Authors: Colin J. O’Shea, MD, MPH (EM Assistant Professor, Vanderbilt University Medical Center) and Matthew Pirotte, MD (EM Program Director, Vanderbilt University Medical Center) // Reviewed by: Summer Chavez, DO, MPH, MPM; Brit Long, MD (@long_brit); Alex Koyfman, MD (@EMHighAK)

Case #1

Your first patient is a 67-year-old male who presents with sudden, painless vision loss of the right eye. He describes total vision loss in all fields that began 12 hours prior to presentation. Four days ago, the patient had 20 minutes of complete vision loss of his right eye like a curtain descending that resolved spontaneously. He has a history of hypertension, type 2 diabetes mellitus, and hyperlipidemia. On exam, his acuity in the affected eye is limited to hand motion only. He has full extraocular movements, and you note that he has asymmetric pupillary response on the right when light is shined back and forth between his eyes.

Case #2

Your second patient is a 65-year-old female who presents with vision loss of the left eye with associated headache. She describes looking through a haze that was noticed when she awoke this morning – around 8 hours ago. The patient notes that she has had intermittent, brief vision loss over the past week and endorses recent headaches, fever, and muscle weakness. On exam, her visual acuity is 20/100 in the left eye and 20/25 in the right eye. Her extraocular movements are intact, and her intraocular pressure is normal.

Introduction

Vision loss can be a challenging ED chief complaint to diagnose and manage because of the difficulty determining which causes are neurological and which are related to intrinsic ocular pathology. This website has previously covered an overview of the causes of vision loss. This article will help to differentiate central (CNS) versus peripheral (ocular) causes of vision loss.

Definitions

The causes of vision loss are vast and include processes in the CNS, the orbit, and systemic toxicities. For this article, we will define central vision loss as causes that arise from the CNS – specifically, the optic nerve, the chiasm, and the retrochiasm. Peripheral etiologies are those that originate in the orbit or systemic processes.

Historical Features

When a patient presents with vision loss, there are important historical features that can help distinguish central versus peripheral causes.

1. Quality of the vision loss – is it a loss of acuity or a field cut?
2. Determine if the vision change is monocular versus binocular.
3. Pain – ask if there is associated globe pain and/or associated headache
4. Determine the time course of the vision change
5. Redness
6. Trauma
7. Associated neurologic symptoms

It is important to qualify the vision loss and determine if it is a field cut, scotoma, or loss of acuity, for example. It is also crucial to determine if the vision change is monocular or binocular – occurring in one eye or both. Binocular diplopia resolves with covering one eye, whereas monocular diplopia persists with covering one eye. In general, any binocular process should increase your suspicion for a central process. Patients may not think to look through one eye at a time before presenting, so this may only become clear through history and exam.

Pain – in the absence of trauma, most central causes of vision loss are painless. The few exceptions to this are optic neuritis, cavernous sinus thrombosis, and idiopathic intracranial hypertension (IIH).^1-5 There are many painful causes of peripheral vision loss, from angle closure glaucoma to endophthalmitis.

Diplopia – although patients with diplopia may not have true vision loss, they may perceive diplopia as blurry vision,⁶ so this may be their chief complaint in the ED. Monocular diplopia persists with closing one eye and usually relates to a refractive error in the eye.⁶

Field cut – the one peripheral cause of a field cut is a retinal detachment. Branch retinal artery occlusion (BRAO) will have a monocular field cut, while optic pathway tumor or ischemia may have binocular field cuts.^7,8

Time course – any sudden vision loss, particularly without trauma, should increase concern for a central cause.^9-11 Vascular pathologies of the retina, such as central retinal artery occlusion (CRAO) and BRAO, or vascular insults of the cerebrum tend to cause acute visual deficits. Many inflammatory or infectious peripheral processes tend to cause more subacute vision loss.

Trauma – trauma can cause vision loss related to both central and peripheral etiologies.¹² Central causes include cervical artery dissection and occipital lobe hemorrhage, while there are multiple peripheral causes of traumatic vision loss.

Redness – associated scleral injection occurs often with many peripheral causes, from iritis to acute glaucoma. Cavernous sinus thrombosis, however, can also cause redness and chemosis of the eye.^3,4

Neurologic symptoms – any associated neurologic symptom raises concern for a central process.^2,6 Cranial nerve palsies with vision loss can be seen in cavernous sinus thromboses and IIH. Optic neuritis may be associated with extremity or facial numbness or weakness if associated with multiple sclerosis.

The Eye Exam

The fundamental eye exam consists of the following: general inspection, visual acuity, pupils, confrontation visual fields, extraocular movements, external exam, eye surface (woods lamp/slit lamp, fluorescein staining), intraocular pressure, and posterior chamber evaluation. The posterior chamber is often evaluated with fundoscopy, which can be difficult to perform in the ED. Ocular ultrasound can be used.

General inspection – evaluate the lids and sclera closely for erythema, tearing, and proptosis.

Visual acuity – remember that if the patient cannot make out the letters on the Snellen chart, acuity is determined by ability to count fingers, detect hand motion, and detect light perception.

Confrontation visual fields – any bilateral field cut is concerning for a central process. As mentioned above, tumors along the optic pathway and strokes involving the occipital lobe can affect visual fields of both eyes.

Pupils – assess for shape, symmetry, and reactivity. Tear drop shaped pupils are classically seen in open globes.¹³ Patients with anisocoria, unequal pupillary sizes, may or may not have true vision loss. However, it is an important feature to note because of the wide differential for this finding.¹⁴ A relative afferent pupillary defect (RAPD) is concerning for optic nerve dysfunction, either from compression, ischemia, or demyelination.^{6, 14} Large retinal detachments and vitreous hemorrhage can also cause a RAPD if severe.

Extraocular movements – diseases affecting vision can also affect extraocular movements. Aside from trauma resulting in ocular muscle entrapment, the one peripheral cause of ophthalmoplegia is orbital cellulitis.¹⁵ More central causes are associated with ophthalmoplegia. Intranuclear ophthalmoplegia (INO) is a disorder of ocular movement causing an inability to perform conjugate lateral gaze and is due to damage at the medial longitudinal fasciculus. There are multiple possible causes of this damage and INO can occur unilaterally or bilaterally, but if INO is found, it should increase your suspicion for multiple sclerosis and optic neuritis.²

Eye Surface – in additional to evaluating for scleral erythema, use of a fluorescein stain can help in the evaluation of corneal abrasions, ulcerations, and keratopathy.

Intraocular pressure – acutely elevated intraocular pressure (IOP) can be seen in multiple peripheral causes of vision loss: angle closure glaucoma, retrobulbar hematoma, endophthalmitis, uveitis, orbital cellulitis.^15-19 Cavernous sinus thrombosis, however, can also cause elevated IOP.⁴ Any measurement above 20 mmHg is abnormal. A measurement above 40 mmHg is an indication to start emergent therapy for acute angle closure glaucoma.¹³ There is not a specific cutoff for diseases other than glaucoma.

Posterior Chamber – bedside ocular ultrasound can be used to evaluate the posterior chamber and is particularly useful in the diagnoses of retinal detachments, vitreous detachments, and vitreous hemorrhage. Point of care ultrasound is fairly sensitive for retinal detachment and vitreous hemorrhage (97% and 88% respectively), but is less sensitive for vitreous detachment (43%).²⁰

Clinical Presentation Differentials

Knowing the initial history and fundamental eye exam can narrow the differential for vision loss. The differentials for the primary complaints of field cut and vision loss have been broken down below using proposed step by step processes. Remember that each patient should have a complete history and a complete ophthalmologic physical exam, however, specific parts of the exam are helpful in distinguishing a central versus a peripheral process. A more complete list of diseases is outlined below (Table 3), but here we present an initial approach to certain chief complaints.

Field Cut

If a patient presents with an isolated field cut without loss of acuity, the differential changes whether the field cut affects one eye or both. Any binocular field cut is concerning for a central process, ischemia or tumor anywhere along the optic tract to the visual cortex.^1,8 If a patient notes a monocular field cut, one helpful adjunct is ultrasound. Ultrasound can detect retinal detachment and vitreous detachment, which may cause a field cut with associated flashes and floaters. If there are no abnormal ultrasound findings, this should increase concern for a central process, such as BRAO. Vision loss in CRAO tends to be profound and involve all fields, however, central vision may be spared if the cilioretinal artery is spared.²¹ Keep in mind that CRAO is considered a form of ischemic stroke and patients with CRAO and BRAO should undergo vascular imaging.²²

Painful Atraumatic Vision Loss

For patients who describe painful vision loss, it is important to note their intraocular pressure (IOP). As mentioned above, elevated IOP is more often seen in peripheral causes of vision loss. If a patient has elevated IOP, painful vision loss, and systemic symptoms, this should increase concern for orbital cellulitis or cavernous sinus thrombosis. There are many peripheral causes of painful vision loss that can be seen with fluorescein stain or close examination of the sclera.

Optic neuritis and IIH are two central causes of painful vision loss, however, these patients will have a normal fluorescein stain, normal intraocular pressure, and normal sclera on exam. Ultrasound may be an additional adjunct to evaluate for papilledema with fair sensitivity.²³ Anterior ischemic optic neuropathy (AION) is a cause of painless vision loss; however, when it is associated with giant cell arteritis (GCA), can cause headaches and other body pain in addition to vision loss. Patients with GCA may have elevated inflammatory markers, jaw claudication, joint pain, and fever, which are unlikely to be seen in optic neuritis or IIH. It is reasonable to order an ESR and CRP on any patient over 50 who presents with the complaint of visual changes, especially if accompanied by a unilateral headache or temporal tenderness to palpation. Under this age, GCA is virtually unheard of.¹

Painless Atraumatic Vision Loss

One helpful tool to use with patients with painless vision loss is ultrasound, which can quickly detect a large retinal detachment or vitreous hemorrhage. Around 25% of patients with GCA will present with painless vision loss without other symptoms;⁸ elevated inflammatory markers can help to make this diagnosis. CRAO and retinal vein occlusion can both present similarly – sudden onset vision loss with an associated APD and otherwise unremarkable exam. Retinal vein occlusion, however, has a different fundoscopic appearance of multiple hemorrhages throughout the retina – so called “blood and thunder”.¹²

Pearls

• For any patients over 50, it is reasonable to obtain an ESR and CRP to evaluate for GCA.
• A RAPD should increase your concern for optic nerve pathology.
• Monocular diplopia is almost always related to a peripheral process, while binocular diplopia should increase your concern for a central process.
• Any binocular field cut is concerning for a central process.
• CRAO should be considered a stroke equivalent.

Case Resolutions

Patient 1: On exam, you note that the patient has a RAPD. Additionally, he describes amaurosis fugax – transient loss of vision. ESR, CRP, and bedside ultrasound are normal. Your fundoscopic exam does not reveal any significant retinal hemorrhages. The patient undergoes CT/CTA of the head and neck, and neurology is consulted given the concern for CRAO. The patient is found to have a large plaque at the internal carotid artery and is admitted to neurology.

Patient 2: This is a patient presenting with vision loss with associated constitutional symptoms. Her intraocular pressure is normal. You send inflammatory markers for this patient and stain with fluorescein, which appears normal. ESR and CRP are both elevated. Given the concern for GCA causing AION, the patient is started on high dose steroids and is admitted for temporal artery biopsy.

Table 3:

References

1. Kidd DP. Neuro-Ophthalmology: Illustrated Case Series. Springer-Verlag London Limited;2017.
2. Hickman SJ, Raoof N, McLean RJ, Gottlob I. Vision and multiple sclerosis. Mult Scler Relat Disord. 2014;3(1):3-16.
3. Frank GS, Smith JM, Davies BW, Mirsky DM, Hink EM, Durairaj VD. Ophthalmic manifestations and outcomes after cavernous sinus thrombosis in children. J AAPOS. 2015;19(4):358-62.
4. Visvanathan V, Uppal S, Prowse S. Ocular manifestations of cavernous sinus thrombosis. BMJ Case Rep. 2010;3doi:10.1136
5. Wall M, Kupersmith MJ, Kieburtz KD, et al. The idiopathic intracranial hypertension treatment trial: clinical profile at baseline. JAMA Neurol. 2014;71(6):693-701.
6. Lemos J, Eggenberger E. Neuro-Ophthalmological emergencies. Neurohospitalist. 2015;5(4):223-33.
7. Mason JO, III, Shah AA, Vail RS, Nixon PA, Ready EL, Kimble JA. Branch retinal artery occlusion: visual prognosis. Am J Ophthalmol. 2008;146(3):455-7.
8. Lawlor M, Perry R, Hunt BJ, Plant GT. Strokes and vision: The management of ischemic arterial disease affecting the retina and occipital lobe. Surv Ophthalmol. 2015;60(4):296-309.
9. Wray SH. Acute visual loss. Semin Neurol. 2016;36:425-432.
10. Gordon LK, Levin LA. Visual loss in giant cell arteritis. JAMA. 1998;280(4):385-6.
11. Heckman JG, Vachalova I, Lang CJG, Pitz S. Neuro-Opthalmology at the Bedside: A Clinical Guide. J Neurosci Rural Pract. 2018;9(4):561-573.
12. Atkins EJ, Newman NJ, Biousse V. Post-Traumatic vision loss. Rev Neurol Dis. 2008;5(2):73-81.
13. Go S. Ocular emergencies. In: Cline DM, Ma OJ, Cydulka RK, Meckler GD, Handel DA, Thomas SH, eds. Tintinalli’s Emergency Medicine Manual 7th Edition. McGraw Hill Medical; 2012:739-51:chap 149.
14. Wilhelm H. Disorders of the pupil. Handb Clin Neurol. 2011;102:427-66.
15. Hamed-Azzam S, AlHashash I, Briscoe D, Rose GE, Verity DH. Common orbital infections – state of the art – part I. J Ophthalmic Vis Res. 2018;13(2):175-182.
16. Lipke KJ, Gümbel HOC. Emergency treatment of ocular trauma. Facial Plast Surg. 2015;31:345-350.
17. Botting AM, McIntosh D, Mahadevan M. Paediatric pre- and post-septal peri-orbital infections are different diseases: A retrospective review of 262 cases. Int J Pediatr Otorhinolaryngol. 2008;72(3):377-83.
18. Prum BE, Jr, Herndon LW, Jr, Moroi SE, et al. Primary angle closure preferred practice patern guidelines. Ophthalmology. 2016;123(1):1-40.
19. Taban M, Behrens A, Newcomb RL, et al. Acute endophthalmitis following cataract surgery: a systematic review of the literature. Arch Ophthalmol. 2005;123(5):613-20.
20. Lahham S, Shniter I, Thompson M, et al. Point-of-Care Ultrasonography in the Diagnosis of Retinal Detachment, Vitreous Hemorrhage, and Vitreous Detachment in the Emergency Department. JAMA Netw Open. 2019 Apr; 2(4): e192162.
21. Grory BM, Lavin P, Kirshner H, Schrag M. Thrombolytic therapy for acute central retinal artery occlusion. Stroke. 2020;51(2):687-695.
22. Sacco RL, Kasner SE, Broderick JP, et al. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013;44(7):2064-89.
23. Teismann N, Lenaghan P, Nolan R, et al. Point-of-care ocular ultrasound to detect optic disc swelling. Acad Emerg Med. 2013;20(9):920-5.

The post Central vs. Peripheral Vision Loss appeared first on emDOCs.net - Emergency Medicine Education.

Author: Rachel Bridwell, MD (@rebridwell, EM Attending Physician) // Reviewed by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital); Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

The post EM@3AM: Retropharyngeal Abscess appeared first on emDOCs.net - Emergency Medicine Education.

Author: Alex Koyfman, MD (@EMHighAK) // Reviewed by: Brit Long, MD (@long_brit) and Manpreet Singh, MD (@MprizzleER)

Welcome back to the EM Educator Series. These posts provide brief mini-cases followed by key questions to consider while working. The featured questions provide important learning points for those working with you, as well as vital items to consider in the evaluation and management of the specific condition discussed.

This week has another downloadable PDF document with questions, links and answers you can share with learners as educators in #MedEd. Please message us over Twitter and let us know if you have any feedback on ways to improve this for you. Enjoy!

Case 1:

A 55-year-old male with a history of cirrhosis and recurrent ascites presents with worsening abdominal pain and distension. He also states he has had a subjective fever with chills. Exam reveals mild, diffuse abdominal tenderness and positive fluid wave. He otherwise appears well.

Case 2:

A 57-year-old female presents with a week of abdominal pain and swelling. The pain worsened the initial 2 days but then improved. However, the pain returned and is more severe.  The patient has also experienced chills, rigors, and fevers the last 2 days.  Exam reveals BP 108/55, HR 122, RR 23, T 38.2 C, and severe abdominal tenderness with palpation. Bedside US reveals evidence of fluid with septations and free air.

