Get With the Guidelines-Resuscitation (formerly National Registry of Cardiopulmonary Resuscitation) Investigators. Crit Care Med 2013; 41: 2688-2697. [PubMed]
Búsqueda en PubMed:
  • Enunciado: Predicción de la supervivencia en la parada cardiaca intrahospitalaria
  • Sintaxis: in-hospital cardiopulmonary resuscitation prediction survival 
  • [Resultados]
       

Lipid Emulsion Therapy

Intro

Intravenous lipid emulsion (ILE, also known as lipid emulsion therapy, lipid resuscitation therapy, lipid rescue, intravenous fat emulsion and Intralipid®) has been used in the past for caloric supplementation and treatment of essential fatty acid deficiency.  Since 1998, ILE has been considered for resuscitative therapy in drug-induced cardiovascular and neurologic toxicity.  The use of ILE has been best described for cardiovascular collapse and seizures caused by local anesthetic systemic toxicity (LAST) with successful animal trials and human case reports.  Subsequent to these findings, the use of ILE in LAST is recommended by the latest guidelines for the American Heart Association, American Society of Regional Anesthesia and Pain Medicine (ASRA), and the Association of Anaesthetists of Great Britain and Ireland.  ILE has also been used as a resuscitative agent for a number of lipid- and water-soluble xenobiotics that induce cardiac and/or neurologic toxicity including tricyclic antidepressants, non-dihydropyridine calcium channel blockers, bupropion, citalopram, venlafaxine, atypical anti-psychotics, beta-blockers, diphenhydramine, etc.  See table 1 for a complete list of xenobiotics for which ILE has been attempted in case reports and abstracts.

Proposed Mechanisms

The exact mechanism of action has yet to be elucidated.  Two theoretical mechanisms of action have been widely described: partitioning and enhanced metabolism.  The partitioning theory or otherwise termed the “lipid sink” theory postulates that the administration of lipids compartmentalizes the offending xenobiotic into lipid phase and away from the target receptors.  Resuscitation of toxicity mediated by xenobiotics with high lipid solubility (defined as log P, octanol:water partition coefficient, greater than 2) are more likely to be successful although the intervention has worked for water-soluble xenobiotics.  The enhanced metabolism theory argues that the infusion of triglyceride and phospholipids are capable of providing fatty acid energy source to myocytes under toxic conditions.  Myocardium is capable of utilizing fatty acids for energy although in stressed states, cardiac myocytes preferentially utilized carbohydrates, a theory that gives credence to the use of high dose insulin therapy in calcium channel and beta blocker toxicity.

Administration Recommendations

Current recommendation from ARSA for 20% lipid emulsion therapy for LAST:

  1. Bolus 1.5 mL/kg (lean body mass) intravenously over one minute (Note that the dose is in volume, not weight)
    • 100 mL for a 70 kg patient
    • Repeat bolus for persistent cardiovascular collapse
  2. Continuous infusion 0.25 mL/kg/min
    • 18 mL/min for a 70 kg patient
    • Can double the infusion rate for persistent hemodynamic instability
    • Continue infusion for at least 10 minutes after hemodynamic recovery

In the setting of persistent cardiovascular collapse or hemodynamic instability, the upper limits of therapy are also not established.  ARSA recommends the upper limits of 10 mL/kg (700 mL in a 70 kg patient) over the first 30 minutes.

Pitfalls

Elevated serum triglycerides may interfere and prevent routine laboratory analysis including serum electrolytes, hematocrit, liver function tests, and coagulation function.  A false negative aspartate transaminase (AST) resulted in the premature discontinuation of n-acetylcysteine in a co-ingestion of acetaminophen, amitriptyline, and diphenhydramine.  A 13-year-old female developed acute pancreatitis and acute respiratory distress syndrome after receiving the ARSA recommended dose of lipid emulsion therapy for a tricyclic antidepressant overdose.  Serum amylase elevations have also been reported.

Bottom Line

Unfortunately, the lack of high-quality controlled human studies precludes lipid emulsion therapy as a first-line agent for indications other than local anesthetic systemic toxicity.  In the setting of severe hemodynamic compromise caused by a lipid-soluble xenobiotic or drugs with cardiovascular and/or neurologic toxicity, lipid emulsion therapy should be considered early in the resuscitation but is not the standard of care at this time.

