By Elizabeth Chen MD PGY-3

Acute Ischemic Stroke (AIS) in the pediatric population is extremely rare, has many mimics, and often presents with signs and symptoms that differ from a typical “adult” stroke.  Because the goal for diagnosis and treatment of AIS in adults is 4 hours, these differences often lead to delayed recognition and treatment. In a Canadian study, median interval from time of onset to diagnosis was 22.7 hours. When a stroke occurred in hospital, it still took 12.7 hours to diagnose.   When a child had a stroke out of the hospital, it took on average 1.7 hours for patients to present to the hospital, indicating that the time delay to diagnosis was often on the part of the medical staff. Currently, only a handful of large, dedicated pediatric centers have pediatric stroke teams similar to the typical adult “code stroke” teams found in most communities.  These pediatric teams are equipped to diagnosis and potentially treat children with AIS quickly but most hospitals are not. The key to improve care for children in the community is for all emergency physicians to be well trained on how to recognize and evaluate children for stroke.
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Recent estimate of the incidence of pediatric stroke is 2-13 per 100,000 children per year. Presentation in children less than a year old, may show up as focal weakness, but more likely to present as seizures and altered mental status. In older children, it is somewhat more similar to adults with hemiparesis or other focal neurologic signs like aphasia, visual disturbances, or cerebellar signs.
According to the International Pediatric Stroke study, half of children with AIS have at least one predisposing factor.   In 676 children from ages 29 days to 18 years with AIS, 9% had no risk factors, 53% had arteriopathies, 31% cardiac disorders, and 24% infection.  When assessing patients for stroke, have a higher clinical suspicion when they have any of the following risk factors:


Arteriopathies:
Focal cerebral arteriopathy of childhood—unilateral focal or segmental stenosis of distal carotid arteries and proximal circle of Willis vessels. The cause is unknown but some have had antecedent viral infections which may potentially cause an inflammation vasculitis.  
Postvaricella arteriopathy—Accounts for nearly 1/3 of childhood AIS. Intraneuronal migration from trigeminal ganglion to cerebral arteries. In a study in Canada with children 6 months to 10 years with confirmed AIS, 31%  had Varicella in the preceding year with a mean interval from varicella infection to AIS being 5.2 months. Patients may experience recurrent varicella associated AIS up to 33 weeks after presentations even with antithrombic prophylaxis.
Moyamoya—a disease process that causes progressive stenosis of the distal intracranial internal carotid artery, and less commonly stenosis of the anterior cerebral artery, middle cerebral artery , basilar artery, and posterior cerebral artery. Peak incidence is at 5 years. Recurrent TIA/AIS are common. Typically, the strokes are ischemic in childhood and then convert to hemorrhagic strokes in young adulthood.


Cervicocephalic arterial dissection—Cervicocephalic arterial dissection accounts for 7.5% of all AIS, half of which are due to trauma. Predisposing factors include trauma, connective tissue abnormalities, fibromuscular dysplasia, and anatomic variations. The cause of intracranial dissection is often spontaneous, while extracranial dissections are associated with trauma. This condition presents with headache, vomiting, dizziness, vertigo, diplopia, confusion, neck pain, and recurrent TIA’s.
Sickle Cell Disease (SCD)—These children are at a very high risk of stroke.  Approximately 11% of SCD patients will have had a clinically significant stroke by age 20, and this increases to 24% by age 45. Transcranial doppler is important in predicting risk for stroke; a mean velocity greater than 170 cm/sec places patients at a marginal risk, while values greater than 200 cm/sec in MC/ICA are highly associated with increased AIS risk.  If a patient with SCD presents with AIS, immediately order transfusion therapy and immediate exchange transfusion for a goal of a HbS fraction less than 30% and a hemoglobin level of 10. Hydroxyurea used by patients with sickle cell disease to reduce the incidence of painful crisis and blood transfusions unfortunately does not prevent stroke recurrence.


Congenital heart disease: Stroke is associated with most types of cardiac lesions but complex congenital heart lesions with right to left shunting and cyanosis are particularly prone to cause stroke. Additionally valvular disease, endocarditis, and arrythmias can lead to stroke. Chronic hypoxia leads to a markedly elevated hematocrit which places patients at higher risk for cerebral venous sinus thrombosis. Although the presence of a PFO increases the risk of stroke, it’s presence should not exclude further investigation into other cardiac abnormalities.


