The use of inhaled nitric oxide is established in certain groups of patients: it improves oxygenation (but not survival) in patients with acute respiratory distress syndrome(1), and it is used in neonatology for management of persistent pulmonary hypertension of the newborn(2). But it can be applied in other resuscitation settings: in arrested or peri-arrest patients with pulmonary hypertension.
Read this (modified) description of a case managed by one of my resuscitationist friends from an overseas location:
A young lady suffered a placental abruption requiring emergency hysterectomy. She arrested twice in the operating room after suspected amniotic fluid embolism. She had fixed dilated pupils.
She developed extreme pulmonary hypertension with suprasystemic pulmonary artery pressures, and she went down the pulmonary HT spiral as I stood there. On ultrasound her distended RV was making her LV totally collapse. She arrested. Futile CPR was started.
I have never had an extreme pulmonary HT survive an arrest. I grabbed a bag and rapidly set up a manual inhaled Nitric Oxide system and bagged and begged…
She achieved ROSC after some minutes. A repeat ultrasound showed a well functioning LV and less dilated RV.
Today, after 12 hours she is opening her eyes and obeying commands. Still a long way to go, but alive.
It sounds impressive. I don’t have more case details, and don’t know how confident they could be about the diagnosis of amniotic fluid embolism but the presentation certainly fits with acute pulmonary hypertension with RV failure. The use of inhaled nitric oxide has certainly been described for similar scenarios before(3). But it raises bigger questions: is this something we should all be capable of? Are there cardiac arrests involving or caused by pulmonary hypertension that will not respond to resuscitation without nitric oxide?
Inhaled nitric oxide is a pulmonary vasodilator. It decreases right-ventricular afterload and improves cardiac index by selectively decreasing pulmonary vascular resistance without causing systemic hypotension(4).
RV failure and pulmonary hypertension
Patients may become shocked or suffer cardiac arrest due to acute right ventricular dysfunction. This may be due to a primary cardiac cause such as right ventricular infarction (always consider this in a hypotensive patient with inferior STEMI, and confirm with a right ventricular ECG and/or echo). Alternatively it could be due to a pulmonary or systemic cause resulting in severe pulmonary hypertension, causing secondary right ventricular dysfunction. The commonest causes of acute pulmonary hypertension are massive PE, sepsis, and ARDS(5).
The haemodynamic consequences of RV failure are reduced pulmonary blood flow and inadequate left ventricular filling, leading to decreased cardiac output, shock, and arrest. In severe acute pulmonary hypertension the RV distends, resulting in a shift of the interventricular septum which compresses the LV and further inhibits LV filling (the concept of ventricular interdependence).
What’s wrong with standard ACLS?
In some patients with PHT who arrest, CPR may be ineffective due to a failure to achieve adequate pulmonary blood flow and ventricular filling. In one study of patients with known chronic PHT who arrested in the ICU, survival rates even for ventricular fibrillation were extremely poor and when measured end tidal carbon dioxide levels were very low. In the same study it was noted that some of the survivors had received an intravenous bolus administration of iloprost, a prostacyclin analogue (and pulmonary vasodilator) during CPR(6).
CPR may therefore be ineffective. Intubation and positive pressure ventilation may also be associated with haemodynamic deterioration in PHT patients(7), and intravenous epinephrine (adrenaline) has variable effects on the pulmonary circulation which could be deleterious(8).
If inhaled nitric oxide (iNO) can improve pulmonary blood flow and reduce right ventricular afterload, it could theoretically be of value in cases of shock or arrest with RV failure, especially in cases of pulmonary hypertension; these are patients who otherwise have poor outcomes and may not benefit from CPR.
Is the use of iNO described in shock or arrest?
Numerous case reports and series demonstrate recovery from shock or arrest following nitric oxide use in various situations of decompensated right ventricular failure from pulmonary hypertension secondary to pulmonary fibrotic disease(9), pneumonectomy surgery(10), and pulmonary embolism(11) including post-embolectomy(12).
Acute hemodynamic improvement was demonstrated following iNO therapy in a series of right ventricular myocardial infarction patients with cardiogenic shock(13).
