All posts by Tim Horeczko

PEM Playbook – Approach to Shock

Originally published at Pediatric Emergency Playbook on June 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

Do we recognize shock early enough?

How do we prioritize our interventions?

Are we making our patient better or worse?

World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately.

So, what is shock?

Simply put, shock is the inadequate delivery of oxygen to your tissues.  That’s it.  Our main focus is on improving our patient’s perfusion.

Oxygen delivery to the tissues depends on cardiac output, hemoglobin concentration, the oxygen saturation of the hemoglobin you have, and the environmental partial pressure of oxygen.

At the bedside, we can measure some of these things, directly or indirectly.  Did you notice, however, that blood pressure is not part of the equation?  The reason for that is that blood pressure is really an indirect proxy for perfusion – it’s not necessary the ultimate goal.

The equation here is a formality:

DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2  x 0.003)

Shock CAN be associated with a low blood pressure,

but shock is not DEFINED by a low blood pressure.

Compensated Shock: tachycardia with poor perfusion.  A child compensates for low cardiac output with tachycardia and a increase in systemic vascular resistance.

Decompensated Shock: frank hypotension, an ominous, pre-arrest phenomenon.

 

Shock is multifactorial, but we need to identify a primary cause to prioritize interventions.

How they “COHDe”: Cardiogenic, Obstructive, Hypovolemic, and Distributive.

Cardiogenic Shock

All will present with tachycardia out of proportion to exam, and sometimes with unexplained belly pain, usually due to hepatic congestion.  The typical scenario in myocarditis is a precipitous decline after what seemed like a run-of-the-mill URI.

Cardiogenic shock in children can be from congenital heart disease or from acquired etiologies, such as myocarditis.  Children, like adults, present in cardiogenic shock in any four of the following combinations:warm, cold, wet, or dry.

“Warm and Dry”

A child with heart failure is “warm and dry” when he has heart failure signs (weight gain, mild hepatomegaly), but has enough forward flow that he has not developed pulmonary venous congestion.  A warm and dry presentation is typically early in the course, and presents with tachycardia only.

“Warm and Wet”

If he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and seesome respiratory distress.  Infants with a “warm and wet” cardiac presentation sometimes show sacral edema – it is their dependent region, equivalent to peripheral edema as we see in adults with right-sided failure.

“Warm” patients – both warm and dry and warm and wet — typically have had a slower onset of their symptoms, and time to compensate partially. Cool patients are much sicker.

“Cold and Dry”

A patient with poor cardiac output; he is doing everything he can to compensate with increased peripheral vascular resistance, which will only worsen forward flow.  Children who have a “cold and dry” cardiac presentation may have oliguria, and are often very ill appearing, with altered mental status.

“Cold and Wet”

The sickest of the group, this patient is so clamped down peripherally that it is now hindering forward flow, causing acute congestion, and pulmonary venous back-up.  You will see cool, mottled extremities.

Cardiogenic Shock: Act

Use point-of-care cardiac ultrasound:

Good Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion.

Pericardial Effusion? Get ready to aspirate.

Ventricle Size? Collapsed, dilated, or normal.

Careful with fluids — patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion.

Pressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg/kg/minute.  The usual adult starting range will end up being 1 to 10 mcg/min.

Avoid norepinephrine, as it increases systemic vascular resistance, may affect afterload.

Just say no to dopamine: increased mortality when compared to epinephrine.

 

Obstructive Shock

Mostly one of two entities: pulmonary embolism or cardiac tamponade.

Pulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors.

Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy.

Tamponade — can be infectious, rheumotologic, oncologic, or traumatic.  It’s seen easily enough on point of care ultrasound.  If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating.

Obstructive Shock: Act

Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial.  PE with symptoms: heparin.

Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.

 

Hypovolemic Shock

The most common presentation of pediatric shock; look for decreased activity, decreased urine output, absence of tears, dry mucous membranes, sunken fontanelle.  May be due to obvious GI losses or simply poor intake.

Rapid reversal of hypovolemic shock: may need multiple sequential boluses of isotonic solutions. Use 10 mL/kg in neonates and young infants, and 20 mL/kg thereafter.

Hypovolemic Shock: Act

Tip: in infants, use pre-filled sterile flushes to push fluids quickly.  In older children, use a 3-way stop cock in line with your fluids and a 30 mL syringe to “pull” fluids, turn the stopcock, and “push them into the patient.

Titrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output.

When concerned about balancing between osmolality, acid-base status, and volume status, volume always wins.  Our kidneys are smarter than we are, but they need to be perfused first.

 

Distributive Shock

The most common cause of distributive shock is sepsis, followed by anaphylactic, toxicologic, adrenal,and neurogenic causes.  Septic shock is multifactorial, with hypovolemic, cardiogenic, and distributive components.

Children with sepsis come in two varieties: warm shock and cold shock.

Distributive Shock: Act

Warm shock is due to peripheral vascular dilation, and is best treated with norepinephrine.

Cold shock is due to a child’s extreme vasoconstriction in an attempt to compensate.  Cold shock is the most common presentation in pediatric septic shock, and is treated with epinephrine.

Early antibiotics are crucial, and culture everything that seems appropriate.

 

Shock: A Practical Approach

“How FAST you FILL the PUMP and SQUEEZE”

 

Sometimes things are not so cut-and-dried.  We’ll use a practical approach to diagnose and intervene simultaneously.

Look at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance.

How FAST you FILL the PUMP and SQUEEZE

First, we look at heart rate — how FAST?

Look at the heart rate – is it sinus?  Could this be a supraventricular tachycardia that does not allow for enough diastolic filling, leading to poor cardiac output?  If so, use 1 J/kg to synchronize cardiovert.  Conversely, is the heart rate too slow – even if the stroke volume is sufficient, if there is severe bradycardia, then cardiac output  — which is in liters/min – is decreased.  Chemically pace with atropine, 0.01 mg/kg up to 0.5 mg, or use transcutaneous pacing.

If the heart rate is what is causing the shock, address that first.

Next, we look at volume status.

How FAST you FILL the PUMP and SQUEEZE

Look to FILL the tank if necessary.  Does the patient appear volume depleted?  Try a standard bolus – if this improves his status, you are on the right track.

Now, we look at contractility.

How FAST you FILL the PUMP and SQUEEZE

Is there a problem with the PUMP?  That is, with contractility?  Is this in an infarction, an infection, a poisoning?  Look for signs of cardiac congestion on physical exam.  Put the probe on the patient’s chest, and look for effusion.  Look to see if there is mild, moderate, or severe decrease in cardiac contractility.  If this is cardiogenic shock – a problem with the pump itself.  Begin pressors.

And finally, we look to the peripheral vascular resistance.

How FAST you FILL the PUMP and SQUEEZE

Is there a problem with systemic vascular resistance – the SQUEEZE?

Troubleshoot

Look for signs of changes in temperature – is the patient flushed?  Is this an infectious etiology?  Are there neurogenic or anaphylactic concerns?  After assessing the heart rate, optimizing volume status, evaluating contractility, is the cause of the shock peripheral vasodilation?  If so, treat the cause – perhaps this is a distributive problem due to anaphylaxis.  Treat with epinephrine. The diagnosis of exclusion in trauma is neurogenic shock.  Perhaps this is warm shock; both are supported with norepinephrine.  All of these affect systemic vascular resistance – and the shock won’t be reversed until you optimize the peripheral squeeze.

 

Summary

The four take-home points in the approach to shock in children:

  1. To prioritize your interventions, remember how patients COHDe: Cardiogenic, Obstructive, Hypovolemic, and Distributive. Your patient’s shock may be multifactorial, but mentally prioritize what you think is the MAIN case of the shock, and deal with that first.
  2. To treat shock, remember: How FAST You FILL The PUMP and SQUEEZE: Look at the heart rate – how FAST.  Look at the volume status – the FILL.  Assess cardiac contractility – the PUMP, and evaluate the peripheral vascular tone – the SQUEEZE.
  3. In pediatric sepsis, the most common type is cold shock – use epinephrine (adrenaline) to get that heart to increase the cardiac output. In adolescents and adults, they more often present in warm shock, use norepinephrine (noradrenaline) for its peripheral squeeze to counteract this distributive type of shock.
  4. Rapid-fire word association:
  • Epinephrine for cardiogenic shock
  • Intervention for obstructive shock
  • Fluids for hypovolemic shock
  • Norepinephrine for distributive shock

References

Agha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department.Pediatrics. 2013 Oct;132(4):663-7.

Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637.

Jaff MR et al. for the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011; Apr 26;123(16):1788-830.

Levy B et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011; 39:450.

