Blunt Abdominal Trauma in Pediatric Patients: A Clinical Decision Rule

A school-age child was brought to the ED by the mother following involvement in an MVC during which the child was restrained with a lap belt.  The child initially complained of abdominal pain while eating, but currently has no complaints, stable vital signs, and a benign abdominal exam.  The mother is concerned and wonders if her child should get imaging.  This prompts you to investigate whether there are any evidence based clinical decision rules for imaging in pediatric blunt abdominal trauma.

Clinical question: 

Do all children with blunt abdominal trauma necessitate abdominal imaging?  Is there a clinical decision rule that can help guide physician and parent shared-decision making when weighing risks vs benefit in evaluation of pediatric patients following blunt abdominal trauma?

Literature:

Injuries secondary to blunt abdominal trauma contribute to a large degree of morbidity in the pediatric patient population.  In assessing these patients following trauma, CT scans have become the reference standard for diagnostic of traumatic injury.  However, we must also weigh the risk of exposing patients to increased dosage of radiation and increasing their risk of radiation-induced malignancy.  This is especially true in the pediatric population given their rapidly developing bodies as well as their propensity to have a continued lifetime of exposure to medical radiation through future diagnostics.  

Clinicians, especially those not accustomed to regularly seeing pediatric patients, trauma patients, or more specifically pediatric trauma patients, often (anecdotally) err on the side of obtaining advanced imaging to assess patients following blunt abdominal trauma.  Dr. James Holmes and his colleagues in the PECARN (Pediatric Emergency Care Applied Research Network) group derived a clinical decision rule to help guide decision making when considering imaging in the pediatric patients.  Using a large, prospective study in 20 EDs, they identified a 7 point rule based solely on history and physical data to help risk stratify the pediatric blunt abdominal patient.  In patients who have no evidence of abdominal wall trauma or a seatbelt sign, a GCS >14, no abdominal tenderness on PE, no thoracic wall trauma, no complaint of abdominal pain, no absence or decreased breath sounds, and no vomiting, the risk of intra-abdominal injury requiring intervention is extremely low (0.1%).  

While these findings require external validation before likely widespread use, they have benefit for current ED practitioners for several reasons.  First, they used a patient oriented outcome of injury requiring intervention rather than a diagnostic outcome of any intra-abdominal injury, so that some patients who perhaps had injury but went on to have a stable clinical course and never received imaging were not a source of bias.  Secondly, their 7 findings were based solely on history and physical findings, something that is available to any clinician regardless of location or resources.  This eliminated the exclusion of validity to centers able to perform FAST scans or obtain more rapid lab results.  It also likely further decreased the “miss rate” for significant intra-abdominal injury when the clinical decision rule is supplemented by these diagnostic studies.  Finally, their rule is not meant as a hard “rule” to force a physician’s hand in obtaining a CT on a patient who carries 1 or 2 of their H&P risk factors.  It is meant to guide the conversation and critical decision process in weighing the radiation exposure risk versus the inherent injury risk when deciding how to continue the workup of the presenting child.  0.1% is a lower risk of injury the risk of a radiation induced malignancy in a young child.  However, as more risk factors accumulate, that may mitigate the difference in risk percentage, increasing the possible benefit of obtaining the CT.

Take home:

All patients, especially pediatric patients are sensitive to the ionizing radiation of medical imaging.  Risk stratifying pediatric patients with decreased likelihood of significant intra-abdominal injury can help physicians to have informed discussions with patients and their guardians and help to decrease the number of CT scans ordered on low risk patients and their exposure to unnecessary radiation.

References:

1) Holmes, JF, et al.  Identifying Children at Very Low Risk of Clinically Important Blunt Abdominal Injuries.  Annals of Emergency Medicine.  2013. 62: 107-16

Kindly contributed by Michael Galante, PGY-3.

#FOAMed Digest No. 1: Total Eclipse of the Heart

Welcome to the very first edition of the WUEMR FOAMed Digest! The Social Media Committee hopes with this segment to parse out from the overwhelming FOAMed universe a few of the most high-yield pieces of highest relevance to the general EM trainee. We hope to deliver this in an easily digestible format that you can realistically work through over a week – even if you’re stuck in an ICU.