A recent systematic review of inhaled nitric oxide in acute pulmonary embolism documented improvements in oxygenation and hemodynamic variables, “often within minutes of administration of iNO”. The authors state that these case reports underscore the need for randomised controlled trials to establish the safety and efficacy of iNO in the treatment of massive acute PE(14).
Why aren’t they telling us to use it?
If iNO may be helpful in certain cardiac arrest patients, why isn’t ILCOR recommending it? Actually it is mentioned – in the context of paediatric life support. The European Resuscitation Council states:
ERC Guideline: (Paediatric) Pulmonary hypertension
There is an increased risk of cardiac arrest in children with pulmonary hypertension.
Follow routine resuscitation protocols in these patients with emphasis on high FiO2 and alkalosis/hyperventilation because this may be as effective as inhaled nitric oxide in reducing pulmonary vascular resistance.
Resuscitation is most likely to be successful in patients with a reversible cause who are treated with intravenous epoprostenol or inhaled nitric oxide.
If routine medications that reduce pulmonary artery pressure have been stopped, they should be restarted and the use of aerosolised epoprostenol or inhaled nitric oxide considered.
Right ventricular support devices may improve survival
Should we use it?
So if acute (or acute on chronic) pulmonary hypertension can be suspected or demonstrated based on history, examination, and echo findings, and the patient is in extremis, it might be anticipated that standard ACLS approaches are likely to be futile (as they often are if the underlying cause is not addressed). One might consider attempts to induce pulmonary vasodilation to improve pulmonary blood flow and LV filling, improving oxygenation, and reducing RV afterload as means of reversing acute cor pulmonale.
Are there other pulmonary vasodilators we can use?
iNO is not the only means of inducing pulmonary vasodilation. Oxygen, hypocarbia (through hyperventilation)(15), and alkalosis are all known pulmonary vasodilators, the latter providing an argument for intravenous bicarbonate therapy from some quarters(16). Prostacyclin is a cheaper alternative to iNO(17) and can be given by inhalation or intravenously, although is more likely to cause systemic hypotension than iNO. Some inotropic agents such as milrinone and levosimendan can lower pulmonary vascular resistance(18).
What’s the take home message?
The take home message for me is that acute pulmonary hypertension provides yet another example of a condition that requires the resuscitationist to think beyond basic ACLS algorithms and aggressively pursue and manage the underlying cause(s) of shock or arrest. Inhaled pulmonary vasodilators may or may not be available but, as always, whatever resources and drugs are used, they need to be planned for well in advance. What’s your plan?
1. Adhikari NKJ, Dellinger RP, Lundin S, Payen D, Vallet B, Gerlach H, et al.
Inhaled Nitric Oxide Does Not Reduce Mortality in Patients With Acute Respiratory Distress Syndrome Regardless of Severity.
Critical Care Medicine. 2014 Feb;42(2):404–12
2. Steinhorn RH.
Neonatal pulmonary hypertension.
Pediatric Critical Care Medicine. 2010 Mar;11:S79–S84 Full text
3. McDonnell NJ, Chan BO, Frengley RW.
Rapid reversal of critical haemodynamic compromise with nitric oxide in a parturient with amniotic fluid embolism.
International Journal of Obstetric Anesthesia. 2007 Jul;16(3):269–73
4. Creagh-Brown BC, Griffiths MJ, Evans TW.
Bench-to-bedside review: Inhaled nitric oxide therapy in adults.
Critical Care. 2009;13(3):221 Full text
5. Tsapenko MV, Tsapenko AV, Comfere TB, Mour GK, Mankad SV, Gajic O.
Arterial pulmonary hypertension in noncardiac intensive care unit.
Vasc Health Risk Manag. 2008;4(5):1043–60 Full text
6. Hoeper MM, Galié N, Murali S, Olschewski H, Rubenfire M, Robbins IM, et al.
Outcome after cardiopulmonary resuscitation in patients with pulmonary arterial hypertension.
American Journal of Respiratory and Critical Care Medicine. 2002 Feb 1;165(3):341–4.
7. Höhn L, Schweizer A, Morel DR, Spiliopoulos A, Licker M.
Circulatory failure after anesthesia induction in a patient with severe primary pulmonary hypertension.
Anesthesiology. 1999 Dec;91(6):1943–5 Full text
8. Witham AC, Fleming JW.
The effect of epinephrine on the pulmonary circulation in man.