Considerations:

• What are the types of bacterial peritonitis?
• How can patients with bacterial peritonitis present?  How do the different types differ in their presentation?
• What laboratory testing is recommended, and what should you expect to find?
• When and what type of imaging should be obtained?
• What is the management of SBP? Who should receive albumin?

Suggested Resources:

• Articles
  • emDOCs SBP
  • Emergency Medicine Cases
  • REBEL EM SBP
  • CORE EM
  • REBEL EM Albumin
  • PulmCrit Secondary Bacterial Peritonitis
• Journal Articles
  • AJEM
  • EM Clin NA

The post The EM Educator Series: Spontaneous Bacterial Peritonitis appeared first on emDOCs.net - Emergency Medicine Education.

Here’s another case from Medical Malpractice Insights – Learning from Lawsuits, a monthly email newsletter for ED physicians. The goal of MMI-LFL is to improve patient safety, educate physicians, and reduce the cost and stress of medical malpractice lawsuits. To opt in to the free subscriber list, click here.

Chuck Pilcher, MD, FACEP

Editor, Med Mal Insights

Transverse myelitis (TM) leaves patient quadriplegic

A melodramatic attorney and a wheelchair-bound patient in the courtroom leads to $8 million settlement.

Facts: A 34-year-old previously healthy and athletic security guard collapses suddenly in his driveway at home and is taken to the ED. He is briefly evaluated, diagnosed with stress and muscle aches and discharged with instructions to follow up with his PCP if not improving. Over the next month, he becomes increasingly weak, but does not seek follow-up. He falls again and is returned to the hospital where he is diagnosed with transverse myelitis (TM). Despite treatment, he is left quadriplegic. He seeks legal advice, and a lawsuit is filed against the EP and the hospital. The case goes to trial.

Plaintiff: You should have diagnosed my client’s TM on his first visit. TM is a horrible disease. My client’s “immune system rebelled… and attacked his spinal cord like a foreign invader, and 100 million forest fires started at the same time.” [Yes, the attorney said that.] Just look at this video of him having to have his mother give him a bath! [Yes, a bath video was shown to the jury.] You should have made the diagnosis when he came to the ER the first time. If you’d have done an MRI, the TM would have been found. If you’d have found it, you should have treated him with steroids, and he’d be fine today. Now you owe him $20 million for missing this life-changing diagnosis.

Defense: TM is an extremely rare condition. It occurs in about 5  people out of a million each year. The EP’s care was reasonable. You spent a month getting worse and did nothing about it. Yes, maybe an MRI would have helped, but it’s normal in in up to 40% of TM cases, especially in the first hours of the disease. Yes, high-dose steroids and other options could have been tried, but no treatment has been proven to make a major difference.  Your case was in its early stages on the first visit and evidence for any treatment is only Class 2C. Grade C evidence has no good randomized controlled studies to support it, i.e., a “very weak” recommendation that’s little more than a “suggestion.” Tx doesn’t work for every patient. Benefits and risks must be balanced and are uncertain. And even if treated, only 1/3 of individuals recover with few or only minor symptoms. Another 1/3 have some permanent disability and 1/3 are left severely disabled. The outcome is worst in patients with rapid onset of symptom like your client. So, you can’t say beyond a reasonable doubt that your client’s outcome would have been good. Our care was not negligent. Even if it were, you cannot say the delayed diagnosis changed the outcome.

Result: After 4 1/2 years of litigation and several days of trial, the treating EP, an independent contractor, was removed from the suit. The matter was then settled during jury deliberations by the hospital for $8 million.

Takeaways:

• Because of its rarity, transverse myelitis will always be missed if one fails to consider it.
• Neuro symptoms associated with back pain should make one think of spinal epidural abscess. Neuro symptoms with little or no back pain should put TM on the differential.
• The defense in this case was very strong and the outcome rather surprising.
• At best, this seems to be a “loss of chance” case, i.e., the plaintiff had lost the opportunity for a better outcome.
• There is no clear protocol that assures a good recovery in patients with TM and little evidence that an earlier MRI and/or treatment would have helped.
• The mere presence of a quadriplegic who is represented by a melodramatic attorney in the courtroom can indeed sway a jury.

References:

1. Misdiagnoses leaves ex-security guard a quadriplegic. Michaud S. MyLANews.com. January 30, 2017. https://mynewsla.com/crime/2017/01/30/misdiagnoses-leaves-ex-security-guard-a-quadriplegic-victim-just-wants-to-walk/
2. Diagnosis and Treatment of Transverse Myelitis-A New Guideline. Wilner A. Wilner on Neurology. Feb 29, 2012. http://boards.medscape.com/forums/?128@@.2a2fc19e!comment=1
3. Transverse Myelitis. Siegel Rare Neuroimmune Association (SRNA). https://wearesrna.org/living-with-myelitis/disease-information/transverse-myelitis/prognosis-management/
4. Transverse Myelitis Information Sheet. The Transverse Myelitis Association. www.myelitis.org http://files.wearesrna.org/resources/Information_Sheets/About_TM.pdf

The post Medical Malpractice Insights: Transverse myelitis leaves patient quadriplegic appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Jamie Zink, MD (EM Resident Physician, Virginia Tech Carilion EM Residency) and Andrew Moore, MD (Assistant Professor of Emergency Medicine, Virginia Tech Carilion School of Medicine) // Reviewed by: Andrew Grock, MD; Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case #1

A 73-year-old male with a past medical history of congestive heart failure (EF 20-25%) and hypertension presents following an episode of loss of consciousness (LOC) while walking 2 hours prior to arrival. He thinks he may be dehydrated and denies the following: a podrome, head trauma, other traumatic injury, chest pain, shortness of breath, or abdominal pain. The LOC lasted about 10 seconds and the patient quickly returned to baseline. He is currently asymptomatic and asking to be discharged.

Vitals: HR 83, RR 18, BP 145/93, Temp 97.9°F, SpO2 94%

Case #2

A 20-year-old female who is 33 weeks pregnant (G1P0) with no known PMHx presents after LOC for approximately 2 minutes. Prior to the episode she reports feeling in her usual state of good health. During her LOC, her eyes reportedly deviated to the left and she had urinary incontinence. The patient took about 15 minutes to return to baseline. Currently endorsing fatigue and blurry vision bilaterally, otherwise denies any symptoms. She denies prodromal symptoms, fevers, chills, nausea, vomiting, shortness of breath, chest pain, or abdominal pain.

Vitals: HR 91, RR 18, BP 173/111, Temp 99.2°F, SpO2 98%

Introduction

Syncope, or brief LOC, is a fairly common presentation, accounting for 1-2% of ED visits annually in the United States.^2,3 Nonetheless, it can be a frustrating chief complaint for emergency medicine (EM) physicians. By the time the patient sees you, most have normal and stable vital signs, and are back to baseline without symptoms. Furthermore, the list of potential etiologies is near endless, as syncope can be caused by an arrhythmia, a benign etiology (e.g., vagal), or near any dangerous diagnosis in the EM textbook. Studies do show the prevalence of syncope etiologies (in descending order of prevalence) are: vasovagal/reflex-mediated (21%), cardiogenic (10%), and syncope caused by orthostatic hypotension (9%).^2–4 Other, less common causes are medication related (7%) and neurologic (4%).³ Of the many causes of syncope, most are benign, with only about 10% being critical.^1,3 Of those critical diagnoses, cardiac etiologies are associated with the worst outcomes, carrying a >10% 6-month mortality rate.³ In the end, over one third of ED syncope patients never discover the etiology.⁴ That said, each cause shares the same common pathway – a brief interruption of blood flow/nutrients to the brain or decrease in cerebral perfusion by >35%, most commonly by a drop in cardiac output.⁵Of note, near syncope (fainting without LOC) shares the same basic pathophysiology and risks as syncope.^6,7

Additionally, syncope can present similarly to several other conditions, further obfuscating the picture. Fortunately, the emergency department’s (ED) job is not necessarily to diagnose the exact cause of syncope (assuming it truly was syncope), but to rule out life threatening conditions and risk stratify for admission versus discharge with outpatient management. As such, having a systematic approach to risk stratifying and working up syncope while considering mimics is absolutely essential.

Of course, some patients will require immediate action, resuscitation, and a targeted history and physical. As with every patient, start with the basics when warranted:

Assess ABCDEs and vital signs. Place the patient on the monitor, obtain an ECG and obtain 2 large bore IV’s. If the patient is hypotensive, consider performing a RUSH exam.¹

Syncope Mimics

Syncope mimics achieve LOC via different physiologic mechanisms and must be identified as management is completely different.⁴

Seizures

One study showed that 40 out of 822 patients presenting with syncope ultimately were diagnosed with seizure.³ While syncope causes LOC through global cerebral hypoperfusion, some seizures cause LOC by decreasing or disorganizing activity in the reticular activating system (RAS).⁸ Seizures are certainly variable in presentation and can sometimes be obvious based on history, however, nonconvulsive seizures can be difficult to clinically distinguish from syncope.⁴Conversely, syncopal episodes may present with reports of “shaking” and are presumed to be seizures, but are actually myoclonic jerks related to cerebral hypoperfusion.⁴

Unfortunately, there are no diagnostic tests in the ED for differentiating syncope from seizure after they have occurred. That said, some clinical signs such as a prolonged return to baseline as well as the presence of tongue lacerations or incontinence can suggest seizure activity.⁹ The most important aspect is complete return to neurologic baseline following the transient loss of consciousness.

Temporal lobe epilepsy, in particular, is associated with ictal asystole and can present with sudden collapse or unexplained falls in some cases.¹⁰ During these episodes, patients may remain unresponsive for 2 to 3 minutes with their eyes closed. Without an EEG during the episode, this is indistinguishable from syncope.¹⁰ That said, EEG monitoring is rarely warranted in the ED if the patient has returned to baseline, and seizure can usually be worked up outpatient.⁴

Metabolic Disorders

Many different metabolic disorders cause LOC and can mimic syncope, including hypoglycemia, hypoxemia, heat stroke, carbon monoxide poisoning, hyperventilation, and toxic ingestions.⁴ Importantly, patients with LOC from metabolic disorders typically remain altered or symptomatic until their underlying metabolic derangement is corrected.⁴

Hypoglycemia is usually associated with autonomic symptoms and should always be considered in patients with diabetes, especially if on insulin or oral hypoglycemics.⁴

Hypoxemia can additionally cause LOC and should be considered in patients with underlying lung pathology, particularly if on home oxygen or if hypoxia is noted in the ED.

Exertional heat stroke (history of strenuous activity in a hot environment for a prolonged time) should be fairly obvious based on history. Non-exertional heat stroke may be less obvious, in which the patient, typically elderly or disabled, inherently lacks the ability to cool themselves.^11,12 Risk factors include lack of air conditioning and social isolation. Non-exertional heat stroke should also be considered in patients with congenital absence of sweat glands or with history of severe burns, progressive systemic scleroderma, hyperthyroidism, and pheochromocytoma.^11,12

Recent exposure to structural fires as well as vehicle exhaust or space heaters in an enclosed environment should raise concern for carbon monoxide toxicity.¹³ Symptoms range from headaches, nausea, and flu like illness to LOC and death.¹³ Consider this especially if multiple patients present from the same area with similar symptoms. Check a co-oximetry on suspected CO toxic patients and treat with exogenous oxygen. If airway/breathing is intact, place on high flow oxygen via nonrebreather and evaluate for possible hyperbaric therapy. If airway/breathing not intact, intubate, place on 100% FiO2, and transfer to a facility with hyperbaric capabilities. LOC secondary to CO poisoning is an indication for hyperbaric oxygen.¹³

Hyperventilation can cause transient LOC secondary to hypocapnia causing cerebral vasoconstriction, and thus, cerebral hypoperfusion.¹⁴ However, because hyperventilation is not always accompanied by a decrease in pCO2, it stands to reason that there may be another mechanism responsible.⁴ If hyperventilation is present, consider infection, salicylate overdose, primary lung etiology, pregnancy, pain, and severe anxiety.⁴

Other toxic ingestions that can present with LOC include salicylates, narcotics, insulin and hypoglycemics, cholinesterase inhibitors, antidepressants, antihypertensives, and vasodilators.⁴

Stroke/TIA

Several stroke presentations can mimic syncope. Acute ischemia of the vertebrobasilar system can cause LOC.⁴ If secondary to a TIA, these symptoms by definition would be transient. One study showed that 38 of 772 (4.9%) patients with stroke or TIA had syncope or presyncope on initial presentation.¹⁵ Another study of 483 patients in the ED with syncope found that 37 (7.7%) had TIA-related syncope, which was highly concomitant with hypertension and ischemic heart disease.¹⁶

Consider TIA in all patients with multiple episodes of unexplained LOC, particularly if they have stroke risk factors, and direct the history and physical exam to thoroughly evaluating for any unidentified resolved or persistent neurologic deficits.⁴

Intracranial Hypertension

Case reports of LOC from increased ICP secondary to mass lesions, subdural hematomas, and cerebral venous sinus thrombosis have been described in the literature.^17,18 Although rare, consider increased ICP if there is a history of recent head trauma, recurrent unexplained headaches, or focal neurologic symptoms.

Psychogenic Pseudosyncope

The appearance of LOC without true loss of consciousness, termed psychogenic pseudosyncope, is a form of conversion disorder and is clinically similar to psychogenic nonepileptic seizures, but without the characteristic bodily movements.⁴One study found 14% of 939 patients referred to an outpatient center with undiagnosed syncope had psychogenic pseudosyncope.¹⁹ It is diagnosed by precipitating an episode during EEG monitoring, which will reveal normal alpha waves without EEG abnormalities.²⁰ True syncope will have background suppression or delta wave slowing.²⁰

Patients tend to be young, female, have other psychiatric comorbidities, and display an increased number of “syncopal” events leading up to their presentation.²¹ Characteristics include prolonged duration, high frequency of episodes, little or no post-ictal state, no injuries sustained from episodes, and unusual triggers, such as exercise or lying supine without typical predisposing factors such as noxious stimuli.^20,21

Cataplexy

Cataplexy, a pathognomonic symptom of narcolepsy, involves sudden onset, transient loss of skeletal muscle tone without loss of consciousness, and may be confused with syncope.⁴ Unlike syncope, patients typically remember the episode as they do not have LOC. Patients will often feel the onset of muscle weakness and can sometimes sit or lie down to avoid injury before reaching maximal intensity.^4,22 Triggers are often easily identified as this is preceded by strong emotions, either positive (more common) or negative.²²

History

Obtain a history from the patient AND witnesses.

Ask about triggering events and prodromal symptoms. What was the patient doing right before their LOC? Exertion preceding syncope in the absence of a prodrome or trigger is highly concerning for a cardiac etiology.^1,3,23

Ask about past medical history (especially cardiac hx and VTE risk factors) to help with risk stratification. Any family history of sudden, unexplained death?

Has the patient syncopized before and if so, was this different?

How long did it take for the patient to return to baseline? A prolonged recovery may be indicative of seizure activity.

Ask about any symptoms that may be associated with syncope. This can be tremendously helpful in elucidating the etiology (see Syncope Plus).

Perform a thorough medication reconciliation.

Syncope Plus

Other symptoms, when present with syncope, can provide important clues to the etiology. Use the following word associations as a guide for considering critical diagnoses. These are of course not absolutes.

Syncope + headache = SAH, elevated ICP, RCVS, cervical vessel dissection

Syncope + chest pain = MI, PE, aortic dissection, aortic stenosis, tamponade

Syncope + shortness of breath = PE, dysrhythmia (when associated with CHF), MI, hypoxia, aortic stenosis, tamponade

Syncope + palpitations = dysrhythmia

Syncope + vomiting = MI, GI bleed

Syncope + abdominal or back pain = AAA, dissection, GI bleed, ectopic pregnancy

Syncope + vaginal bleeding = ectopic pregnancy

Physical Exam

The physical exam should focus primarily on cardiovascular and neuro systems. Commonly, the following are performed: bilateral upper extremity blood pressures, cardiac auscultation for murmurs, a complete neuro exam to evaluate for any focal deficits, mental status assessment as a sustained alteration may suggest a post-ictal state or metabolic encephalopathy.¹ Evaluate for tongue lacerations as well as abdominal tenderness and/or a pulsatile mass. Lastly, consider a rectal exam if the history suggests GI bleed. Occult blood testing is poorly evidence based; however, the presence of gross blood is important to note.

Of course, don’t forget to rule out traumatic injuries during the exam that may have been sustained during the syncopal episode.

