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Pediatric Emergency Playbook

You make tough calls when caring for acutely ill and injured children. Join us for strategy and support, through clinical cases, research and reviews, and best-practice guidance in our ever-changing acute-care landscape. This is your Pediatric Emergency Playbook.
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Now displaying: Category: general
Jul 1, 2016

"She won't walk", or "He just looks like he's limping".

So many things can be going on -- how do we tackle this chief complaint?

You’re dreading a big work-up.  You almost want to tell the kid – please, STOP LIMPING...

STOP LIMPING!

S – Septic Arthritis 

The most urgent part of our differential diagnosis. The hip is the most common joint affected, followed by the knee.  Lab work can be helpful, as well as US of the hip to look for an effusion,  but sometimes, regardless of the results, the joint just has to be tapped to know for sure.

T – Toddler’s fracture

This is usually a torque injury when the wobbling toddler pivots quickly or trips and falls.  Toddler’s fractures happen in children 1 to 3 years of age, and occur in the distal 1/3 of the tibia.  Sometimes a cast is needed, but currently there is a new trend in foregoing casting in mild cases.

O – Osteomyelitis

Bacteremia – from any source – can seed into any bone.  It’s not very common, but it happens: approximately 2% of children who present to an ED with limp will have osteomyelitis.  Plain films, ESR, and CRP are a fair screen to start.  For more than the casual concern, MRI is the best modality to evaluate, followed by radionuclide scintigraphy.  Although not the first choice modality, CT can show periosteal changes, such as inflammatory new bone formation or periosteal purulence.

P – Perthes disease

This is the famous Legg-Calvé-Perthes idiopathic avascular necrosis of the hip, usually affecting children from 3 to 12 years. They present with a slow onset pain and with an antalgic gait.  Patients will have trouble with internal rotation and abduction of the hip.  Radiographs may be initially normal.  MRI can show the culprit: decreased perfusion to the femoral head and subsequent necrosis.

L – Limb-Length Discrepancy

Parents may notice that he seems “wobblier” than he should be.  It may be that we are just now appreciating a congenital anomaly.  Get out the paper tape, and measure from the anterior superior iliac spine to the medial malleolus and compare both sides.   Children with limb-length discrepancy only need a non-urgent referral to pediatric orthopedics to look for congenital dysplasia of the hip, or other growth abnormalities.  Some are treated with orthotics.  Surgical options vary.  Epiphysiodesis destroys the growth plate on the unaffected side, which evens out the growth.  Other options are limb-lengthening or limb-shortening procedures.

I – Inflammatory

Transient Synovitis.  This is what we want them to have right?  The typical age is between 3 and 6 years, sometimes just after a URI.  To be comfortable with this diagnosis, we should have considered all of the dangerous diagnoses, the child should be well, afebrile, in minimal discomfort, and he should respond almost completely to an NSAID.  He’s the one running up and down the department after treatment – or just from sheer boredom after observation.

M – Malignancy

Primary bone tumors such as Ewing’s sarcoma or osteogenic sarcoma typically affect older children.  Limping, however, may be a presenting symptom of leukemia.  If you have any suspicion of the general wellness of the child, get a screening CBC, and perhaps a peripheral blood smear.  Whatever you do, make sure you get close follow up for these kids that are on your malignancy radar -- the blast crisis may not have occurred yet – but it can happen hours to days later.

Plain films are insensitive for leukemic involvement of bone but they may show diffuse osteopenia, or metaphyseal bands – symmetrical high-uptake markings around the joint.  They look like stacks of paper within normal bone – you can see them also in anemia, lead poisoning, and other causes.  Also look for periosteal new bone formation, sclerosis, or lysis.

P – Pyomyositis

This usually presents with vague irritability, pain, and fever, and sometimes with a subacute minor trauma.  These children don’t look to well.

Also think about just run-of-the-mill myositis, usually from a viral cause, such as influenza.  Typically the calves are affected and are always tender.  Hydration and supportive therapy are indicated for viral causes.

For bacterial focal pyomyositis, give empiric antibiotics, admit them for major inpatient workup, and think about early surgical consultation if you think you need sepsis source control.