J Clin Invest. 1951 Jul;30(7):707–17 Full text
9. King R, Esmail M, Mahon S, Dingley J, Dwyer S.
Use of nitric oxide for decompensated right ventricular failure and circulatory shock after cardiac arrest.
Br J Anaesth. 2000 Oct;85(4):628–31. Full text
10. Fernández-Pérez ER, Keegan MT, Harrison BA.
Inhaled nitric oxide for acute right-ventricular dysfunction after extrapleural pneumonectomy.
Respir Care. 2006 Oct;51(10):1172–6 Full text
11. Summerfield DT, Desai H, Levitov A, Grooms DA, Marik PE.
Inhaled Nitric Oxide as Salvage Therapy in Massive Pulmonary Embolism: A Case Series.
Respir Care. 2012 Mar 1;57(3):444–8 Full text
12. Schenk P, Pernerstorfer T, Mittermayer C, Kranz A, Frömmel M, Birsan T, et al.
Inhalation of nitric oxide as a life-saving therapy in a patient after pulmonary embolectomy.
Br J Anaesth. 1999 Mar;82(3):444–7 Full text
13. Inglessis I, Shin JT, Lepore JJ, Palacios IF, Zapol WM, Bloch KD, et al.
Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock.
Journal of the American College of Cardiology. 2004 Aug;44(4):793–8 Full text
14. Bhat T, Neuman A, Tantary M, Bhat H, Glass D, Mannino W, Akhtar M, Bhat A, Teli S, Lafferty J.
Inhaled nitric oxide in acute pulmonary embolism: a systematic review.
Rev Cardiovasc Med 2015;16(1):1–8.
15. Mahdi M, Joseph NJ, Hernandez DP, Crystal GJ, Baraka A, Salem MR.
Induced hypocapnia is effective in treating pulmonary hypertension following mitral valve replacement.
Middle East J Anaesthesiol. 2011 Jun;21(2):259-67
16. Evans S, Brown B, Mathieson M, Tay S.
Survival after an amniotic fluid embolism following the use of sodium bicarbonate.
BMJ Case Rep. 2014;2014
17. Fuller BM, Mohr NM, Skrupky L, Fowler S, Kollef MH, Carpenter CR.
The Use of Inhaled Prostaglandins in Patients With ARDS: A Systematic Review and Meta-analysis.
Chest. 2015 Jun;147(6):1510–22 Full text
18. LITFL: Right Ventricular Failure
Life In The Fast Lane iNO info
Comments Off on Post-arrest hypothermia in children did not improve outcome
Many clinicians extrapolate adult research findings to paediatric patients because there’s no alternative, and until now we’ve had to do that with post-cardiac arrest therapeutic hypothermia after paediatric cardiac arrest.
However the THAPCA trial in the New England Journal of Medicine now provides child-specific data.
It was a multicentre trial in the US which included children between 2 days and 18 years of age, who had had an out-of-hospital cardiac arrest and remained comatose after return of circulation. They were randomised to therapeutic hypothermia (target temperature, 33.0°C) or therapeutic normothermia (target temperature, 36.8°C) within 6 hours after the return of circulation.
Therapeutic hypothermia, as compared with therapeutic normothermia, did not confer a significant benefit with respect to survival with good functional outcome at 1 year, and survival at 12 months did not differ significantly between the treatment groups.
These findings are similar to the adult TTM trial, although there are some interesting differences. In the paediatric study, the duration of temperature control was longer (120 hrs vs 36 hrs in the adult study), respiratory conditions were the predominant cause of paediatric cardiac arrest (72%), and there were only 8% shockable rhythms in the paediatric patients, compared with 80% in the adult study.
The full text is available here.
Therapeutic Hypothermia after Out-of-Hospital Cardiac Arrest in Children
N Engl J Med. 2015 Apr 25
Background: Therapeutic hypothermia is recommended for comatose adults after witnessed out-of-hospital cardiac arrest, but data about this intervention in children are limited.