Evaluation 

An ECG is required on every suspected syncope case. Admit any patient with ischemia, conduction abnormalities, prolonged QT or QTc, dangerous syncope syndrome (Wolf-Parkinson-White, Brugada, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia), or other concerning dysrhythmias.²⁴ Consider echocardiography in patients with significant cardiac history or with ECG abnormalities.⁴

Blood glucose should be checked if you suspect hypoglycemia, particularly if the patient is diabetic. A pregnancy test is commonly performed in women of childbearing age, and absolutely must be done if there is any abdominal, flank, or pelvic pain or vaginal bleeding to rule out ectopic pregnancy.

More advanced labs and imaging should be ordered as clinically indicated but are often nondiagnostic.¹

Disposition

In cases of actual syncope, once other life-threatening etiologies have been ruled out, the patient’s arrythmia risk determines disposition. Limited data for clinical decision rules exist as most of them failed external validation. One option is the Canadian Syncope Risk tool which has been externally validated. Generallypatients that are low risk (no cardiovascular risk factors) with a normal ECG, normal vitals, and a clear vasovagal mechanism may be discharged without labs or imaging.¹ Patients that are low risk but without clear cause may be observed with or without labs prior to discharge and do not necessarily require outpatient follow up. Intermediate-risk patients (elderly with a likely vasovagal mechanism or young patients with some cardiovascular risks and no clear cause) with a normal ECG may be observed with or without labs and may be considered for a short admission to a monitored bed vs outpatient follow up with ambulatory monitoring.¹

Admit all patients that are high risk for an arrythmia as well as those found to have an underlying etiology requiring specific treatment (PE, ACS, AAA rupture, etc.).¹

Case Wrap Up and Conclusion

Case #1 is very concerning for cardiogenic syncope, especially given the patient’s history of heart failure, exertion preceding syncope, and the reported lack of prodrome. The patient’s ECG met voltage criteria for LVH and additionally revealed nonspecific repolarization abnormalities.  A chest X-ray was performed revealing cardiomegaly. A troponin, CBC and CMP were unremarkable. Pro-BNP was moderately elevated but unchanged from baseline. The patient had two runs of non-sustained ventricular tachycardia while on telemetry and was ultimately admitted for AICD placement. This patient should not be sent home, despite being asymptomatic!

Case #2 is consistent with eclampsia. Pay attention to the history of pregnancy, the story concerning for seizure (eye deviation, urinary incontinence, and prolonged return to baseline), and the hypertension on arrival. The patient’s ECG was normal sinus without abnormality.  A CBC, CMP, and UA were performed. The CBC and CMP were unremarkable, however the UA revealed heavy proteinuria. The patient was given 6 grams of magnesium through intravenous bolus and admitted to OB.

Syncope can be a difficult chief complaint as it can be challenging to differentiate from mimics. That said, take a good history and perform a thorough physical exam to appropriately risk stratify patients and tailor therapy. Everyone gets an ECG. Further testing may be warranted based on H&P.

Take Home Points

– Every syncope patient deserves an ECG and telemetry monitoring while in the ED. Additional targeted testing may be warranted based on elements from the history and physical exam. There is no role for broadly ordering screening labs on every syncope patient.

– Up to one-third of patients with syncope will be undiagnosed after their ED evaluation.

– The job of an EM physician is not to diagnose the exact etiology of syncope, but to risk stratify patients, rule out critical diagnoses, and treat as needed. Determine who can go home and who needs to stay.

– Rule out traumatic injuries that may have been sustained during the syncopal episode.

– Consider syncope mimics, especially emergencies such as seizures, metabolic disorders, stroke/TIA, and intracranial hypertension.

References

1. Quinn J, D’Souza P. Syncope. EM:RAP CorePendium. Accessed November 30, 2021. https://www.emrap.org/corependium/chapter/recn9iTEoblED2hWk/Syncope
2. Chen LY, Shen WK, Mahoney DW, Jacobsen SJ, Rodeheffer RJ. Prevalence of syncope in a population aged more than 45 years. Am J Med. 2006;119(12):1088.e1-7. doi:10.1016/j.amjmed.2006.01.029
3. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885. doi:10.1056/NEJMoa012407
4. Coleman DK, Long B, Koyfman A. Clinical Mimics: An Emergency Medicine–Focused Review of Syncope Mimics. J Emerg Med. 2018;54(1):81-89. doi:10.1016/j.jemermed.2017.09.012
5. Thiruganasambandamoorthy V, Quinn J. Syncope. In: Tintinalli JE, Ma OJ, Yealy DM, et al., eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020. Accessed November 30, 2021. accessemergencymedicine.mhmedical.com/content.aspx?aid=1181478598
6. Grossman SA, Babineau M, Burke L, et al. Do outcomes of near syncope parallel syncope? Am J Emerg Med. 2012;30(1):203-206. doi:10.1016/j.ajem.2010.11.001
7. Bastani A, Su E, Adler DH, et al. Comparison of 30-Day Serious Adverse Clinical Events for Elderly Patients Presenting to the Emergency Department With Near-Syncope Versus Syncope. Ann Emerg Med. 2019;73(3):274-280. doi:10.1016/j.annemergmed.2018.10.032
8. Yu L, Blumenfeld H. Theories of impaired consciousness in epilepsy. Ann N Y Acad Sci. 2009;1157:48-60. doi:10.1111/j.1749-6632.2009.04472.x
9. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol. 2002;40(1):142-148. doi:10.1016/s0735-1097(02)01940-x
10. Fincham RW, Shivapour ET, Leis AA, Martins JB. Ictal bradycardia with syncope: a case report. Neurology. 1992;42(11):2222-2223. doi:10.1212/wnl.42.11.2222
11. Atha WF. Heat-related illness. Emerg Med Clin North Am. 2013;31(4):1097-1108. doi:10.1016/j.emc.2013.07.012
12. Hifumi T, Kondo Y, Shimizu K, Miyake Y. Heat stroke. J Intensive Care. 2018;6:30. doi:10.1186/s40560-018-0298-4
13. Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
14. Cipolla MJ. Control of Cerebral Blood Flow. Morgan & Claypool Life Sciences; 2009. Accessed November 30, 2021. https://www.ncbi.nlm.nih.gov/books/NBK53082/
15. Ryan DJ, Kenny RA, Christensen S, Meaney JFM, Fagan AJ, Harbison J. Ischaemic stroke or TIA in older subjects associated with impaired dynamic blood pressure control in the absence of severe large artery stenosis. Age Ageing. 2015;44(4):655-661. doi:10.1093/ageing/afv011
16. Davidson E, Rotenbeg Z, Fuchs J, Weinberger I, Agmon J. Transient ischemic attack-related syncope. Clin Cardiol. 1991;14(2):141-144. doi:10.1002/clc.4960140210
17. Bruner DI, Jamros C, Cogar W. Subdural Hematoma Presenting as Recurrent Syncope. J Emerg Med. 2015;49(3):e65-68. doi:10.1016/j.jemermed.2015.01.037
18. Larimer P, McDermott MW, Scott BJ, Shih TT, Poisson SN. Recurrent syncope due to refractory cerebral venous sinus thrombosis and transient elevations of intracranial pressure. The Neurohospitalist. 2014;4(1):18-21. doi:10.1177/1941874413493183
19. Iglesias JF, Graf D, Forclaz A, Schlaepfer J, Fromer M, Pruvot E. Stepwise evaluation of unexplained syncope in a large ambulatory population. Pacing Clin Electrophysiol PACE. 2009;32 Suppl 1:S202-206. doi:10.1111/j.1540-8159.2008.02291.x
20. Raj V, Rowe AA, Fleisch SB, Paranjape SY, Arain AM, Nicolson SE. Psychogenic pseudosyncope: diagnosis and management. Auton Neurosci Basic Clin. 2014;184:66-72. doi:10.1016/j.autneu.2014.05.003
21. Benbadis SR, Chichkova R. Psychogenic pseudosyncope: an underestimated and provable diagnosis. Epilepsy Behav EB. 2006;9(1):106-110. doi:10.1016/j.yebeh.2006.02.011
22. Dauvilliers Y, Siegel JM, Lopez R, Torontali ZA, Peever JH. Cataplexy–clinical aspects, pathophysiology and management strategy. Nat Rev Neurol. 2014;10(7):386-395. doi:10.1038/nrneurol.2014.97
23. Writing Committee Members, Shen WK, Sheldon RS, et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2017;14(8):e155-e217. doi:10.1016/j.hrthm.2017.03.004
24. Sud S, Klein GJ, Skanes AC, Gula LJ, Yee R, Krahn AD. Predicting the cause of syncope from clinical history in patients undergoing prolonged monitoring. Heart Rhythm. 2009;6(2):238-243. doi:10.1016/j.hrthm

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Welcome back to Small Talk; a new monthly section from emDOCs.  Every first Wednesday of the month we will release high yield PEM content written by PEM talent from around the country.  We hope you enjoy these reviews. Comments, questions, accolades or concerns: feel free to reach out to Joe Ravera, MD (pemgemspod@gmail.com).

Author: Joe Ravera, MD (@pemuvm1, Director of Pediatric Emergency Medicine, Assistant Professor of Surgery, Division of Emergency Medicine, University of Vermont Medical Center) // Reviewed by Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Cases

Case 1:  A 6-month-old presents with fussiness and difficulty feeding.  On exam there the infant is tachypneic and tachycardic.  The initial triage heart rate is 210.

Case 2:  A 4-year-old presents with a “funny feeling” in his chest.  He has a history of a repaired VSD but no cardiac restrictions. His triage heart rate is 200.

Case 3:  A 16-year-old presents with palpitations after drinking an energy drink.  The patient has no previous cardiac history.  The initial triage heart rate is 180.

Epidemiology, Evaluating Risk, and Expanding the Diagnosis of “SVT”

Pediatric narrow complex tachycardia, commonly referred to as Supraventricular Tachycardia (SVT), is the most common rhythm disturbance in pediatrics, with an estimated prevalence of 1 in 250-1000. The range of presentations varies from subtle fussiness to palpitations. The spectrum of disease also varies from well-tolerated palpitations to fulminant cardiogenic shock – particularly in children with a history of structural congenital heart disease (CHD). Dysrhythmia disproportionately effects children with CHD – up to 7% of children with CHD have dysrhythmia, as opposed to less than 1% without it – and, moreover, these children may not have the cardiac reserve to tolerate sustained tachycardia.^1,2 Children with both structural disease and rhythm disturbance are a high-risk population and early consultation with pediatric cardiology/PICU is recommended.

In a crisis, a PALS algorithm card can be extremely helpful for quick reference and management (Figure 1).³

As clinicians we often use the term “supraventricular tachycardia” (SVT) as shorthand for discussing narrow complex tachydysrhythmias. The classification of SVT is helpful to make rapid decisions with a deteriorating patient in critical situations. However, when there is time to think about the underlying disorder it is important to remember that SVT encompasses multiple different rhythms, each with a different pathophysiology.

SVT includes the rhythms:

• Sinus Tachycardia
• Atrial Fibrillation
• Atrial Flutter
• Multifocal Atrial Tachycardia
• Junctional Ectopic Tachycardia
• Atrial Ectopic Tachycardia
• AV Nodal Reentrant Tachycardia (AVNRT)
• Atrioventricular Reciprocating Tachycardia (AVRT)

SVT often refers to either atrial ectopic tachycardia or, more commonly, to a reentrant tachycardia like AV nodal reentrant tachycardia (AVNRT) or atrioventricular reciprocating tachycardia (AVRT) (Figure 2). While they sound similar, there is a major physiologic difference between AVRT and AVNRT – AVRT has a bypass tract which has implications for therapy with AV nodal blockade. Making this distinction on a dysrhythmic EKG can be extremely difficult, if not impossible.  It should be noted that age is a strong predictor of AVRT since most children under 8 and nearly all children under 1 have a bypass tract (Figure 3).⁴ 

Infant Tachydysrhythmia: The Challenge is Recognition

The main difficulty in managing infant SVT is actually making the diagnosis. There are several factors which make recognition challenging: infants have higher resting heart rates and can tolerate tachycardia; they are non-verbal; and they do not have the exertional demands of older children. Given these factors, the presentation can vary from subtle symptoms like fussiness or fatigue to the more overt increased work of breathing and tachycardia mediated cardiomyopathy. A percentage of infants with SVT can be sub-clinically symptomatic or asymptomatic for an extended period of time.⁵

To make matters more difficult, infants’ naturally higher heart rate can be exacerbated by stress such as fever or pain, so the challenge becomes differentiating sinus tachycardia from a pathologic reentrant tachycardia. Several EKG features, notably the rate, variability, and presence of p-waves, can help make the distinction (Table 1).

After diagnosing reentrant tachycardia, patient management and disposition are straightforward. Nearly all reentrant tachycardia in this age group is associated with a bypass tract. While AV nodal blockade is the initial treatment, it must be respected – and these patients should have electrical cardioversion pads in place before chemical cardioversion is attempted.

Before trying chemical cardioversion, vagal maneuvers (such as a placing a bag of ice on the face or taking a rectal temperature) can be attempted. If this is unsuccessful, pharmacologic cardioversion with adenosine (0.1 mg/kg) should be attempted. If there is no rhythm change at all, attempts should be made at better access, a faster mediation push, and/or an increased dose to 0.2 mg/kg. Occasionally, if access is difficult and there is no pause in the rhythm achieved with 0.2 mg/kg, the dose can be increased to 0.3 mg/kg.⁵

If this is a first episode, the child will almost certainly be admitted even if ED cardioversion is successful. Discharge may be possible but only in consultation with pediatric cardiology.

Older Children and Adolescents with SVT: Easier to Diagnosis, Straightforward to Manage, but More Nuanced Dispositions

As opposed to infants, diagnosing SVT in verbal children is usually not subtle. They will often present with palpitations. Moreover, in the absence of structural cardiac disease, they will often be relatively stable with normal perfusion.

Initial history taking should focus on the presence of structural cardiac disease, any previous episodes, and an underlying diagnosis like Wolf-Parkinson-White. Absent those, the history can focus on other cardiac questions such as the child’s baseline exercise tolerance.

The electrocardiographic distinction of a bypass tract is typically not possible from the dysrhythmic EKG (Figure 6). A post conversion EKG (Figure 7) and during conversion rhythm strip will be the most helpful in determining the presence of a bypass tract. It should be noted that a normal post-conversion EKG does not exclude the diagnosis of a bypass tract.

The initial treatment for a reentrant tachycardia, regardless of the presence of a bypass tract, is adenosine 0.1 mg/kg (adult dose 6 mg) increasing to 0.2 mg/kg (adult dose 12 mg) if the lower dose is unsuccessful. While there is concern about using medications that cause AV nodal blockade in patients with an undiagnosed bypass tract, proper preparation can help manage these concerns. One study examining children in the cath lab with known bypass tract found a transient run of atrial fibrillation in approximately 12% of patients receiving adenosine. Atrial fibrillation in patients with a bypass tract is a risk factor for ventricular fibrillation and, as such, this needs to be a consideration.^1,3,6 The current recommendations are that adenosine is a reasonable choice for SVT in the presence of a bypass tract, as long as appropriately sized resuscitative equipment is readily available, and the patients are prepared with pads on. In short, respect these kids when you give them adenosine.

Assuming these patients are successfully cardioverted, the next question that comes up is disposition. In patients with a known diagnosis, a discussion with their pediatric cardiologist can be helpful, and most of these kids should be able to go home.

If this is a first presentation, the critical question is often- Do these children have underlying structural heart disease? In the absence of structural heart disease, the risk of sudden cardiac death in children with Wolf-Parkinson-White and dysrhythmia is low.⁷ In this case, a discussion with pediatric cardiology to assure follow-up may be appropriate if there are no red flags for undiagnosed structural disease (e.g. cardiac murmurs or exercise intolerance).

Failed Cardioversion and Special Circumstances

While most patients presenting with SVT will be stable and will convert with adenosine. There is a subset of patients who are either unstable or will have a rhythm that does not respond to adenosine. Unstable patients with hypotension or poor perfusion are straightforward and require emergent cardioversion with 0.5-2 J/kg for a narrow complex tachycardia.³

Patients who don’t convert with adenosine usually fall in to one of two categories. The first did not have a pause and, in this case, they simply need a higher dose of adenosine given as fast and as close to the heart as possible. The second category – when there was a noticeable pause, but the patients then re-enter the abnormal rhythm – is more challenging. In these patients, look for an underlying etiology such as sepsis, a toxidrome, or concomitant structural heart disease.

Patients with an underlying etiology will require longer acting rhythm control, which can be done in consultation with a pediatric cardiologist. As a quick guideline, this author recommends avoiding AV nodal blocking agents in patients with a known or suspected bypass tract, which makes procainamide a good first line agent. In patients without a bypass tract, a longer acting AV nodal blocking agent like diltiazem could be considered.

Lastly, it is important to remember that electrical cardioversion is always an option and, while there may be a mental block to performing this procedure in children, functionally it is no different than adults. Occasionally, patients have a rhythm that adenosine will not terminate such as atrial flutter (Figure 8 and 9) and cardioversion after sedation may be a reasonable option.