I – Iliopsoas Abscess

Children most often will develop a primary abscess from bacteremia from an unresolved infection.   Adults more commonly form secondary abscesses from Crohn’s disease, post-op complications, a vertebral infection, or even a bad chronic urinary tract infection.  Lest you think this is a dramatic presentation, think again: iliopsoas abscesses present also with vague symptoms of back, flank, abdominal, or hip pain, sometimes with fever.  The median time from symptoms to diagnosis in children is a whopping 20+ days, according to one study.  If iliopsoas abscess is starting to get your attention, get the CT or MRI.

N – Neurologic

Not to scare you, but children do have strokes; unlike adults, half are hemorrhagic, half are thromboembolic.  Typically they’ll have some underlying pathology that will alert you, such as a cardiac lesion, sickle cell disease, or some infectious or metabolic history.  The good news is that it won’t just be a limp – you’ll have some other neuro sign or symptom to go after.

Guillain Barré is another thing to consider – early lower extremity weakness may present as a limp or refusal to walk.  Maybe it’s not the hip that should be tapped, but the spinal canal.

Think also about muscular dystrophy or peripheral neuropathy and its possible underlying etiology.

G – Gastrointestinal and Genitourinary

What else could be going on?  Appendicitis may be faking you out here.  Perhaps there is a hernia, or testicular or ovarian torsion, all of which can present as lateralizing pain and not wanting to walk.  Think outside the box.

Phases of Gait

The gait cycle has three phases: contact, stance, and propulsion. Contact is the time from heel strike to just when the foot is flat.  Stance is from the foot being flat to lifting the heel from the ground.  The stance phase is when you bear most of your weight.  The propulsion phase is when your weight transfers to your toes, and you push off.

Gait Cycle_Horeczko_Tim

Abnormal Gaits

Antalgic Gait -- "hobbling" gait; normal contact phase, but stance phase is abbreviated; propulsion is normal.  The patient is trying to limit the time spent bearing weight on that side.

Trendelenburg Gait -- the affected side's hip abductor muscles are too weak or painful to stabilize the pelvis; the unaffected side dips to the floor. May be superior gluteal neuropathy, or a biomechanical problem, such as avascular necrosis, congenital dysplasia of the hip, or slipped capital femoral epiphysis.

Circumduction Gait -- the patient swings his foot laterally (due to a foot or ankle pathology), or to avoid tripping in limb-length discepancy.

Stiff-leggged Gait -- the patient walks with knees locked, in an attempt to avoid using the gastrocnemius muscles; concerning for myositis.

Equinus Gait -- toe-walking, as seen in myositis, also to avoid exacerbating pain from the calves.

Hip Internal Rotation_Horeczko TimLag of Internal Rotation of the Hip

Look for symmetry of internal rotation, or lateralizing pain or "guarding" with range of motion.

Keep the pelvis flush to the bed, and simultaneously rotate the lower extremity laterally, which will cause internal rotation of the hip.

Avascular necrosis will not allow full internal rotation, since the joint space is narrowed with this maneuver, causing impingement of the sensitive necrotic head of the femur.

Note any pain, asymmetry, and angle of internal rotation achieved.

 

Kocher Criteria

In their original paper in 1999, Dr Kocher et al. performed a retrospective analysis of children who were being evaluated for a septic joint versus transient synovitis over a 15 year period, in a major referral center.  They came up with four independent predictors of a septic joint, and calculated the probability of septic arthritis based on the number of features present.  In 2004 the same group validated their prediction tool, with a slightly decreased sensitivity and specificity in the validation population.

In short, the Kocher criteria are not perfect, but it’s the best evidence we have at the moment.

The four predictors are:

Inability to walk

Fever of 38.5 C of greater

ESR > 40 mm/h

WBC > 12,000

 

Bonus mnemonic: Walk FEW: Inability to Walk | Fever | ESR | WBC

 

The probability of septic arthritis increases with increasing predictor. In this prediction model, each predictor has the same weight.

Probability of Septic Arthritis (Kocher et al. 1999)

0 Predictor – <0.2 %

1 Predictor – 3%

2 Predictors – 40%

3 Predictors – 93.1%

4 Predictors – 99.6%

Now, remember, this is to be used in children in whom you already have some suspicion of a septic joint.  So, 0 predictors, generally you’re alright.  1 predictor, you may start to worry.  Once you have 2 predictors, your chances jump for 3% to 40%.  You really have to go looking.