Each post will contain several sections:

1. Three Stars: Three of the best-of-the-best from the FOAMed world published in the past week or so.

2. Oldie But Goodie: The FOAMed universe has been around long enough that there’s already a good number of very well-done and highly informative blog posts and podcasts.

3. Free (For Now) Open Access Med Ed: F(FN)OAMed for short. There are some great resources out there that are not free to the vast majority of EM practitioners but, due to your EMRA membership being graciously covered via the residency and MoCEP, you have access to them. Most notably, your EMRA membership allows you subscription to the EM:RAP podcast and the EB Medicine resources – EM Practice, EM Critical Care, etc. You should take advantage of this opportunity while you can, and this section will help you do so. (Contact your friendly local Social Media Committee member if you need help setting up your access.)

4. The Gunner Files: The Social Media Committee recognizes that, with this being Wash U and all, some of you will always be overachieving. So we’ll include a few extra selections for those of you that have a more insatiable FOAMed appetite.

Without further ado, let’s kick the tires and light the fires.

This week, “Total Eclipse of the Heart,” will focus on care of various cardiac conditions.

Three Stars:

1. Ever heard of Wellens’ Syndrome? If you have any hope of passing your boards one day, you should. Not mention that whole “you shouldn’t miss a critical EKG finding that portends certain doom” thing. Never fear, Salim Reazie, author of the excellent R.E.B.E.L.-EM blog, has you covered. 

(Don’t miss the links list at the bottom that highlights posts from other top-notch FOAMed resources!)

2. Syncope is one of those presenting complaints that really must be approached in a systematic manner. The grandmaster of EM EKG interpretation, Amal Mattu, reviews the differential while highlighting the characteristic EKG findings of a can’t-miss diagnosis.

3. Okay, so DKA isn’t exactly a “cardiac” condition – but the worst-case-scenario is still hemodynamic collapse, right? It counts. The EBM gurus over at Anand Swaminathan’s blog EMLyceum give you the latest & greatest when it comes to evidence-based care of DKA.

Oldie But Goodie:

So you’ve achieved the nigh-impossible – achieved sustained ROSC in an OHCA patient. Now what? The reigning American Idol of EM Critical Care, Scott Weingart, tells you what in an excellent two-part interview with one of the lead authors of the TTM trial, Stephen Bernard.

F(FN)OAM:

Worst-case scenario #137: Running ACLS on a patient brought in with PEA arrest. As CPR continues, the staff looks to you. “Uhhhhhh…more Epi?” Like all things resus, you need a systematic approach. The smart dudes over at EM:RAP, along with EM cardiology expert Amal Mattu, review a newly published paper that will help you do just that in the August 2014 edition.

PubMed link to the paper itself here.

(Once again, contact the Social Media Committee if you need helping subscribing to EM:RAP.)

The Gunner Files:

1. Excellent review article from the journal Emergency Medicine Australasia covering that bane of the overnight Deuce shift. No, not vaginal discharge – dental pain.

2. EMLyceum deals in pearls once again when addressing ocular emergencies.

3. Ryan Radecki over at EMLitofNote looks at a very interesting paper just published in JAMA regarding the use of pulse oximetry and dispo of bronchiolitis patients. 

(And as always, be sure to read the original paper for yourself!)

4. My FOAMed man-crush, Rory Spiegel of EMNerd, tackles the C-spine injury algorithm debate.

5. The Aussies over at St. Elmyn’s get you straightened out when dealing with the breathless patient in the ED. Incredibly high-yield for new ‘terns, but useful for docs of all ages.

Now get to FOAMing! 

As always, comments/concerns/criticisms are appreciated!

C. Sam Smith, PGY-3

Emergency Department management of myasthenic crisis

A 23 year old woman with a history of myasthenia gravis presented with several days of worsening generalized weakness, shortness of breath, and difficulty speaking.  She denies infectious symptoms such as fevers, chills, cough, dysuria, vomiting, or diarrhea.  Given her presentation, there is concern for myasthenic crisis.  She has had multiple similar episodes of these symptoms in the past and is currently being treated with prednisone, cyclosporine, and pyridostigmine.  She has needed IVIG and plasma exchange in the past for myasthenia exacerbations.   Her vital signs were within normal limits, but she was in mild distress from shortness of breath. 