Micek ST, McEvoy C, McKenzie M, Hampton N, Doherty JA, Kollef MH. Fluid balance and cardiac function in septic shock as predictors of hospital mortality. Crit Care. 2013; 17:R246.

Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med. 2007; 35:64-8.

Ventura AM, Shieh HH, Bousso A, Góes PF, de Cássia F O Fernandes I, de Souza DC, Paulo RL, Chagas F, Gilio AE. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit Care Med. 2015;43(11):2292-302.



This post and podcast are dedicated to Natalie May, MBChB, MPHe, MCEM, FCEM for her collaborative spirit, expertise, and her super-charged support of #FOAMed.  You make a difference.  Thank you.



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Undifferentiated Shock

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

Pediatric; Emergency Medicine; Pediatric Emergency Medicine; Podcast; Pediatric Podcast; Emergency Medicine Podcast; Horeczko; Harbor-UCLA; Presentation Skills; #FOAMed #FOAMped #MedEd

PEM Playbook – Altered Mental Status in Children

Originally published at Pediatric Emergency Playbook on May 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

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How do you approach the child who may be altered?

Altered mental status in children can be subtle.  Look for age-specific behaviors that range from irritability to anger to sleepiness to decreased interaction.

In the altered child, anchoring bias is your biggest enemy.  Keep your mind open to the possibilities, and be ready to change it, when new information becomes available.

For altered adults, use AEIOU TIPS (Alcohol-Epilepsy-Insulin-Overdose-Uremia-Trauma-Infection-Psychosis-Stroke).

Try this for altered children: remember that they need their VITAMINS!

V – Vascular (e.g. arteriovenous malformation, systemic vasculitis)

I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis)

T – Toxins (e.g. environmental, medications, contaminated breast milk)

A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma)

M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders)

I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy)

N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch)

S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)

Case One: Sleepy Toddler

16-month-old who chewed on his grandmother’s clonidine patch

Clonidine is an alpha-2 agonist with many therapeutic indications including hypertension, alcohol withdrawal, smoking cessation, perimenopausal symptoms.  In children specifically, clonidine is prescribed for attention deficit hyperactivity disorder, spasticity due to cerebral palsy and other neurologic disorders, and Tourette’s syndrome.

The classic clonidine toxidrome is altered mental status, miosis, hypotension, bradycardia, and bradypnea.  Clonidine is on the infamous list of “one pill can kill”.

Treatment is primarily supportive, with careful serial examinations of the airway, and strict hemodynamic monitoring.

Naloxone can partially counteract the endogenous opioids that are released with clonidine’s pharmacodynamics.

Start with the usual naloxone dose of 0.01 mg/kg, up to the typical adult starting dose of 0.4 mg.

In clonidine overdose, however, you may need to increase the naloxone dose (incomplete and variable activity) up to 0.1 mg/kg.  Titrate to hemodynamic stability and spontaneous respirations, not full reversal of all CNS effects.

Case Two: In Bed All Day

A 7-year-old with fever, vomiting, body aches, sick contacts.  Altered on exam.

Should you get a CT before LP?

If you were going to perform CT regardless, then do it.

Adult guidelines: age over 60, immunocompromised state, history of central nervous system disease, seizure within one week before presentation, abnormal level of consciousness, an inability to answer two consecutive questions correctly or to follow two consecutive commands, gaze palsy, abnormal visual fields, facial palsy, arm drift, leg drift, and abnormal language.

Children: if altered, and your differential diagnosis is broad (especially if you may suspect tumor, bleed, obvious abscess).

Influenza is often overlooked as a potential cause of altered mental status.  Many authors report a broad array of neurological manifestations associated with influenza, such as altered mental status, seizures, cranial nerve abnormalities, hallucinations, abnormal behavior, and persistent irritability.  All of this is due to a hypercytokinemic state, not a primary CNS infection.

Case Three: “Terrible Teenager”

14-year-old brought in for “not listening” and “acting crazy”; non-complaint with medications for systemic lupus erythematosus (SLE).

SLE is rare in children under 5. When school-age children present with SLE, they typically have more systemic signs and symptoms.  Teenagers present like adults.  All young people have a larger disease burden with lupus, since they have many more years to develop complications.

Lupus cerebritis: high-dose corticosteroids, and possibly IV immunoglobulin.  Many will need therapeutic plasma exchange (TPE), a type of plasmapheresis, where the patient’s plasma is replaced with donor plasma, to remove auto-antibodies and cytokines.

Summary

  • In altered mental status, keep your differential diagnosis open
  • Pursue multiple possibilities until you are able to discard them
  • Be ready to change your mind completely with new information
  • Make sure your altered child gets his VITAMINS (Vascular, Infectious, Toxins, Accident/Abuse, Metabolic, Intussusception, Neoplasm, Stroke)

References

Beckman HB, Frankel RM. The effect of physician behavior on the collection of data. Ann Intern Med 1984; 101:692.

Fujita K, Nagase H, Nakagawa T et al. Non-convulsive seizures in children with infection-related altered mental status. Pediatrics International. 2015; 57(4):659–664.

Gallagher J, Luck RP, Del Vecchio M. Altered mental status – a state of confusion. Paediatr Child Health. 2010 May-Jun; 15(5): 263–265.

Hasbun R, Abrahams J, Jekel J, Quagliarello VJ. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. N Engl J Med. 2001; 345(24):1727-33.

Oliver WJ, Shope TC, Kuhns LR. Fatal Lumbar Puncture: Fact Versus Fiction—An Approach to a Clinical Dilemma. Pediatrics. 2003; 112(3)

Schwartz J et al. Guidelines on the Use of Therapeutic Apheresis in Clinical Practice—Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Sixth Special Issue. Journal of Clinical Apheresis. 2013; 28:145–284.

Zorc JJ. A lethargic infant: Ingestion or deception? Pediatr Ann 2000; 29: 104–107


This post and podcast are dedicated to Teresa Chan, HBSc, BEd, MD, MS, FRCPC for her boundless passion for and support of #FOAMed, for her innovation in education, and for her dedication to making you and me better clinicians and educators.  Thank you, T-Chan.


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Altered Mental Status

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

PEM Playbook – Big Labs, Little People: Troponin, BNP, D-Dimer, and Lactate

Originally published at Pediatric Emergency Playbook on April 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

It’s a busy shift.  Today no one seems to have a chief complaint.

Someone sends a troponin on a child.  Good, bad, or ugly, how are you going to interpret the result?

And while we’re at it – what labs do I need to be careful with in children – sometimes the normal ranges of common labs can have our heads spinning!

Read on for bread-and-butter pediatric blood work and further, to answer the question – what’s up with troponin, lactate, d-dimer, and BNP in kids?

big-labs-little-people_handout_229

A fundamental tenet of emergency medicine:

We balance our obligation to detect a dangerous condition with our suspicion of the disease in given patient.

Someone with a cough and fever may simply have a viral illness, or he may have pneumonia.  Our obligation is to evaluate for the pneumonia.  It’s ok if we “miss” the diagnosis of a cold. It could be bad if we don’t recognize the pneumonia.


How do we decide?  Another fundamental concept:

The threshold.

Depending on the disease and the particular patient, we have a threshold for testing, and a threshold for treating.  Every presentation – and every patient for that matter – has a complicated interplay between what we are expected to diagnose, how much we suspect that particular serious diagnosis, and where testing and treating come into play.


What’s wrong with “throwing on some labs”?

Easy to do right?  They are but a click away…

Often a good history and physical exam will help you to calibrate your investigational thresholds.  This is especially true in children – the majority of pediatric ambulatory visits do not require blood work to make a decision about acute care.  If your patient is ill, then by all means; otherwise, consider digging a bit deeper into the history, get collateral information, and make good use of your general observation skills.

First, a brief word about basic labs.

The punchline is, use a pediatric reference.

If you don’t have a trusted online reference available during your shift, make sure you have something like a Harriett Lane Handbook accessible to you. Don’t rely on your hospital’s lab slip or electronic medical record to save you, unless you are sure that they use age-specific pediatric reference ranges to flag abnormal values. Believe it or not, in this 21st century of ours, some shops still use adult reference ranges when reporting laboratory values on children.


Notable differences in basic chemistries

Potassium: tends to run a bit higher in infants, because for the first year of life, your kidneys are inefficient in excreting potassium.

BUN and creatinine: lower in children due to less muscle mass, and therefore less turnover (and usually lack of other chronic disease)

Glucose: tends to run lower, as children are hypermetabolic and need regular feeding (!)

