The Technologically Dependent Child in the ED
EMS is bringing you a child with a VP shunt, port-a-cath, trached on a vent, seizing, hypotensive, and now desaturating â€“ ETA â€“ 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.Â Before we go further, remember to assess the parent and the child as a unit.Â The caregiver who is usually the parent, is a rich source of knowledge about the childâ€™s particular condition and past experience.Â 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.Â The obstruction may be a tumor, post-infectious, or addressing a congenital anomaly.Â Children may have bronchopulmonary dysplasia, a restrictive lung disease such as scoliosis. A wide array of neurologic problems can result in a childâ€™s having a trach, such as cerebral palsy, TBI, or spinal muscular atrophy.
Early complications of trachs especially in the first few months â€“ 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 â€œnot acting her usual selfâ€.Â 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.Â 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.Â 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.Â The slit-ventricle syndrome results from overdrainage, causing headaches and ataxia and the slit-ventricle syndrome.Â 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.Â 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 â€“ the irises look like a setting sun against the prominent bulbar conjunctiva.Â 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.Â 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.Â 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.Â 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.Â 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 Durantâ€™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.Â You can put the US probe on and look for a whirlwind of tiny bubbles to confirm â€“ it is very sensitive and can detect as little as 0.05 ml/kg of air.Â Some references advocate for hyperbarics to allow the embolus to resolve, others comment on using a needle to aspirate air.Â 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.Â Insufficient intake may be due to anatomical problems, prematurity, or failure to thrive.Â Increased demand may be temporary, such as in burns, s/p cardiac surgery, or ay prolonged recovery.Â Increased losses may be from enteropathies, or short gut syndrome.
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 â€“ 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.
â€œBuried bumper syndromeâ€ 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 â€“ causing pain, inadequate feeds, obstruction, and sometimes peritonitis.Take Home Messages
Tracheostomy: the stoma matures in one month â€“ 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 â€“ be aware of the painful, obstructed, poorly mobile g-tube. The stoma matures in one month is open, three months of itâ€™s a PEG. If it has fallen out, you have 1-3 hours before the stoma begins to close â€“ temporize with a foley catheter.
When it comes to the technologically dependent child in the ED, familiarity breedsâ€¦confidence!
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) 1343â€“1358
Garton HJ. Piatt JH. Hydrocephalus. Pediatr Clin N Am 51 (2004) 305â€“ 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; 106:164â€“77
Marks JH. Pulmonary Care of Children and Adolescents with Developmental Disabilities. Pediatr Clin N Am 55 (2008) 1299â€“1314
Munck A et al. Follow-up of 452 totally implantable vascular devices in cystic fibrosis patients. Eur Respir J 2004; 23: 430â€“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, 162â€“168
Wright SE,VanDahm K. Long-term care of the tracheostomy patient. Clin Chest Med 24 (2003) 473â€“ 487…
Intranasal medications, if understood and employed properly, are a great choice to avoid and IV or as a bridge until IV access is obtained.Â Learn the strengths and limits of intranasal fentanyl, midazolam, ketamine, and dexmedetomidine.
Pain Management in Children
Goal: the â€œouchless EDâ€.Â
Two main barriers in pain treatment in children:
1. We consistently under-recognize childrenâ€™s pain.Â 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.Â 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 â€“ Not every medication is easily amenable to intranasal administration.Â We can use intranasal drugs for analgesia, for anxiolysis, for seizures â€“ but not all drugs used for those purposes will perform well â€“ or at all â€“ via the IN route.
Right Dose â€“ Dosing with IN meds will vary considerably from the IV route.Â Rule of thumb:Â the IN dose is 2-3 times the IV dose.
Right Patient â€“ Is this patient and family appropriate for â€œjust taking the edge offâ€?Â What is the level of anxiety in the room?Â How is the child relating to the parent, usually itâ€™s the mother there.Â What else is going on in that clinical snapshot as you walk in?
Right Timing â€“ Mostly IV and IN onset times are very similar.Â Notable exception:Â intranasal midazolam may take 10-15 minutes to take effect â€“ 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.Â Â 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 â€“ you have to push the drug as fast as you can to atomize the solution.Â
Safe, effective at 2 mcg/kg.Â Most commonly stocked concentration of fentanyl is 50 mcg/mL.Â A 40-kg-child will reach the maximum volume possible for administration (40 kg x 2 mcg/kg = 80 mcg; at 50 mcg/mL â€“ that makes 1.6 mL â€“ if we divide the dose, itâ€™s not ideal, but is still under our maximum of under 1 mL per naris.)Â You graduate from intranasal fentanyl in elementary school.
Sufentanil for adults (half the volume of fentanyl) â€“ 0.5 mcg/kg, which can be repeated as needed.Â
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.Â The IV preparation for midazolam is 5 mg/5 mL â€“ this a very dilute solution.Â 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).Â Kindergarten graduation is when to drop the intranasal midazolam.
The IV dose for ketamine for pain control is 0.15 to 0.3 mg/kg, usually as an infusion over an hour.Â 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.
Dexmedetomidine is an alpha-2 receptor agonist, a smarter clonidine.Â Clonidine is also an alpha-2 agonist, and it can cause a marked decrease in blood pressure with some mild sedation.Â Dexmedetomidine targets receptors in the CNS and spinal cord, and so it provides deep sedation, with very minimal blood pressure effects.Â It induces a sleep-like state.Â In fact, EEGs done under dex show the same pattern as seen in stage II sleep.Â 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:Â The â€œSemmelweiss reflexâ€.