Methods: We conducted this trial of two targeted temperature interventions at 38 children’s hospitals involving children who remained unconscious after out-of-hospital cardiac arrest. Within 6 hours after the return of circulation, comatose patients who were older than 2 days and younger than 18 years of age were randomly assigned to therapeutic hypothermia (target temperature, 33.0°C) or therapeutic normothermia (target temperature, 36.8°C). The primary efficacy outcome, survival at 12 months after cardiac arrest with a Vineland Adaptive Behavior Scales, second edition (VABS-II), score of 70 or higher (on a scale from 20 to 160, with higher scores indicating better function), was evaluated among patients with a VABS-II score of at least 70 before cardiac arrest.
Results: A total of 295 patients underwent randomization. Among the 260 patients with data that could be evaluated and who had a VABS-II score of at least 70 before cardiac arrest, there was no significant difference in the primary outcome between the hypothermia group and the normothermia group (20% vs. 12%; relative likelihood, 1.54; 95% confidence interval [CI], 0.86 to 2.76; P=0.14). Among all the patients with data that could be evaluated, the change in the VABS-II score from baseline to 12 months was not significantly different (P=0.13) and 1-year survival was similar (38% in the hypothermia group vs. 29% in the normothermia group; relative likelihood, 1.29; 95% CI, 0.93 to 1.79; P=0.13). The groups had similar incidences of infection and serious arrhythmias, as well as similar use of blood products and 28-day mortality.
Conclusions: In comatose children who survived out-of-hospital cardiac arrest, therapeutic hypothermia, as compared with therapeutic normothermia, did not confer a significant benefit in survival with a good functional outcome at 1 year.
Comments Off on CPR in Pectus Excavatum
Some pectus excavatum patients have a metal ‘Nuss bar’ inserted below the sternum which can make chest compressions more difficult. In those without one, standard compression depths compress the left ventricle more than in non-pectus subjects, and might lead to myocardial injury.
This has led to a recommendation in the journal Resuscitation:
“Until further studies are available, we recommend strong chest compressions, according to the current guidelines, in PE patients with a sternal Nuss bar and, to minimize the risk of myocardial injury, we suggest a reduced chest compression depth (approximately 3–4 cm) at the level of lower half of the sternum in PE patients who have not had corrective surgery.“
Cardiopulmonary resuscitation in pectus excavatum patients: Is it time to say more?
Resuscitation. 2014 Dec 10.[Epub ahead of print]
Almost two-thirds of patients with extradural haematoma and bilateral fixed dilated pupils survived after surgery, with over half having a good outcome
Neurosurgeon, HEMS doctor, and all round good egg Mark Wilson was on the RAGE podcast recently and mentioned favourable outcomes from neurosurgery in patients with extradural (=epidural) haematomas who present with bilateral fixed dilated pupils (BFDP). Here’s his paper that gives the figures – a systematic review and meta-analysis.
A total of 82 patients with BFDP who underwent surgical evacuation of either subdural or extradural haematoma were identified from five studies – 57 with subdural (SDH) and 25 with extradural haematomas (EDH).
In patients with EDH and BFDP mortality was 29.7% (95% CI 14.7% to 47.2%) and 54.3% had a favourable outcome (95% CI 36.3% to 71.8%).
Only 6.6% of patients with SDH and BFDP had a good functional outcome.
Clearly there is potential for selection bias and publication bias, but these data certainly suggest an aggressive surgical approach is appropriate in some patients with BFDP.
The authors comment on the pessimism that accompanies these cases, which potentially denies patients opportunities for recovery:
“We believe that 54% of patients with extradural haematoma with BFDPs having a good outcome is an underappreciated prognosis, and the perceived poor prognosis of BFDPs (from all causes) has influenced decision making deeming surgery inappropriately futile in some cases.”
Scotter J, Hendrickson S, Marcus HJ, Wilson MH.
Prognosis of patients with bilateral fixed dilated pupils secondary to traumatic extradural or subdural haematoma who undergo surgery: a systematic review and meta-analysis.
Emerg Med J 2014 e-pub ahead of print Nov 11;:1–7
Primary objective To review the prognosis of patients with bilateral fixed and dilated pupils secondary to traumatic extradural (epidural) or subdural haematoma who undergo surgery.