Hypercoagulable disorders: Prothrombotic states alone are rarely a cause of AIS; however, combined with other mechanisms such as protein C deficiency, antiphospholipid antibodies, and elevated lipoprotein, the odds ratio increases.   


Vasculitis: Primary vasculitides include Takayasu, giant cell arteritis, polyarteritis nodosa, Kawasaki disease,  and primary angiitis of the CNS. Diseases associated with secondary vasculitides include infection (bacterial meningitis, HIV, varicella, syphilis, fungal infections, CNS tuberculosis), malignancy, and collagen vascular diseases.  


Metabolic: Conditions such as Fabry disease, homocystinuria, and Menkes disease affect the cerebral vessel walls and increase the risk of AIS.


Presentation:
Infants and toddlers may present with headaches, seizures, altered mental status, behavioral/personality changes, sleepiness or decreased level of consciousness. While older children may present more similarly to adults with severe/sudden headache with vomiting and drowsiness, Vision loss/double vision, severe intractable dizziness, loss of balance/coordination, seizures on one side of the body, numbness/weakness on one side of body, difficulty speaking/understanding others.
There are also many stroke mimics in pediatrics that can make the diagnosis difficult.
Stroke Mimics n=287 Children (Mackay, Stroke 2017)


Migraine-28%
Febrile/Afebrile Seizure-15%
Bell’s Palsy-10%
Stroke-7%
Conversion Disorder-6%
Syncope-5%
Headache NOS-4%
Other CNS conditions-10%

Diagnosis:  Because of the difficulty of making the ultimate diagnosis of AIS in children an MRI and MRA of the brain and neck must be done, after an initial CT.  This often increases the time to diagnosis because of the logistics required to provide sedation for an MRI.


Management: The goal of treating children with AIS is to minimize morbidity and mortality and if possible to improve perfusion to the ischemic areas of the brain.  The system for adults is well organized and shown to improve outcomes. Thrombolysis (tPA) is well documented for use in adults, however it is not FDA approved for anyone under 18 years of age.  Attempts have been made to show efficacy and safety in children. There was a large NIH funded study started in 2015, Thrombolysis in Pediatric Stroke Study (TIPS). It was an international multicenter study with a total of 17 different sites.  A total of 93 patients were screened; 43 had a confirmed stroke, but only 1 child was enrolled. Almost half the stroke patients did not meet enrollment criteria because of missing the time limit (4.5 hours) to receive tPA. The study was discontinued because of a lack of enrollment.  Although there are still no large scale trials showing efficacy and safety there are some case reports showing positive results of tPA in teenage patients. Therefore, management to date should include rapid diagnosis and stabilization to minimize morbidity. Thrombolysis should be considered on a case-by-case basis.  


Future of AIS evaluation in children:  We need to improve awareness of stroke signs and symptoms in pediatric patients in order to diagnose and transport more quickly to a Pediatric Stroke Center.

Here is an example of a pediatric stroke evaluation protocol from Boston Children's Hospital:

By Emerson Posadas MD MBA PGY-2

This is the first of a series of blog posts about administrative and management aspects of the Emergency Department. The first blog in this series describes the transition from one electronic medical record (EMR) system to a new one in our own Emergency Department and all the challenges we faced.

As part of the American Recovery and Reinvestment Act, all pubic and private healthcare providers were required to adopt electronic medical records in 2014. There have been multiple articles on the transition from paper charting to EMR. However, not much has been discussed regarding the transition from one EMR system to another one. With an ever-increasing amount of electronic platforms available, EMR transitions are a common challenge faced by many hospital systems. At University Medical Center of Southern Nevada (UMC) we recently transitioned from McKesson software to EPIC software as our primary EMR system. With this, there were multiple opportunities to improve our workflow and operations in the emergency department. However, as with all transitions this was not as seamless as envisioned.

This transition period was preceded by months of preparation, as we customized the EMR system to our needs. We attempted to develop efficient pathways in the EMR to improve patient care and bring efficiency benefits. This involved multiple meetings with the EMR representatives, gathering input from all staff including physicians, nurses, and pharmacists. We received several notifications in the preceding months that we were “going live” on December 1st 2017. Staff was informed that there would be multiple EPIC “Superusers” available to us in the emergency department during the first month of transition period. Luckily, I was scheduled to work the night we went live.

I was in the middle of a busy night shift. We had been informed that at 3:00 am our current EMR system would be disabled, and there would be a downtime before the new EMR went live. However, we found that the downtime started to occur much earlier than we expected, and by 1:00 am our original EMR had gone down. Orders were no longer going through the computer system. Radiology reports were not being received. Further, there was no electronic tracking board to display which patients had been placed in a bed, discharged, or admitted. In the already chaotic environment of the Emergency Department, another layer of disarray had been added.