Discussion Questions

  • What is the evidence supporting the use of intravenous lipid emulsion (ILE) in this patient?
  • Under what other acute poisonings should emergency department providers consider the use of ILE?
  • How should ILE be administered?
  • What are reported and potential adverse effects of ILE?
  • How does ILE adversely impact laboratory monitoring?
  • What are the considerations for stocking ILE in emergency departments?

Further Reading

  1. Weinberg GL. Lipid emulsion infusion: resuscitation for local anesthetic and other drug overdose. Anesthesiology. 2012;117:180-7.
  2. Neal JM, Mulroy MF, Weinberg GL, American Society of Regional A, Pain M. American Society of Regional Anesthesia and Pain Medicine checklist for managing local anesthetic systemic toxicity: 2012 version. Regional Anesthesia and Pain Medicine. 2012;37:16-8.
  3. American College of Medical Toxicology. ACMT position statement: interim guidance for the use of lipid resuscitation therapy. Journal of Medical Toxicology. 2011;7:81-2.
  4. http://www.ncbi.nlm.nih.gov/pubmed/24338451
  5. http://www.ncbi.nlm.nih.gov/pubmed/23518248
  6. http://www.ncbi.nlm.nih.gov/pubmed/23992445
  7. http://www.ncbi.nlm.nih.gov/pubmed/23685061
  8. http://www.ncbi.nlm.nih.gov/pubmed/20923546
  9. http://www.ncbi.nlm.nih.gov/pubmed/20688937
Edited by Alex Koyfman

 

Table 1: Xenobiotic overdose responses to ILE from 2006 to 2013 in case reports and abstracts.

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Mystery Bleed (M&M)

Time 12:25

Triage Note: 35M referred from Coumadin clinic for headache, dizziness and weakness.

Triage Vitals: BP 89/53 HR 89 RR 19 T 95.6 (oral) O2 98% Pain 5/10 (headache)

Time 13:40

Intern HPI

35M Jehovah’s witness with PMH of aortic valve repair at age 9 and aortic arch replacement 2 weeks ago at OSH for aortic aneurysm with dissection. Sent from Coumadin clinic for lightheadedness and headache. +dull headache and progressive lightheadedness x 2 days. His INR was 2.7 and Hbg 10mg/dL a few days ago. Denies active chest pain, palpitations, SOB, fever, head trauma. He has had significant weight loss since hospitalization.

  • PMHX: prosthetic valve, aortic dissection s/p repair 2 weeks ago
  • Meds: Coumadin, Metoprolol, Cozar, ASA
  • ROS: otherwise negative
  • Allergies: none

Exam

  • Vitals: BP 93/52 HR 87 RR 16, 98% on RA
  • Gen: Well-developed male
  • HEENT: Pale conjunctiva and dry mucous membranes, OP clear
  • Cardiac: RRR, valvular click, pulses equal bilaterally
  • Lungs: CTAB, no wheeze or crackles. Surgical scar c/d/i
  • Abd: Soft abdomen no masses
  • Neuro: CN intact, strength equal bilateral

Labs

  • Hbg 5.7
  • INR 3.60

CXR

Sternotomy wires, no effusions, no pneumothorax or infiltrate

FAST

Negative

Assessment/Plan

35M s/p recent aortic arch repair, with supra-therapeutic INR, now with 2-3 days of lightheadedness on standing, increasing fatigue, and SBP of low 90s, concerning for anemia or hemorrhage 2/2 post-op cardiovascular pathology.

  • ECHO
  • HEAD CT
  • CHEST CT
  • CT Surgery Consult

Time 15:02

ECHO being performed. Tentative results: No bleeding source; AV function WNL; graft intact; EF WNL; no effusions; no dissection

Time 16:40

Head CT nml

mysteryBleedBrain

Time 17:08

CTA Chest and Abdomen: no evidence of active extravasation/mediastinal hematoma. Multiple vascular embolization coils in abdomen.