Methods A systematic review and meta-analysis was performed using random effects models. The Cochrane Central Register of Controlled Trials and PubMed databases were searched to identify relevant publications. Eligible studies were publications that featured patients with bilateral fixed and dilated pupils who underwent surgical evacuation of traumatic extra-axial haematoma, and reported on the rate of favourable outcome (Glasgow Outcome Score 4 or 5).
Results Five cohort studies met the inclusion criteria, collectively reporting the outcome of 82 patients. In patients with extradural haematoma, the mortality rate was 29.7% (95% CI 14.7% to 47.2%) with a favourable outcome seen in 54.3% (95% CI 36.3% to 71.8%). In patients with acute subdural haematoma, the mortality rate was 66.4% (95% CI 50.5% to 81.9%) with a favourable outcome seen in 6.6% (95% CI 1.8% to 14.1%).
Conclusions and implications of key findings Despite the poor overall prognosis of patients with closed head injury and bilateral fixed and dilated pupils, our findings suggest that a good recovery is possible if an aggressive surgical approach is taken in selected cases, particularly those with extradural haematoma.
Comments Off on Blunt traumatic arrest in kids
Traumatic cardiac arrest outcomes are not great, but they’re not so bad that resuscitation is futile – a subject I’ve ranted about before.
The largest study on blunt traumatic arrest in children to date has been published, showing that 340 / 7766 kids without signs of life in the field survived to hospital discharge. Neurological status at discharge was not documented. However, this represents 4.4%, or in other words for every 22 blunt traumatically arrested children who underwent prehospital resuscitation, one survived to discharge. The authors describe this survival as ‘dismal’. It’s not great, but my take on it is that survival is possible and in most cases resuscitation should be attempted.
The authors state:
“Based on these data, EMS providers should not be discouraged from resuscitating blunt pediatric trauma patients found in the field with no signs of life“
While the major focus should be on injury prevention, it is worthwhile considering whether more advanced resuscitation in the field could be provided to further increase the number of neurologically intact survivors.
Survival of pediatric blunt trauma patients presenting with no signs of life in the field
J Trauma Acute Care Surg. 2014 Sep;77(3):422-6
BACKGROUND: Prehospital traumatic cardiopulmonary arrest is associated with dismal prognosis, and patients rarely survive to hospital discharge. Recently established guidelines do not apply to the pediatric population because of paucity of data. The study objective was to determine the survival of pediatric patients presenting in the field with no signs of life after blunt trauma.
METHODS: We conducted a retrospective analysis of the National Trauma Data Bank research data set (2002-2010). All patients 18 years and younger with blunt traumatic injuries were identified (DRG International Classification of Diseases-9th Rev. codes 800-869). No signs of life (SOL) was defined on physical examination findings and included the following: pulse, 0; respiratory rate, 0; systolic blood pressure, 0; and no evidence of neurologic activity. These same criteria were reassessed on arrival at the emergency department (ED). Furthermore, we examined patients presenting to the ED who underwent resuscitative thoracotomy (Current Procedural Terminology code 34.02). Our primary outcome was survival to discharge from the hospital.
RESULTS: There were a total of 3,115,597 pediatric patients who were found in the field after experiencing blunt trauma. Of those, 7,766 (0.25%) had no SOL. Seventy percent of the patients with no SOL in the field were male. Survival to hospital discharge of all patients presenting with no SOL was 4.4% (n = 340). Twenty-five percent of the patients in the field with no SOL were successfully resuscitated in the field and regained SOL by the time they arrived to the ED (n = 1,913). Of those patients who regained SOL, 13.8% (n = 265) survived to hospital discharge. For patients in the field with no SOL, survival to discharge was significantly higher in patients who did not receive a resuscitative thoracotomy than in those who did.
CONCLUSION: Survival of pediatric blunt trauma patients in the field without SOL is dismal. Resuscitative thoracotomy poses a heightened risk of blood-borne pathogen exposure to involved health care workers and is associated with a significantly lower survival rate.
Patients in cardiac arrest due to severe hypothermia benefit from extracorporeal rewarming, and it is often recommended that they are treated at centres capable of providing cardiopulmonary bypass or extracorporeal membrane oxygenation (ECMO).
But what if they’re brought to a centre that doesn’t have those facilities?
If you work in such a centre do you have a plan, and are you familiar with what equipment you could use?