The Kocher caveat is that there is no single test or single decision rule that will stop you from investigating if you are concerned enough.  Don’t have too much faith in this imperfect decision tool – we use it because we need somewhere to start.  Treat and push for the aspiration of the hip if you are left in doubt.  Septic arthritis can be devastating if not identified early.

Summary

  • Fever and limp? – do not pass go – especially with 2 or more Kocher criteria – or if there is any doubt, tap that joint.
  • Refusal to walk after adequate analgesia? Admit for observation, MRI, further workup, blood cultures, and much more.
  • Remember some developmental concerns to help you to decide whether to continue the investigation urgently as an inpatient, or non-urgently as an outpatient.
  • After all of that, try to get them them to STOP LIMPING!

 

References

Jain S et al. A stiff-legged gait: benign acute childhood myositis. CMAJ. 2009 Nov 10; 181(10): 711–713.

Julien L et al. Pyogenic Sacroiliitis in a 13-Month-Old Child: A Case Report and Literature. Medicine (Baltimore). 2015 Oct; 94(42): e1581.

Kocher MS et al. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999 Dec;81(12):1662-70.

Kocher MS et al. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am. 2004 Aug;86-A(8):1629-35.

Lindsay D, D'Souza S. A limping child. BMJ. 2016 Feb 9;352:i476.

Navarro López V et al. Microbiology and outcome of iliopsoas abscess in 124 patients. Medicine (Baltimore). 2009;88(2):120.

Rennie LM et al. Benign acute childhood myositis in an Accident and Emergency setting. Emerg Med J 2005;22:686-688

Sapru K, Cooper JG. Management of the Toddler's fracture with and without initial radiological evidence. Eur J Emerg Med. 2014 Dec;21(6):451-4.

Schuh AM, Whitlock KB, Klein EJ. Management of Toddler's Fractures in the Pediatric Emergency Department. Pediatr Emerg Care. 2015 Jun 17. [Epub ahead of print]

Stoica Z et al. Imaging of Avascular Necrosis of Femoral Head: Familiar Methods and Newer Trends. Curr Health Sci J. 2009 Jan-Mar; 35(1): 23–28.

Verma S. Pyomyositis in Children. Curr Infect Dis Rep. 2016 Mar;18(4):12.

 

This post and podcast are dedicated to the estimable yet graciously humble Andrew Tagg BSC(Hons), MBBS, MRCSEd, ACEM for his dedication to #FOAMed, Emergency Medicine, Pediatric Emergency Medicine, and all things caffeinated.  Thank you for your dedication, generosity, and your example.

Don't Forget the Conference!   #DFTB17   #DFTB

 

Jun 1, 2016

Do we recognize shock early enough?

How do we prioritize our interventions?

How can we tell whether we’re 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.  But did you notice 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 see some 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,

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.  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 stop cock, 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?

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 innterventions, 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

May 1, 2016

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 is 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 on 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.

 

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

 

Mar 1, 2016

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 decompensates and needs blood.

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)

Direct 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.

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

Feb 1, 2016

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 grace – 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 be proactive. 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.


Pediatric Trauma on WikEM

 

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

Dec 1, 2015

Victims of electrical injuries present either in extremis or as the seeming well patient with insidious, developing disease.

A targeted history usually gets you the information you need.

 


 

Four main things to find out:

1. Household or Industrial electricity?

Household electricity uses alternating current, or AC.  Voltages across the world range anywhere from 100 to 240 V.  Here in North America, most outlets and appliances use 120 volts, which is the measure of electrical tension, or the potential difference in electrical charge.

Cut-off between low voltage and high voltage is 1000 V.

Industrial energy may be AC or direct current, DC.  DC current propels the victim -- think of this as a blast injury.  The same voltage in AC is three times as damaging as that voltage at DC, because AC causes muscle tetany, and prolonged contact time.

2. What was the likely pathway that current took?

Did the current pass through the thorax?  -- Think dysrhythmias.  Through the head or neck?  -- Think damage to the CNS and risk for later central respiratory arrest; acoustic nerve damage; cataract formation.  Did the current pass along an extremity? -- Think compartment syndrome and rhabdomyolysis.

