November 01, 2015

Adventures in RSI

51 minutes

Pediatric airway management is a skill that integrates the three types of knowledge as described by the ancient Greeks: episteme, or theoretical knowledge, techne, or technical knowledge, and phronesis, or practical wisdom, also called prudence.

Here we’ll invoke each type of knowledge and understanding as we go beyond the anatomical issues in pediatric airway management – to the advanced decision-making aspect of RSI and the what-to-do-when the rubber-hits-the road.

Case 1: Sepsis

Laura is a 2-month-old baby girl born at 32 weeks gestational age who today has been “breathing fast” per mother. On arrival she is in severe respiratory distress with nasal flaring and intercostal retractions. Her heart rate is 160, RR 50, oxygen saturation is 88% on RA. She has fine tissue-paper like rales throughout her lung fields. Despite a trial of a bronchodilator, supplemental oxygen, even nasal CPAP and fluids, she becomes less responsive and her heart rate begins to drop relatively in the 80s to 90s – this is not a sign of improvement, but of impending cardiovascular collapse.

She is in respiratory failure from bronchiolitis and likely viral sepsis. She needs her airway taken over.

Is this child stable enough for intubation?

We have a few minutes to optimize, to resuscitate before we intubate.

Here’s an easy tip: use the sterile flushes in your IV cart and push in 20, 40, or 60 mL/kg NS. Just keep track of the number of syringes you use – it is the fastest way to get a meaningful bolus in a small child.

Alternatively, if you put a 3-way stop-cock in the IV line and attach a 30 mL syringe, you can turn the stop cock, draw up stream from the IV bag into the syringe, turn te stop cock, and push the fluid in the IV.

Induction Agent in Sepsis

The consensus recommendation for the induction agent of choice for sepsis in children is ketamine.

Etomidate is perfectly acceptable, but ketamine is actually a superior drug to etomidate in the rapid sequence intubation of children in septic shock. It rapidly provides sedation and analgesia, and supports hemodynamic stability by blocking the reuptake of catecholamines.

Paralytic Agent in Sepsis

The succinylcholine versus rocuronium debate…

Succinylcholine and its PROS

82% of RSI in the ED used succinylcholine (According to the National Emergency Airway Registry, in 2005). We know it, we are comfortable with it.

Succinylcholine produces superior intubating conditions when comparing 1 mg/kg succinylcholine versus 0.6 mg/kg rocuronium, succinylcholine is that at 45 seconds.

Succinylcholine and its CONs

Raises serum potassium in everyone, typically 0.5 to 1 mEq/L. That is not usually a problem, but for those with preexisting or inducible hyperkalemia, it can precipitate an arrest, as in renal failure, underlying neurologic or myopathic conditions like multiple sclerosis, muscular dystrophy, ALS, or those who had a stroke or a burn more than 72 hours prior. We often have limited information in critical situations.

Succinylcholine gives us a false sense of security. In children, there really is no “safe apnea” period.

Succinylcholine’s effect on the nicotinic receptors results in mydriasis, tachycardia, weakness, twitching and hypertension, and fasciculations (Think nicotine overdose: M/T/W/Th/F).

Succinylcholine’s effect on muscarinic receptors manifest (as in organophosphate overdose): SLUDGE – salivation, lacrimation, urination, defecation, GI upset or more apropos here: DUMBBELLS – diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation.

Second dose of succinylcholine – beware of the muscarinic effects and bradycardia. Co-administer atropine, 0.01 mg/kg, up to 0.5 mg IV.

Coda: succinylcholine is not that bad – we would not have had such great success with it during the early years of our specialty if it were such a terrible drug. The side effects are rare, but they can be deadly. So, what’s the alternative?

Rocuronium and its PROs

It has none of the side-effects of succinylcholine

Rocuronium and its CONs

Argument 1: the duration is too long if there is a difficult airway, since rocuronium can last over an hour. Still need to intubate, and now your patient is potentially worse.

Argument 2: succinylcholine produces better intubating conditions at 45 seconds compared to rocuronium. At 0.6 mg/kg, rocuronium is inferior to succinylcholine at all time intervals. At 1.0 mg/kg, rocuronium is still inferior at 45 seconds. At 1.2 mg/kg rocuronium – the dose now commonly recommended – there was no difference in intubating conditions, per a study by Heier et al. in Anethesia and Analgesia in 2000.

Case 2: Multitrauma

Joseph is a 3-year-old boy who is excited that there are so many guests at his house for a family party and when it’s starting to wind down and the guests begin to leave, he is unaccounted for. An unsuspecting driver of a mini-van backs over him.

He is brought in by paramedics, who are now bagging him.

Induction Agent in Trauma

Need something that is hemodynamically stable – agents such as midazolam or propofol would cause too many problems.

Etomidate is a short-acting imidazole derivative that acts on GABA-A receptors to induce loss of consciousness in 5-15 seconds. It can cause apnea, pain on injection, and myoclonus.

Etomidate reduces cerebral blood flow, reduces intracranial pressure, and reduces cerebral oxygen consumption, all while maintaining arterial blood pressure and cerebral perfusion pressure.

Ketamine is reasonable as well: there is no contraindication to ketamine except for known hydrocephalus. It is safe in head trauma. It is a good choice for the hypotensive trauma patient. TBI is not a contraindication.