One option if you have an ICU is to provide extracorporeal warming using a haemofiltration machine used for renal replacement therapy(1). A double lumen haemofiltration catheter is inserted into a central vein and an ICU nurse can often do the rest, although some variables have to be set by the intensivist, often aided by a standard renal replacement therapy prescription chart. The machines are mobile and can be wheeled into the resus room (I have practiced this set up in resus). It might be worth discussing and practicing this option with your ICU.
Another extracorporeal option is to rig up a rapid infusion device such as a ‘Level 1’ to connect to arterial and venous catheters so that blood from the patient flows through and is warmed by the machine before being returned to the patient(2). Rapid rewarming has been achieved by this method but it requires some modification to the usual set up and so is much less likely to be a realistic option for most teams doing this on very rare occasions.
Less technical options are the traditionally taught warm saline lavage of body cavities such as the thorax and the peritoneal cavity. These can be achieved with readily available catheters and of course should be combined with ventilation with warmed gas and administration of warm intravenous fluid.
Thoracic lavage can be achieved with open thoracotomy or tube thoracostomy. One or two chest tubes can be placed on each side. One technique was described as:
Two 36 French chest tubes were placed in each hemithorax. One tube was placed in the fourth intercostal space in the mid-clavicular line. Another tube was placed into the sixth intercostal space in the mid-axillary line. Sterile saline at 39.0◦C was infused by gravity into each superior chest tube and allowed to drain passively through each inferior tube.(3)
Rapid rewarming at a rate of 6.8◦C per hour was achieved in an arrested hypothermic man using peritoneal lavage. It was done in the operating room with peritoneal lavage (saline 40◦C) with a rapid infusion system (Level 1) through two laparoscopic access sites. It was combined with external forced air rewarming and warm intravenous infusions(4).
Finally some devices manufactured for inducing hypothermia in post-cardiac arrest patients can also be used to rewarm patients, which might be endovascular devices, such as the Cool Line® catheter(5), or external, such as the Arctic Sun® Temperature Management System(6). It’s definitely worth finding out what your critical care services have as far as this equipment goes.
In summary, although the ‘exam answer’ for cardiac arrest due to profound hypothermia is often ECMO/cardiopulmonary bypass, in most centres that’s not an option. It’s helpful to remind ourselves that (1) other extracorporeal rewarming options exist and (2) non-extracorporeal techniques can provide rapid rewarming.
1. Spooner K, Hassani A. Extracorporeal rewarming in a severely hypothermic patient using venovenous haemofiltration in the accident and emergency department. J Accid Emerg Med. 2000 Nov;17(6):422–4. Full text
2. Gentilello LM, Cobean RA, Offner PJ, Soderberg RW, Jurkovich GJ. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. The Journal of Trauma: Injury, Infection, and Critical Care. 1992 Mar;32(3):316–25 PubMed
3. Plaisier BR. Thoracic lavage in accidental hypothermia with cardiac arrest — report of a case and review of the literature. Resuscitation. 2005 Jul;66(1):99–104. PubMed
4. Gruber E, Beikircher W, Pizzinini R, Marsoner H, Pörnbacher M, Brugger H, et al. Non-extracorporeal rewarming at a rate of 6.8°C per hour in a deeply hypothermic arrested patient. Resuscitation. 2014 Aug;85(8):e119–20. PubMed
5. Kiridume K, Hifumi T, Kawakita K, Okazaki T, Hamaya H, Shinohara N, et al. Clinical experience with an active intravascular rewarming technique for near-severe hypothermia associated with traumatic injury. Journal of Intensive Care. BioMed Central Ltd; 2014;2(1):11. link to abstract
6. Cocchi MN, Giberson B, Donnino MW. Rapid rewarming of hypothermic patient using arctic sun device. Journal of Intensive Care Medicine. 2012 Mar;27(2):128–30. PubMed
Comments Off on When to Stop Resuscitation
My talk at the SmaccGOLD conference in March 2014
Here are the slides:
‘Traditional’ rapid sequence induction of anaesthesia is often described with inclusion of cricoid pressure and the strict omission of any artifical ventilation between paralytic drug administration and insertion of the tracheal tube. These measures are aimed at preventing pulmonary aspiration of gastric contents although there is no convincing evidence base to support that. However it is known that cricoid pressure can worsen laryngoscopic view and can occlude the paediatric airway. We also know that children desaturate quickly after the onset of apnoea, and although apnoeic diffusion oxygenation via nasal cannula can prevent or delay that, in some cases it may be preferable to bag-mask ventilate the patient while awaiting full muscle relaxation for laryngoscopy.