Clinical question: 

What should be done in the ED for patients presenting with signs and symptoms of a myasthenia gravis exacerbation?

Literature:

Myasthenia gravis (MG) is an autoimmune disorder characterized by antibodies to post-synaptic acetylcholine receptors which results in fluctuating weakness.  In severe cases where weakness results in respiratory failure or the inability to swallow, the term myasthenic crisis is used.  Facial weakness, diaphragmatic and accessory muscle weakness may mask typical symptoms of respiratory distress.  Myasthenic crisis and impending respiratory failure is heralded by a forced vital capacity (FVC) of less than 1L and negative inspiratory force (NIF) less than 20 cm of water.  Blood gas measurements are poor indicators of impending respiratory failure since hypoxia and hypercarbia are late indicators of respiratory failure.  Common precipitants of myasthenic crises include infection, certain antibiotics, iodinated contrast agents, surgery, and weaning of immunosuppressants.  

Treatment in the emergency department should focus on frequent evaluation (e.g. every 2 hours) of the patient’s respiratory status with serial FVC and NIF and intubating promptly at signs of respiratory failure.  Sitting the patient upright may help temporize the patient’s dyspnea while preparing for intubation.  Even if not intubated, patients presenting with myasthenic crises will need admission to the ICU.  First line therapies include IVIG and plasmapheresis, both of which take several days to reach full clinical effect by removing acetylcholine receptor antibodies from the circulation.  High dose glucocorticoid therapy and other immunosuppresants such as azathioprine and cyclosporine can be initiated but are intended as long-term therapies and do not provide any benefit in the emergent setting.  Anticholinesterase use, such as pyridostigmine, remains controversial because of the risk of coronary artery vasospasm (resulting in MI) and arrhythmia.  A basic infectious workup, including a chest x-ray and urinalysis, should be considered.  

Take home:

Emergency department management of a patient with myasthenic crisis should focus on frequent and repeated assessment of respiratory status (including NIF, FVC) +/- intubation as necessary and disposition to an ICU.  Medical intervention helps over the longer term, but provides little benefit in the emergency department setting.

References:

1) Chaudhuri A and Behan PO.  Myasthenic crisis.  Q J Med 2009; 102:97–107.

2) Jani-Acsadi A and Lisak RP.  Myasthenic crisis: Guidelines for prevention and treatment. J Neurological Sciences 2007; 261:127–133. 

Kindly contributed by Philip Chan, PGY-2.

Rigid Backboard for Spinal Immobilization?

You are working a busy overnight shift when you see EMS bring in a “trauma packaged” patient – a young, healthy-appearing female, on a hard backboard and with a C-collar in place. Per their report, she was the restrained driver of a vehicle struck from behind at a low rate of speed while stopped at a red light. The patient denies LOC, but is endorsing pain in her neck and all the way down her back. She is complaining that the backboard is uncomfortable and making her back pain worse.

Clinical Question: 

What are the indications for prehospital rigid spine immobilization? Could it have been deferred in this patient?

Literature:

Despite the dogmatic and traditional use of rigid backboards for extrication and transport of patients with possible blunt traumatic injury of the spine, it is not an altogether benign intervention. The discomfort associated with bumpy ambulance rides while secured to a rigid board may worsen a patient’s initial presentation to the ED providers such that unnecessary spinal imaging is ordered. Prolonged transport times on rigid boards have been associated with pressure sore formation and respiratory compromise.

The use of rigid spine immobilization by prehospital providers has become based largely on mechanism of injury and concern for possible spinal cord compromise, rather than being based on signs or symptoms of spinal injury itself. This is the opposite of how diagnosis of such injuries is handled once the patient arrives to the ED. As the validation studies of the NEXUS and Canadian C-spine rules have shown, the risk of a C-spine fracture in a patient with normal mental status and without clinical signs or symptoms of spinal cord injury or distracting injury is vanishingly small.

With this in mind, the National Association of EMS Physicians (NAEMSP) and the American College of Surgeons Committee on Trauma published a position paper in the journal Prehospital Emergency Care entitled “Indications for Prehospital Spinal Immobilization.” This paper (and the accompanying resource document) outlines who should and should not be immobilized based on best evidence.