In the case of the critically injured child who is normotensive, ketamine will raise his blood pressure and perhaps foster further bleeding. The goal is a good general perfusion and a balanced resuscitation, ensuring enough cerebral perfusion without disrupting nascent clots. On the other side of the spectrum, permissive hypotension is not described in children, as hypotension is a late and dangerous sign of shock.

Paralytic Agent in Trauma

Are your surgeons in an uproar about a long-acting agent and the pupillary response? Relax, it’s a myth.

Caro et al in Annals in 2011 reported that the majority of patients undergoing RSI preserved their pupillary response. Succinylcholine actually performed worse than rocuronium. In the rocuronium group, all patients preserved their pupillary response.

In the critically ill, we rethink your dosing of both the sedative and the paralytic.

In a critically ill child or adult, perfusion suffers and it affects how we administer medications. The patient’s arm-brain time or vein-to-brain time is less efficient; additionally, as the patient’s hemodynamic status softens, he becomes very sensitive to the effects of sedatives.

We need to adjust our dosing for a critically ill patient:

Decrease the sedative to avoid falling over the hemodynamic compensation cliff.

Increase the paralytic to account for prolonged arm-brain time.

Case 3: Cardiac/myocarditis/congenital heart disease

Jacob is a 6-year-old-boy with tricuspid atresia s/p Fontan procedure who’s had one week of runny nose, cough, and now 2 days of high fever, vomiting, and difficulty breathing.

The Fontan procedure is the last in a series of three palliative procedures in a child with complex cyanotic congenital heart disease with a single-ventricle physiology.

The procedure reroutes venous blood to flow passively into the pulmonary arteries, because the right ventricle has been surgically repurposed to be the systemic pump. The other most common defect with an indication for a Fontan is hypoplastic left heart syndrome.

Typical “normal” saturations are 75 and 85% on RA. Ask the parents or caregiver.

Complications of the Fontan procedure include heart failure, superior vena cava syndrome, and hypercoagulable state, and others. A patient with a Fontan can present in cardiogenic shock from heart failure, distributive shock from an increased risk of infection, hypovolemic shock from over-diuresis or insensible fluid loss – or just a functional hypovolemia from the fact that his venous return is all passive – and finally obstructive shock due to a pulmonary thromboembolism.

Types of shock mnemonic: this is how people COHDe – Cardiogenic, Obstructive, Hypovolemic, Distributive.

Do we give fluids?

Children after palliative surgery for cyanotic heart disease are volume-dependent. Even if there is a component of cardiogenic shock, they need volume to drive their circuit. Give a test dose of 10 mL/kg NS.

Pressors in Pediatric Shock

Children compensate their shock state early by increasing their SVR.

Epinephrine (adrenaline) is great at increasing the cardiac output (with minimal increase in systemic vascular resistance; tachycardia) In children the cardiac deleterious effects are not pronounced as in adults. Later when the child is stabilized, other medication such as milrinone (ionotrope and venodilator) can be used.

Epinephrine is also fantastic for cold shock when the patient is clamped down with cold extremities – the most common presentation in pediatric septic shock.

Norepinephrine (noradrenaline) is best used when you need to augment systemic vascular resistance, such as in warm shock, where the patient has loss of peripheral vascular tone.

Induction Agent in Cardiogenic Shock

A blue baby – with a R –> L shunt – needs some pinking up with ketamine

A pink baby – with a L –> R shunt – is already doing ok – don’t rock the boat – give a neutral agent like etomidate.

Myocarditis or other acquired causes of cardiogenic shock – etomidate.

Case 4: Status Epilepticus

Jessica is a 10-year-old girl with Lennox-Gastaut syndrome who arrives to your ED in status epilepticus. She had been reasonably controlled on valproic acid, clonazepam, and a ketogenic diet, but yesterday she went to a birthday party, got into some cake, and has had stomach aches – she’s been refusing to take her medications today.

On arrival, she is hypoventilating, with HR 130s, BP 140/70, SPO2 92% on face mask. She now becomes apneic.

Induction Agent in Status Epilepticus

Many choices, but we can use the properties of a given agent to our advantage. She is normo-to-hypertensive and tachycardic. She has been vomiting. A nice choice here would be propofol.

Propofol as both a sedative and anti-epileptic agent works primarily on GABA-A and endocannabinoid receptors to provide a brief, but deep hypnotic sedation. Side effects can include hypotension, which is often transient and resolves without treatment. Apnea is the most common side-effect.

Ketamine would be another good choice here, for its anti-epileptic activity.

Paralytic Agent in Status Epilepticus

Rocuronium (in general), as there are concerns of a neurologic comorbidity.

Housekeeping in RSI

What size catheter doe I use? If you know your ETT size, then it is just a matter of multiplication by 2, 3, 4, or 5.

Remember this: 2, 3, 4 – Tube, Tape, Tap

The NG/OG/Foley is 2 x the ETT – tube

The ETT should be taped at a depth of 3 x the ETT size – tape

A chest tube size 4 x the ETT – tap

In summary, in these cases of sepsis, multitrauma, cardiogenic shock, and status epilepticus:

Resuscitate before you intubate

Use the agent’s specific properties and talents to your benefit

Adjust the dose in critically ill patients: decrease the sedative, increase the paralytic

Have post-intubation care ready: sedation, verification, NG/OG/foley

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By Tim Horeczko, MD, MSCR, FACEP, FAAP

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