However, what occurred next was actually a marvelous display of problem solving and teamwork that was a testament to the preparedness of our Emergency Department. We dusted off old containers that held old paper order forms. The clerks got in contact with the radiology reading room to fax over any reads, and the nursing staff constantly printed and brought them to the physicians. The charge nurse created a makeshift tracking board on a white board that was constantly updated. We were going old school, and it was working. I credit the staff and administration for converting what could have been a terrible situation into something that was manageable. Further, I was able to peer into a time before computers and electronics dominated the healthcare environment. It was simple, but it worked. Over the next few hours, our new EMR system slowly started to become “live.”

​Over the next few weeks, there were growing pains with incorporating the new system to our workflow, but I believe the transition has been a good thing. It has been an opportunity to address core issues in the emergency department to increase efficiency, processes, and ultimately deliver the best possible patient care.

By M. Subramanian, MD and J. Haber, MD

​Image by Alessandro M via flickr

With Punxsutawney Phil predicting another 6 weeks of winter, it’s time for a review of literature on resuscitation of the hypothermic patient. Hypothermia can be a source of anxiety for the emergency physician. The risk of malignant arrest or arrhythmia is very high (and should be expected to occur) in any patient with a core body temperature under 32 degrees Celsius, despite rewarming and resuscitation; this is due to a phenomenon called Rescue Collapse or Afterdrop. Morbidity and mortality are very high in these patients, with less than 50-60% of patients survive neurologically intact after experiencing hypothermic arrest. While there are very few studies on hypothermia resuscitation, there exists some interesting opinions on protocols.
Let’s start at the beginning….
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Many of the protocols start with recognizing hypothermia, either by measuring core temperature (which is difficult to do in the field) or by feeling a cold trunk.  Hypothermia is defined as a core temperature of less than 35 degrees Celsius. A few studies show that esophageal measurement of core body temperature is equivocal to rectal and bladder temperature, but rectal and bladders temperatures may lag behind core temperatures during the process of rewarming.
The next step should be assessment of vital signs. Hypothermic patients may have cardiac instability or irritability, which places them at a very high risk of developing a malignant arrhythmia. Initiation of CPR in an altered hypothermic patient with a bradycardic pulse may actually cause cardiac arrest. Many of the protocols recommend gentle handling of the altered hypothermic patient, and one even recommends checking for a plus for 60 seconds before initiating CPR. Staging the degree of hypothermia is important to determine management; the standard scale used is the Swiss Hypothermia Scale. 

Classification depends more on clinical symptoms rather than core temperature. A patient with a core temperature less than 35 degrees Celsius who is alert (Stage 1) can be treated with passive rewarming measures, such as blankets, heat lamp, and active movement. It is important that the patient have a shivering response as this is key to recovery.

For the altered hypothermic patient with a pulse (Stage 2 or 3), many protocols recommend passive and minimally invasive rewarming.  These include blankets/Bair huggers and warm lights. It is generally not recommended to attempt bladder lavage, peritoneal lavage or thoracic lavage in these patients as such practices may aggravate the cardiac membrane and initiate malignant arrhythmia. Warm IV fluids does not substantially contribute to rewarming, but may be used for volume resuscitation as hypothermia may cause cold-diuresis. One protocol recommends normal saline boluses of 500 ml. Other protocols, however, recommend using crystalloids other than normal saline as patients may require massive amounts of fluids and large boluses of normal saline may worsen acidosis. Warmed humidified air has been seen in multiple studies to improve rewarming rates and is recommended by most protocols. Early airway management was also generally recommended as endotracheal intubation had low rates of instigating arrhythmias in hypothermic patients. As providers should expect a fatal arrhythmia to occur, securing the airway, placing of defibrillating pads and adequate IV access is recommended. Different protocols recommended rewarming the patient to 32-34 degrees Celsius, and then following therapeutic hypothermia rewarming protocols over the next 24 hours. Sinus bradycardia is a normal physiological process in the setting of hypothermia. It is not necessary to use atropine or cardiac pacing, as this will resolve with rewarming. Hypotension or ventricular arrhythmias reflect cardiac irritability, and while supportive management is the mainstay, providers must prepare for a probable malignant arrhythmia.