Time: 17:40

(5 hours and 15 minutes since triage)
Rectal Exam done. Bright red blood in vault.

Time 17:59

Attending Update Note: CT head (for HA) negative; CT chest to look for aortic graft leakage negative. + guaiac noted-possible blood loss is in GI tract . GI consulted 1746. Patient has acute life threat risk from bleeding, He is a Jehovah’s Witness and refuses blood or blood products even if he might die without them. Critical need to localize the bleeding site and if GI have scope or IR stop bleeding.

Time 18:09

Nexium 80mg in 100ml NS over 30 minutes

Time 19:05

Admitting Resident’s Plan

  • GI: EGD patient in ICU ASAP; continue Nexium gtt; 1L NS bolus; defer serial CBCs; patient refusing all blood/synthetic products; will consult Heme re: possible reversal agents ddAVP? Tranexamic acid? Bebulin?; spoke with Critical Care fellow via phone, aware of pt; holding off transfer to ICU given no opportunity to intervene
  • CV: aggressive fluid resuscitation with NS; HR management diltiazem gtt if necessary; INR supra-therapeutic – will hold anticoagulation given acute bleed
  • PPX: Nexium gtt; scds
  • Dispo: to ICU; FULL CODE; NO BLOOD PRODUCTS

Esophagogastroduodenoscopy (EGD)

Normal EGD
Normal EGD
Patient's EGD
Patient’s EGD

Teaching Points

Look early for all possible reversible causes of hypotension.

  • In this case, GI bleed was only considered 5 hours after arrival to the ED.
  • On further history patient reports that stool was newly JET black and STICKY for several days

Think about possible reversal or correction agents in patients who cannot accept human-donor blood products.

  • Vitamin K, TXA, ddAVP, Protamine, PPI, Aprotinin for hemorrhage
  • Iron, Folate, B12, Erythropoietin for anemia
    • This patient received 5mg IV Vit K to reduce INR to 2. ddAVP was also given 2/2 hx of aspirin use.

Speak with Jehovah’s Witness patients about what is permitted for use.

  • Usually, whole blood, RBC, plt, plasma is not allowed
  • Cell Saver, plasma proteins, clotting factors MAY be tolerated
  • Knowing this, limit phlebotomy and still get Type and Screen x TWO
  • Cohort study of JW surgical patients who refused RBC transfusions found 2.5x odds increase in mortality for every 1g/dL drop post-operatively. (1)
  • Ethical concerns about patients refusing blood products when altered. (2)
    • Biblical basis:
      • Genesis 9:3-5: “But you must not eat blood that has its lifeblood still in it.”
      • Leviticus 17: “You must not eat the blood of any creature, because the life of every creature is its blood; anyone who eats it must be cut off.”

Areas of Improvement

  • Communication: There was no inter-facility hand-off done between hospitals. Patient arrived without records of procedure, name of surgeon and a poor understanding of his own medical history. ED team spent valuable time getting surgical history from outside hospital.
  • Improper Triage: Patient triaged to level 3 despite being hypotensive and complaining of weakness.
  • Cognitive Bias: MD was anchored to the recent surgical procedure as source of blood loss leading to premature closure of other causes of hypotension and anemia.
  • Rule-Based Issues: Patient only had single IV placed and single Type and Screen sent. Patient was hypotensive, supra-therapeutic and anemic…with presumed bleeding. Rule is generally that 2 IVs and 2 Type and Screens should be placed and sent on hypotensive/bleeding patients.

References

  1. Tobian AA, Ness PM, Novick H, Carson PL. Time course and etiology of death in patients with severe anemia.Transfusion, Jul2009 Part 1 of 2, Vol. 49 Issue 7, p1395-1399, 5p, p1397.
  2. Megan L. Panico, Grace Y. Jenq, and Ursula C. Brewster. When a Patient Refuses Life-Saving Care: Issues Raised When Treating a Jehovah’s Witness. American Journal of Kidney Diseases, 2011-10-01, Volume 58, Issue 4, Pages 647-653.
Edited by Adaira Landry. As with all of the emDocs cases, this is a fictional account intended for educational purposes, and any resemblance to any person living or dead is purely coincidental.