Pearls and Pitfalls:

• The presentation of SVT varies by age and can be subtle in infants
• Most children and nearly all infants have an associated bypass tract
• Beware the child with structural and dysrhythmic heart disease – call for help early
• Adenosine is first line in SVT, even in known WPW, but respect the cardioversion and have pads on.
• Have a plan if the adenosine fails – don’t be afraid of electrical cardioversion if needed.

References:

1. Manole MD, Saladino RA. Emergency department management of the pediatric patient with supraventricular tachycardia. Pediatr Emerg Care. 2007 Mar;23(3):176-8
2. Tripathi A, Black GB, Park YM, Jerrell JM. Factors associated with the occurrence and treatment of supraventricular tachycardia in a pediatric congenital heart disease cohort. Pediatr Cardiol. 2014 Feb;35(2):368-73.
3. Topjian AA, Raymond TT, Atkins D, et al. Pediatric Basic and Advanced Life Support Collaborators. Part 4: Pediatric Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020 Oct 20;142(16_suppl_2):S469-S523.
4. Ko JK, Deal BJ, Strasburger JF, Benson DW Jr. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol. 1992 Apr 15;69(12):1028-32.
5. Moak JP. Supraventricular tachycardia in the neonate and infant. Prog Pediatr Cardiol. 2000 May 1;11(1):25-38.
6. Strickberger SA, Man KC, Daoud EG et. al. Adenosine-induced atrial arrhythmia: a prospective analysis. Ann Intern Med. 1997 Sep 15;127(6):417-22.
7. Pappone C, Vicedomini G, Manguso F, et. al. Risk of malignant arrhythmias in initially symptomatic patients with Wolff-Parkinson-White syndrome: results of a prospective long-term electrophysiological follow-up study. Circulation. 2012 Feb 7;125(5):661-8.

The post Pediatric Small Talk – The Rhythm Is Gonna Get Ya’: Age Based Approach to Pediatric Narrow Complex Tachydysrhythmia appeared first on emDOCs.net - Emergency Medicine Education.

Today on the emDOCs cast with Brit Long, MD (@long_brit), we cover another oncologic complication, immune-related adverse events (irAE) from immune checkpoint inhibitor therapy.

Episode 44: Immune-Related Adverse Events from Immune Checkpoint Inhibitors

Background

• A variety of cancer treatments are available. Immunotherapy encompasses several treatments that enhance, regulate, or supplement the immune system.
• These therapies may be used in isolation or in combination with chemotherapy and radiation.
• Immune checkpoint inhibitors (ICIs) are one such class of novel cancer therapy.
• ICIs are used for several cancers (Table 1), with 7 having FDA approval by 2021.
• Patients receiving ICI therapy may experience several adverse events due to T cell activation and immune system dysregulation.
• These immune-related adverse events (irAEs) usually occur 3-6 months after initiation of therapy and affect organs with high cell turnover (dermatologic, GI, renal, endocrine). However, any system may be affected at any time after treatment.
• The risk of irAE depends on the malignancy, medication, and use of other therapies.

Pathophysiology

• T cells possess an important role in the immune system by recognizing and destroying abnormal cells (infected and malignant).
• Several cancers suppress T cell function through activation of checkpoint signals. These signals normally result in activation of T cells to destroy abnormal cells (cancer).
• ICIs prevent this suppression signal from malignant cells, which allows T cells to attack cancer cells.
• ICIs include inhibitory ligands for the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1), as well as programmed cell death ligand 1 (PD-L1).
  • CTLA-4 protein receptors are present on T cell surfaces and act as competitive receptor for CD28, responsible for cytokine production.
  • PD-1 is a receptor that stops T-lymphocyte proliferation, decreases proinflammatory cytokine production, and decreases T-lymphocyte survivability. Tumor cells take advantage of this by producing PD-L1.
• Because of the disinhibition of the immune system, ICIs can result in organ injury, most commonly organs with rapid cell turnover. These are known as an immune related adverse event (irAE).
• An irAE may occur in 60-90% of those on an anti-CTLA-4 medication and 20-70% of those on an anti-PD-1/PD-L1 medication.

Immune-Related Adverse Events

• IrAEs are graded based on the National Cancer Institute (NCI) scale: mild (grade 1), moderate (grade 2), severe (grade 3), life-threatening (grade 4), and death (grade 5).
  • Most patients experience grade 1 or 2 irAE, with < 10% experiencing grade 3 or worse.
• Consultation with patient’s oncologist is recommended in those with suspected irAE. In most cases, consultation with the organ-specific specialist is recommended as well.

• Dermatologic:
  • Occurs in up to 50% of patients, typically 2-3 weeks after treatment initiation.
  • Most common findings: non-severe rashes (e.g., maculopapular, lichenoid, psoriasiform, eczematous), pruritus, and vitiligo.
  • Bullous reactions and severe cutaneous adverse reactions (SCARs) including SJS, TEN, and DRESS are rare.
  • Grading:
    • Non-severe rashes: symptoms not affecting quality of life (grade 1), symptoms affecting quality of life requiring initiation of interventions (grade 2), failure of treatment for grade 2 toxicity (grade 3), and unmanageable or intolerable toxicity (grade 4).
    • Bullous diseases are primarily graded by body surface area (BSA) affected: <10% (grade 1), 10-30% (grade 2), >30% or limiting activities of daily living (ADL) (grade 3), and >30% with electrolyte or fluid status abnormalities (grade 4)
    • SCARs start at grade 2 with the following grades: non-sloughing maculopapular rash with 10-30% BSA and systemic symptoms (grade 2), sloughing of <10% BSA with mucosal involvement (grade 3), and sloughing of >10% BSA and/or systemic symptoms (grade 4).
  • Treatment:
    • Patients with non-severe rashes with grade 1 or 2 toxicities and bullous reactions of grade 1 toxicity can continue ICI therapy and treat symptoms with topical emollients and steroids.
    • Patients with grade 2 bullous reactions or grades 2-3 SCARs should be started on lower-dose systemic steroids with 0.5-1 mg/kg/day of prednisone or equivalent in addition to topical therapies.
    • Grade 3 or higher bullous reactions and grade 4 SCARs require high-dose systemic steroids at 1-2 mg/kg/day of prednisone or equivalent.  Any patient requiring systemic steroids or experiencing a SCAR of any grade should stop ICI therapy and receive a dermatology consultation. Patients with SCAR should be considered for transfer to burn center.

• Pulmonary:
  • Occur in up to 19% of patients undergoing ICI therapy. Most common irAE is pneumonitis (also most common cause of death due to irAE).
  • Presents with dyspnea, chest pain, cough, decreased activity tolerance, hypoxia. Productive cough is uncommon. Symptoms usually begin 3 months after treatment initiation.
  • Grading: asymptomatic or limited disease (defined as only one lung lobe or <25% of parenchymal involvement) (grade 1); symptomatic or more extensive disease (defined as more than one lobe or up to 50% of parenchymal involvement) with mild hypoxemia (grade 2); severe symptoms, hypoxemia requiring hospitalization or oxygen supplementation, or severe disease (defined as all lung lobes or >50% of parenchymal involvement) (grade 3); and life-threatening complications or requirement for intubation (grade 4).
  • Imaging with x-ray or CT recommended. Evaluate for infection.
  • Treatment: Empiric antibiotics recommended in grade 2 severity or higher, with pulmonology consultation. Patients with grade 2 severity and higher require steroids 1-2 mg/kg/day of prednisone or equivalent. Patients with grades 3-4 may ultimately need non-ICI immunomodulators.

• Gastrointestinal:
  • Hepatotoxicity and colitis most common. Colitis includes diarrhea and abdominal pain, while hepatotoxicity involves asymptomatic mild elevations in liver function tests, with severe cases including jaundice, weakness, and fever.
  • Typically starts 8-12 weeks after beginning therapy.
  • Colitis:
    • Occurs in up to 33% of patients. Chronic diarrhea with steatorrhea is one of the most common manifestations.
    • Grading: up to 3 additional stools from baseline or mild increase ostomy output (grade 1); 4-6 additional stools from baseline or moderate increase ostomy output (grade 2); 7 or more additional stools from baseline, severe increase in ostomy output, or requiring hospitalization (grade 3); and life-threatening complications associated with colitis (grade 4).
    • Evaluation includes fecal studies such as cultures, infectious stool polymerase chain reaction panels, if available, and fecal leukocytes. Obtain CBC, lipase, renal and liver function, electrolytes.
    • CT can assist in evaluating for severity of irAE and complications.
    • Treatment: Grade 1 – hold ICI; grade 2: start steroids; grade 3 or higher: other immunomodulators.
    • Severe colitis: surgery consultation and antibiotics.
  • Hepatotoxicity:
    • Occurs in up to 7% of patients.
    • Hepatoxicity grading: asymptomatic with AST/ALT levels up to 3 times the ULN or total bilirubin up to 1.5 times the ULN (grade 1); asymptomatic with AST or ALT 3-5 times the ULN or total bilirubin 1.5-3 times the ULN (grade 2); symptomatic liver toxicity, AST/ALT 5-20 times the ULN, or total bilirubin 3-10 times the ULN (grade 3); and decompensated liver failure (e.g., synthetic dysfunction, metabolic encephalopathy, ascites), AST/ALT greater than 20 times the ULN, or total bilirubin greater than 10 times the ULN (grade 4).
    • Evaluation includes LFTs, ruling out causes of liver enzyme abnormalities, imaging with ultrasound of liver, biliary tract, gallbladder.
    • Treatment: Grade 1 – hold ICI; grade 2: start steroids; grade 3 or higher: other immunomodulators.

• Renal:
  • Affects up to 29% of patients receiving immunotherapy.
  • Includes AKI, interstitial nephritis, glomerulonephritis, and IgA nephritis.
  • ICI-associated renal injury commonly presents as hematuria, pyuria, worsening hypertension, or rising serum creatinine levels, with most cases having an onset of symptoms within the first 2-3 months.
  • Grading: increase of >0.3 mg/dL or 1.5-2.0 times above baseline (grade 1); creatinine 2.0-3.0 times above baseline (grade 2); creatinine >3.0 times above baseline, creatinine value of  >4.0 mg/dL, or hospitalization (grade 3); and any life-threatening complications or need for dialysis (grade 4).
  • Evaluation: CK to evaluate for rhabdomyolysis and myositis, electrolytes, renal and liver function, CBC and blood smear to evaluate for microangiopathic anemias, and urinalysis.  Urinalysis can be normal but may show sterile pyuria, microscopic hematuria, mild proteinuria, and granular casts. Obtain renal ultrasound.
  • Treatment: avoidance of nephrotoxic agents and cessation of ICI therapy, with permanent discontinuation for severity grade 3 or higher. When grade 2 or higher ICI-induced renal toxicity is suspected, administer steroids.

• Endocrine:
  • Occurs in up to 17% of patients.
  • Includes hypophysitis, or pituitary gland inflammation, both hyper- and hypothyroidism, adrenal insufficiency (AI), and diabetes mellitus (DM).
  • Hypophysitis ranges from 2-3 months, thyroid dysfunction ranges from 2 weeks to 5 months, and DM ranges from 1 week to 1 year after therapy initiation.
  • Hypophysitis:
    • Symptoms are often vague, including headache, blurry vision, generalized weakness, fatigue, mood changes, dizziness, and loss of libido.
    • Graded in terms of ADLs: asymptomatic or mild symptoms (grade 1), moderate symptoms but still able to perform ADLs (grade 2), severe symptoms causing life-threatening conditions or inability to perform ADLs (grades 3-4).
    • Evaluation typically includes CBC, renal and liver function, TSH, FT4, electrolytes, morning cortisol, and ACTH. Neuroimaging with brain MRI is recommended.
    • Treatment of hypophysitis includes holding ICI therapy for all grades, initiation of replacement hormone therapy depending on which pituitary axis is affected, and endocrinology consultation. Patients with secondary AI or grades 3-4 toxicity should receive systemic steroids at a dose of 1-2 mg/kg/day of prednisone or equivalent.
  • Thyroid:
    • Patients with symptomatic hyperthyroidism can present with weight loss, fatigue, palpitations, anxiety, heat intolerance, and increased bowel movements.  Patients with hypothyroidism can present with nonspecific symptoms including weakness, fatigue, dizziness, weight change, and mood changes.
    • Hypothyroidism grading also includes TSH levels with a TSH <10 mIU/L for grade 1 and a TSH  >10 mIU/L for grade 2.
    • Treatment: Patients with grade 1 toxicities for both hyper- and hypothyroidism can continue ICI therapy.  Patients with grade 2 or higher hyperthyroidism should have ICI therapy held and begin treatment with beta-blockers and consideration for methimazole or propylthiouracil.  Grades 3 or 4 hyperthyroidism also require systemic steroids at a dose of 1-2 mg/kg/day of prednisone or equivalent.  Patients with grade 2 or higher hypothyroidism should have ICI therapy held and initiate thyroid replacement therapy, which should include intravenous therapy in grades 3-4.
  • Diabetes:
    • DKA is a common presentation.
    • Evaluation: basic metabolic panel, ketone levels, venous blood gas,, and the addition of DM autoantibody levels (if available).
    • Grading: asymptomatic or mild symptoms (e.g., polyuria, polydipsia) and a fasting blood glucose (FBG) >160 mg/dL without evidence of ketosis (grade 1), moderate symptoms with a FBG >160-250 mg/dL or ketosis (grade 2), and severe symptoms with life-threatening complications with a FBG >250-500 mg/dL (grade 3) or FBG > 500 mg/dL (grade 4).
    • Treatment: patients with grade 2 toxicity or higher should have the ICI therapy held until blood glucose is controlled with initiation of insulin therapy for grades 3-4. Treatment of DKA is similar to patients without ICI therapy.
  • Adrenal insufficiency:
    • Very rare, with case reports.
    • Presents with fatigue, dehydration, nausea, vomiting, and weight loss, though distributive shock can be present in adrenal crisis.
    • Grading of AI is the same as the grade for hypophysitis and includes ADLs.
    • Treatment will include steroids.

• Neurologic:
  • Occurs in up to 6%.
  • Headaches, sleep disturbances, psychiatric symptoms most common.
  • The more severe neurologic complications associated with ICI therapy (e.g., myasthenia gravis, non-infectious encephalitis, Guillain-Barre syndrome [GBS], aseptic meningitis, transverse myelitis) are much less frequent.
  • Myasthenia gravis and non-infectious encephalitis have a reported mortality rate of up to 20%.

• Cardiac:
  • Rare overall, occurring in less than 1%.
  • Includes myocarditis, pericarditis, coronary artery disease, heart failure, and arrhythmias.
  • Evaluate with ECG, renal and liver function, electrolytes, troponin, BNP, imaging.

• Hematologic:
  • Rare overall.
  • Includes drug-induced hemolytic anemia, immune thrombocytopenia, lymphopenia, acquired hemophilia, thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS).

Disposition:

• Consult the patient’s oncologist to assist with evaluation, management, and disposition.
• Admit those with neurologic toxicity, cardiac toxicity, toxicity above grade 2 of any organ system, or patients requiring the initiation of high-dose systemic steroids. These patients require coordination of further evaluation and irAE-specific therapy, steroid tapering, electrolyte trending, close monitoring for progression to higher grade toxicities, and consideration of continued ICI treatment.
• Outpatient management for grade 1-2 toxicities may be reasonable in coordination with oncology, specialists based on the affected organ system(s), and assessment of the patient’s clinical trend in the ED.
• Disposition decisions may also be influenced by time from ICI induction, duration of symptoms, stability of symptoms, comorbid conditions, social support, and access to care.

Take Home Points:

• ICIs are a mainstay in cancer treatment, and the indications have significantly broadened. These medications are used in a wide range of malignancies as both single medications and combination therapies.
• ICI therapy is typically well tolerated. However, ICIs can cause significant toxicities requiring their cessation, initiation of systemic steroids, and potentially additional immunosuppressant medications.
• Each organ system and irAE possesses its own toxicity grading and associated treatment recommendations, making the approach to patients on ICI drugs challenging. 

The post emDOCs Podcast – Episode 44: Immune-Related Adverse Events from Immune Checkpoint Inhibitors appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Cameron Jones, MD, MPH (EM Resident Physician, Northwestern Memorial Hospital, Chicago, IL) and Dana Loke, MD (Clinical Instructor and Medical Education Fellow, Department of Emergency Medicine, Northwestern Memorial Hospital, Chicago, IL) // Reviewed by: Alexander Y. Sheng, MD, MHPE (@TheShenger); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case

Emergency Medicine Services (EMS) arrives with a 63-year-old male with a history of head/neck cancer, s/p tracheostomy, in respiratory distress. His initial oxygen saturation was 82%, which improved to 87% after EMS applied oxygen to his face and stoma. Upon arrival, the patient is sleepy but arousable, receiving oxygen by non-rebreather on the face and BVM at his stoma. As staff begin placing him on the monitor, you note a medical alert bracelet on the patient that informs you he has had a laryngectomy. How does this change your approach and what are your next steps?