Alkaline phosphatase: is always high in normal, growing children, due to bone turn over (also found in liver, placenta, kidneys)

Ammonia: high in infancy, due to immature liver, trends down to normal levels by toddlerhood

ESR and CRP: low in healthy children, as chronic inflammation from comorbidities is not present; both increase steadily with age

Thyroid function tests: all are markedly high in childhood, not as a sign of disease, but a marker of their increased metabolic activity



Big Labs



Troponin

Reliably elevated in myocarditis, and may help to distinguish this from pericarditis (in addition to echocardiography)

Other causes of elevated troponin in children include: strenuous activity, status epilepticus, toxins, sepsis, myocardial infarction (in children with congenital anomalies).  Less common causes of troponemia are: Kawasaki disease, pediatric stroke, or neuromuscular disease.

Don’t go looking, if you won’t do anything with the test.


Brain natriuretic peptide (BNP)

In adults, we typically think of a BNP < 100 pg/mL as not consistent with symptoms caused by volume overload.

Luckily, we have data in children with congenital heart disease as well.  Although each company’s assay reports slightly different cut-offs, in general healthy pediatric values match healthy adult values.

One exception is in the first week of life, when it is high even in healthy newborns, due to the recent transition from fetal to newborn circulation.

Use of BNP in children has been studied in both clinic and ED settings. Cohen et al. in Pediatrics used BNP to differentiate acute heart failure from respiratory disease in infants admitted for respiratory distress. They compared infants with known CHF, lung disease, and matched them with controls.

Later, Maher et al. used BNP in the emergency department to differentiate heart failure from respiratory causes in infants and children with heart failure and those with no past medical history.

The bottom line is:

BNP reliably distinguishes cardiac from respiratory causes of shortness of breath in children with a known diagnosis of heart failure.


D-dimer

To cut to the chase: d-dimer for use as a rule-out for pulmonary embolism has not been studied in children.

The only data we have in using d-dimer in children is to prognosticate in established cases. It is only helpful to track therapy for children who have chronic clots.

This is where our adult approach can get us into trouble. Basically, think of the d-dimer in children like it doesn’t even exist. It’s not helpful in our setting for our indications.   An adult may have an idiopathic PE – in fact, up to a third of adults with PE have no known risk factor, which makes decision tools and risk stratification important in this population.

Children with PE almost always have a reason for it.

Slide41

There is at least one identifiable risk factor in up to 98% of children with pulmonary embolism. The majority have at least two risk factors.

If you’re suspecting deep venous thrombosis, perform ultrasonography, and skip the d-dimer.

If you’re worried about PE, go directly to imaging. In stable patients, you may elect to use MR angiography or VQ scan, but most of us will go right to CT angiography. Radiation is always a concern, but if you need to know, get the test.

This is yet another reminder that your threshold is going to be different in children when you think about PE – they should have a reason for it. After you have excluded other causes of their symptoms, if they have risk factors, and you are still concerned, then do the test you feel you need to keep this child safe.

You are the test.

Risk factors only inform you, and you’ll have to just pull the trigger on testing in the symptomatic child with risk factors.


Lactate

A sick child with sepsis syndrome?

The short answer – yes.

In the adult literature, we know that a lactate level above 4 mmol/L in patients with severe sepsis was associated with the need for critical care. This has been studied in children as well, and an elevated lactate in children – typically above 4 – was a predictor of prolonged ICU course and mortality in septic patients.

The acute recognition and treatment of sepsis is first and foremost, clinical.

Our goal is to promote perfusion and provide oxygen to the tissues. Laboratory testing is not a substitute for clinical assessment – it should be used as an extension of your assessment.  There are two main reasons for an elevated lactate: the stress state and the shock state.

The stress state is due to hypermetabolism and an increase in glycolysis, as an example, in early sepsis. The shock state is due to tissue hypoxia, seen in septic shock. The confusion and frustration with lactate is that we often test the wrong people for it.

We could use it to track treatment, and see if we can clear the lactate; decreased lactate levels are associated with a better outcome in adults. Serial clinical assessments are even more useful to gauge your success with treatment.

We should use lactate to detect occult shock. Children compensate so well for shock, that subtle tissue hypoxia may not be detected until later. It may inform your decision for level of care, intensive care versus some other lower level.

Have you every been in this situation:

“Why, oh why, did we send a lactate?”

There are times when a lactate is ordered – maybe by protocol or maybe accidentally – or maybe in retrospect, the patient didn’t need it. Here is a quick mnemonic to remember the reasons for an elevated lactate: LACTATES

Slide52

Lliver – any liver disease affects how lactate is metabolized by the Cori cycle
Aalbuterol (or for our international friends, salbutamol), beta-agonists like albuterol, increase lactate production via cyclic amp
C“can’t breathe” – respiratory distress and increased work of breathing shifts the ratio of aerobic and anerobic repiration
Ttoxins – all kinds of wonder drugs and recreational drugs do it – look up your patient’s list if you’re suspicious
Aalcohol, not an infrequent offender
Tthiamine deficiency – think of this in your cachectic or malnourished patients
Eepinephrine – a by-product of the Cori cycle, how lactate is metabolized. Difficult to interpret lactates when a patient is on an epinephrine drip.
Sseizure or shock – most commonly septic, but can be any type: cardiogenic, bstructive, hypovolemic, distributive.

Bottom line: high serum lactate levels have been associated with morbidity and mortality in children with sepsis and trauma, the two best-studied populations.


A summary of how labs can help you – or hurt you – in pediatric emergency medicine:

  1. Have a good reference for normal values and always be skeptical of how your lab reports them.
  2. Troponin testing is great for the child with suspected cardiogenic shock, myocarditis, or in unwell children with congenital heart disease.
  3. BNP in children can be used just like you do in adults – to get a sense of whether the presenting symptoms are consistent with heart failure.
  4. D-dimer is mostly a waste of time in the PED.
  5. Lactate can be useful in the right patient – use it to risk-stratify the major trauma patient or the patient with sepsis that may be suffering from occult shock.
  6. And lastly, make sure that you are mindful of your threshold for testing, and our threshold for treatment. If will vary by disease and by the patient at hand.

References

Troponin

Gupta SK, Naheed Z. Chest Pain in Two Athletic Male Adolescents Mimicking Myocardial Infarction. Pediatr Emer Care. 2014;30: 493-495.

Kelley WE, Januzzi JL, Christenson RH. Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure. Clinical

Chemistry. 2009; (55) 12:2098–2112.

Kobayashi D, Aggarwal S, Kheiwa A, Shah N. Myopericarditis in Children: Elevated Troponin I Level Does Not Predict Outcome. Pediatr Cardiol. 2012; 33:1040–1045.

Koerbin G, Potter JM, Abhayaratna WP et al. The distribution of cardiac troponin I in a population of healthy children: Lessons for adults. Clinica Chimica Acta. 2016; 417: 54–56.

Liesemer K, Casper TC, Korgenski K, Menon SC. Use and Misuse of Serum Troponin Assays in Pediatric Practice. Am J Cardiol. 2012;110:284 –289.

Newby KL et al. for the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. J Am Coll Cardiol. 2012; 60(23): 2427-2463.

Schwartz MC, Wellen S, Rome JJ et al. Chest pain with elevated troponin assay in adolescents. Cardiology in the Young; 2013. 23: 353–360.

BNP

Auerbach SR, Richmond ME, Lamour JM. BNP Levels Predict Outcome in Pediatric Heart Failure Patients Post Hoc Analysis of the Pediatric Carvedilol Trial. Circ Heart Fail. 2010;3:606-611.

Cohen S, Springer C, Avital A et al. Amino-Terminal Pro-Brain-Type Natriuretic Peptide: Heart or Lung Disease in Pediatric Respiratory Distress? Pediatrics. 2005;115:1347–1350.

Fried I, Bar-Oz B, Algur N et al. Comparison of N-terminal Pro-B-Type Natriuretic Peptide Levels in Critically Ill Children With Sepsis Versus Acute Left Ventricular Dysfunction. Pediatrics. 2006; 118(4): 1165-1168.

Koch A, Singer H. Normal values of B type natriuretic peptide in infants, children, and adolescents. Heart. 2003;89:875–878.

Maher KO, Reed H, Cuadrado A et al. , B-Type Natriuretic Peptide in the Emergency Diagnosis of Critical Heart Disease in Children. Pediatrics. 2008;121:e1484–e1488.

Mir TS, Marohn S, Laeer S, Eistelt M. Plasma Concentrations of N-Terminal Pro-Brain Natriuretic Peptide in Control Children From the Neonatal to Adolescent Period and in Children With Congestive Heart Failure. Pediatrics. 2002;110(6)1:6.

Mir TS, Laux R, Hellwege HH et al. Plasma Concentrations of Aminoterminal Pro Atrial Natriuretic Peptide and Aminoterminal Pro Brain Natriuretic Peptide in Healthy Neonates: Marked and Rapid Increase After Birth. Pediatrics. 2003;112:896–899.