3. What was the contact time?

The electrical charge meets resistance and converts to thermal energy, which causes tissue necrosis, increasing with the contact time.  Was your patient extricated?  Was there tetany?  Was he found in a pool of water or liquid?  Longer contact time correlates with extensive injuries that may only be apparent hours later.

4. Are there any associated injuries?

Think of electrical injury as a trauma – major trauma rarely occurs in isolation.   Was the patient flung after contact?  Did he have a syncopal episode? -- Think precipitated dysrhythmia and fall.   Was there any chest pain?   -- Consider stress-induced ischemia.

 

Pearl: Patients may be confused initially or unable to localize symptoms because of CNS disruption.  Get collateral information, re-interview, and re-examine as needed.

 


 Case 1: Toddler with an oral commissure burn

An electrical burn to the angle of the mouth cauterizes superficial bleeding vessels, and hours later the wound becomes covered with a white layer of fibrin, surrounded by erythema.  Edema and thrombosis will continue, and at 24 hours there is typically a significant margin of tissue necrosis.  Most patients do well, and the burn heals by secondary intention.  The eschar will slough off in 1 to 2 weeks.  The labial artery is just deep to the burn, and as the eschar sloughs off, it can be exposed.  It’s a high-flow artery to the face, and if disrupted, the child may have significant bleeding and possibly hemorrhagic shock.

These children need close wound care follow-up, and potentially outpatient coordination with Head and Neck Surgery and/or Plastic Surgery consultants.

Precautionary advice:  take the moment to talk to parents about the risk, and show them how to apply pressure to the wound, pinching the inner and outer cheek together with the thumb and index finger until the child arrives to the hospital.


Case 2: School-age child with knife versus electrical outlet

A a “kissing burn” occurs when the electrical charge creates an arc and jumps to a more proximal portion of the extremity.

The kissing burn typically occurs at flexor creases such as the wrist or the antecubital fossa.  There is often extensive underlying tissue damage even under the skin where it doesn’t appear to be involved.  Compartment syndrome and subsequent rhabdomyolysis and renal failure are the highest-risk complications.


Case 3: Adolescent after a taser exposure

Nitrogen capsules propel two barbs into the dermis, which deliver short bursts of energy; most patients have no harm from the electricity delivered.

How to remove a dart:  The darts are typically 9 mm long, but the small barb is typically not buried very deep in the skin.  Hold the skin taught, use a hemostat to grasp the end as close to the skin as possible, align the dart perpendicularly to the skin, and pull quickly and firmly.

If the patient can’t tolerate this or the barb appears particularly embedded, inject with local lidocaine and make a small superficial incision with an 11-blade scalpel just large enough to allow passage.   Ultrasound can be used to troubleshoot when needed.

Taser dispo:  People who have been tased do remarkably well and complications are rare.   In a review of tasers used by law enforcement, Vilke et al. found that there was no need for routine laboratory testing or observation, as there was ‘no evidence of dangerous laboratory abnormalities, physiologic changes, or immediate or delayed cardiac ischemia or dysrhythmias after exposure to electrical discharges of up to 15 s.”  Subsequent studies with minors less than 16 years of age found similar results.

Special note on the patient with agitated delirium or stimulant intoxication: treat these patients carefully, as the organic problem that got them tased in the first place still needs to be addressed, and substances such as PCP, cocaine, and methamphetamines are all cardiac irritants and may predispose them to dysrythmias.


Case 4: Adolescent in full arrest after lightening strike

Patients who are struck by direct current like lightening should be treated aggressively, because the reason for their cardiac arrest is often reversible if treated quickly.  Either the current sent the victim into a dysrhythmia, or it caused a temporary paralysis of the thoracic muscles, resulting in a primary respiratory arrest.

For victims of a lightning strike, classically we use reverse triage – normally, those in full arrest are triaged as black, deceases.  In high-voltage and lightening injuries, we tend to those in full arrest first, because you might quickly reverse them, and can move on to the next patient triaged red, or immediate.

High-voltage injuries are a multi-trauma – other sequelae include pulmonary edema, paralysis, ileus, and cataracts, in addition to the more immediate cardiac, musculoskeletal, neurologic, and renal considerations.