Background

The primary indication for total laryngectomy is laryngeal cancer and thus, the vast majority of post-laryngectomy patients the emergency physician (EP) sees will have a history of head and neck cancer. Other, less common, indications for laryngectomy include severe laryngeal stenosis or chronic aspiration refractory to other treatments.¹

Total laryngectomy involves surgical removal of the entire larynx resulting in discontinuity between the trachea and oropharynx. With removal of the larynx, the end of the patient’s proximal trachea is mobilized and brought to the skin to create a stoma in the lower anterior neck. Therefore, patients who have undergone laryngectomy are obligate stoma-breathers and can only be oxygenated via the stoma.^1,2 An understanding of the anatomy involved can help provide clues to recognizing that a patient has undergone a laryngectomy rather than a simple tracheostomy if unable to obtain history from the patient or family members. Post-laryngectomy patients will typically have larger stomas and examination of the stoma and tracheal inlet will reveal a blind ending superior to the stoma.³

What devices or tubes might ED physicians encounter with laryngectomies?

Patients will most commonly have a simple heat/moisture exchanger (HME) over the stoma to help with humidification. These often look like a flat button with a housing to hold it in place, and these devices can usually be easily removed. Additionally, many patients with laryngectomies will have a tracheo-esophageal prosthesis (TEP), a one-way valve between the superior trachea and the patient’s esophagus to allow speech and which can usually be visualized through the stoma on the posterior-superior trachea. Finally, some patients may have a soft, flexible tube in place to maintain the stoma tract, especially in the initial days or weeks after surgery.^2,4 These silicone tubes, often referred to as Larytubes (though this is actually a commercial name) can be attached directly to an HME.⁵

Less commonly, patients may have an adjunctive airway such as a tracheostomy tube or an endotracheal tube in place, which can make it more challenging to initially recognize a laryngectomy stoma vs a tracheostomy. Understanding and trouble-shooting various tracheostomy tubes is outside the scope of this article (please refer to this previous emDocs post on airway emergencies and this emDocs and CORE EM post on tracheostomy care).

How can providers differentiate a laryngectomy from a tracheostomy?

In many ways, ED care for the patient with a laryngectomy relies primarily on staff recognizing and appreciating their distinction from tracheostomy patients. Unfortunately, many emergency personnel struggle to recognize the anatomical differences and how this impacts their care.^6,7  Most patients will be able to provide this information themselves if they are stable enough to do so. While laryngectomy patients lose the ability to speak using their native vocal cords due to removal of the voicebox, those with TEPs or electrolarynxes can learn to speak using these devices. It is important to have a patient-centered approach and first attempt to communicate directly with them via one of these methods or an alternative, such as writing.⁸ Family or friends accompanying the patient can also provide valuable information. If unable to obtain information from the patient, a relation, or electronic medical records, physical inspection may also alert providers that the patient has had a laryngectomy. Look for medical alert bracelets or medical cards many patients are given after their surgery.³ Many of these patients may initially receive supplemental oxygen at both the face and stoma while gathering further history, and the absence of end-tidal capnography (EtCO2) waveform measured at the face indicates absence of upper airway respirations. Next, inspect the stoma site itself. Laryngectomy patients will typically have a larger stoma, and palpation or visualization of trachea superior to the stoma will reveal a blind pouch in post-laryngectomy patients.^2-4 The presence of a TEP also indicates a laryngectomy.

What are the most common complications after laryngectomy?

Pharyngocutaneous fistulas are one of the more common post-op issues, especially in patients who have undergone pre-operative radiation therapy. These fistulas can present with salivary leakage into the soft tissues and erythema around the patient’s stoma or incision or worsening tenderness at the incision site, most often between 7-10 days after surgery. Wound dehiscence and local hematomas can also occur, which, depending on their severity, may require otolaryngology (ENT) consultation.^3,9,10

However, for the EP, the most important complications to recognize are those that may lead to hypoxia or ventilatory failure. Given the absence of airway exchange through the nose and mouth, patients with laryngectomies are especially susceptible to obstruction of the airway. If a trach device is present, removing the entire device or the inner cannula (if a mature stoma) and passing a suction catheter can often alleviate this obstruction. TEPs can occasionally become dislodged and partially obstruct a patient’s distal trachea or proximal bronchi. A visible tracheo-esophageal fistula site with no button/prosthesis in place on exam should prompt this consideration, which can typically be diagnosed with x-ray.⁴  For those patients with thick secretions in the distal trachea or proximal small bronchi, small aliquots (around 5 cc) of normal saline expressed through the stoma can help break up these secretions and induce a cough reflex to help them.

Bleeding around the stoma site in tracheostomy patients should be immediately addressed, as it may be the herald of significant hemorrhage. Tracheo-innominate fistulas (TIFs) are one of the most feared complications of tracheostomies. However, TIFs are extremely rare in laryngectomy patients due to their altered anatomy and the absence of a trach tube in place for any significant period of time, thus preventing erosion into the innominate artery.¹⁰ Instead, providers should be alert for carotid-blowout syndrome (CBS), in which the carotid or branch vessels are threatened or eroded, which is more common in irradiated patients due to poor tissue integrity. The first sign may be new bruising/hematoma, or oozing from the neck or intra-orally. If suspected, a secure airway (ideally via intubation of the stoma with cuffed endotracheal tube) should be established immediately as bleeding can quickly lead to aspiration and stoma/airway compromise. Providers should activate massive transfusion protocols and perform resuscitation as they would for other significant hemorrhage, and direct pressure should be applied over any external bleeding and intraorally using packing and forceps. Definitive management will require surgical treatment or IR embolization, and therefore, specialty consultation should occur early.^11,12

Resuscitating the patient with a laryngectomy

In the crashing patient, especially one with altered anatomy that will be less familiar to most ED personnel, it is important to have an algorithmic approach to allow rapid and systematic assessment and stabilization (see figure below). As noted above, the most important step in this evaluation is recognizing that a patient has a laryngectomy stoma rather than a tracheostomy. This recognition will allow all providers to focus on oxygenating, supporting and troubleshooting the stoma rather than attempting to ventilate or establish a definitive airway via the mouth and upper airway. Even if the patient is found to have a tracheostomy, rather than a laryngectomy, it is also important to know why their tracheostomy was performed. Some patients with tracheostomies have essentially non-patent upper airways due to severe stenosis or other anatomic abnormalities and must be functionally treated as laryngectomy patients in the ED.  However, there is little harm in applying oxygen to the face/nose and stoma initially while gathering information and making this determination.² As with any unstable patient, you should try to mobilize resources and personnel as quickly as possible. If given advance notice by a pre-arrival call, providers should gather all necessary equipment (Table 1), ensure appropriate nursing/tech staff is available, and notify respiratory therapy (RT) staff if available.¹³ Some larger academic hospitals may have trach specialists among their RTs, and, in a facility with ENT available, they should be consulted as soon as possible in the unstable post-laryngectomy patients.

Once you have recognized the patient has a laryngectomy, all oxygenation efforts should be focused on the patient’s stoma. A bag-valve mask fitted with a pediatric mask or a supraglottic airway device, such as a laryngeal mask airway (LMA), will allow for a good seal around the stoma (see video linked below).¹⁴ While providing oxygen and ventilatory support as needed, providers should begin their assessment of the stoma itself.

Video from National Tracheostomy Safety Project on Stoma Ventilation

This process begins with examining the devices in or around the stoma and attempting to determine how recently the patient’s laryngectomy was performed. With tracheostomy tubes, traditional teaching emphasizes that EPs and emergency responders should try to avoid removal of in-situ devices or re-cannulation of the stoma within 7-10 days of surgery, as the tract may not yet be mature.  Most post-laryngectomy patients remain hospitalized for around a week and are not typically sent home with a tracheostomy tube in place.⁹ However, the presence of sutures in place around the stoma site may suggest a more recent procedure, and, if possible, in these scenarios exploration of the stoma and airway should be performed under direct fiberoptic visualization or with specialty consultants at the bedside.¹⁵

Next, attempt to determine the patency of the stoma or devices present. HMEs or similar button devices should be removed, and if the patient does have a trach in place, the inner cannula should be removed. Next, attempt to gently pass a suction catheter or bougie through the stoma, trach tube, or patency tube. If a suction catheter cannot be passed through a tube in place, any present cuff should be deflated and the tube should be removed. In general, patency at the stoma itself is less often an issue than with the tracheostomy patient, and, once all cuffs have been deflated and devices removed, reassess by listening and feeling at the stoma for respirations and using end-tidal capnography. If the patient is breathing and oxygen levels have stabilized, continue applying oxygen at the stoma and continue your usual assessment to determine alternative causes of respiratory distress.^2,3 If encountering obstruction in the proximal respiratory tract, use of a fiberoptic scope (reusable or single-use bronchoscopes or shorter nasopharyngeal scopes) can be extremely helpful for direct visualization of the airway.¹⁶

If at any point the patient decompensates, stops breathing, or arrests, a definitive airway must be established via the stoma. For the EP, the fastest and safest way to do so will most likely be via intubation of the stoma with an endotracheal tube (ETT). A size 6.0 ETT will easily pass through most stomas and should be the first size in most adults. Placement of a tracheostomy tube is likely to be similarly effective, though most EPs will find use of an ETT to be more familiar and also eliminates the cognitive load of choosing a trach tube size. Intubation over a bougie or fiberoptic will allow the provider to maintain a ready tract into the airway and can allow for rapid down-sizing if meeting resistance with a 6.0 tube. The tube should only be advanced a few centimeters past the cuff, as it is very easy to accidentally pass into a mainstem (similar to when performing a cricothyrotomy).^3,15

Take-Home Points

• Patients who have undergone laryngectomies have no connection between their lower and upper airway and can only be oxygenated and ventilated via their stoma.
• Some tracheostomy patients must be functionally treated as laryngectomy patients, as they have a very limited or non-patent upper airway due to stenosis, mass, etc.
• In all patients with anterior neck stomas who present to the ED, initially apply O2 to both the face and neck but immediately attempt to determine upper airway patency via history, examination of the stoma, or absence of end-tidal CO2 waveform at the face.
• Emergency oxygenation at a tracheal stoma is best applied with a BVM fitted with a pediatric facemask or with a laryngeal mask airway (LMA).
• For the patient with a laryngectomy in respiratory distress, the primary tasks are to apply supportive oxygen, assess stoma patency and establish a definitive airway if necessary.
• If the patient stops breathing, arrests, or decompensates, intubate the tracheal stoma using a 6.0 ETT over a bougie or fiberoptic device.

References

1. Ceachir O, Hainarosie R, Zainea V. Total Laryngectomy – Past, Present, Future. Mædica. 2014;9(2):210.
2. Mcgrath, BA, Atkinson D, Moore JA, Bates L. Comprehensive Tracheostomy Care. National Tracheostomy Safety Project. 2013. Accessed September 10, 2021. https://www.tracheostomy.org.uk/storage/files/Comprehensive%20Tracheostomy%20Care.pdf
3. Townsley RB, Baring DEC, Clark LJ. Emergency department care of a patient after a total laryngectomy. Eur J Emerg Med. 2014;21(3):164-169. doi:10.1097/MEJ.0B013E32835ED735
4. Bryant CD.  Complications of Airway Devices. In: Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed September 22, 2021. https://accessmedicine-mhmedical-com.turing.library.northwestern.edu/content.aspx?bookid=2353&sectionid=221180267
5. University of Mississippi Medical Center. Laryngectomy: What to Expect. Accessed September 23, 2021. https://www.umc.edu/Healthcare/ENT/Patient-Handouts/Adult/Head_Neck/HN%20_PDF/Laryngectomy%20_What%20to%20Expect_Fin.pdf.
6. Darr A, Dhanji K, Doshi J. Tracheostomy and laryngectomy survey: do front-line emergency staff appreciate the difference? 2021. doi:10.1017/S0022215112000618
7. Whitcroft KL, Moss B, Mcrae A. ENT and airways in the emergency department: national survey of junior doctors’ knowledge and skills. J Laryngol Otol. 2016;130(2):183-189. doi:10.1017/S0022215115003102
8. Lee MT, Gibson S, Hilari K. Gender Differences in health-related quality of life following total laryngectomy. International Journal of Language & Communication Disorders. 2010;45(3):287-294.
9. Goepfert RP, Hutcheson KA, Lewin JS, et al. Complications, hospital length of stay, and readmission after total laryngectomy. Cancer. 2017;123(10):1760-1767. doi:10.1002/CNCR.30483
10. Hasan Z, Dwivedi RC, Gunaratne DA, Virk SA, Palme CE, Riffat F. Systematic review and meta-analysis of the complications of salvage total laryngectomy. European Journal of Surgical Oncology. doi:10.1016/j.ejso.2016.05.017
11. Miguel C, Estomba C, Alberto F, et al. Carotid blowout syndrome in patients treated by larynx cancer. Braz J Otorhinolaryngol. 2017;83(6):653-658. doi:10.1016/j.bjorl.2016.08.013
12. Carotid Artery Rupture Precautions. Head and Neck Protocols. University of Iowa Healthcare. 2017. Accessed September 24, 2021. https://medicine.uiowa.edu/iowaprotocols/carotid-rupture-precautions.
13. Morris LL, Whitmer A, Mcintosh E. Tracheostomy care and complications in the intensive care unit. Crit Care Nurse. 2013;33(5):18-30. doi:10.4037/CCN2013518
14. Bhalla RK, Corrigan A, Roland NJ. Comparison of two face masks used to deliver early ventilation to laryngectomized patients. Ear Nose and Throat Journal 2004; 83: 414.
15. Long B, Koyfman A. Resuscitating the tracheostomy patient in the ED. American Journal of Emergency Medicine. doi:10.1016/j.ajem.2016.03.049
16. McGrath, B. A., Bates, L., Atkinson, D., & Moore, J. A. (2012). Multidisciplinary guidelines for the management of tracheostomy and laryngectomy airway emergencies. Anaesthesia, 67(9), 1025–1041. https://doi.org/10.1111/j.1365-2

The post ED Management of the Post-Laryngectomy Patient appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Brit Long, MD (@long_brit – EM Attending Physician, San Antonio, TX); Manpreet Singh, MD (@MPrizzleER – Assistant Professor of Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center); and Alex Koyfman, MD (@EMHighAK – EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) 

Thank you for everything you do! Despite all the difficulties, we have the awesome privilege of caring for patients no matter what. You are heroes!

Thank you as well for your support of our site and podcast this past year. We cannot do what we do without your views, feedback, and assistance. This last year saw several amazing posts and resources.

Now, without further ado, here is our list of top posts from 2021 based on viewership from you, the readers:

Lactated Ringers versus Normal Saline: Myths and Pearls in the ED

This post from Gabrielle Leonard and Aaron Lacy evaluates the continuous debate of LR vs. NS, as well as pearls and pitfalls in their use. You don’t want to miss this one!

Evaluation and Management of Hematuria in the Emergency Department

Taylor Goller and Sarah Klemencic look at the presentation, diagnosis, and management of hematuria in the ED.

Syncope in the ED: Who can go home?

We are experts in evaluating and managing the patient with syncope, but who can be discharged safely from the ED? Aaron Blau and Richard Bounds provide you with pearls and pitfalls, as well as a look at the most recent risk scores.

Ostomy complications: ED presentations, complications, and management

Ostomies can have several complications. Jonathan Bornstein, Jennifer Liao, Marzena Sroczynski, and Carlos Rodriguez provide you with key points concerning the care of ostomies in the ED.

Tympanic Membrane Rupture

Tympanic membrane rupture can cause significant morbidity. What do you need to consider in evaluating and managing these patients?

Oliguria and Anuria: ED Presentations, Evaluation, and Management

Daniel Weidner and Michael Yoo cover the differential and etiologies, evaluation, and management of oliguria and anuria.

Pulmonary Hypertension: ED Presentation, Evaluation, and Management

Pulmonary hypertension is extremely challenging, and a mistake in the evaluation or management can result in patient harm. Rachel Bridwell covers what you need to expertly handle these patients in the ED.

Evidence-based Approach to Nailbed Injuries: ED Presentations, Evaluation, and Management

Erik Sherman and Chin He look at the potentially challenging nailbed injury. How should you examine these patients, and when should you consider trephination or other nailbed repairs?