D-Dimer

Goldenberg NA, Knapp-Clevenger RA, Manco-Johnson MJ. Elevated Plasma Factor VIII and d-Dimer Levels as Predictors of Poor Outcomes of Thrombosis in Children for the Mountain States Regional Thrombophilia Group. Pediatrics. 2003;112:896–899.

Manco-Johnson MJ. How I treat venous thrombosis in children. Blood. 2006; 107(1)21-31.

Naqvi M, Miller P, Feldman L, Shore BJ. Pediatric orthopaedic lower extremity trauma and venous thromboembolism. J Child Orthop. 015;9:381–384.

Parasuraman S, Goldhaber SZ. Venous Thromboembolism in Children. Circulation. 2006;113:e12-e16.

Strouse JJ, Tamma P, Kickler TS et al. D-Dimer for the Diagnosis of Venous Thromboembolism in Children. N Engl J Med. 2004;351:1081-8.

Lactate

Andersen LW, Mackenhauer J, Roberts JC et al. Etiology and therapeutic approach to elevated lactate. Mayo Clin Proc. 2013; 88(10): 1127–1140.

Bai et al. Effectiveness of predicting in-hospital mortality in critically ill children by assessing blood lactate levels at admission. BMC Pediatrics. 2014; 14:83.

Scott HF, Donoghue AJ, Gaieski DF et al. The Utility of Early Lactate Testing in Undifferentiated Pediatric Systemic Inflammatory Response Syndrome. Acad Emerg Med. 2012; 19:1276–1280.

Shah A, Guyette F, Suffoletto B et al. Diagnostic Accuracy of a Single Point-of-Care Prehospital Serum Lactate for Predicting Outcomes in Pediatric Trauma Patients. Pediatr Emer Care. 2013; 29:715-719.

Topjian AA, Clark AE, Casper TC et al. for the Pediatric Emergency Care Applied Research Network. Early Lactate Elevations Following Resuscitation From Pediatric Cardiac Arrest Are Associated With Increased Mortality. Pediatr Crit Care Med. 2013; 14(8): e380–e387.


This post and podcast are dedicated to Daniel Cabrera, MD for his vision and his leadership in thinking ‘outside the box’.



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Troponin     |     BNP     |     D-Dimer     |     Lactate

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

PEM Playbook – Multisystem Trauma in Children Part II: Massive Transfusion, Trauma Imaging, and Resuscitative Pearls

Originally published at Pediatric Emergency Playbook on March 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

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A 5-year-old boy was playing with his older brother in front of their home when he was struck by a car. He sustained a femur fracture, splenic laceration, and blunt head trauma – the so-called Waddell’s triad.

On arrival, he was in compensated shock, with tachycardia. He needs blood.

He decompensates…

How do we manage his hemodynamics and when do we perform massive transfusion?

Pediatric Massive Transfusion

40 mL/kg of blood products given at any time within the first 24 hours.

Adolescents and Adult Massive Transfusion

6-8 units of packed red blood cells (PRBCs)

  • Adults have about 5 L of circulating blood.
  • Not including plasma, one could replace all circulating erythrocytes with about 10 units of PRBCs
  • The best ratio of PRBCs:Plasma:Platelets is unknown, but consensus is 1:1:1.
  • 1 unit of PRBCS is typically 300 mL of volume.

The typical initial transfusion of PRBCs in children is 10 mL/kg.

Massive transfusion in children is defined as 40 mL/kg of any blood product.

Once you start to give a child with major trauma the second 10 mL/kg dose of PRBCs – start thinking about other blood components, and ask yourself whether you should initiate your massive transfusion protocol.

The goal is to have the products ready to use in the case of the dynamic trauma patient.

The Thromboelastogram (TEG)

TEG directly measures the four components of clot formation. When there is endolethial damage and bleeding, the sequence that your body takes to address it is as follows:

  1. Platelets migrate and form a plug
  2. Clotting factors aggregate and reinforce the platelets
  3. Fibrin arrives an acts like glue
  4. Other cells migrate and support the clot.

R time – reaction time – the initial line in the tracing that shows time to beginning of clot formation.

  • Treated with platelets

K factor – kinetics of the clot –how much the clot allows the pin to move, or the amplitude.

  • Treated with cryoprecipitate

Alpha angle – the slope between the R and K measurements – reflects how quickly the fibrin glue is working.

  • Treated with cryoprecipitate

Ma – maximum amplitude – reflects the overall strength of the clot.

  • Treated with platelets

LY30 – the clot lysis at 30 min – is the decrease in strength of the clot’s amplitude at 30 min.

  • Treated with an antifibrinolytics (tranexamic acid)

Shape Recognition

Red wine glass: a normal tracing with a normal reaction time and a normal amplitude. That patient just needs support and monitoring.

Champagne glass: a coagulopathic TEG tracing – thinned out, with less amplitude. This patient needs specific blood products.

Puffer fish or blob: a hyperfibrinolytic tracing. That patient will needs clot-stablizer.

TEG – like the FAST – can be repeated as the clinical picture changes.

The Trauma Death Spiral

Lethal triad of hypothermia, acidosis, and coagulopathy.

Keep the patient perfused and warm.

Each unit of PRBCs contains 3 g citrate, which binds ionized calcium, causing hypotension. In massive transfusion, give 20 mg/kg of calcium chloride, up to 2 g, over 15 minutes. Calcium chloride is preferred, as it is ionically readily available – just use a larger-bore IV and watch for infiltration. Calcium gluconate could be used, but it requires metabolism into a bioavailable source of calcium.

Prothrombin complex concentrate (PCC)

Prothrombin complex concentrate (PCC) is derived from pooled human plasma and contains 25-30 times the concentration of clotting factors as FFP. Four-factor PCCs contain factors II, VII, IX and X, while 3-factor PCCs contain little or no factor VII.

The typical dose of PCC is 20-50 units/kg

In the severely hemorrhaging patient – you don’t have time to wait for the other blood products to thaw – PCC is a powder that is reconstituted instantly at the bedside.

Tranexamic acid (TXA)

Tranexamic acid (TXA), is an anti-fibrinolytic agent that functions by stopping the activation of plasminogen to plasmin, and the degradation of fibrin. The Clinical Randomisation of an Antifibrinolytic in Significant Hemorrhage (CRASH-2) investigators revealed a significant decrease in death secondary to bleeding when TXA was administered early following trauma.

Based on the adult literature, one guideline is to give 15 mg/kg loading dose of TXA with a max 1 g over 10 minutes followed by 2 mg/kg/h for at least 8 h or until bleeding stops.

Resuscitative Pearls

Our goal here is damage control. Apply pressure whenever possible. Otherwise, resuscitate, identify the bleeding source, and slow or stop the bleeding with blood products or surgery.

How Children are Different in Trauma

In adults, we speak of “permissive hypotension” (also called “balanced resuscitation” or “damage control resuscitation”). The idea is that if we bring the adult patient’s blood pressure up to normal, we may be promoting clot rupture. To avoid this, we target a MAP of 65 and look for clinical signs of sufficient perfusion. Adults tolerate hypotension relatively well, and is sufficient until we send them to the OR or interventional radiology suite.

In children, this is simply not the case. Hypotension in children is a sign of pre-arrest. Remember, they compensate with an increased systemic vascular resistance and tachycardia to maintain blood pressure.

We should not allow children to become hypotensive – severe tachycardia alone should prompt us to resuscitate.

In other words, permissive hypotension is not permissible for children.

FAST is not sensitive enough to rule-out abdominal trauma.

Fox et al. in Academic Emergency Medicine found a sensitivity of 52%; with a 95% confidence interval [CI] = 31% to 73%.

Often children even with high-grade splenic and liver lacerations can be managed non-operatively. If they are supported adequately, they are observed in the ICU and can avoid surgery in many cases. Unfortunately, a negative FAST cannot help with detecting or grading the laceration for non-operative management. In other words, feel free to use ultrasound – especially for things that we in the ED will react to and intervene on – but CT may help to manage the traumatized child non-operatively.

General Guideline for Imaging in Pediatric Trauma

CT Head and Neck, non-contrast: in concerning mechanisms of injury, patients that are difficult to assess (especially those under 3 months), those with a GCS of 13 or lower.

CT Chest, IV contrast: for suspicion of vascular injury that needs exploration, especially in penetrating trauma. Otherwise, chest xray will tell you everything you need to know in children – especially in blunt trauma. Hemo or pneumothoraces are readily picked up by US or CXR. Rib fractures on CXR predict pulmonary contusions. If you are concerned about great vessel injury, then CT Chest may be helpful; otherwise consider omitting it.