The hypothermic arrest patient provides a challenge to the typical ACLS resuscitation. The physiology of medication metabolism and the cardiac myocyte response to electricity in hypothermia decreases success of current practices. European guidelines recommend trying 3 rounds of epinephrine and cardiac defibrillation before core body temperature is rewarmed to 32 degrees Celsius. Other sources say to only give one round of epinephrine and one defibrillation attempt before core temperature reaches 32 degrees Celsius. Dr. Doug Brown recommends a combination of the two; one dose of epinephrine and one defibrillation attempt (in the setting of a shockable rhythm) at first, then continuous CPR with rewarming. With every 5 degree Celsius increase in core body temperature, he recommends checking for pulse and shockable rhythm, and if pulseless with shockable rhythm, giving another round of epinephrine and defibrillation. If that does not work, continue CPR and rewarming until core body temperature is 32 degrees Celsius, and a last round of epinephrine and defibrillation. If at that point the arrest is not reversed, the patient is presumed dead and CPR may be terminated. As the emergency medicine adage goes- “the patient is not dead, until warm and dead”. This alteration to the typical ACLS process allows for fewer interruptions of CPR and defined end point. Unfortunately, there is no solid evidence defining what is “warm enough”, but consensus appears to settle around 30-32 degree Celsius.

It is in the setting of Stage 3-4 that invasive rewarming techniques is found to be most beneficial. Multiple case reports and series have shown an advantage to patients who received extracorporeal warming. Techniques include continuous venovenous, continuous arteriovenous (which can be done in the ED), hemodialysis and cardiac bypass. Other techniques of invasive rewarming include lavages of the bladder, peritoneum (similar to a DPL) and thoracic cavities. While these latter techniques are recommended by a few protocols, Dr. Weingart of EMCrit discourages against bladder and peritoneal lavage. He states the risk of complications with peritoneal lavage is not worth the benefit of rewarming. Also, bladder lavage rewarming rates are not aggressive enough to justify the intervention. However, given the high mortality of stage 3 and stage 4, it may be reasonable for clinicians to decide to perform these procedures, as a last resort if all else has failed. Almost all protocols agree that extracorporeal warming is the best for rapid rewarming. Mortality rates improve from below 37% survival to 50-60% survival. Unfortunately many community practices do not have facilities to achieve this, and transfer to such facilities may be difficult to ensure. Hemodialysis is more readily available and has rewarming rates of 1.5 degrees Celsius/hour. Dr. Gentilello created a machine that took blood from an arterial line to a level 1 infuser, warming the blood and connecting it to a venous catheter. However it is difficult to find this adapter anymore.

If a patient does not rewarm at the established rates (given the rewarming interventions), providers should consider other causes preventing an increase in core body temperature. Most common causes of failure to rewarm include hypoglycemia, alcohol intoxication, infection/sepsis, Addison’s, malnutrition and myxedema coma. It is important to check a fingerstick glucose as well as labs for CBC, metabolic panel, thyroid function tests and blood cultures.
While there are many case reports of successful return of spontaneous circulation in hypothermic arrest patients, slow or stagnant neurologic recovery is a significant part of morbidity. Stage 1 patients have the best chances of survival with rates up to 100% neurologically intact. Organ failure is common within the first 24 hours of Stage 4 hypothermic patients, with pulmonary edema as the leading cause of death. Resuscitated hypothermic patients have an in-hospital mortality of 40%. However, given the existence of case reports highlighting the rare patient with full neurologic recovery from Stage 3 or 4 hypothermia, it is difficult to counsel family on withdrawing care. One study found that patients with hypothermia that were found indoors had worse outcomes. Other prognostic factors include serum potassium. A significantly elevated serum potassium is indicative of hypoxia and traumatic cell death. One protocol suggested termination if serum potassium was greater than 12 mmol/liter. Another factor is hypothermia from avalanche burial; indications that hypoxia preceded hypothermia (and therefore not likely to respond to CPR) include snow in the airway, asystole and burial time greater than 35 minutes.

While there are multiple protocols addressing the management of the hypothermic patient, there is little evidence to support one protocol versus another. More research is needed to determine the best evidence based approach to hypothermic patients. Therefore, consider contributing your hypothermia cases to the International Hypothermia Registry, and increase available data to help establish a standard of practice.  