Small Talk – Hot Off The Presses: The Latest AAP Guidelines for the Febrile Neonate

The American Academy of Pediatrics updated their guidelines concerning the evaluation and management of the febrile neonate this year. Nathaniel White, Michele McDaniel, and Joe Ravera provide you with the key takeaways that change our practice.

Anemia in the ED Setting: Pearls and Pitfalls

We routinely see patients with anemia in the ED. This post from Brandon Carius looks at the ED evaluation and management for these patients.

Stay tuned for 2022! We have more exciting posts and changes that will improve your practice of EM!

The post Top emDOCs Posts of 2021 appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Welcome back to The EM Thinker series. This series will provide important considerations for the practice of emergency medicine.

1) Multiple visits for nephrolithiasis: CT renal colic is not needed each and every time. What’s the patient history like – co-morbidities with higher risk for kidney diseases, type of stone, antibiotic courses, complications, interventions, etc.? What it boils down to is severe sepsis/septic shock +/- in setting of obstruction. Consider serious mimics when appropriate. Master interpretation of lab work and urinalysis, and know their limitations. Bedside ultrasound can be helpful, but also has its limitations. Bottom line: it’s not a one-size-fits-all disease.

2) Female with abdominal pain + you’re obtaining a CT. Did you consider OB/Gyn pathology and do a complete exam? The answer may lie there and a CT may be unnecessary.

3) When should you obtain stool studies: ill patient in front of you with systemic sympotms, immunocompromised, grossly bloody diarrhea, > 1 week of symptoms and not improving. There are nuances to antibiotics and antimotility agents; look them up each time. With a WBC > 20 in patient with no source, consider C. diff colitis.

4) If you’re able to obtain a cohesive patient story, it will likely jive with your work-up. If not, consider expanding what you’re doing. Language/communication barriers add a lot of complexity.

5) If pneumomediastinum is identified => consider esophageal and pulmonary sources. The major conditions to not miss include esophageal perforation and tracheal perforation.

6) Small puncture wound in vicinity of fracture, give a dose of antibiotics and don’t look back. Type I is what burns emergency physicians along with not considering the environment the injury occurred in.

7) Beware reflexive use of propranolol in patients with thyroid storm, especially in cases of undiagnosed cardiomyopathy. We likely over-diagnose this entity as Burch-Wartofsky scale has its limitations. Perform a bedside echocardiogram and save a life. Esmolol may be a better option, but we don’t have great data.

8) Don’t anchor on equivocal or contaminated urinalysis as source of infection in patients with diabetes. Do a thorough history and exam and consider the list of sneaky infections.

9) Find a way that works for you to stay up-to-date on meaningful clinical changes. 1 recent example: https://www.cdc.gov/std/treatment-guidelines/urethritis-and-cervicitis.htm and https://www.cdc.gov/std/treatment-guidelines/pid.htm

10) ECG with low or wide rhythm: consider hyperkalemia. Management approach to bradycardic periarrest includes electrical and medical arms. Simplify your approach to etiology and look up the rest: DIE (Drugs, Ischemia, Electrolytes).

Further reading:

• emDocs The Sick Kidney Stone Patient
• Amazon The EM Mindset
• emDocs Incidental Pneumomediastinum
• EM@3AM Open Fracture
• IBCC Thyroid Storm
• emDocs DKA Sneaky Triggers
• IBCC Bradycardia

The post EM Thinker: Pearls from the Frontlines appeared first on emDOCs.net - Emergency Medicine Education.

Author: Brit Long, MD (@long_brit) // Reviewed by: Alex Koyfman, MD (@EMHighAK)

The Surviving Sepsis Campaign published updated guidelines for the management of sepsis and septic shock, with 93 recommendations. We will not cover all 93 here. Instead, we will break this post into the EM Top Changes, with some discussion of the literature behind these changes, as well as other changes that impact our practice.

EM Top Changes:

• For adults with septic shock, we suggest using capillary refill time to guide resuscitation as an adjunct to other measures of perfusion. Weak, low quality of evidence, NEW.
  • The ANDROMEDA SHOCK trial evaluated resuscitation using capillary refill time and found it to be more effective than a resuscitation strategy using lactate in reducing organ dysfunction (1).
• For patients with sepsis-induced hypoperfusion or septic shock we suggest that at least 30 mL/kg of IV crystalloid fluid should be given within the first 3 hr of resuscitation. Weak, low quality of evidence DOWNGRADE from Strong, low quality of evidence.
  • This is a change from “recommended” due to low quality of evidence. There are no prospective interventional studies looking at different volumes for the initial resuscitation of those with sepsis or septic shock. A retrospective study including ED adult patients with sepsis or septic shock found failure to receive 30 mL/kg of crystalloids was associated with higher mortality (2). Guidelines also cite the PROCESS, PROMISE, and ARISE trials, which provided fluid in the 30 mL/kg range (3-5).
• For adults with sepsis or septic shock, we suggest using balanced crystalloids instead of normal saline for resuscitation. Weak, low quality of evidence, CHANGED from weak recommendation, low quality of evidence.
  • Normal saline may result in hyperchloremic metabolic acidosis. The SMART and SALT ED trials support the use of balanced crystalloids, with a network meta-analysis demonstrating decreased mortality with balanced fluids (6-8).
• For adults with septic shock on vasopressors, we recommend an initial target mean arterial pressure (MAP) of 65 mm Hg over higher MAP targets. Strong, moderate-quality evidence.
  • An RCT evaluating patients in septic shock randomized to MAP targets of 65-70 mm Hg versus 80-85 mm Hg found no difference in mortality. There was reduced risk of renal replacement therapy in patients with chronic hypertension and higher rates of atrial fibrillation in the group randomized to the higher MAP target group (9).
• For adults with septic shock, we suggest starting vasopressors peripherally to restore mean arterial pressure rather than delaying initiation until central venous access is secured. Weak, very low quality of evidence, NEW.
  • Vasopressors play an important role in treatment of septic shock. Peripheral administration of vasopressors is generally safe if infused in the antecubital fossa for a short period of time (< 6 hours) (10,11). Peripheral infusion is associated with shorter time to administration and time to achieving a MAP > 65 (12).
• For adults with sepsis-induced hypoxemic respiratory failure, we suggest the use of high flow nasal oxygen (also known as HFNC) over noninvasive ventilation (NIV). Weak, low quality of evidence, NEW.
  • One RCT demonstrates improved 90-day survival with HFNC compared with NIV (OR 0.42, 95% CI 0.21-0.85), with more days from mechanical ventilation (13). In another study including those with severe hypoxemia, HFNC was resulted in lowered rates of intubation when compared with conventional oxygen therapy (14-16).
• For adults with sepsis or septic shock we suggest against using IV vitamin C. Weak, low quality of evidence, NEW.
  • One before and after study published in 2017 reported reduced mortality with vitamin C, thiamine, and hydrocortisone (17). However, the VITAMINS trial found no impact on mortality with this regimen (18), and a meta-analysis evaluating high dose vitamin C also found no mortality impact (19).
• For adults with septic shock and an ongoing requirement for vasopressor therapy we suggest using IV corticosteroids. Weak, moderate-quality evidence, UPGRADE from Weak recommendation, low quality of evidence.
  • Since the 2016 guidelines, several large RCTs have been published, with a meta-analysis finding faster resolution of shock and increased vasopressor-free days in those receiving systemic steroids (20-23). However, steroids are associated with increased neuromuscular weakness and have no clear effect on mortality (23).

The Rest:

• We recommend against using qSOFA compared with SIRS, NEWS, or MEWS as a single screening tool for sepsis or septic shock. Strong, moderate-quality evidence, NEW.
• For adults suspected of having sepsis, we suggest measuring blood lactate. Weak, low quality of evidence.
• Sepsis and septic shock are medical emergencies, and we recommend that treatment and resuscitation begin immediately. Best practice statement.
• For adults with sepsis or septic shock, we suggest using dynamic measures to guide fluid resuscitation, over physical examination, or static parameters alone. Weak, very low quality of evidence.
• For adults with sepsis or septic shock, we suggest guiding resuscitation to decrease serum lactate in patients with elevated lactate level, over not using serum lactate. Weak, low quality of evidence.
• For adults with sepsis or septic shock, we recommend using crystalloids as first-line fluid for resuscitation. Strong, moderate-quality evidence.
• For adults with sepsis or septic shock, we suggest using albumin in patients who received large volumes of crystalloids. Weak, moderate-quality evidence.
• There is insufficient evidence to make a recommendation on the use of restrictive versus liberal fluid strategies in the first 24 hr of resuscitation in patients with sepsis and septic shock who still have signs of hypoperfusion and volume depletion after the initial resuscitation. No recommendation.
• For adults with septic shock, we recommend using norepinephrine as the first-line agent over other vasopressors. Strong Dopamine. High-quality evidence Vasopressin. Moderate-quality evidence Epinephrine. Low quality of evidence Selepressin. Low quality of evidence Angiotensin II. Very low-quality evidence.
• For adults with septic shock on norepinephrine with inadequate mean arterial pressure levels, we suggest adding vasopressin instead of escalating the dose of norepinephrine. Weak, moderate quality evidence.
• For adults with septic shock and inadequate mean arterial pressure levels despite norepinephrine and vasopressin, we suggest adding epinephrine. Weak, low quality of evidence.
• For adults with septic shock and cardiac dysfunction with persistent hypoperfusion despite adequate volume status and arterial blood pressure, we suggest either adding dobutamine to norepinephrine or using epinephrine alone. Weak, low quality of evidence.
• For adults with septic shock and cardiac dysfunction with persistent hypoperfusion despite adequate volume status and arterial blood pressure, we suggest against using levosimendan. Weak, low quality of evidence, NEW.
• For adults with possible septic shock or a high likelihood for sepsis, we recommend administering antimicrobials immediately, ideally within 1 hr of recognition. Strong, low quality of evidence (Septic shock), CHANGED from previous.
• For adults with possible sepsis without shock, we recommend rapid assessment of the likelihood of infectious versus noninfectious causes of acute illness. Best practice statement.
• For adults with possible sepsis without shock, we suggest a time-limited course of rapid investigation and if concern for infection persists, the administration of antimicrobials within 3 hr from the time when sepsis was first recognized. Weak, very low quality of evidence, NEW from previous.
• For adults with suspected sepsis or septic shock, we suggest against using procalcitonin plus clinical evaluation to decide when to start antimicrobials, as compared to clinical evaluation alone. Weak, very low quality of evidence.
• For adults with sepsis or septic shock at high risk of MRSA, we recommend using empiric antimicrobials with MRSA coverage over using antimicrobials without MRSA coverage. Best practice statement, NEW from previous.
• For adults with sepsis or septic shock at low risk of MRSA, we suggest against using empiric antimicrobials with MRSA coverage, as compared with using antimicrobials without MRSA coverage. Weak, low quality of evidence, NEW from previous.
• For adults with sepsis or septic shock and high risk for multidrug resistant (MDR) organisms, we suggest using two antimicrobials with gram-negative coverage for empiric treatment over one gram-negative agent. Weak, very low quality of evidence.
• For adults with sepsis or septic shock and low risk for multidrug resistant (MDR) organisms, we suggest against using two gram-negative agents for empiric treatment, as compared to one gram-negative agent. Weak, very low quality of evidence.
• For adults with sepsis or septic shock, we suggest against using double gram-negative coverage once the causative pathogen and the susceptibilities are known. Weak, very low quality of evidence.
• For adults with sepsis or septic shock at high risk of fungal infection, we suggest using empiric antifungal therapy over no antifungal therapy. Weak, low quality of evidence, NEW from previous.
• We make no recommendation on the use of antiviral agents. No recommendation.
• For adults with sepsis or septic shock, we recommend rapidly identifying or excluding a specific anatomical diagnosis of infection that requires emergent source control and implementing any required source control intervention as soon as medically and logistically practical. Best practice statement.
• For adults with sepsis or septic shock, we recommend prompt removal of intravascular access devices that are a possible source of sepsis or septic shock after other vascular access has been established. Best practice statement.
• There is insufficient evidence to make a recommendation on the use of noninvasive ventilation in comparison to invasive ventilation for adults with sepsis-induced hypoxemic respiratory failure. No recommendation.
• For adults with sepsis-induced ARDS, we recommend using a low tidal volume ventilation strategy (6 mL/kg), over a high tidal volume strategy (> 10 mL/kg). Strong, high-quality evidence.
• For adults with sepsis-induced severe ARDS, we recommend using an upper limit goal for plateau pressures of 30 cm H2O, over higher plateau pressures. Strong, moderate-quality evidence.
• For adults with moderate to severe sepsis induced ARDS, we suggest using higher PEEP over lower PEEP. Weak, moderate-quality evidence.
• For adults with septic shock and an ongoing requirement for vasopressor therapy we suggest using IV corticosteroids. Weak, moderate-quality evidence, UPGRADE from Weak recommendation, low quality of evidence.
• For adults with sepsis or septic shock we recommend using a restrictive (over liberal) transfusion strategy. Strong, moderate-quality evidence.
• For adults with sepsis or septic shock we suggest against using IV immunoglobulins. Weak, low quality of evidence.
• For adults with sepsis or septic shock, we recommend using pharmacologic venous thromboembolism (VTE) prophylaxis unless a contraindication to such therapy exists. Strong, moderate-quality evidence.
• For adults with sepsis or septic shock, we recommend initiating insulin therapy at a glucose level of ≥ 180mg/dL (10 mmol/L). Strong, moderate-quality evidence.
• For adult survivors of sepsis or septic shock, we recommend assessment and follow-up for physical, cognitive, and emotional problems after hospital discharge.

The Guidelines:

• Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021 Nov 1;49(11):e1063-e1143.
• Evans L, Rhodes A, Alhazzani W, et al. Executive Summary: Surviving Sepsis Campaign: International Guidelines for the Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021 Nov 1;49(11):1974-1982.

References:

1. Hernandez G, Ospina-Tascon GA, Damiani LP, et al; The ANDROMEDA SHOCK Investigators and the Latin America Intensive Care Network (LIVEN). Effect of a resuscitation strategy targeting peripheral perfusion status vs serum lactate levels on 28-day mortality among patients with septic shock: The ANDROMEDA-SHOCK randomized clinical trial. JAMA 2019; 321:654–664.
2. Kuttab HI, Lykins JD, Hughes MD, et al. Evaluation and Predictors of Fluid Resuscitation in Patients With Severe Sepsis and Septic Shock. Crit Care Med 2019; 47:1582–1590.
3. Yealy DM, Kellum JA, Huang DT, et al; ProCESS Investigators. A randomized trial of protocol-based care for early septic shock. N Engl J Med 2014; 370:1683–1693.
4. Investigators A, Group ACT, Peake SL, et al. Goal-directed resuscitation for patients with early septic shock. N Engl J Med 2014; 371:1496−1506.
5. Mouncey PR, Osborn TM, Power GS, et al; ProMISe Trial Investigators. Trial of early, goal-directed resuscitation for septic shock. N Engl J Med 2015; 372:1301–1311.
6. Semler MW, Self WH, Wanderer JP, et al; SMART Investigators and the Pragmatic Critical Care Research Group. Balanced Crystalloids versus Saline in Critically Ill Adults. N Engl J Med. 2018 Mar 1;378(9):829-839.
7. Self WH, Semler MW, Wanderer JP, et al; SALT-ED Investigators. Balanced Crystalloids versus Saline in Noncritically Ill Adults. N Engl J Med. 2018 Mar 1;378(9):819-828.
8. Rochwerg B, Alhazzani W, Sindi A, et al. Fluids in Sepsis and Septic Shock Group: Fluid resuscitation in sepsis: a systematic review and network meta-analysis. Ann Intern Med 2014; 161:347–355.
9. Asfar P, Meziani F, Hamel JF, et al; SEPSISPAM Investigators. High versus low blood-pressure target in patients with septic shock. N Engl J Med 2014; 370:1583–1593.
10. Tian DH, Smyth C, Keijzers G, et al. Safety of peripheral administration of vasopressor medications: A systematic review. Emerg Med Australas 2020; 32:220–227.
11. Loubani OM, Green RS. A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters. J Crit Care 2015; 30:653.e9–653.17.
12. Delaney A, Finnis M, Bellomo R, et al. Initiation of vasopressor infusions via peripheral versus central access in patients with early septic shock: A retrospective cohort study. Emerg Med Australas 2020; 32:210–219.
13. Frat JP, Thille AW, Mercat A, et al. FLORALI Study Group; REVA Network: High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N Engl J Med 2015; 372:2185–2196.
14. Ni YN, Luo J, Yu H, et al. The effect of high-flow nasal cannula in reducing the mortality and the rate of endotracheal intubation when used before mechanical ventilation compared with conventional oxygen therapy and noninvasive positive pressure ventilation. A systematic review and metaanalysis. Am J Emerg Med 2018; 36:226–233.
15. Ou X, Hua Y, Liu J, et al. Effect of high-flow nasal cannula oxygen therapy in adults with acute hypoxemic respiratory failure: A meta-analysis of randomized controlled trials. CMAJ 2017; 189:E260–E267.
16. Rochwerg B, Granton D, Wang DX, et al. High-flow nasal cannula compared with conventional oxygen therapy for acute hypoxemic respiratory failure: Author’s reply. Intensive Care Med 2019; 45:1171.
17. Marik PE, Khangoora V, Rivera R, et al. Hydrocortisone, Vitamin C, and Thiamine for the Treatment of Severe Sepsis and Septic Shock: A Retrospective Before-After Study. Chest 2017; 151:1229–1238.
18. Fujii T, Luethi N, Young PJ, et al; VITAMINS Trial Investigators. Effect of Vitamin C, Hydrocortisone, and Thiamine vs Hydrocortisone Alone on Time Alive and Free of Vasopressor Support Among Patients With Septic Shock: The VITAMINS Randomized Clinical Trial. JAMA. 2020 Feb 4;323(5):423-431.
19. Sato R, Hasegawa D, Prasitlumkum N, et al. Effect of IV High-Dose Vitamin C on Mortality in Patients With Sepsis: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Crit Care Med. 2021 Dec 1;49(12):2121-2130.
20. Annane D, Renault A, Brun-Buisson C, et al; CRICSTRIGGERSEP Network. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock. N Engl J Med 2018;378:809–818.
21. Venkatesh B, Finfer S, Cohen J, et al. Adjunctive Glucocorticoid Therapy in Patients with Septic Shock. N Engl J Med 2018; 378:797−808.
22. Gordon AC, Mason AJ, Thirunavukkarasu N, et al; VANISH Investigators. Effect of Early Vasopressin vs Norepinephrine on Kidney Failure in Patients With Septic Shock: The VANISH Randomized Clinical Trial. JAMA 2016; 316:509–518.
23. Rygad SL, Butler E, Granholm A, et al. Low-dose corticosteroids for adult patients with septic shock: a systematic review with meta-analysis and trial sequential analysis. Intensive Care Med 2018; 44:1003–1016.