CT Abdomen and Pelvis, IV contrast: helpful in grading splenic and liver lacerations with goal to manage non-operatively. Abdominal tenderness to palpation, significant bruising, or a seat belt sign are concerning and would generally warrant a CT. Also, consider in liver function test abnormalities, or hematuria.

Extremity injuries: in general can be evaluated with physical exam and plain films. However, some injuries in high-risk anatomically complex areas such as the hand and wrist, tibial plateau, and midfoot may be missed by plain films, and CT may be helpful here.

Remember: you can help to mitigate post-traumatic stress and risk for adult healthcare aversion.

Summary

  1. Massive transfusion in children is at 40 mL/kg of total blood products. Think about it if you are giving your second transfusion to the traumatized child.
  2. Do everything you can to support perfusion and avoid the death spiral of hypothermia, coagulopathy, and acidosis. Keep the child perfused with blood as needed, correct coagulopathy, avoid too much crystalloid, and make sure to use the least high-tech of all of these interventions – keep him dry and covered with warm blankets.
  3. Do a careful physical exam, and use CT selectively with an end-point in mind – the default is not the pan-scan – evaluate possible injuries depending on your suspicions from history, physical, and lab tests.
  4. Become familiar with the relatively new modalities in trauma such as TXA, cryoprecipitate and the emerging technology of thromboelestogram – red wine is good for you, champagne is weak, and a puffer fish is trouble.

Selected References

Dehmer JJ, Adamson WT. Massive transfusion and blood product use in the pediatric trauma patient. Semin Pediatr Surg. 2010 Nov;19(4):286-91. doi: 10.1053/j.sempedsurg.2010.07.002.

Fox JC, Boysen M, Gharahbaghian L, Cusick S, Ahmed SS, Anderson CL, Lekawa M, Langdorf MI. Test characteristics of focused assessment of sonography for trauma for clinically significant abdominal free fluid in pediatric blunt abdominal trauma. Acad Emerg Med. 2011 May;18(5):477-82.

Harvey V, Perrone J, Kim P. Does the use of tranexamic acid improve trauma mortality? Ann Emerg Med. 2014 Apr;63(4):460-2.

Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.

Nosanov L, Inaba K, Okoye O, Resnick S, Upperman J, Shulman I, Rhee P, Demetriades D. The impact of blood product ratios in massively transfused pediatric trauma patients. Am J Surg. 2013 Nov;206(5):655-60.

Ryan ML, Van Haren RM, Thorson CM, Andrews DM, Perez EA, Neville HL, Sola JE, Proctor KG. Trauma induced hypercoagulablity in pediatric patients. J Pediatr Surg. 2014 Aug;49(8):1295-9.

Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.

This post and podcast are dedicated to Larry Mellick, MS, MD, FAAP, FACEP. Thank you for your dedication to medical education, and sharing your warm bedside manner, extensive knowledge and talents, and your patient interactions with the world.


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Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

PEM Playbook – Multisystem Trauma in Children Part I: Airway, Chest Tubes, and Resuscitative Thoracotomy

Originally published at Pediatric Emergency Playbook on February 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

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Traumatized children need your full attention.

Protocols work well for adults, but trauma in children requires that we exercise our clinical muscles just a bit more.

Two main reasons:

  1.  Children have specific injury patterns.

  2.  Their physiologic response to trauma is unique.

Crash course in pediatric anatomy and physiology in trauma

When you think of trauma in children, think of Charlie Brown. Large head, no neck, his chest and abdomen form an underdeveloped, amorphous shape.

Alternatively, think of children as apples – they are rounder than they are tall, with a large increased surface area. Apples don’t have a hard shell or thick rind to protect them. If you drop them, you may not see any evidence of damage to the outside, but there can be considerable bruising just under the surface.

  • A child has thin skin, less subcutaneous deposits than an adult, and a non-calcified, pliable thorax that deforms more than it protects or shields.
  • The child’s abdominal muscles are not yet developed. There is less peritoneal fat to cushion a blow, and so traumatic forces transmit readily into internal organs, often without external bruising.
  • The child’s large surface area also causes him to dissipate heat more quickly. He may be wet from urine or blood, and in a major trauma, this faster cool-down predisposes him to coagulopathy.

Case

A 5-year-old boy who was playing with his older brother in front of their home when the ball rolled into the street. He ran after it, and was struck by a sedan going approximately 30 mph.

This is the so-called Wadell’s triad  that occurs in a collision of auto versus pedestrian or auto versus bicycle. The initial impact is the greatest, and will vary depending on the child’s height and what part of his body reaches up to the bumper of the car. Depending on the height of the child and the height of the car, the initial impact will cause a femur fracture, a pelvic fracture, or direct abdominal trauma. The second impact happens as the child is flung onto the grill or the hood of the car, causing usually thoracic trauma. The third impact can be the coup de grâce – to add insult to major injury, the child is then propelled forward, worsening the two previous impacts’ injuries and adding a third – severe blunt head trauma.

Intubation Pearl #1:

If your patient has any subtle change in mental status, intubate early. In pediatric trauma, we need to beproactive. Hypoxia is our enemy.

Intubation Pearl #2:

Thankfully cervical spine injuries in children are uncommon, and when they do occur, they typically occur at the child’s fulcrum, which is at C2. Compare this with an adult’s injury pattern with our fulcrum at C7. Be careful and minimize manipulation of the cervical spine, but do what you must to visualize the chords and place the tube. Keep the neck midline, and realize that the child’s usual decrease respiratory reserve is even more affected by trauma. Preoxygenate and pass that tube quickly.

Chest Tube Pearl #1:

Chest tube sizing in pediatrics is straightforward if we remember that the traditional chest tube size is 4 x the ETT size.

Chest Tube Pearl #2:

Try using a pigtail catheter.

Safety Triangle

  • Lateral edge of the pectoral muscle
  • Lateral edge of the latisimus dorsi
  • Line along the fifth intercostal space at the level of the nipple.

It’s roughly where you would put on a generous dose of deodorant. Insertion here minimizes the risk of damage to nerves, vessels and organs.

Resuscitative Thoracotomy in Children

In a 40-year review of ED thoracotomy, Moore et al. analyzed 1,691 patients who received ED thoracotomy. Overall all-cause adult survival was 6.1%. In children ? 15 years of age, overall all-cause survival was considerably less, at 3.4%.

In a large case series and review of the literature for pediatric ED thoracotomy, Allen et al. found a survival rate in penetrating trauma of 10.2%, with a much lower survival rate in blunt pediatric arrest, at 1.6%. Adolescents had more penetrating injuries, and younger children had more blunt trauma.

To synthesize, the rarity of ED thoracotomy in children is due to the fact that:

  1. Traumatic full arrest in children is uncommon.
  2. It is most often blunt trauma.
  3. Blunt traumatic arrest in children is mostly non-survivable.

REBOA

If you have access to resuscitative endovascular balloon occlusion of the aorta or REBOA, this may be an option to temporize the child to get him to the relative control of the operating room. REBOA involves accessing the common femoral artery, passing a vascular sheath, floating a balloon catheter to the appropriate section of the aorta, and inflating the balloon to occlude blood flow.

Brenner et al. described a case series of 6 patients from two Level I trauma centers. They used REBOA for refractory hemorrhagic shock due to either blunt or penetrating injury. After balloon occlusion, blood pressure improved sufficiently to take the patient either to interventional radiology or to the OR. Four patients lived, two died. The AORTA trial is underway to investigate its use in trauma.

Summary:

  1. Children are like Charlie Brown – large head, no neck, amorphous, underdeveloped and unprotected thorax and abdomen. Or, if you like, they’re like, apples – they have a large surface area and are easily internally bruised, often without overt signs of external bruising.
  2. Chest tubes for children are very similar to the adult procedure – the traditional chest tube size is 4 x the child’s ETT size. Try to use smaller pigtail catheters, available in commercial kits, whenever possible. They’re easy, safe, and effective.
  3. Resuscitative thoracotomy is for penetrating trauma with signs of life wthin 10-15 minutes of arrival. Find the correctable surgical cause of the arrest. Resuscitative thoracotomy for blunt trauma has a dismal prognosis in children.

Selected References

Allen CJ, Valle EJ, Thorson CM, Hogan AR, Perez EA, Namias N, Zakrison TL, Neville HL, Sola JE. Pediatric emergency department thoracotomy: a large case series and systematic review. J Pediatr Surg. 2015 Jan;50(1):177-81.

American College of Surgeons Committee on Trauma; American College of Emergency Physicians Pediatric Emergency Medicine Committee; National Association of Ems Physicians; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Fallat ME. Withholding or termination of resuscitation in pediatric out-of-hospital traumatic cardiopulmonary arrest. Pediatrics. 2014 Apr;133(4):e1104-16.

Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.