A Swiss study looked at 1001 children undergoing RSI for non-cardiac surgery. They used a ‘controlled rapid sequence induction and intubation (cRSII)’ approach for children assumed to have full stomachs. This procedure resembled RSI the way it is currently done in many modern critical care settings, including the retrieval service I work for:
- No cricoid pressure
- Ketamine for induction if haemodynamically unstable
- A non-depolarising neuromuscular blocker rather than succinylcholine
- No cricoid pressure
- Gentle facemask ventilation to maintain oxygenation until intubation conditions achieved
- Intubation with a cuffed tracheal tube
- Still no cricoid pressure
The authors comment:
The main finding was that cRSII demonstrated a considerably lower incidence of oxygen desaturation and consecutive hemodynamic adverse events during anesthesia induction than shown by a previous study on classic RSII in children. Furthermore, there was no incidence of pulmonary aspiration during induction, laryngoscopy, and further course of anesthesia.
Looks like more dogma has been lysed, and this study supports the current trajectory away from traditional teaching towards an approach more suitable for critically ill patients.
Controlled rapid sequence induction and intubation – an analysis of 1001 children
Paediatr Anaesth. 2013 Aug;23(8):734-40
BACKGROUND: Classic rapid sequence induction puts pediatric patients at risk of cardiorespiratory deterioration and traumatic intubation due to their reduced apnea tolerance and related shortened intubation time. A ‘controlled’ rapid sequence induction and intubation technique (cRSII) with gentle facemask ventilation prior to intubation may be a safer and more appropriate approach in pediatric patients. The aim of this study was to analyze the benefits and complications of cRSII in a large cohort.
METHODS: Retrospective cohort analysis of all patients undergoing cRSII according to a standardized institutional protocol between 2007 and 2011 in a tertiary pediatric hospital. By means of an electronic patient data management system, vital sign data were reviewed for cardiorespiratory parameters, intubation conditions, general adverse respiratory events, and general anesthesia parameters.
RESULTS: A total of 1001 patients with cRSII were analyzed. Moderate hypoxemia (SpO2 80-89%) during cRSII occurred in 0.5% (n = 5) and severe hypoxemia (SpO2 <80%) in 0.3% of patients (n = 3). None of these patients developed bradycardia or hypotension. Overall, one single gastric regurgitation was observed (0.1%), but no pulmonary aspiration could be detected. Intubation was documented as ‘difficult’ in two patients with expected (0.2%) and in three patients with unexpected difficult intubation (0.3%). The further course of anesthesia as well as respiratory conditions after extubation did not reveal evidence of ‘silent aspiration’ during cRSII.
CONCLUSION: Controlled RSII with gentle facemask ventilation prior to intubation supports stable cardiorespiratory conditions for securing the airway in children with an expected or suspected full stomach. Pulmonary aspiration does not seem to be significantly increased.
Comments Off on Palpating neonatal tracheal tubes
A technique was evaluated involving palpation of the tube tip in the suprasternal notch, which in this small study was superior to insertion length based on a weight-based nomogram.
The suprasternal notch was chosen because it anatomically corresponds to vertebral level T2, close to the optimal position at the mid-tracheal point. Correct position on the chest radiograph was defined as any position <0.5 cm above the interclavicular midpoint and more than 1 cm above the carina.
During tracheal tube placement, the tip was gently palpated in the suprasternal notch with the index or little finger of the left hand while holding the body of the tube with the fingers of the right hand. The tube tip was adjusted until the bevelled edge was just palpable in the the suprasternal notch.
Digital palpation of endotracheal tube tip as a method of confirming endotracheal tube position in neonates: an open-label, three-armed randomized controlled trial.
Paediatr Anaesth. 2013 Oct;23(10):934-9
OBJECTIVE: To compare the malposition rates of endotracheal tubes (ETTs) when the insertional length (IL) is determined by a weight-based nomogram versus when IL is determined by palpation of the ETT tip.