To begin, patients must first be assessed for a mechanism of injury capable of causing spinal cord injury. This is somewhat open to interpretation by EMS providers, and can vary for different patient populations (i.e., a fall from standing would be a very low-risk mechanism for healthy young adult male but much higher risk in an elderly, frail female). The document specifically addresses penetrating wounds, based on evidence published in a paper in the Journal of Trauma in 2010. Basically, if a penetrating wound to the head, neck, or torso does not obviously affect the area of the spine and is not associated with evidence of spinal injury (including focal neurologic deficits), there is no need for rigid immobilization.

If the mechanism is determined to be a risk for spinal cord injury, the EMS provider must then perform a spinal assessment, which is largely derived from the NEXUS and Canadian rules for C-spine imaging. The spinal assessment is “positive” if there is any midline tenderness, palpable/visible midline deformity, or a new neurologic deficit. Immobilization must also be considered for those in which a spinal assessment is unreliable. This includes patients with altered mental status, who are intoxicated with alcohol or drugs, who have a painful distracting injury (by NAESMP criteria, a long bone fracture proximal to the wrists or ankles), or who are otherwise unable to fully participate in the exam due to a language barrier or due to age (i.e., pre-verbal pediatric patients).

If this assessment is negative, NAESMP recommends a C-collar should still be placed if the patient is over 65 (due to increased risk of C-spine injury in this population), but the patient does not require further spinal immobilization and can be transported in position of comfort. Obviously, a C-collar should be placed on any patient if there is midline tenderness in the C-spine.

Interestingly, a study from the Journal of Emergency Medicine published in 2013 reported data from a high-speed infrared motion analysis of healthy volunteers that showed those who extricated themselves with a C-collar in place had less spinal motion than those who were told to hold still while EMS crews attempted extrication themselves. Thus, if the patient is able to extricate themselves and able to ambulate, they should be allowed to do so. If their spinal assessment is positive, they can then be secured to the stretcher with seatbelts, which has been shown to be as effective at immobilizing the T- and L-spine as a rigid backboard. If the patient cannot self-extricate, they can be extricated using standard equipment and transported to the stretcher via a hard backboard. However, he or she should be logrolled off the backboard once reaching the stretcher to minimize time spent on the hard board. The safety of this approach is reinforced by data from other studies which have shown an extremely remote risk of significant (i.e., surgical) T- or L-spine injury in restrained persons in low-risk MVCs.

Take home: 

Remember that securing to the stretcher is an effective mode of spinal immobilization. Rigid backboards should probably be reserved for transfer of a nonambulatory patient from the scene to the stretcher, and should be removed as soon as possible.

References:

1) Prehosp Emerg Care. 2014;18(2):306-14.
2) J Trauma. 2010;68(1):115-20.
3) J Emerg Med. 2013;44(1):122-7.
4) Spine J. 2014. PMID 24486471 [EPub].
5) J Emerg Med. 2006;31(4):403-5.
6) Injury. 2006;36(4):519-25.

Kindly contributed by Sam Smith, PGY-3.

Valproic acid and status epilepticus

You are working in trauma when a patient arrives with altered mental status requiring intubation, and a negative work-up who seemingly wakes up after a trial of ativan, trying to grab his endotracheal tube. You consult Neurology with concern for status epilepticus, who suggest a fosphenytoin load. As the patient has systolic blood pressure in the 80s, you consider valproic acid as the next intervention for presumed status epilepticus.

Clincal Question: 

Is VPA an effective next-line therapy for status epilepticus after benzodiazepines?

Literature:

One of the first articles found with a quick pubmed search is from 2006 in Neurology, a small unblinded RCT of 68 patients in status epilepticus as defined as 2 or more convulsive seizures w/o full recovery of consciousness between the seizures or continuous convulsive seizures lasting for more than 10 minutes. Patients were consecutively enrolled then randomized to a VPA group (n=35) which received sodium valproate 30 mg/kg in 100 mL saline infused over 15 minutes, or the PHT group (n=33) which received phenytoin sodium 18 mg/kg in 100 mL saline infused immediately at a rate of 50 mg/minute. They found that SE was aborted by VPA in 23 (66%) and by PHT in 14 (42%) (p = 0.046), and in refractory patients, as a second choice, VPA was effective in 15 of 19 patients (79%), whereas PHT was effective in 3 of 12 patients (25%) (p value = 0.004). As for side effects and relating to my case, 2 patients who received PHT had CV effects (not elaborated) while 0 of the VPA group though this was not significant.