The post Surviving Sepsis Campaign: 2021 Updates appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Sean Griffiths, DO (Emergency Physician, USAF); Josh Lowe, MD (Emergency Physician, USAF); Rachel Bridwell, MD (Emergency Physician, USA) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

“Trauma team to the trauma room, trauma team to the trauma room.” This is a call every emergency medicine (EM) physician has experienced countless times. It is often met by an exasperated sigh as the critically ill patients are transported from scene, allowing you only a few moments to put on your game face and then shoot expressive looks at teammates to move quickly. You and your team spring into action; the patient is in extremis from multiple gunshot wounds to the head and chest.  Ultimately despite everyone’s best efforts and through no one’s fault, the patient dies. You conduct a short, perfunctory debrief with the team which, as usual, leads to pretty minimal effective feedback from anyone. This one patient is just another body to add to the long list of bodies in your career and finally you head back to the pod to pick up the next chart in the heaping pile of patients waiting to be seen.

You tell yourself the patient was always going to die no matter what you did and you mostly believe yourself. In that moment, you relive every order, procedure, disagreement with nursing staff or consultants, the debrief, and your documentation. Then the family arrives. You take an extra moment to reapply your game face, grab a swig of coffee, straighten out your scrubs, and take off your stupid Patagonia vest because you’re sweating. As you deliver the bad news, the family delivers their own death blow to you, wailing that their only other child died of leukemia this week and the funeral was today. Another far more painful sigh comes bubbling up, but you contain it because it doesn’t have the cathartic effect it had on your anxiety an hour before. You stumble through a few more sterile “I’m sorry’s” and several “We did everything we could’s” then hastily retreat to your desk. Your shift is now over and time to go home to your spouse and children.

You’re numb, you put on a different but equally important game face – the “parent face” and walk in with a smile. You fumble through the rest of the evening in a fog, drink a little too much after dinner, and tell your spouse work was “fine”. Then as you lay down in bed, for some reason that exists only within the rambling minds of EM physicians trying to fall asleep, you remember a movie quote from the 2001 cinematic classic Training Day – “When you kill someone on duty, they have to be your slave in the afterlife”. You didn’t kill anyone but that night you dream about an eerily similar young male patient with multiple gunshot wounds to the head and chest, his family, and the rest of your slaves.

Residue

Residue is the focus of an article by Preston Cline, Ed.D., a researcher, podcaster, medic, expeditionary team leader and cofounder of the Mission Critical Team Institute (MCTI). The paper focuses on changing the paradigm of how high-performance individuals deal with the intense experiences that are the foundation of the extraordinary lives they have chosen.

Residue is neither good nor bad, it is not traumatic or atraumatic; it is the residual emotions, thoughts, anxiety, successes, identity, and dreams that stick tightly to us from our experiences. It is the splattered blood on your shoes from the trauma bay, the moon dust of the Middle East still clinging to your backpack, the cup ring on your back porch after beers with your best friends, or the mud stubbornly caked on your wheel well from driving to a friend’s funeral two weeks ago. It is inconsequential in isolation, barely affecting you, but cumulatively over years of exposure, it gums up the works of your mind rendering you less effective in your mission, whatever that may be.

Residue shifts the approach to trauma and wellness from a pathological (deficit) based approach to a strength (asset) based approach with several fundamental truths:

• You are not broken. You are not a victim. You are not a survivor.
• You have chosen a hard path full of extreme experiences, both good and bad.
• These experiences leave residue that if dealt with appropriately, fuel greater achievement. If neglected, they can lead to worsened performance and feelings of failure, alienation, and resentment.

This strength-based approach avoids the problem-focused approach of other wellness techniques. Instead, residue management leads to self-directed, opportunity-focused, changes in behavior. Those who are struggling are often labeled, diagnosed, prescribed and treated in a manner which says, “something is wrong with you and here is how you fix it”. The inherent flaw in this approach is that there is no fixing it. Tomorrow someone else on shift is going to come across a critically ill patient, get a patient complaint, or argue with a consultant. No matter what SSRI they’re prescribed, how much they talk to a therapist, or how understanding their family is – the residue on their life will continue to build, gumming the gears of progress. Each person needs a way internalize this residue, release yourself from its sticky attachment, and move forward through life.

From one EM physician to another

You may not think you need this. From one physician to another, you do. We all process these important experiences differently, but we still all NEED to process them. There’s an apt metaphor for dealing with stress that is attributed to COL (ret) David Hackworth, a highly decorated Korea and Vietnam veteran. It basically states that everyone has a cup they can fill with trauma. Some cups are thimbles, others are swimming pools, but they all have limits. If you manage your experiences appropriately while embracing the residue left by positive experiences, you can dump out some of your cup to make room for future stressors. But if you let your cup overflow, there’s no going back or reversing damage; you have burned out to an irrecoverable state. This is the end state we are always looking to avoid, the forever burnout. We will cover some particularly salient points specific to the EM physician in coping with residue.

 1. Suffering as a Privilege

Dr. Cline quotes a military EM physician ruminating on this quote from Portrait of a Lady, “You must have suffered first, have suffered greatly, have gained some miserable knowledge. In that way your eyes are opened to it”. You’re suffering with regards to the trials of medical school and residency, the personal relationships that have withered on the vine, and the countless numbers of dead and dying you have laid hands on is not a weight you drag around your ankles to and from shift. It is a badge of honor shared between you and your brothers and sisters in medicine. Dan Dworkis, MD, PhD and an EM physician at USC Medical Center stated in a MCTI podcast, “Don’t let suffering go to waste”. Your suffering lets you know you still care deeply. If examined through the appropriate lens, your suffering teaches you how and in what direction to grow. Examining your suffering through a strength-based approach reframes the narrative. It helps you examine tragedy or loss through the framework of improvement, not through the view of damage done to your psyche from which you need to convalesce or run. Look at your shortcomings as opportunities to learn and build upon, not as an exposé on why you’re a terrible doctor.

2. Improving your inner dialogue and self-awareness

Similar to before a big resuscitation arrives, we all have particular self-talk phrases to keep us calm and confident right before to perform our best. We use our square breathing and tell ourselves “you got this, kid” or whatever your phrase is to get you in the mindset of conquering the task at hand.  Our inner dialogue after these events is equally critical for processing our residue. Balancing the honest critique of performance with the protection of your self-esteem is a precarious tight rope to walk, especially while on shift when the next patient we see after these moments is the scariest. We will often look elsewhere to place external blame, thereby preserving our self-image. However, this can lead us down the road of self-pity and a finger pointing, deflective, narcissistic path. Practicing self-compassion or “allowing yourself some grace”, will allow you to evaluate your performance in a non-accusatory way that can lead to the notation of areas of improvement. Scott Weingart, MD discusses his thoughts on self-reflection, “Let the real negative voices speak to you because they may say something valuable that you wouldn’t hear otherwise… but don’t let them speak too long”. Protracted negative self-talk leads to pathologic imposter syndrome and decision-making paralysis from fear of repeated failure. This will mature into an inability to search internally for legitimate shortcomings and the hindrance of our professional growth. Failure is an inevitable part of medicine, how we debrief ourselves after failure to handle and internalize the lessons learned is a choice.

3. The third thing

Residue delves into many other tools to help digest and cope with our experiences but the final point we will cover is the development of your “third thing”. The first thing is your job, the second thing is your family, and the third thing is anything that brings you to new learning and self-improvement. This third thing is a way to disconnect from your professional world and bring fulfillment away from medicine. This concept of the third thing is non-negotiable for your mental longevity and residue processing capability. Our job in medicine will one day end and if your entire internal picture is “the doctor”, this end in clinical medicine will wreak havoc on your unidimensional self-image. It is a fallacy to think that dedicating time to woodworking, fitness, a small business startup, or a Dungeons and Dragons clan will take away from your professional development as a physician. The lessons learned in these other endeavors are directly applicable to your life in medicine and give you a source of joy completely independent of EM.

The world may be on fire, but you don’t have to be

Every day it seems that there’s a new article about the slow death of EM and the pandemic of EM burnout as the COVID pandemic persists. We cannot begin to imagine solutions on a macroscale, but we are tired of articles and papers painting us as defeated victims in our burning EDs. Finally, at least for us, we have found an approach that has the solutions buried within our conscious thoughts.  All we want to be able to do is help other physicians improve their lives. We have to believe that a workforce full of motivated and mentally healthy physicians can overcome any obstacle that we collectively face. Please read Residue and hopefully it will help you process the experiences you face daily in EM as it has for us.

Disclaimer:  The views expressed in this post are those of the authors and do not reflect the official views or policy of the United States Government, Defense Health Agency, United States Army, United States Navy, United States Air Force, SAUSHEC, or the Department of Defense or its Components.

References

https://missioncti.com/wp-content/uploads/2020/06/RESIDUE-V.4-PUBLIC-DISTRIBUTION-4.20.20-1.pdf

Cline P, Dworkis D. MCTI Teamcast. Season 2 Episode 5. The Emergency Mind. July 19, 2021. https://teamcast.missioncti.com/episode/s2-ep5-the-emergency-mind

Orman R, Weingart S. Stimulus with Rob Orman, MD. Episode 55. June 28, 2021. https://www.stimuluspodcast.com/post/53-the-five-fears-of-scott-weing

The post You’re not broken: a Commentary on Residue appeared first on emDOCs.net - Emergency Medicine Education.

Here’s another case from Medical Malpractice Insights – Learning from Lawsuits, a monthly email newsletter for ED physicians. The goal of MMI-LFL is to improve patient safety, educate physicians and reduce the cost and stress of medical malpractice lawsuits. To opt in to the free subscriber list, click here.

This month’s case is another reminder to think of spinal epidural abscess in back pain patients. This diagnosis continues to be missed far too often. Doing the right thing, while not always keeping one from getting sued, will (almost always) keep a jury on your side. We are not responsible for foreseeing the future. We are responsible for keeping an open mind, developing a broad differential, testing appropriately and documenting our findings.

Chuck Pilcher, MD, FACEP

Editor, Med Mal Insights

Excited delirium: A medical problem, not a police problem

Patient removed from ICU at physician’s request, dies in jail. 

Facts: A 26-year-old male alcoholic and meth addict well-known to the police and hospital staff is brought to the ED with extreme agitation, violent outbursts and seizures. After a brief stay in the ED, he is admitted to the ICU where he is given low doses of lorazepam (3 mg total IV) and haloperidol (10 mg IM). His violent and erratic behavior remains uncontrolled for the next 2 1/2 hours, at which time the physician asks that the police be called to remove him from the hospital. He is placed in a wheelchair with difficulty, taken out of the hospital and left in a nearby park without any discharge meds or instructions. The physician documents his condition on discharge as “stable,” despite a CO2 level of 16 and a sodium 126. Five hours later he is found in the park naked, arrested for lewd conduct and booked into jail. He is placed in a “restraint chair” for several hours, then moved to a cell. The next morning he asks to go to the hospital. The request is denied. He has a seizure and dies in his cell 24 hours later. His estate files a lawsuit.

Plaintiff: You told the police I was “stable” for discharge when I was anything BUT stable. In fact, had the police found me somewhere other than in the hospital in my condition, they would have considered me unstable and brought me TO the hospital. I had already had 2 seizures in the previous 12 hours. You gave me ridiculously low doses of lorazepam and haloperidol during my stay. In fact, you gave me the haloperidol only 20 minutes before the police took me out. It didn’t have time to work. Even if you had given me the right dosages, you could have done more to bring my behavior under control. You could have called an anesthesiologist and/or used propofol, ketamine, or even chemical paralysis and intubation. My labs were out of whack, and you didn’t check my VS on discharge. In fact, I wasn’t discharged. I was kicked out, even though I was getting worse, not better. You never checked my old record. It contains a virtual “recipe” of the drug regimen that other doctors had used for my prior similar episodes. It worked so well that they could discharge me from the ED without admission. I would not have died if you’d given me appropriate doses of medications for my condition, controlled my seizures and let me calm down.

Defense: I wrote orders for “2 mg IV lorazepam q3h prn anxiety and agitation.” I included a plan to “transfer [you] to an inpatient detox facility as soon as [you became] stable enough to be discharged.” I determined that you were medically cleared to be in police custody.

Result: After an expert reviewed the record and submitted a declaration supporting the patient’s claims, a pre-trial settlement was reached for an undisclosed amount.

Takeaways:

1. Controlling medically unstable behavior is the responsibility of the physician, not the police.
2. A variety of options may be utilized for chemical restraint, including haloperidol or droperidol and/or benzodiazepines.
3. Ketamine 4-5 mg/kg IM or 1-2 mg/kg IV can provide rapid control. If this is utilized, the patient requires close monitoring.
4. Medical ethics and the standard of care do not allow a patient to be “discharged” because his behavior is inconvenient or otherwise unacceptable.
5. Having the police remove a patient with excited delirium from the ICU is not a discharge plan.

References:

1. Assessment and emergency management of the acutely agitated or violent adult. Moore G, Pfaff JA. UpToDate Online, updated Sep 21, 2021. https://www.uptodate.com/contents/assessment-and-emergency-management-of-the-acutely-agitated-or-violent-adult?source=search_result&search=acute agitation&selectedTitle=1~150
2. emDocs Cases: ED Approach to Agitation. Brit Long. emDocs.net, Feb 5, 2018. http://www.emdocs.net/emdocs-cases-ed-approach-agitation/
3. A 5-step approach to the agitated patient Anton Helman. ACEP Now. November 16, 2018. https://www.acepnow.com/article/a-5-step-approach-to-the-agitated-patient/
4. Excited Delirium: The ED Minefield. Gabrielle Bunney. emDocs.net, Jun 21, 2021. http://www.emdocs.net/excited-delirium-the-ed-minefield/

The post Medical Malpractice Insights: Excited Delirium appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Scott Fitter, PharmD, BCCCP (Clinical Pharmacy Specialist-ED, Loma Linda University Medical Center, Assistant Professor, Loma Linda University School of Pharmacy); Kimberly Won, PharmD, BCCCP, (Assistant Professor- Department of Pharmacy Practice, Chapman University School of Pharmacy); Kayvan Moussavi, PharmD, BCCCP (Assistant Professor- Department of Pharmacy Practice, Marshall B. Ketchum University College of Pharmacy) // Reviewed by Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case:

You are working in a rural ED when a 55-year-old, 80 kg male is brought in with sudden onset chest pain. He is diaphoretic and clutching his chest. An EKG shows ST-segment elevations in leads II, III, and aVF.  You highly suspect STEMI and begin further workup.  Due to an ongoing snowstorm, the closest PCI center is a four-hour drive and three-hour helicopter flight. If this patient were found to have a STEMI, would he be a candidate for systemic thrombolysis?