Regardless of the exposure, obtain an ECG and look for bundle branch block, heart block, and dysrhythmias, since those will change disposition.  In those who are injured, consider a basic metabolic panel, looking for potassium, calcium, and creatinine.  A creatine phosphokinase or total CK will screen for rhabdomyolysis.  Troponin is not predictive of the extent of direct myocardial damage, but get it if you think there might be a stress-induced, or type II MI.  Radiography as needed depending on the presenting associated trauma.


 

Take Home Points

1. Injury from electrical burns can be subtle.   Think of patients as having occult multi-trauma.   Be thorough in history and examination.  Plan to re-examine either during observation in the ED, or in close outpatient follow-up.

2. Discharge patients with low-voltage injury, no symptoms, and a normal ECG.  Counsel outpatients and provide close follow-up as appropriate.

3. Admit patients with low-voltage injury with signs or symptoms such as loss of consciousness, ECG changes, or evidence of end-organ damage on laboratory screening.  Admit all patients with high-voltage injury, even if asymptomatic and a normal laboratory screen.

4. Transfer patients with high-voltage injury or significant burns to a regional burn center or trauma center.


References

Celik A, Ergün O, Ozok G. Pediatric electrical injuries: a review of 38 consecutive patients. J Pediatr Surg. 2004;39(8):1233-1237.

Ericsson KA. Deliberate Practice and Acquisition of Expert Performance: A General Overview. Acad Emerg Med. 2008; 15:988-994.

Fish RM. Electric injury, part I: treatment priorities, subtle diagnostic factors, and burns. J Emerg Med. 1999;17(6):977-983. doi:10.1016/S0736-4679(99)00127-4.

Fish RM. Electric injury, part II: Specific injuries. J Emerg Med. 2000;18(1):27-34. doi:10.1016/S0736-4679(99)00158-4.

Fish RM. Electric injury, part III: cardiac monitoring indications, the pregnant patient, and lightning. J Emerg Med. 2000;18(2):181-187. doi:10.1016/S0736-4679(99)00190-0.

Horeczko T. “Electrical Injuries: Shocking or Subtle?” In Avoiding Common Errors in the Emergency Department, 2nd Edition. Mattu M, Swadron SP (eds). Lippincott, Williams & Wilkins. Phiadelphia. 2016. (In Press).

Rai J, Jeschke MG, Barrow RE, Herndon DN. Electrical Injuries: A 30-Year Review. J Trauma Acute Care Surg. 1999;46(5):933-936.

Vilke GM, Bozeman WP, Chan TC. Emergency department evaluation after conducted energy weapon use: review of the literature for the clinician. J Emerg Med. 2011; 40(5):598-604.


This post and podcast are dedicated to Joelle Donofrio, MD, FAAP for her tireless care of children, in the ED and in the field.  A special thank you and dedication to Cliff Reid, BM, FRCP(Glasg), FRCSEd(A&E), FRCEM, FACEM, FFICM, FCCP, EDIC, DCH, DipIMC, RCSEd, DipRTM, RCSEd, CCPU, CFEU for his transformative intelligence and educational verve.

Nov 1, 2015

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 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 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 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 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 ETTtube
  • The ETT should be taped 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: sedation, verification, NG/OG/foley
Oct 1, 2015

EMS is bringing you a child with a VP shunt, port-a-cath, trached on a vent, seizing, hypotensive, and now desaturating – ETA – 3 minutes. Are you ready?

Medicine is evolving. As technology advances, we need to meet the challenge of taking care of our patients who have come to rely on this technology for their basic needs.  Before we go further, remember to assess the parent and the child as a unit.  The caregiver who is usually the parent, is a rich source of knowledge about the child’s particular condition and past experience.  Take them seriously, and be on the lookout for caregiver burnout.

Tracheostomy Troubles

4-month-old baby boy born full term with Pierre Robin Sequence, febrile, not eating anything, now with breathing difficulty.
Place on trach collar oxygen, suction those secretions; flush with small amounts of saline, and repeat.

Any child symptomatic with a trach? Remember to monitor for hypoxia and bradycardia.