Another article from 2008 by Gilad et al., similarly prospectively enrolled 74 patients in SE (2 or more consecutive clinical seizures, or continued seizure activity >30min) or acute repetitive seizure/acute refractory seizure (ARS) (2 or more w/in 5-6hrs) and gave either VPA as 30mg/kg over 20min in 50mL saline or PHT as 18mg/kg over 20min in 100mL saline. They found seizure discontinued in 43/49 (87.8%) of the VPA patients, with similar results in the PHT group in which seizures of 22/25 (88%) patients were well controlled. They noted that 3 pts had side fx of cardiac arrhythmia, hypoNa, or vertigo in the PHT group, and none in the VPA (p 0.035). This study was certainly small, but I think it should be noted that of the PHT group 12/25 had exposure to PHT in the past while only 11/49 of the VPA group (p = .03).

Furthermore, in April 2014 ACEP released its policy on the valuation and management of adult patients with seizures in the emergency department. Item #4 “In ED patients with generalized convulsive status epilepticus who continue to have seizures despite receiving optimal dosing of a benzo, which agent or agents should be administered next to terminate seizures?” directly applies to my question. As a Level B recommendation, they state “Valproate appears to be safe and effective in refractory status epilepticus and was not associated with hypotension. In conclusion, it appears that IV valproate is an acceptable treatment option for refractory status epilepticus and may work as well as phenytoin.” My last comment is that I was unable to find any studies w/ direct comparison of fosphenytoin vs VPA, and the ACEP literature review did not find any as well. The policy and lit review does cite a number of articles detailing CV effects of both PHT and fosphenytoin.

Take Home: 

In the setting of hypotension, valproic acid may be considered instead of fosphenytoin for the treatment of status epilepticus.

References: 

1) Misra UK1, Kalita J, Patel R. Sodium valproate vs phenytoin in status epilepticus: a pilot study.Neurology. 2006 Jul 25;67(2):340-2.
2) Gilad R, Izkovitz N, Dabby R, Rapoport A, Sadeh M, Weller B, Lampl Y. Treatment of status epilepticus and acute repetitive seizures with i.v. valproic acid vs phenytoin.Acta Neurol Scand. 2008 Nov;118(5):296-300
3) American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Seizures:, Huff JS, Melnick ER, Tomaszewski CA, Thiessen ME, Jagoda AS, Fesmire FM. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Seizures. Ann Emerg Med. 2014 Apr;63(4):437-447.

Does a cervical seatbelt sign mandate advanced imaging?

You are working in the emergency department when EMS brings in a middle aged female who was the restrained driver in a low speed head-on MVC. In the emergency department, she is slightly hypertensive and complaining of generalized stiffness. Her physical exam (including C-spine exam and neurologic exam) is unremarkable with the exception of an abrasion to the left side of her neck without surrounding hematoma concerning for a cervical seat belt sign.

Clinical Question:

In this otherwise well appearing patient you wonder – what is the best course of action? Does the physical finding of a cervical seat belt sign warrant additional imaging for vascular injury, such as a CT-A?

Literature:

One study that addressed this question was a retrospective review of patients who received neck CT angiograms based on the presence of a seatbelt sign alone at a Level I trauma center from 2008-2010. Over this time period, 418 patients underwent a CT-A. Eleven patients had positive vascular findings, two with blunt carotid injury (BCA) – giving an overall frequency vascular injury of 2.6%. Importantly, all of the patients who were found to have vascular injuries had a cervical spine fracture, rib fracture, thoracic spine fracture, facial fracture, skull fracture, large hematoma on the neck or a combination of the above injuries. The correlation between seatbelt sign and positive CT-A finding was overall very weak (r = .007). The above findings lead the authors to reasonably conclude that CT-A of the neck vascular injury can be “safely reserved for patients with a seatbelt sign and obvious injuries on physical examination and/or positive findings on standard trauma imaging.”