DESIGN: Open-label, randomized controlled trial (RCT).
SETTING: Level III neonatal intensive care unit (NICU).
SUBJECTS: All newborn babies admitted in NICU requiring intubation.
INTERVENTIONS: Subjects were randomly allocated to one of three groups, wherein IL was determined by (i) weight-based nomogram alone, (ii) weight-based nomogram combined with suprasternal palpation of ETT tip performed by specially trained neonatology fellows, or (iii) combination of weight-based and suprasternal methods by personnel not specially trained.
PRIMARY OUTCOME: Rate of malposition of ETT as judged on chest X-ray (CXR).
RESULTS: Fifty seven babies were randomized into group 1(n = 15), group 2 (n = 20), and group 3 (n = 22). The proportion of correct ETT placement was highest in group 2, being 66.7%, 83.3%, and 66.7% in groups 1 through 3, respectively (P value = 0.58). No complication was attributable to palpation technique.
CONCLUSION: Suprasternal palpation shows promise as a simple, safe, and teachable method of confirming ETT position in neonates.
Comments Off on Atropine for Paediatric RSI?
In some areas it has been traditional to pre-medicate or co-medicate with atropine when intubating infants and children, despite a lack of any evidence showing benefit. It is apparently still in the American Pediatric Advanced Life Support (PALS) Provider Manual when age is less than 1 year or age is 1–5 years and receiving succinylcholine. However it is not recommended with rapid sequence intubation in the British and Australasian Advanced Paediatric Life Support manual and course.
A French non-randomised observational study compares intubations with and without atropine in the neonatal and paediatric critical care setting. Atropine use was associated with significant acceleration of heart rate, and no atropine use was associated with a higher incidence of new dysrhythmia, the most common being junctional rhythm, but with none appearing to be clinically significant.
The incidence of the most important peri-intubation cause of bradycardia – hypoxia – is not reported. It is also not clear how many intubation attempts were required. The authors admit:
“it is not possible using our methodology to deduce whether bradycardia was due to hypoxia, laryngoscopy, or sedation drugs.“
Actual rapid sequence was rarely employed – their use of muscle relaxants was low – making this difficult to extrapolate to modern emergency medicine / critical care practice.
My take home message here is that this study provides no argument whatsoever for the addition of atropine in routine RSI in the critically ill child. Why complicate a procedure with an unnecessary tachycardia-causing drug when the focus should be on no desat / no hypotension / first look laryngoscopy?
The Effect of Atropine on Rhythm and Conduction Disturbances During 322 Critical Care Intubations
Pediatr Crit Care Med. 2013 Jul;14(6):e289-97
OBJECTIVES: Our objectives were to describe the prevalence of arrhythmia and conduction abnormalities before critical care intubation and to test the hypothesis that atropine had no effect on their prevalence during intubation.
DESIGN: Prospective, observational study.
SETTING: PICU and pediatric/neonatal intensive care transport.
SUBJECTS: All children of age less than 8 years intubated September 2007-2009. Subgroups of intubations with and without atropine were analyzed.
MEASUREMENT AND MAIN RESULTS: A total of 414 intubations were performed in the study period of which 327 were available for analysis (79%). Five children (1.5%) had arrhythmias prior to intubation and were excluded from the atropine analysis. Atropine was used in 47% (152/322) of intubations and resulted in significant acceleration of heart rate without provoking ventricular arrhythmias. New arrhythmias during intubation were related to bradycardia and were less common with atropine use (odds ratio, 0.14 [95% CI, 0.06-0.35], p < 0.001). The most common new arrhythmia was junctional rhythm. Acute bundle branch block was observed during three intubations; one Mobitz type 2 rhythm and five ventricular escape rhythms occurred in the no-atropine group (n = 170). Only one ventricular escape rhythm occurred in the atropine group (n = 152) in a child with an abnormal heart. One child died during intubation who had not received atropine.
CONCLUSIONS: Atropine significantly reduced the prevalence of new arrhythmias during intubation particularly for children over 1 month of age, did not convert sinus tachycardia to ventricular tachycardia or fibrillation, and may contribute to the safety of intubation.