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Resources:
Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. N Engl J Med. 2012;367(20):1930-8.
Gervais J, Sholl M, Holmes J. Accidental Hypothermia Guideline. Maine Medical Center. Jan 2013. < http://www.mainehealth.org/workfiles/mmc_em/Accidental-hypothermia-v2.pdf>
Mulcahy A, Watts M. Accidental Hypothermia: An Evidence Based Approach. Emergency Medicine Practice. 2009;11(1).
Van der ploeg GJ, Goslings JC, Walpoth BH, Bierens JJ. Accidental hypothermia: rewarming treatments, complications and outcomes from one university medical centre. Resuscitation. 2010;81(11):1550-5.
Boue Y, Lavolaine J, Bouzat P, Matraxia S, Chavanon O, Payen JF. Neurologic recovery from profound accidental hypothermia after 5 hours of cardiopulmonary resuscitation. Crit Care Med. 2014;42(2):e167-70.
Roeggla, M., Holzer, M., Roeggla, G., Frossard, M., Wagner, A. and Laggner, A. N. (2001), Prognosis of Accidental Hypothermia in the Urban Setting. Journal of Intensive Care Medicine, 16: 142–149.
Jones AI, Swann IJ. Prolonged resuscitation in accidental hypothermia: use of mechanical cardio-pulmonary resuscitation and partial cardio-pulmonary bypass. Eur J Emerg Med. 1994;1(1):34-6.
Weingart, Scott. "Podcast 66 – …Until They Are Warm and Dead: Severe Accidental Hypothermia." Review. Audio blog post. EMCrit. Scott Weingart, 7 Feb. 2012. Web. 27 Feb. 2014.
Brown, Doug, and Mel Herbert. "Accidental Hypothermia- Part 2." Review. Audio blog post. EM:RAP. Mel Herbert, Jan. 2014. Web. 27 Feb. 2015.
Petrone P, Asensio JA, Marini CP. Management of accidental hypothermia and cold injury. Curr Probl Surg. 2014;51(10):417-31.
Kosiński S, Darocha T, Gałązkowski R, Drwiła R. Accidental hypothermia in Poland – estimation of prevalence, diagnostic methods and treatment. Scand J Trauma Resusc Emerg Med. 2015;23:13.
Gordon L, Ellerton JA, Paal P, Peek GJ, Barker J. Severe accidental hypothermia. BMJ. 2014;348:g1675.
Paal P, Gordon L, Strapazzon G, et al. Accidental hypothermia-an update : The content of this review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM). Scand J Trauma Resusc Emerg Med. 2016;24(1):111.
Walpoth B, Meyer M. International Hypothermia Registry. University Hospital Geneva, Switzerland. Accessed 12/14/17. <https://www.hypothermia-registry.org/>

By Schon Roberts MD PGY-3

61yo M with h/o of metastatic adenocarcinoma p/w numbness, tingling, and weakness in B/L UE and LE X 3 weeks. This has worsened in the past 3 days. He is now unable to walk or feed himself. He denies bowel/bladder incontinence, HA, fevers, chills, N/V/D, abdominal pain.  He denies any IVD. He was 3 weeks ago able to work full time as an electrician. He complains also of chronic neck and back pain.
Vital Signs are unremarkable.  Back is normal appearance. Pt has 4/5 strength in B/L UE and LE. He has rigidity of R arm with spasm. Decreased sensation B/L UE and LE R>L.  What is the best treatment option for this pt?

A. Discharge home. This is chronic back pain.
B. Refer patient to both pain management and a spinal surgeon to evaluate for disc herniation
C. Obtain consults from nuclear medicine, spinal surgery, and admit pt. Give steroids
D. Place pt in a TLSO brace and admit to the hospital
E. Start broad spectrum antibiotics: pt has an epidural abscess  

By Schon Roberts MD PGY-3

14 mo F, seen 3 days ago in ED with fever and possible UTI p/w new onset rash. She was placed on Omnicef and followed up with her regular doctor today. He sent her for evaluation. Parents state that she has had swelling of her hands and feet. Mother states that she has had a fever for 5 days. Fever was TMax 103 F. She has had adequate PO intake with good urine output and stooling. Parents deny URI Symptoms, N/V/D, or recent travel. Vital Signs show a pulse of 179, RR of 28, Temperature of 102.1 F, and patient has a spO2 of 99% on RA. Physical exam is remarkable for injected sclera, swelling of her hands and the dorsum of her feet. She has an erythematous rash on her trunk and extremities that blanches. It spares the palms and soles. Lungs are CTABL and cardiac exam is unremarkable. What is the best treatment option for this child?
 