A second study prospectively evaluated trauma patients with cervical or thoracic seatbelt signs at a level I trauma center over a 17 month period. Out of 131 trauma pts with cervical or thoracic seatbelt signs, four (3%) were found to have carotid artery injuries. The presence of a carotid injury was strongly associated with a GCS < 14 (p< 0.0003), ISS > 16 (p < .0001), and the presence of a clavicle or first rib fracture (p < .0037). No vascular injuries were identified in patients with thoracic-only seatbelt signs. Each of the four patients had at least one identifiable significant injury ranging from scalp laceration + extremity fracture to clavicle + bilateral superior rib fractures. The authors of this study concluded that the cervical-thoracic seatbelt sign combined with an abnormal physical examination is an “effective screening combination for cervico-thoracic vascular injury.”

Take Home:

CT-angiogram is not necessarily indicated based on the finding of a cervical seatbelt sign alone in the absence of significant hematoma, neurologic symptoms, or other traumatic injuries.

References:

1) Dhillon, Ramandeep Singh, et al. "Seatbelt sign as an indication for four-vessel computed tomography angiogram of the neck to diagnose blunt carotid artery and other cervical vascular injuries." The American Surgeon 79.10 (2013): 1001-1004.
2) Rozycki, Grace S., et al. "A prospective study for the detection of vascular injury in adult and pediatric patients with cervicothoracic seat belt signs." The Journal of Trauma and Acute Care Surgery 52.4 (2002): 618-624.

Insulin bolus in DKA?

A middle aged male with a history of IDDM presents with 2 days of nausea and vomiting. He reports running out of his insulin. In triage, FSBS is critical high, FS ketones are 5.0. You start to treat for DKA with bolus of IVF and draw basic labs. You order your insulin infusion and give a 0.10U/kg bolus prior to starting the drip. Your attending questions your actions. 

Clinical Question:

Is there any evidence to support giving an insulin bolus prior to starting a drip in DKA patients?

Literature:

The latest ADA recommendations last updated in 2009 still recommend giving a 0.1U/kg bolus prior to initiating an insulin infusion at 0.1U/kg/hr. This recommendation is based on the theory that DKA represents a significant "insulin resistant" state, and a bolus of insulin is needed to overcome this resistance and effectively reduce serum glucose and suppress gluconeogensis. Much of these recommendations are based on limited studies from the 1980's, measuring active levels of insulin in serum, and none were prospective comparing continuous insulin infusion with and without the bolus. (1) In 2008, Kitbachi Et al performed a randomized prospective study with three arms, those on an insulin infusion at 0.07U/kg/hr with and without a bolus, and those who were only on a infusion at 0.14U/kg/hr. Kitbachi effectively demonstrated that an insulin bolus is unnecessary in those who were started on a infusion at 0.14U/kg/hr. There was no difference in time to optimal glucose, pH, Anion Gap, or bicarbonate. (2) In 2010, Goyal Et al performed a similar study but had two arms, insulin infusion at 0.1U/kg/hr and those with an infusion and a bolus. He showed no difference in length of ED stay or hospital stay, and no difference in time to goal glucose or anion gap closure. (3)

Take Home:

In summary, there appears to be a paucity of evidence supporting the ADA recommendation for an insulin bolus prior to infusion, however there seems to be robust evidence showing at least a noninferiority with insulin infusion alone. Therefore I find there is no reason to continue using an insulin bolus during my standard treatment of DKA.

References:

1) Diabetes in the Emergency Department: Acute Care of Diabetes Patients. Clinical Diabetes April 1, 2011 29:51-59 http://care.diabetesjournals.org/content/32/7/1335.short
2) Kitabchi Et al, Is a priming dose of insulin necessary in a low-dose insulin protocol for the treatment of diabetic ketoacidosis? Diabetes Care. 2008 Nov;31(11):2081-5
3) Goyal Et al, Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. 2010 May;38(4):422-7. doi: 10.1016/j.jemermed.2007.11.033. Epub 2008 Jun 2.

Submitted by Louis Jamtgaard, PGY-3