Moore HB, Moore EE, Bensard DD. Pediatric emergency department thoracotomy: A 40-year review. J Pediatr Surg. 2015 Oct 19.

Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.

Stannard A, Eliason JL, Rasmussen TE. Resuscitative endovascular balloon occlusion of the aorta (REBOA) as an adjunct for hemorrhagic shock. J Trauma. 2011 Dec;71(6):1869-72.


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This post and podcast are dedicated to Dr Al Sacchetti, MD, FACEP. Thank you for promoting the emergency care of children and for spreading the message that you don’t need subspecialty training to take good care of acutely ill and injured children.

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

 

PEM Playbook – Adventures in RSI

Originally published at Pediatric Emergency Playbook on November 1,
2015 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

Aairwayjawthrust

Pediatric airway management is a skill that integrates the three types of knowledge as described by the ancient Greeks:

Episteme — theoretical knowledge

Techne — technical knowledge

Phronesis — 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

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.  1.2 mg/kg rocuronium is the dose now commonly recommended; per a study byHeier et al. in Anesthesia and Analgesia in 2000, rocuronium produced excellent intubating conditions in higher doses.

Case 2: Multitrauma

Joseph is a 3-year-old boy who is excited that there are so many guests at his home 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 bleedingThe 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 of Emergency Medicine 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, 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 for post-operative CHD can be 75 and 85% on RA.  The Fontan procedure improves saturations, which are typically 88-95%.  Ask the parents or caregiver.

Complications of the Fontan procedure include heart failure, superior vena cava syndrome, 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: this is how people COHDeCardiogenic, 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 shuntneeds 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 likeetomidate.

Myocarditis or other acquired causes of cardiogenic shock – etomidate.  Ketamine is an acceptable alternative, but watch for tachydysrythmias.

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 do I use?  Based on ETT size, it is just a matter of multiplication by 2, 3, or 4.

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

The NG/OG/Foley is 2 x the ETTtube

The ETT should be secured at a depth of 3 x the ETT sizetape

A chest tube size 4 x the ETTtap

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: analgesia, sedation, verification, NG/OG/foley

Selected References

Adelson PD, Srinivas R, Chang Y, Bell M, Kochanek PM. Cerebrovascular response in children following severe traumatic brain injury. Childs Nerv Syst ChNS Off J Int Soc Pediatr Neurosurg. 2011;27(9):1465-1476.

Baird CRW, Hay AW, McKeown DW, Ray DC. Rapid sequence induction in the emergency department: induction drug and outcome of patients admitted to the intensive care unit. Emerg Med J EMJ. 2009;26(8):576-579.

Choi S-H, Yi J-W, Rha Y-H. Rocuronium anaphylaxis in a 3-year-old girl with no previous exposure to neuromuscular blocking agents. Asian Pac J Allergy Immunol Launched Allergy Immunol Soc Thail. 2013;31(2):163-166.

Chon JY. In the hour of Sugammadex. Korean J Anesthesiol. 2013;64(1):3-5.

De Backer D, Biston P, Devriendt J, et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. N Engl J Med. 2010;362(9):779-789.

Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.

Denmark TK, Crane HA, Brown L. Ketamine to avoid mechanical ventilation in severe pediatric asthma. J Emerg Med. 2006;30(2):163-166. doi:10.1016/j.jemermed.2005.09.003.

Diaz LK, Jones L. Sedating the child with congenital heart disease. Anesthesiol Clin. 2009;27(2):301-319.

Dmello D, Taylor S, O’Brien J, Matuschak GM. Outcomes of etomidate in severe sepsis and septic shock. Chest. 2010;138(6):1327-1332.

Green SM, Clark R, Hostetler MA, Cohen M, Carlson D, Rothrock SG. Inadvertent ketamine overdose in children: clinical manifestations and outcome. Ann Emerg Med. 1999 Oct;34(4 Pt 1):492-7.

Gu H, Zhang M, Cai M, Liu J. Comparison of Adrenal Suppression between Etomidate and Dexmedetomidine in Children with Congenital Heart Disease. Med Sci Monit Int Med J Exp Clin Res. 2015;21:1569-1576.

Hardcastle N, Benzon HA, Vavilala MS. Update on the 2012 guidelines for the management of pediatric traumatic brain injury – information for the anesthesiologist. Paediatr Anaesth. 2014;24(7):703-710.

Henderson J, Popat M, Latto P, Pearce A. Difficult Airway Society guidelines. Anaesthesia. 2004;59(12):1242-1243; author reply 1247.

Henderson JJ, Popat MT, Latto IP, Pearce AC, Difficult Airway Society. Difficult Airway Society guidelines for management of the unanticipated difficult intubation. Anaesthesia. 2004;59(7):675-694.

Hildreth AN, Mejia VA, Maxwell RA, Smith PW, Dart BW, Barker DE. Adrenal suppression following a single dose of etomidate for rapid sequence induction: a prospective randomized study. J Trauma. 2008;65(3):573-579.

Ilina MV, Kepron CA, Taylor GP, Perrin DG, Kantor PF, Somers GR. Undiagnosed heart disease leading to sudden unexpected death in childhood: a retrospective study. Pediatrics. 2011;128(3):e513-e520.

Jang YH, Kim SG, Son YH, Park JM. Rocuronium bromide induced anaphylaxis in a child -A case report-. Korean J Anesthesiol. 2010;59(6):411-415.

Kerrey BT, Mittiga MR, Rinderknecht AS, et al. Reducing the incidence of oxyhaemoglobin desaturation during rapid sequence intubation in a paediatric emergency department. BMJ Qual Saf. July 2015. doi:10.1136/bmjqs-2014-003713.
50.

Kochanek PM, Carney N, Adelson PD, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents–second edition. Pediatr Crit Care Med J Soc Crit Care Med World Fed Pediatr Intensive Crit Care Soc. 2012;13 Suppl 1:S1-S82.

Kogan A, Efrat R, Katz J, Vidne BA. Propofol-ketamine mixture for anesthesia in pediatric patients undergoing cardiac catheterization. J Cardiothorac Vasc Anesth. 2003;17(6):691-693.

Lee C. Goodbye suxamethonium! Anaesthesia. 2009;64 Suppl 1:73-81.

Lin C-C, Yu J-H, Lin C-C, Li W-C, Weng Y-M, Chen S-Y. Postintubation hemodynamic effects of intravenous lidocaine in severe traumatic brain injury. Am J Emerg Med. 2012;30(9):1782-1787. doi:10.1016/j.ajem.2012.02.013.

Malik M, Malik V, Chauhan S, Dhawan N, Kiran U. Ketamine-etomidate for children undergoing cardiac catheterization. Asian Cardiovasc Thorac Ann. 2011;19(2):143-148. doi:10.1177/0218492311402132.

Mallon WK, Keim SM, Shoenberger JM, Walls RM. Rocuronium vs. succinylcholine in the emergency department: a critical appraisal. J Emerg Med. 2009;37(2):183-188.

Marsch SC, Steiner L, Bucher E, et al. Succinylcholine versus rocuronium for rapid sequence intubation in intensive care: a prospective, randomized controlled trial. Crit Care Lond Engl. 2011;15(4):R199.

McRae ME. Long-term issues after the Fontan procedure. AACN Adv Crit Care. 2013;24(3):264-282; quiz 283-284.

Metterlein T, Frommer M, Ginzkey C, et al. A randomized trial comparing two cuffed emergency cricothyrotomy devices using a wire-guided and a catheter-over-needle technique. J Emerg Med. 2011;41(3):326-332.

Metterlein T, Frommer M, Kwok P, Lyer S, Graf BM, Sinner B. Emergency cricothyrotomy in infants–evaluation of a novel device in an animal model. Paediatr Anaesth. 2011;21(2):104-109.

Metterlein T, Haubner F, Knoppke B, Graf B, Zausig Y. An unexpected ferromagnetic foreign body detected during emergency magnetic resonance imaging: a case report. BMC Res Notes. 2014;7(1):808.

Morray JP, Lynn AM, Stamm SJ, Herndon PS, Kawabori I, Stevenson JG. Hemodynamic effects of ketamine in children with congenital heart disease. Anesth Analg. 1984;63(10):895-899.

Nakao S, Kimura A, Hagiwara Y, Hasegawa K, Japanese Emergency Medicine Network Investigators. Trauma airway management in emergency departments: a multicentre, prospective, observational study in Japan. BMJ Open. 2015;5(2):e006623.

Neuhaus D, Schmitz A, Gerber A, Weiss M. Controlled rapid sequence induction and intubation – an analysis of 1001 children. Paediatr Anaesth. 2013;23(8):734-740.