Tracheostomy indications: obstruction, primary respiratory compromise, or a neurologic disorder.  The obstruction may be a tumor, post-infectious, or addressing a congenital anomaly.  Children may have bronchopulmonary dysplasia, a restrictive lung disease such as scoliosis. A wide array of neurologic problems can result in a child’s having a trach, such as cerebral palsy, TBI, or spinal muscular atrophy.

Early complications of trachs especially in the first few months – include bleeding, pneumomediastinum, accidental decanulation, wound breakdown, and subcutaneous emphysema. The most common later complications include infection and granuloma formation. Tracheo-esophageal fistulas and trachea-innominate fistulas are thankfully very rare.

VP Shunt Shudderings

11-year-old girl with a history of prematurity, intraventricular hemorrhage, and subsequent flaccid paralysis with neurogenic bladder. She is brought in by her mother because of constipation and “not acting her usual self”.  She is afebrile, abdomen is soft, full of stool.

The most common shunt is the ventriculoperitoneal shunt, originating in a lateral ventricle and tracking subcutaneously down the neck and chest until the distal end enters and coils in the peritoneal space.  Less common types include ventriculoatrial, ventriculopleural, ventriculocisternal, ventriculo-vesicular (to gall bladder) and the lumbo-peritoneal, usually reserved for spina bifida.

The common denominator: hydrocephalus.  The most common causes are tumor, congenital anomalies, hemorrhage, or post-infectious obstructions.

The two most common complications of VP shunts are malfunction (due to obstruction, fracture, or kinking) or infection.  The slit-ventricle syndrome results from overdrainage, causing headaches and ataxia and the slit-ventricle syndrome.  An abdominal pseudocyst forms when cells floating in the peritoneal cavity aggregate on the distal tip of the VP shunt, forming a biofilm that fills with CSF.  VP shunts, like any foreign body, can migrate and erode through intestines and skin.

Classically in severe hydrocephalus an infant or toddler will have sun-setting eyes – the irises look like a setting sun against the prominent bulbar conjunctiva.  However, the presentation is usually much more subtle; if the child just feels off or if the parent tells you he is not acting right, this is a shunt malfunction until proven otherwise.

Garton et al. in the Journal of Neurosurgery followed 344 children with shunts, and found that in the first six months after a shunt is placed, the presence of nausea or vomiting carried a positive LR pf 10.4 for shunt malfunction.  Irritability conveyed a positive LR of 9.8 for shunt malfunction. Decreased LOC was 100% predictive.

Most shunt infections occur within a few weeks after placement. 90% of infections occur within the first 9 months. Fever is only 60% sensitive, but CRP is 95% specific.

If the child has severe mental status changes, hypertension, and/or bradycardia, tap the shunt emergently.

Head of the bed is 30 degrees; sterile fashion: don a cap, mask, faceshield, and sterile gloves, chlorhexidine or betadine to clean.  Use a 23 or 25 g butterfly attached to a manometer, and advance slowly. Pressures above 25 mmH20 are reliably indicative of a distal shunt obstruction. If there is no return of CSF, or there is poor flow, there probably is a proximal obstruction.  Make note of the pressure you get, allow the pressure to equilibrate, remove the needle, and dress it sterilely. Be ready to take over the airway if needed, and use standard ICP lowering temporizing tactics until a neurosurgeon is found.

Vascular Device Dilemmas

A 3-year-old boy with ALL undergoing consolidation chemotherapy has had vomiting with abdominal pain since yesterday; he is febrile, tachycardic, and pale; there is mild tenderness to palpation in the right lower quadrant, and his capillary refill is 3 seconds. He is in compensated shock.

The Huber needle is not a resuscitative line.  Obtain proper access to give fluids -- do not rely on the port-a-cath.

Vascular devices are notoriously troublesome. In the European Respiratory Journal, Munck et al. reviewed cases of patients who needed to have their vascular devices out. 43% of them got them out for was for occlusion, 21% infection; other reasons included displacement, rupture, and skin necrosis. Only 2.5% of them were removed for clinical improvement.