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Clinical Case 103: Midnight MacGyver Medicine

This is an exercise in medical minimalism.  I am going to throw you a case and a set of resources – you need to say how you would manage it.  I am going to release my strategy in a few days.  So here we go – here is the case…

Firstly, a little bit of background you get from the old file:

Monica is a 49 yo woman who has had a long history of renal trouble.

She was diagnosed with type 2 DM at age 21, with early nephropathy.

By age 40 she was on CAPD, and by 43 was dependent on haemodialysis.

She got lucky and was the recipient of a cadaveric transplant at age 45…..  but, that kidney isn’t doing so well. She has had multiple episodes of threatened rejection and ongoing renal impairment.

In the last year her new kidney started to pack it in and she has had yet another AV fistula formed… in anticipation of ongoing HD.

So here we are – most recently her creatinine was 500, with normal K+ and bicarb of 18.  She has advanced renal osteodystrophy, hypertension, anaemia [on darbopoeitin],  also has chronic asthma / COPD.  Oh, and her BMI is 40, with really tough IV access due to previous fistulae surgery…  good luck.

On the bright side – she has no documented ischemic / valvular heart disease.

Meds: prednisolone 5 mg, ramipril 10 mg, amlodipine 5 mg,  tacrolimus 1 mg, salmeterol inhaler, CaCO3, cinacalcet 30mg and aspirin 150 mg.

It is 5 minutes to midnight on your night shift at “Janus General” hospital in a remote location.  You are on your own.

Here is the scenario:

The Ambos roll in the door with Monica on the stretcher – she is looking pretty crook.  She called ’000′  as she was getting increasingly ‘short-winded’ and her puffers were not helping.

The ambulance crew have her on 8 L/min via a nebuliser mask with salbutamol nebs over the last 20 minutes.

Obs are:  Resp rate 36/min, pulse 110/min, SpO2 = 94%, BP is 180/110, she is afebrile and coughing with green sputum.  She is alert and oriented.  Her new fistula is buzzing nicely

A quick auscultation of her chest reveals diffuse, bilateral, coarse crackles.  A few scattered wheezes but reasonable air entry.  She is working pretty hard – tripoding.

In between gasps she indicates some (R) sided chest pain  - it appears to be pleuritic.

Her legs are both really oedematous – with pitting oedema up to her kneess… maybe a little more on the right.

The monitor shows sinus tachycardia and an ECG the same  - with maybe some slight depression of the ST segments laterally.

The differential diagnosis is looking pretty broad at the moment!  Take a moment to contemplate the possibilities….

Here is what you have:

  • A well stocked, small, rural ED
  • Oxylog ventilator – capable of NIV
  • a POC blood gas analyser (basic biochem and gas panel + lactate)
  • a bedside ultrasound machine [ of course ;-)  ]
  • two really great nurses
  • a telephone to phone a friend / specialist  - but none will be able to attend.

Here is what you do not have:

  • Any formal radiology
  • Any laboratory tests other than the POC machine
  • Any immediate, physical backup
  • Any way of transferring Monica anywhere in the next 12 hours. [ though the sun will rise in 6- usually makes things seem better!]

So – here is the challenge:

  1. Get IV access somehow!
  2. Initiate empirical therapy – what would you use up front
  3. make some sort of diagnosis (es)
  4. Make a plan for the next 12 hours (the lab and Xray department will be available then…)

Welcome to Broome.    Go!

Casey

A Prehospital Transfusion Confusion

Which is to say – endorsing conclusions founded on sparse data is worse than simply admitting the limitations of our knowledge.

Clearly, if a patient requires blood, the more, the sooner, the better with severe injury.  However, starting that transfusion outside a setting fully capable of assessing injury severity and physiology can mean wasted or inappropriate product use.

These authors attempt to show patients receiving blood in the pre-trauma center setting have markedly decreased mortality and traumatic coagulopathy.  However, they do so using a retrospective database of patients from 2003 to 2010, of which only 50 patients received pre-trauma center transfusion, compared with 1,365 who did not.  Additionally, there were diverse differences in ISS, base deficit, and total crystalloid and product transfusion.  They subsequently attempt to control for this using logistic regression and by deriving a propensity-matched cohort – which then compares 35 patients with pre-hospital transfusion with 78 patients without, but still has diverse significant differences in initial physiology and total product transfusion.