Oklü E, Bulutcu FS, Yalçin Y, Ozbek U, Cakali E, Bayindir O. Which anesthetic agent alters the hemodynamic status during pediatric catheterization? Comparison of propofol versus ketamine. J Cardiothorac Vasc Anesth. 2003;17(6):686-690.

Patanwala AE, McKinney CB, Erstad BL, Sakles JC. Retrospective Analysis of Etomidate Versus Ketamine for First-pass Intubation Success in an Academic Emergency Department. Acad Emerg Med. 2014;21(1):87-91.

Perry JJ, Lee JS, Sillberg VAH, Wells GA. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev. 2008;(2):CD002788.

Prunty SL, Aranda-Palacios A, Heard AM, et al. The ‘Can’t intubate can’t oxygenate’ scenario in pediatric anesthesia: a comparison of the Melker cricothyroidotomy kit with a scalpel bougie technique. Paediatr Anaesth. 2015;25(4):400-404.

Reddy JI, Cooke PJ, van Schalkwyk JM, Hannam JA, Fitzharris P, Mitchell SJ. Anaphylaxis is more common with rocuronium and succinylcholine than with atracurium. Anesthesiology. 2015;122(1):39-45.

Reynolds SF, Heffner J. Airway management of the critically ill patient: rapid-sequence intubation. Chest. 2005;127(4):1397-1412.

Rinderknecht AS, Mittiga MR, Meinzen-Derr J, Geis GL, Kerrey BT. Factors associated with oxyhemoglobin desaturation during rapid sequence intubation in a pediatric emergency department: findings from multivariable analyses of video review data. Acad Emerg Med Off J Soc Acad Emerg Med. 2015;22(4):431-440.

Robinson N, Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emerg Med J EMJ. 2001;18(6):453-457.

Schaefer R, Hueter L, Preussler N-P, Schreiber T, Schwarzkopf K. Percutaneous transtracheal emergency ventilation with a self-made device in an animal model. Paediatr Anaesth. 2007;17(10):972-976.

Scherzer D, Leder M, Tobias JD. Pro-con debate: etomidate or ketamine for rapid sequence intubation in pediatric patients. J Pediatr Pharmacol Ther. 2012;17(2):142-149.

Scrase I, Woollard M. Needle vs surgical cricothyroidotomy: a short cut to effective ventilation. Anaesthesia. 2006;61(10):962-974.

Sigurtà A, Zanaboni C, Canavesi K, Citerio G, Beretta L, Stocchetti N. Intensive care for pediatric traumatic brain injury. Intensive Care Med. 2013;39(1):129-136.

Sokolove PE, Price DD, Okada P. The safety of etomidate for emergency rapid sequence intubation of pediatric patients. Pediatr Emerg Care. 2000;16(1):18-21.

Stocchetti N, Maas AIR, Chieregato A, van der Plas AA. Hyperventilation in head injury: a review. Chest. 2005;127(5):1812-1827.

Strayer RJ. Rocuronium versus succinylcholine: Cochrane synopsis reconsidered. Ann Emerg Med. 2011;58(2):217-218.

Sunder RA, Haile DT, Farrell PT, Sharma A. Pediatric airway management: current practices and future directions. Paediatr Anaesth. 2012;22(10):1008-1015.

Umesh G, Jasvinder K, Shetty N. Suxamethonium stands the test of time: it is too early to say goodbye. Anaesthesia. 2009;64(9):1023; author reply 1023-1024.

Warner KJ, Cuschieri J, Jurkovich GJ, Bulger EM. Single-dose etomidate for rapid sequence intubation may impact outcome after severe injury. J Trauma. 2009;67(1):45-50.

Weiss M, Engelhardt T. Proposal for the management of the unexpected difficult pediatric airway. Paediatr Anaesth. 2010;20(5):454-464.

Zuckerbraun NS, Pitetti RD, Herr SM, Roth KR, Gaines BA, King C. Use of etomidate as an induction agent for rapid sequence intubation in a pediatric emergency department. Acad Emerg Med Off J Soc Acad Emerg Med. 2006;13(6):602-609.

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Rapid Sequence Intubation Portal on WikEM

 

This podcast and post are dedicated to Minh Le Cong, MBBS, FRACGP, FACRRM, FARGP, GDRGP, GCMA,GEM, Dip AeroMedical Retrieval & Transport, for his humble brilliance, fine example, and for being the life of the FOAMed party; and to Diane Birnbaumer, MD, FACEP, for her steadfast dedication to clinical and educational excellence, her stellar example, and her hard-won clinical prudence.

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

PEM Playbook – The Undifferentiated Sick Infant

Originally published at Pediatric Emergency Playbook on September 1,
2015 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

Image courtesy of @srrezaie
Image courtesy of @srrezaie

You have all of the skills you need to care for an acutely ill infant. Learn a few pearls to make this a smoother endeavor.

The Pediatric Assessment Triangle is a rapid, global assessment tool using only visual and auditory clues to make determinations on three key domains: appearance, work of breathing, and circulation to the skin.

The combination of abnormalities determines the category of pathophysiology: respiratory distress, respiratory failure, CNS or metabolic problem, shock, or cardiopulmonary failure.

Pediatric Assessment Triangle

Appearance

TICLS
Tone – the newborn should have a normal flexed tone; the 6 month old baby who sits up and controls her head; the toddler cruises around the room.

Interactiveness – Does the 2 month old have a social smile? Is the toddler interested in what is going on in the room?

Consolability – A child who cannot be consoled at some point by his mother is experiencing a medical emergency until proven otherwise.

Look/gaze – Does the child track or fix his gaze on you, or is there the “1000-yard stare”?

Speech/cry – A vigorously crying baby can be a good sign, when consolable – when the cry is high-pitched, blood-curling, or even a soft whimper, something is wrong.

If the child fails any of the TICLS, then his appearance is abnormal.

Work of Breathing

Children are respiratory creatures – they are hypermetabolic – we need to key in on any respiratory embarrassment.
Look for nasal flaring. Uncover the chest and abdomen and look for retractions. Listen – even without a stethoscope – for abnormal airway sounds like grunting or stridor. Grunting is the child’s last-ditch effort to produce auto-PEEP. Stridor is a sign of critical upper airway narrowing.

Look for abnormal positioning, like tripodding, or head bobbing

Circulation to the skin

Infants and children are vasospastic – they can change their vascular tone quickly, depending on their volume status or environment.

Without even having to touch the child, you can see signs of pallor, cyanosis, or mottling. If any of these is present, this is an abnormal circulation to the skin.

Pattern of Abnormal Arms = Category of Pathophysiology

THE MISFITS at play

Differential Diagnosis in a Sick Infant: “THE MISFITS

Trauma – birth trauma, non-accidental – check for a cephalohematoma which does not cross suture lines and feels like a ballotable balloon, as well as for subgaleal hemorrhage, which is just an amorphous bogginess that represents a dangerous bleed. Do a total body check.

Heart disease or Hypovolemia – is there a history of congenital heart disease? Was there any prenatal care or ultrasound done? Does this child look volume depleted?

Endocrine Emergencies – Could this be congenital adrenal hyperplasia with low sodium, high potassium, and shock? Look for clitoromegaly in girls, or hyperpigmented scrotum in boys. Could this be congenital hypothyroidism with poor tone and poor feeding? Any history of maternal illness or medications? Congenital hyperthyroidism with high output failure?

Metabolic – What electrolyte abnormality could be causing this presentation? Perhaps diGeorge syndrome with hypocalcemia and seizures?

Inborn Errors of Metabolism – there are over 200 inborn errors of metabolism, but only four common metabolic pathways that cause a child to be critically ill. Searching for an inborn error of metabolism is like looking for A UFO – amino acids, uric acids, fatty acids, organic acids. If the child’s ammonia, glucose, ketones, and lactate are all normal in the ED, then his presentation to the ED should not be explained by a decompensation of an inborn error of metabolism.

Seizures – Neonatal seizures can be notoriously subtle – look for little repetitive movements of the arms, called “boxing” or of the legs, called “bicycling”.

Formula problems – Hard times sometimes prompt parents to dilute formula, causing a dangerous hyponatremia, altered mental status, and seizures. Conversely, concentrated formula can cause hypovolemia.

Intestinal disasters – 10% of necrotizing enterocolitis occurs in full-term babies – look for pneumatosis intestinalis on abdominal XR; also think about aganglionic colon or Hirschprung disease; 80% of cases of volvulus occur within the 1st month of life.

Toxins – was there some maternal medication or ingestion? Is there some home remedy or medication used on the baby? Check a glucose ad drug screen.

Sepsis – Saved for last – You’ll almost always treat the sick neonate empirically for sepsis – think of congenital and acquired etiologies.