When a child or an adult is at risk for a massive air embolism, we should do three things: clamp the device proximal to the fracture or defect, hyperoxygenate, and perform Durant’s maneuver, or left lateral decubitus in Trendelenberg. This forces a presumed air embolus to stay in the apex of the right ventricle until we figure out what to do.  You can put the US probe on and look for a whirlwind of tiny bubbles to confirm – it is very sensitive and can detect as little as 0.05 ml/kg of air.  Some references advocate for hyperbarics to allow the embolus to resolve, others comment on using a needle to aspirate air.  The main thing for us is to suspect it, detect it, control it, and if the child arrests, to do vigorous CPR to mechanically disrupt the bubbles.

G-tube Tumult

A 17-year-old boy with a history of botulism had a rough ICU course, home after rehabilitation, with some residual dysmotility issues, still partially g-tube dependent. No complaints in the ED, but there is irritation around the stoma, and discomfort with g-tube manipulation.

G-tubes are placed for one of three reasons: insufficient intake, increased demand, or increased loss.  Insufficient intake may be due to anatomical problems, prematurity, or failure to thrive.  Increased demand may be temporary, such as in burns, s/p cardiac surgery, or ay prolonged recovery.  Increased losses may be from enteropathies, or short gut syndrome.

Alphabet Tube

Gastrostomy or g-tubes end directly in the stomach. Whatever you can take by mouth can go into the g-tube, including medications and bolus feeds.

Jejunostomy tubes, or J-tubes are placed by IR or surgery for babies with severe reflux – this is for drip feeds, usually done at night.

Gastro-jejunostomy tubes or G-J tubes use the G port for medications, and the J port for continuous feeds.

We do not pull or replace or touch G-J or J tubes in the ED, but we can place a Foley catheter in the stoma to keep it patent if needed.

Buried bumper syndrome” occurs when the patient has not changed his g-tube for much longer than recommended, or if there is a dramatic change in habitus. The inner balloon is pulled up and away from the stomach lumen, so that it is displaced and fixed – causing pain, inadequate feeds, obstruction, and sometimes peritonitis.

Take Home Messages

Tracheostomy: the stoma matures in one month – you can change out after that, suction, suction, suction, and you can place an ETT if the patient is critical.

Ventriculoperitoneal Shunts: 90% of infections occur within the first 9 months.

Vascular Devices: assume the line is not functional, and use another to resuscitate, especially in port-a-caths.

Gastrostomy Tubes: buried bmpers are bad business – be aware of the painful, obstructed, poorly mobile g-tube. The stoma matures in one month is open, three months of it’s a PEG. If it has fallen out, you have 1-3 hours before the stoma begins to close – temporize with a foley catheter.

When it comes to the technologically dependent child in the ED, familiarity breeds…confidence!

Selected References

Babu R, Spicer RD. Implanted vascular devices (ports) in children: compications and their prevention. Pediatr Surg Int (2002) 18: 50-53

DiBaise JK, Scolapio JS. Home Parenteral and Enteral Nutrition. Gastroenterol Clin N Am 36 (2007) 123-144l

Feinberg A et al. Gastrointestinal Care of Children and Adolescents with Developmental Disabilities. Pediatr Clin N Am 55 (2008) 1343–1358

Garton HJ. Piatt JH. Hydrocephalus. Pediatr Clin N Am 51 (2004) 305– 325

Kusminsky RE. Complications of Central Venous Catheterization. J Am Coll Surg. January 17, 2007.

Marek A. Mirski MA et al. Diagnosis and Treatment of Vascular Air Embolism. Anesthesiology 2007; 106:164–77

Marks JH. Pulmonary Care of Children and Adolescents with Developmental Disabilities. Pediatr Clin N Am 55 (2008) 1299–1314

Munck A et al. Follow-up of 452 totally implantable vascular devices in cystic fibrosis patients. Eur Respir J 2004; 23: 430–434

Shinkwin CA, Gibbin KP. Tracheostomy in children. J Royal Soc Med. Volume 89 April 1996

Simpkins C. Ventriculoperitoneal Shunt Infections in Patients with Hydrocephalus. Pediatr Nurs Nov 2005 Vol 31, No 6

Trachsel D, Hammer J. Indications for tracheostomy in children. Paediatric Resp Rev (2006) 7, 162–168

Wright SE,VanDahm K. Long-term care of the tracheostomy patient. Clin Chest Med 24 (2003) 473– 487

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