So, because of all these intrinsic differences, all their reported odds ratios are adjusted after “controlling for confounders”.  After all the statistical wrangling, "covariate-adjusted" 30 day survival was ~95% in the cohort with pre-trauma center transfusion, and ~88% in others.  The propensity-matched results showed similar odds ratios.  Unadjusted mortality in the cohorts is not presented.

Who knows what this really shows?  The data used is retrospective, heterogenous and collected over the course of 8 years, their sample of pre-trauma center transfusions is tiny, and all their reported odds ratios required huge statistical adjustments.  Pre-trauma center transfusions are probably helpful, if used judiciously, but this is not the study that shows it.

“Pretrauma Center Red Blood Cell Transfusion Is Associated With Reduced Mortality and Coagulopathy in Severely Injured Patients With Blunt Trauma”

Ethical CPR Decisions

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We spend a lot of time thinking about saving lives, and becoming expert at interventions to maximise survival.  But sometimes we need to take a step back and consider why we are doing this… what are the outcomes we would like to achieve for this patient? For this family?  It may be appropriate to set some boundaries of care.  So how do we go about having this discussion with patients and families?

EMPEM-Hayes-CPR-decisions

We are honoured to be joined by an expert in the field of ethical decision making in CPR, Dr Barbara Hayes.  Join us for a lively discussion as we navigate the perils of talking about death and dying, and the role of CPR.

Apologies for the variable audio quality on this episode.  Hopefully you will still enjoy the discussion.

 


Outline: Ethical decision-making in CPR

Intro [cp]: welcome, disclaimer
[bh]: Barbara Hayes introduction
[cp]: Relevant publication: Hayes B. Clinical model for ethical cardiopulmonary resuscitation decision-making. Internal Medicine Journal. 2013; 43:77-83.
[nl]: Nicole background / interest in ‘dying well’

[bh]: Framework for ethical decisions relating to treatment options

Examples of ethical challenges in CPR decision making:
[nl]: diabetic asthma patient
[bh]: examples from palliative care

Trust:
Sometimes there is a difference of opinion between the patient and family on the one hand, and the treating team on the other hand, about whether CPR should be provided. This is often occurring when the patient is very unwell, and the family are emotional and frightened. How do you work with this?
[nl], [bh], [cp]

Discussion:
Differences in Palliative Care vs ED
Added issues / stressors with dying child

Practical tips for the ‘less experienced’ (ie everyone):

  • Patient first
  • Family (& their grieving) second
  • Think about salvageable quality of life (cf some religious/cultural beliefs re sanctity of life regardless of quality)
  • Be honest in your communication
  • We are the medical experts, family are the expert about the patient (and what they would want, if unable to communicate)
  • Aim to all contribute to the shared pool of understanding, to reach best outcome for the patient
  • What does the patient, family, treating staff want?
  • Use the framework (for any ethical treatment decision, not just CPR)
  • Do not (completely) defer the medical decisions to the family or patient – they need to make an informed decision; guide them when appropriate
  • Remember organ donation as a positive outcome in death

Summary & final ‘take-home’ thoughts:
[cp],[nl],[bh]

Goodbye & invite comments [cp]

 

References and further reading

Hayes B.
Clinical model for ethical cardiopulmonary resuscitation decision-making.
Internal Medicine Journal. 2013; 43:77-83.
PubMed PMID: 22646807

Ehlenbach WJ et al.
Epidemiologic study on in-hospital cardiopulmonary resuscitation in the elderly.
New England Journal of Medicine. 2009; 361: 22–31.
PubMed PMID: 19571280

Hayes B.
Trust and distrust in CPR decisions.
Journal of Bioethical Inquiry. 2010; 7:111-122.

Emanuel EJ & Emanuel LL.
Four models of the physician-patient relationship.
JAMA. 1992; 267(16): 2221-2226 Review.
PubMed PMID: 1556799

 

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