A. Broaden antibiotic coverage for meningitis to include listeria coverage, LP, and admit to the hospital
B. Discharge home; Pt has a URI
C. PO Tylenol, wait for defervescence, and D/C if improved
D. Obtain an echocardiogram, start on high dose ASA, IVIG, and admit
E. Start on steroids and admit with nephrology consult

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By Emerson Posadas MD PGY-1
 
Aaron Heckleman, MD
The Crashing Heart
Heart Failure

• if nitroglycerine helps, be aggressive with it, but maintain blood pressure MAP >=65
• start the nitroglycerine drip at 100 mcg/min, go up by 50 q5min
• critical aortic stenosis is preload dependent

 
Adenosine

• Safe for everyone except Afib with WPW (Wide, irregular)
• If giving through central line cut the initial dose in half to 3 mg

 
Ross Berkeley, MD
Advanced Documentation

• don’t forget to document patient reassessments, interventions performed, discussion with patient/family, chaperone in the room, informed consent, conversations with consultants, review of EMS/nursing notes
• document due diligence, that you reassessed

 
 
Kelly Morgan, MD
Traumatic Brain Injury

• Mild Traumatic Brain Injury – GCS 13-15 with no structural change
• Second Impact Syndrome – rare condition caused by rapid brain swelling/herniation after a second concussion in close succession to a prior MTBI
• Explain expected course and possibility of post-concussive symptoms to patients

 
 

Dr. Tony Zitek offers his evidence-based approach to pregnant and non-pregnant vaginal bleeding in this lecture. This lecture is a nice evidence-based complement to the most recent EMRAP C3 project on this topic.

​Certainly, a more in depth review will reveal a more complete understanding of the methodology, however, here are a few takeaways: First, a thorough history and physical is necessary in these cases. If my patient meets the definition of BRUE, they are in the low risk category and I find no worrisome characteristics on physical and history and can have follow up the next day, then I plan to discharge them. I would consider keeping the patient hooked up to a cardiorespiratory and pulse ox monitor during my evaluation and would consider getting an EKG, as there is a 4% incidence of cardiac disease found in ALTE patients in one study. Beyond those things, I would not do any more for my low risk BRUE patients.  With this guideline in place, the hope is more specific research and studies can be done to further guide practitioners in dealing with BRUE patients.
 
References
1.     Tieder JS, Bonkowsky JL, Etzel RA, et al. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants. Pediatrics. 2016 May;137(5).
2.     McGovern MC, Smith MB. Causes of apparent life threatening events in infants: a systematic review. Arch Dis Child. 2004;89(11):1043–1048pmid:15499062
3.     Tieder JS, Altman RL, Bonkowsky JL, et al. Management of apparent life-threatening events in infants: a systematic review. J Pediatr. 2013;163(1):94–99, e91–e96
4.     Brand DA, Altman RL, Purtill K, Edwards KS. Yield of diagnostic testing in infants who have had an apparent life-threatening event. Pediatrics. 2005;115(4):885–893pmid:15805360
5.     Green M. Vulnerable child syndrome and its variants. Pediatr Rev. 1986;8(3):75–80pmid:3332339
6.     Claudius I, Keens T. Do all infants with apparent life-threatening events need to be admitted? Pediatrics. 2007;119(4):679–683pmid:17403838
7.     Bonkowsky JL, Guenther E, Filloux FM, Srivastava R. Death, child abuse, and adverse neurological outcome of infants after an apparent life-threatening event. Pediatrics. 2008;122(1):125–131pmid:18595995
8.     Al-Kindy HA, Gelinas JF, Hatzakis G, Cote A. Risk factors for extreme events in infants hospitalized for apparent life-threatening events. J Pediatr. 2009;154(3):332–337, 337.e1–337.e2
9.     Ramanathan R, Corwin MJ, Hunt CE, et al; Collaborative Home Infant Monitoring Evaluation (CHIME) Study Group. Cardiorespiratory events recorded on home monitors: comparison of healthy infants with those at increased risk for SIDS. JAMA. 2001;285(17):2199–2207pmid:11325321
10.  Mittal MK, Sun G,, Baren JM. A clinical decision rule to identify infants with apparent life-threatening event who can be safely discharged from the emergency department. Pediatr Emerg Care. 2012;28(7):599–605pmid:22743742
11.  Hoki R, onkowsky JL, Minich LL, Srivastava R, Pinto NM. Cardiac testing and outcome in infants after an apparent life-threatening event. Arch Dis Child. 2012;97(12):1034-1038pArchmid:23012307