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.
The Undifferentiated Sick Infant
You have all of the skills you need to care for an acutely ill infant.Â 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.Â
The combination of abnormalities determines the category of pathophysiology: respiratory distress, respiratory failure, CNS or metabolic problem, shock, or cardiopulmonary failure.
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?Â Is the toddler interested in what is going on in the room?Â
Consolability - A child who cannot be consoled at some point by his mother is experiencing a medical emergency until proven otherwise.Â
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.Â
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.Â Â Uncover the chest and abdomen and look for retractions.Â Listen - even without a stethoscope - for abnormal airway sounds like grunting or stridor.Â Grunting is the child's last-ditch effort to produce auto-PEEP.Â 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.Â Without even having to touch the child, you can see signs of pallor, cyanosis, or mottling.Â 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"
Â Â Â 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.Â Do a total body check.
Â Â Â Heart disease or Hypovolemia - is there a history of congenital heart disease? Was there any prenatal care or ultrasound done?Â Does this child look volume depleted?
Â Â Â 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.Â Could this be congenital hypothyroidism with poor tone and poor feeding?Â Any history of maternal illness or medications? Congenital hyperthyroidism with high output failure?
Â Â Â Metabolic - What electrolyte abnormality could be causing this presentation? Perhaps diGeorge syndrome with hypocalcemia and seizures?Â
Â Â Â 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.Â Searching for an inborn error of metabolism is like looking for A UFO - amino acids, uric acids, fatty acids, organic acids.Â 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.Â
Â Â Â Seizures - Neonatal seizures can be notoriously subtle - look for little repetitive movements of the arms, called "boxing" or of the legs, called "bicycling"
Â Â Â Formula problems - Hard times sometimes prompt parents to dilute formula, causing a dangerous hyponatremia, altered mental status, and seizures.Â Conversely, concentrated formula can cause hypovolemia
Â Â Â 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
Â Â Â Toxins - was there some maternal medication or ingestion?Â Is there some home remedy or medication used on the baby?Â Check a glucose ad drug screen
Â Â Â Sepsis - Saved for last - You'll almost always treat the sick neonate empirically for sepsis - think of congenital and acquired etiologies.
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.Â Place the child on a non-rebreather mask, and after several minutes, perform an ABG.Â (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.Â If the pO2 on supplemental oxygen is less than 100, then this is extremely predictive of hemodynamically significant congenital heart disease.Â 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.Â
Give prostaglandin if the patient is less than 4 weeks old (typical presentation is within the first 1-2 weeks of life).Â Start at 0.05 mcg/kg/min.Â PGE keep the systemic circulation supplied with some mixed venous blood until either surgery or palliation is decided.Â
* 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
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.
Pediatric Status Epilepticus
Do you have a plan for your little patient when he just wonâ€™t stop seizing?Â 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
â€“ OR â€“
Recurrent activity without recovery between intervals.Â (This definition includes clinically apparent seizures as well as those seen only on EEG.)
During a seizure, GABA receptors in the neuronâ€™s membrane are internalized and destroyed.Â Seizure activity itself starts this self-defeating process â€“ 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 â€“ the NMDA receptors â€“ are acutely upregulated and mobilize to the neuronâ€™s surface.Â This is the second reason to act quickly and avoid this kindling effect.
In other words â€“ time is brain.
Orâ€¦ is it something else as well?
Pediatric status epilepticus is analogous to the multi-organ dysfunction syndrome in severe sepsis.Â Status epilepticus affects almost every organ system.Â
Cardiac â€“ dysrhythmias, high output failure, and autonomic dysregulation resulting in hypotension or hypertension.Â
Respiratory â€“ apnea and hypoxia, ARDS, and potentially aspiration pneumonia.Â
Renal â€“ rhabdomyolysis, myoglobinuria, and acute renal failure.
Metabolic â€“ lactic acidosis, hypercapnia, hyperglycemia, sometimes hypoglycemia, hyperkalemia, and leukocytosis.
Autonomic â€“ hyperpyrexia and breakdown of cerebral circulation.Â
DeLorenzo et al.: Mortality correlated with time seizing.Â Once the seizure has met the 30 min mark, Delorenzo reported a jump from 4.4% mortality to 22%!Â If the seizure lasts greater than 2 hours, 45%.Â Time spent seizing is a vicious cycle: itâ€™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.Â If we know the amount of ingestion in adults or children, we give a gram-for-gram replacement, up to 5 grams.Â
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.Â
The differential is vast: cardiac, hematologic, infectious, vascaulr, syndromic, metabolic, oncologic, traumatic, toxic.Â
Treatment: stabilization, embolization by interventional radiology, elective extirpation when more stable.Â 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.Â 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.Â Also, a prolonged post-ictal state or prolonged altered mental status.Â Other considerations are those who had a seizure and cardiac arrest -Â ROSC without RONF, those with traumatic brain injury, and those needing ECMO â€“ all within the context of seizures.
The longer the seizure lasts, the harder it is to break â€“ 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
â€œHealing is a matter of time, but it is sometimes also a matter of opportunity.â€
â€œExtreme remedies are very appropriate for extreme diseases.â€
Â â€“ Hippocrates of Kos
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: 222â€“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.Â Arch Pediatr Adolesc Med. 1998 Oct;152(10):1037-8
Trommer BL, Pasternak JF.Â 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).
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.