Hyperoxia Test

The hyperoxia test is the single most important initial test in suspected congenital heart disease – we can test the child’s circulation by his reaction to oxygen on an arterial blood gas. Place the child on a non-rebreather mask, and after several minutes, perform an ABG. (Ideally you obtain a preductal ABG in the right upper extremity, and compare that with one on the lower extremity, but this may not be practical.)

In a normal circulatory system, the pO2 should be high – in the hundreds – and certainly over 250 torr. This effectively excludes congenital heart disease as a factor. If the pO2 on supplemental oxygen is less than 100, then this is extremely predictive of hemodynamically significant congenital heart disease. Between 100 and 250, you have to make a judgement call, and I would side on worst first.

If you are giving this child 100% O2, and he doesn’t improve 100% — that is, his ABG is not at least 100 – then he has congenital heart disease until proven otherwise.

Give prostaglandin if the patient is less than 4 weeks old (typical presentation is within the first 1-2 weeks of life). Start at 0.05 mcg/kg/min. PGE keep the systemic circulation supplied with some mixed venous blood until either surgery or palliation is decided.

Neonatal Shock Algorithm

Summary Points

  • When you see a sick infant, keep THE MISFITS around to keep you out of trouble.
  • Before you decide on sepsis, ask yourself, could this be a cardiac problem?
  • When in doubt, perform the hyperoxia test.
  • All the rest, you have time to look up.

Before You Go: The Availability Heuristic

Selected References

Brousseau T, Sharieff GQ. Newborn Emergencies: The First 30 Days of Life. Pediatr Clin N Am. 2006; 53:69-84.

Cloherty JP, Eichenwald EC, Stark AR: Manual of Neonatal Care, 5th edition. Philadelphia, PA, Lipincott Williams & Wilkins, 2004.

Gausche-Hill M, Eckstein M, Horeczko T, McGrath N, Kurobe A, Ullum L, Kaji AH, Lewis RJ. Paramedics Accurately Apply the Pediatric Assessment Triangle to Drive Management. Prehospital Emergency Care. 2014; doi: 10.3109/10903127.2014.912706

Horeczko T, Gausche-Hill M. The Pediatric Assessment Triangle: A Powerful Tool for the Prehospital Provider. J Paramedic Prac. 2011; (3)1:20-25.

Horeczko T, Young K: Congenital Heart Disease, in Pediatric Emergency Medicine-A Comprehensive Study Guide, 4th Ed. ACEP/McGraw-Hill, 2013.

Horeczko T, Enriquez B, McGrath N, Gausche-Hill M, Lewis RJ. The Pediatric Assessment Triangle: Accuracy of its Application by Nurses in the Triage of Children. J Emerg Nurs. 2013; 39(2):182-9.

McGowan et al. Part 15: Neonatal Resuscitation: 2010 American Heart Association Guidelines. Circulation. 2010;122:S909-S919.

Okada PJ, Hicks B. Neonatal Surgical Emergencies. Clin Ped Emerg Med. 2002; 3:3-13.

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Neonatal Resuscitation on WikEM

 

This episode and post are dedicated with gratitude and admiration to Marianne Gausche-Hill, MD, Rob Orman, MD, and Mel Herbert MD MBBS.  You make the world a better place.  Thank you.

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

PEM Playbook – Intranasal Medications and You

Originally published at Pediatric Emergency Playbook on September 1,
2015 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

Image obtained from prehospitalresearch.eu
Image obtained from prehospitalresearch.eu

Intranasal medications, if understood and employed properly, are a great choice to avoid an IV or as a bridge until IV access is obtained.

Learn the strengths and limits of intranasal fentanyl, midazolam, ketamine, and dexmedetomidine.

Pain Management in Children

Traditionally, “brutaine”.

Goal: the “ouchless ED”.

Two main barriers in pain treatment in children:

  1. We consistently under-recognize children’s pain. We may not detect the typical behaviors that children exhibit when they are in pain, especially in the pre-verbal child: crankiness or fussiness; changes in appetite or sleep; decreased activity; or physiologic findings such as dull eyes, flushed skin, rapid breathing, or sweating.
  2. We under-treat pain in children. This is mostly from an old culture of misunderstanding or fear of overdose.
    Four Components to Successful Pain Management and Intranasal Medication Administration

Right drug, right dose, right patient, right timing

Right Drug – Not every medication is easily amenable to intranasal administration. We can use intranasal drugs for analgesia, for anxiolysis, for seizures – but not all drugs used for those purposes will perform well – or at all – via the IN route.

Right Dose – Dosing with IN meds will vary considerably from the IV route. Rule of thumb: the IN dose is 2-3 times the IV dose.

Right Patient – Is this patient and family appropriate for “just taking the edge off”? What is the level of anxiety in the room? How is the child relating to the parent, usually it’s the mother there. What else is going on in that clinical snapshot as you walk in?

Right Timing – Mostly IV and IN onset times are very similar. Notable exception: intranasal midazolam may take 10-15 minutes to take effect – something to keep in mind when you plan your procedure.

Intranasal Medications bypass first-pass metabolism, and a portion of the drug is delivered into the CSF immediately via the nose-brain pathway.

Ideal Volume for Intranasal Medication: 0.25 to 0.3 mL per naris

Absolute maximum: 1 mL per naris (but expect some run-off)

Preload the device with 0.1 mL solution for dead space

Administer intranasal medications in the sniffing position. Lie the patient flat with occiput posterior, put patient in the sniffing position, seat the mucosal atomizing device cushion in the naris, aim toward the pinna of the ear, and shoot fast – you have to push the drug as fast as you can to atomize the solution.

Intranasal Fentanyl
Safe, effective at 2 mcg/kg. Most commonly stocked concentration of fentanyl is 50 mcg/mL. A 40-kg-child will reach the maximum volume possible for administration (40 kg x 2 mcg/kg = 80 mcg; at 50 mcg/mL – that makes 1.6 mL – if we divide the dose, it’s not ideal, but is still under our maximum of under 1 mL per naris.) You graduate from intranasal fentanyl in elementary school.

Sufentanil for adults (half the volume of fentanyl) – 0.5 mcg/kg, which can be repeated as needed.

Intranasal Midazolam
Intranasal Midazolam or versed for anxiolysis is dosed at 0.3 mg/kg (up to 0.5 mg/kg for procedural sedation)
Here, another practicality weighs in. The IV preparation for midazolam is 5 mg/5 mL – this a very dilute solution. You need to use the 5 mg/mL concentration to have any success with intransal midazolam because of the volume needed for the right effect.

A 20-kg-child will near the maximum volume for intranasal midazolam (0.3 mg/kg is 6 mg, at 5 mg/ml, 1.2 mL, or 036 mL per naris). Kindergarten graduation is when to drop the intranasal midazolam.

Intranasal Ketamine
The IV dose for ketamine for pain control is 0.15 to 0.3 mg/kg, usually as an infusion over an hour. The intranasal dose of ketamine for pain control is 1 mg/kg.

Low-dose ketamine may be used for pain control as an adjunct and opioid-sparing agent.

Intranasal Dexmedetomidine
Dexmedetomidine is an alpha-2 receptor agonist, a smarter clonidine. Clonidine is also an alpha-2 agonist, and it can cause a marked decrease in blood pressure with some mild sedation. Dexmedetomidine targets receptors in the CNS and spinal cord, and so it provides deep sedation, with very minimal blood pressure effects. It induces a sleep-like state. In fact, EEGs done under dex show the same pattern as seen in stage II sleep. Dex is safe, if titrated, and does not depress airway reflexes or respiration. Dose is 2.5 mcg/kg IN, and can add another 1 mcg/kg if needed. The downside is that it can last 30 minutes or more, but it may be a good choice for an abdominal ultrasound or CT head in unruly toddlers.

Before You Go: The “Semmelweiss reflex”.

Selected References

Anand KJ, Scalzo FM. Can adverse neonatal experiences alter brain development and subsequent behavior? Expert Opin Drug Deliv. 2008 Oct;5(10):1159-68. doi: 10.1517/17425247.5.10.1159 .

Stephen R, Lingenfelter E, Broadwater-Hollifield C, Madsen T. Intranasal sufentanil provides adequate analgesia for emergency department patients with extremity injuries.

Weisman SJ, Bersnstein B, Schechter NL. Consequences of Inadequate Analgesia During Painful Procedures in Children. Biol Neonate. 2000 Feb;77(2):69-82.

Wu H, Hu K, Jiang X. From nose to brain: understanding transport capacity and transport rate of drugs. J Opioid Manag. 2012 Jul-Aug;8(4):237-41. doi: 10.5055/jom.2012.0121.

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Intranasal Sedation on WikEM

 

This episode and post are dedicated to Ken Milne, MD, MSc, a man of fervor, ardor, and wit.  Thank you for your intellect and your style.

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP