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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: 2015
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

Sep 1, 2015

Intranasal medications, if understood and employed properly, are a great choice to avoid and 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


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


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 .


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.


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

Sep 1, 2015

Do you have a plan for your little patient when he just won’t stop seizing?  What do you do when your typical treatment is not enough? Get up-to-date in the understanding and management of pediatric status epilepticus.


Definition of status epilepticus:

Continuous seizure activity of 5 minutes or greater


– OR –


Recurrent activity without recovery between intervals.  (This definition includes clinically apparent seizures as well as those seen only on EEG.)


During a seizure, GABA receptors in the neuron’s membrane are internalized and destroyed.  Seizure activity itself starts this self-defeating process – this is the first reason we need to act as quickly as possible and take advantage of the GABA receptors that are still recruitable.


Excitatory receptors – the NMDA receptors – are acutely upregulated and mobilize to the neuron’s surface.  This is the second reason to act quickly and avoid this kindling effect.


In other words – time is brain.


Or… is it something else as well?


Pediatric status epilepticus is analogous to the multi-organ dysfunction syndrome in severe sepsis.  Status epilepticus affects almost every organ system. 


Cardiac – dysrhythmias, high output failure, and autonomic dysregulation resulting in hypotension or hypertension. 


Respiratory – apnea and hypoxia, ARDS, and potentially aspiration pneumonia. 
Renal – rhabdomyolysis, myoglobinuria, and acute renal failure.


Metabolic – lactic acidosis, hypercapnia, hyperglycemia, sometimes hypoglycemia, hyperkalemia, and leukocytosis.


Autonomic – hyperpyrexia and breakdown of cerebral circulation. 


DeLorenzo et al.: Mortality correlated with time seizing.  Once the seizure has met the 30 min mark, Delorenzo reported a jump from 4.4% mortality to 22%!  If the seizure lasts greater than 2 hours, 45%.  Time spent seizing is a vicious cycle: it’s harder to break the longer it goes on, and the longer it goes on, the higher the mortality.


Think about treatment of pediatric status epilepticus in terms of time: prehospital care, status epilepticus (greater than 5 min), initial refractory status epilepticus (greater than 10 min), later refractory status (at 20 min), and coma induction (at 25 minutes).


Case 1: Hyponatremic Status Epilepticus


Give 3 mL/kg of 3% saline over 30 min.


Stop the infusion as soon as the seizure stops.


Case 2: INH toxicity


Empiric treatment -- you are the test.  If we know the amount of ingestion in adults or children, we give a gram-for-gram replacement, up to 5 grams. 


If a child under 2 years of age arrives to you in stats epilepticus, give 100 mg of IV pyridoxime for potentially undiagnosed congenital deficiency.


Case 3: Headache and Arteriovenous Malformation


Unlike in adults, stroke in children is divided evenly between hemorrhagic and ischemic etiologies. 

The differential is vast: cardiac, hematologic, infectious, vascaulr, syndromic, metabolic, oncologic, traumatic, toxic. 


Treatment: stabilization, embolization by interventional radiology, elective extirpation when more stable.  Other options for stable patients include an endovascular flow-directed microcatheter using cyanoacrylate. Radiosurgery is an options for others.


Non-convulsive Status Epilepticus


Risk factors include age < 18, especially age < 1, no prior history of seizures, and traumatic brain injury.  This would prompt you to ask for continuous EEG monitoring for non-convulsive status epilepticus, especially when there is a change in mental status for no other reason.  Also, a prolonged post-ictal state or prolonged altered mental status.  Other considerations are those who had a seizure and cardiac arrest -  ROSC without RONF, those with traumatic brain injury, and those needing ECMO – all within the context of seizures.


SUMMARY POINTS


The longer the seizure lasts, the harder it is to break – act quickly


Have a plan for normal escalation of care, and Search for an underlying cause


Recognize when the routine treatment is not enough.

Before You Go


“Healing is a matter of time, but it is sometimes also a matter of opportunity.”


“Extreme remedies are very appropriate for extreme diseases.”


 – Hippocrates of Kos

Selected References


Abend NS et al. Nonconvulsive seizures are common in critically ill children. Neurology. 2011; 76(12):1071-7


Baren J. Pediatric Seizures and Strokes: Beyond Benzos and Brain Scans. ACEP Scientific Assembly. October 8th, 2009. Boston, MA.


Brophy et al. Guidelines for the Evaluation and Management of Status Epilepticus. Neurocrit Care. 2012; DOI 10.1007/s12028-012-9695-z


Capovilla G et al. Treatment of convulsive status epilepticus in childhood: Recommendations of the Italian League Against Epilepsy. Epilepsia. 2013; 54 Suppl 7:23-34


Chin RFM et al., for the NLSTEPSS Collaborative Group. Incidence, cause, and short-term outcome of convulsive status epilepticus in childhood: prospective population-based study. Lancet. 2006; 368: 222–29.


Chen JW, Chamberlain CG. Status epilepticus: pathophysiology and management in adults. Lancet Neurol. 2006; 5:246-256.


DeLorenzo RJ. Comparison of status epilepticus with prolonged seizure episodes lasting from 10 to 29 minutes. Epilepsia. 1999 Feb;40(2):164-9.


LaRoche SM, Helmers SL. The New Antiepileptic Drugs: Scientific Review. JAMA. 2004;291:605-614.


Minns AB, Ghafouri N, Clark RF. Isoniazid-induced status epilepticus in a pediatric patient after inadequate pyridoxine therapy. Pediatr Emerg Care. 2010; 26(5):380-1.


Ogilvy CS et al. Recommendations for the Management of Intracranial Arteriovenous Malformations: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Stroke Council. Stroke. 2001; 32: 1458-1471


Rosati A et al. Efficacy and safety of ketamine in refractory status epilepticus in children. Neurology. 2012; 79:2355-2358.


Schwartz ID. Hyponatremic seizure in a child using desmopressin for nocturnal enuresis.  Arch Pediatr Adolesc Med. 1998 Oct;152(10):1037-8


Trommer BL, Pasternak JF.  NMDA receptor antagonists inhibit kindling epileptogenesis and seizure expression in developing rats. Brain Res Dev Brain Res. 1990 May 1;53(2):248-52.


Waterhouse EJ et al. Prospective population-based study of intermittent and continuous convulsive status epilepticus in Richmond, Virginia. Epilepsia. 1999 Jun;40(6).

Sep 1, 2015

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.


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


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. 


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.


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


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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