Introduction:

Mechanism of Action

Thrombolytics (also called fibrinolytics) serve as plasminogen activators (convert plasminogen to plasmin), which break the crosslinks between fibrin molecules to destabilize the structural integrity of blood clots [1-3].  Thrombolytics can be categorized as fibrin non-selective (e.g. urokinase and streptokinase) or fibrin-selective (e.g. alteplase, tenecteplase, reteplase) [1]. Fibrin-non-selective agents degrade both fibrinogen and fibrin, which produces broad lytic action throughout the body [1].  This widespread fibrin degradation and fibrinogen generation (fibrinogenesis) may increase the risk of hemorrhage, thrombosis, and tissue edema [1].  Fibrin-selective agents (also referred to as tissue plasminogen activators [tPA]) convert plasminogen to plasmin more effectively in the presence of fibrin [1,4,5].  A thrombus is composed of fibrin monomers that are cross-linked via lysine side chains [1].  tPA binds to lysine, which helps localize effects to a thrombus, minimize activation of circulating plasminogen, and can decrease unwanted effects (e.g. hemorrhage) [1].  Once bound, tPA catalyzes plasminogen conversion to plasmin by cleaving an arginine-valine bond [1].  This leads to plasmin break down of a clot by degrading the fibrin matrix of the thrombus [1].

Available Agents

Currently or previously available thrombolytics in the United States include the first-generation agents urokinase (Kinlytic) and streptokinase, second generation tPA alteplase (Activase®), and third generation tPA agents tenecteplase (TNKase®) and reteplase (Retavase®) [1].  Although streptokinase (not available in United States) and urokinase may be less costly than newer agents, their lack of specificity and less favorable adverse effect profiles (i.e. higher risk of hemorrhage) limits their clinical utility [1-3].  Therefore, this article will primarily focus on newer agents (e.g. alteplase, tenecteplase, reteplase).

Indications

Current labeled indications for thrombolytics include [5-7]:

• Acute ischemic stroke
• Pulmonary embolism
• Acute myocardial infarction
• Catheter clearance

Off-label indications include [8-11]:

• Prevention of limb amputation due to frostbite
• Mechanical prosthetic valve thrombosis
• Clearance of pleural effusions
• Management of plastic bronchitis

Contraindications

Contraindications for the use of thrombolytics vary depending upon their indication [5-7].  In general, thrombolytics should be avoided in the following scenarios [5-7]:

• Active bleeding
• Recent intraspinal surgeries (within 2 months) or head trauma (within 3 months)
• Presence of intracranial conditions that could increase the risk of bleeding
• Known bleeding disorders
• Severe, uncontrolled hypertension (unresponsive to therapy)
• Suspected aortic dissection

The list of additional relative and absolute contraindications for use of thrombolytics is extensive and primarily relates to the diagnosed condition, severity of symptoms, symptom onset, conditions that increase the risk of bleeding (e.g. recent prior ischemic stroke, gastrointestinal (GI) malignancy or bleed, infective endocarditis, aortic arch dissection, resistant hypertension), coagulopathy, and concurrent anticoagulant or antiplatelet usage (Table 1) [5-7,12-14].

Table 1.

Complications and Their Treatments

Bleeding is the most notable complication associated with the use of thrombolytics [12,15]. Intracranial hemorrhage (ICH) is the most common and most concerning bleeding event, with reported incidence of 1-2% and 2-7% of patients receiving alteplase for acute myocardial infarction and acute ischemic stroke, respectively [15-18].  Bleeding can be internal or external and develop at any site (e.g. GI, genitourinary, arterial or venous puncture, etc.) [5,12].  Additionally, the effects of thrombolytics may persist for longer than expected based on the individual drug half-lives (Table 2) [1,15]. For example, the effects of alteplase on the coagulation system may last for more than 24 hours despite alteplase having a half-life of only 4-8 minutes [1,15].  If life-threatening hemorrhage (e.g. ICH) develops, general acute management recommendations (i.e. within 24 hours of thrombolytic administration) include [4,12,15]:

• Stop thrombolytic infusion
• Order relevant labs or imaging (e.g. CBC, PT/INR, fibrinogen, head CT)
• Administer cryoprecipitate (contains fibrinogen, factor VIII, fibronectin, factor XIII, and von Willebrand Factor) or antifibrinolytic (e.g. tranexamic acid, aminocaproic acid) if cryoprecipitate contraindicated or unavailable
• Order relevant consults (e.g. hematology, neurosurgery)
• Provide supportive care (e.g. blood pressure management, intracranial pressure management, temperature, glucose control)

Table 2: Summary of Thrombolytic Agents 

Hypersensitivity, including urticarial or anaphylactic reactions, can also occur after thrombolytic administration [5,12,19].  Angioedema has been observed 5 to 720 minutes after alteplase infusions for the treatment of acute ischemic stroke and acute myocardial infarction; however, median onset is typically 60 minutes [5,20,21].  tPAs like alteplase can increase bradykinin production because plasmin cleaves bradykinin from high-molecular-weight kininogen [22]. Bradykinin can lead to vasodilation, plasma extravasation, and mucosal edema, which characterize angioedema [22].  The incidence of orolingual angioedema secondary to alteplase use ranges from 1.3-5.1% [19,22,23]. Patients using angiotensin-converting enzyme (ACE) inhibitors prior to alteplase may be at higher risk of angioedema, possibly due to ACE inhibitors increasing bradykinin concentrations prior to treatment [19,22].  Severity may range from mild to life-threatening with mild orolingual angioedema typically limited to the anterior tongue and lips and more severe cases involving the larynx, palate, floor of mouth, or oropharynx [12].  Recommendations for management of orolingual angioedema include [12,19,24]:

• Discontinue thrombolytic and hold ACE inhibitors
• Maintain airway
  • Edema involving larynx, palate, floor of mouth, or oropharynx with rapid progression (within 30 minutes) poses higher risk of requiring intubation
• Administer methylprednisolone, diphenhydramine, and famotidine
• Administer epinephrine if further increases in angioedema
  • Because epinephrine may worsen coronary ischemia due to inotropic and chronotropic effects, consider using routes with less systemic absorption (e.g. nebulization) or less likely to result in inadvertent overdose (e.g. subcutaneous or intramuscular) [12,25]
• Agents used for hereditary or ACE inhibitor-related angioedema (e.g. icatibant, C1 esterase inhibitor) can also be considered
• Supportive care

Thrombolytic Use in STEMI:

Scenarios for Use

Though primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy for acute ST-elevation myocardial infarction (STEMI), thrombolytic therapy is recommended by the American Heart Association (AHA), American College of Cardiac Foundation (ACCF), American College of Emergency Physicians (ACEP), Society for Cardiovascular Angiography and Interventions, and the European Society of Cardiology (ESC) when a patient, without contraindications to thrombolytic therapy, presents within 12 hours of ischemia symptom onset to an institution without PCI capability, or if the anticipated time that PCI can be performed at a PCI-capable institution is greater than 120 minutes from the first medical contact [13,14,26].  When thrombolytic therapy is administered within 6 hours of symptom onset, it can decrease the incidence of major adverse cardiac events (MACE) and prevent approximately 30 early deaths per 1000 patients [13,14,26,27].  Additionally, the AHA/ACCF and ESC guidelines state that thrombolytic therapy may also be considered for patients who present with ongoing ischemia within 12-24 hours of symptom onset and are hemodynamically unstable or have a large area of myocardium at risk [13,14]. Thrombolytic therapy should NOT be administered to patients with ST depression, except when a true posterior (inferobasal) MI is suspected or when associated with ST elevation in lead aVR [13,27].  Contraindications to use in STEMI are similar to those for other indications (Table 1).

Patients who receive thrombolytic therapy should be immediately transferred to a PCI-capable institution and assessment of reperfusion should be conducted at 60 to 90 minutes post-thrombolytic therapy [13,14].  Lack of resolution of ST elevations is associated with a worse prognosis, and immediate coronary angiography and rescue PCI should be considered in those patients [13,14].

Clinical Pearls and Pitfalls:

Timing and Benefits of Thrombolytic Therapy

If the decision is made for thrombolytic therapy, the thrombolytic agent should be administered as soon as possible, ideally within 30 minutes of first medical contact, since the mortality benefit of fibrinolysis decreases as the time from symptom onset to thrombolytic administration increases [27-31].  The 2017 ESC guideline suggests a goal of 10 minutes from STEMI diagnosis to thrombolytic administration based on findings from the STREAM trial [14,32].  Delays in thrombolytic therapy have been associated with impaired myocardial perfusion grades and poorer epicardial flow grades [28,33].  The greatest benefit of thrombolytic therapy is seen in high-risk patients when the thrombolytic agent is given within 2 hours of symptom onset demonstrated significant reductions in mortality [31,34].

To shorten the symptom onset to thrombolytic administration, some areas allow thrombolytic therapy to be administered in the pre-hospital setting after a STEMI is determined by a 12-lead electrocardiogram [13,14].  Though prehospital thrombolytic therapy is not common in the United States due to lack of resources and specialty-trained emergency medical responders, there are some regions in other countries, including the United Kingdom and Europe, where prehospital thrombolytics are administered due to increase transit times to a PCI-capable facility [13,14,34-40].

Several studies have demonstrated the safety and benefits of administering prehospital thrombolytic therapy for STEMI, including an approximately 60-minute reduction in administering thrombolytic therapy from symptom onset and a 17% risk reduction in all-cause hospital mortality [32,34,35,38,41-47].  In the CAPTIM trial, there was no significant difference in the composite outcome (death, nonfatal reinfarction, and nonfatal disabling stroke within 30 days) or mortality between patients who received PCI or prehospital fibrinolytics [43].  However, a subgroup analysis of the CAPTIM study showed a significantly lower 5-year mortality rate for patients who received thrombolytics within 2 hours of symptom onset compared to primary PCI, but there was no difference in those who received thrombolytics after 2 hours [45].  In contrast, the ASSENT-4 trial, which compared primary PCI versus facilitated PCI (patients received tenecteplase prior to PCI) was stopped early due to it showing a higher in-hospital mortality and higher stroke rate in patients randomized to the facilitated PCI group [48].  Additionally, the STREAM trial, a multicenter, open-label, randomized, parallel-group trial comparing thrombolytic therapy followed by timely coronary angiography to primary PCI reported no difference in the primary end point of 30-day composite death from any cause, shock, congestive heart failure, or reinfarction between the two groups (12.4% vs. 14.3%, p=0.21) [32].  Though the overall rate of intracranial hemorrhage was significantly greater in the fibrinolysis group (1% vs 0.2%, p=0.04), after amending the protocol for a lower dose of tenecteplase in patients 75 years old and greater, the difference between the groups was not statistically significant (0.5% vs. 0.3%, p=0.45) [32].  More recently, the EARLY-MYO trial, a multicenter, randomized noninferiority trial in China comparing early catheterization after half-dose alteplase compared to primary PCI, found that half-dose alteplase plus rescue PCI was noninferior (and even superior) to primary PCI for the primary endpoint of complete epicardial and myocardial reperfusion after PCI (thrombolysis in myocardial infarction [TIMI] flow grade 3) and ST-segment resolution 70% [49].

Adjunctive Agents Given with Thrombolytic Therapy

The 2013 AHA/ACCF and 2017 ESC guidelines recommend that dual antiplatelet therapy with aspirin (162-325 mg loading dose) and clopidogrel (300 mg loading dose in patients <75 years old or 75 mg in patients ≥75 years old) should be administered before or with thrombolytic therapy [13,14].  Aspirin 81 mg daily should be continued indefinitely, and clopidogrel 75 mg daily should be continued for at least 14 days, or one year if patient undergoes rescue PCI after receiving thrombolytic therapy [13].  If patients undergo subsequent PCI after thrombolytic therapy, patients can be switched from clopidogrel to another P2Y₁₂ inhibitor (e.g. ticagrelor, prasugrel) 48 hours after thrombolytic therapy [13]. The TREAT trial, an international, multicenter, randomized, open-label trial that randomized STEMI patients less than 75 years old to receive either ticagrelor or clopidogrel after undergoing thrombolytic therapy, found no difference between groups for the combined outcome of cardiovascular mortality, myocardial infarction or stroke, as well as major, fatal and intracranial bleeding [50].  However, patients who received ticagrelor had a significantly higher rate of any bleeding (10.2% vs. 6.2%; p<0.01), bleeding that required medical attention (3.8% vs. 2.1%; p<0.01), and minimal bleeding based on the TIMI, PLATO, and Bleeding Academic Research Consortium classifications (p<0.01) [50].  These findings further support current recommendations for use of clopidogrel over other P2Y₁₂ inhibitors in patients receiving thrombolytic therapy for acute myocardial infarction [13,14].  Notably, patients older than 75 years were excluded from major trials that established the safety of antiplatelet dosing during thrombolysis [50,51].  In these older patients, providers may wish to skip the loading dose and start with a maintenance dose instead (i.e. administer clopidogrel 75 mg instead of 300 mg) [50,51].

Anticoagulation therapy is also recommended to help improve vessel patency and prevent re-occlusion [13,14]. Anticoagulation with enoxaparin (< 75 years old: 30 mg IV bolus, followed in 15 minutes by 1 mg/kg subcutaneouslyevery 12 hours [maximum of 100 mg for the first 2 doses]; in 75 years old: no IV bolus, 0.75 mg/kg subcutaneously every 12 hours [maximum 75 mg for the first two doses]) or unfractionated heparin (UFH) (60 units/kg loading dose [maximum 4000 units] IV, followed by 12 units/kg/hour IV [maximum initial infusion rate 1000 units/h] adjusted to maintain aPTT 1.5-2 times control) should be given for at least 48 hours or until revascularization, or for the duration of the patient’s hospital stay up to 8 days [13,14]. For anticoagulation therapy extending beyond 48 hours, the ACC/ACCF guidelines recommend enoxaparin due to low molecular weight heparins demonstrating better outcomes compared to UFH [13,52-56].  In the ASSENT-3 trial, patients who received full-dose tenecteplase with weight-adjusted UFH for 48 hours had a significantly higher rate of in-hospital infarction, in-hospital refractory ischemia and non-intracranial hemorrhage bleeding compared those who received full-dose tenecteplase and enoxaparin for 7 days or half-dose tenecteplase with weight-adjusted low-dose UFH plus a 12-hour infusion of abciximab [55].  Compared to UFH, low-molecular weight heparins are less protein-bound and have less platelet activation, thus, making their effects more predictable and potentially more favorable to use in combination with thrombolytic agents [55].  Patients who have a history of heparin-induced thrombocytopenia (HIT) can receive bivalrudin; however, bivalrudin has not been studied with thrombolytic agents [13,14].  Fondaparinux should not be used as the sole anticoagulant for patients referred for PCI and is contraindicated for patients with a creatinine clearance <30 mL/min [13,14].  If patients qualify for fondaparinux use, 2.5 mg IV followed by 2.5 mg subcutaneously daily starting the following day is recommended [13].

Glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors have been investigated with reteplase, alteplase, and tenecteplase [55,57-62].  Overall, GP IIb/IIIa inhibitors significantly reduce the risk for recurrent infarction, but significantly increase the risk of bleeding and are not recommended for routine adjunct therapy with thrombolytic agents with or without anticoagulants [13,14,29].

Thrombolytic Agents of Choice for STEMI

Streptokinase, tenecteplase, alteplase, and reteplase are all approved for reperfusion therapy in STEMI (streptokinase only available outside the United States) [5-7,63].  The AHA/ACCF and ESC guidelines recommend fibrin-specific agents (e.g. alteplase, reteplase, tenecteplase) over the non-fibrin-specific agents (e.g. streptokinase) due to their associated increased risk of all-cause mortality [13,14,28,29,64].  Details of fibrin-specific agents used for STEMI are summarized in Table 2.  In general, fibrin-specific agents have prolonged half-lives compared to streptokinase and are less likely to cause allergic reactions [65].  A large systematic review and network meta-analysis of randomized controlled trials concluded that there was no significant difference in mortality risk between tenecteplase, reteplase or accelerated infusion alteplase plus parenteral anticoagulants; however, streptokinase and non-accelerated infusion alteplase were associated with an increased risk of all-cause mortality [29].

Streptokinase is the proto-typical tissue plasminogen activator (tPA) that was discovered in 1933 [66].  The GISSI and ISIS trials were among the first landmark studies to demonstrate its mortality benefit compared to placebo in AMI [67,68].  Though streptokinase demonstrated a significant decrease in mortality when compared to placebo, it was found to be associated with an increase in all-cause mortality in comparison to other fibrin-specific agents [28,29].  Furthermore, streptokinase is antigenic (i.e. high risk for allergic reaction) and should not be given to a patient who has received streptokinase (or anistreplase) within the prior 6 months due to increased risk of a serious allergic reaction [13,63].  Thus, streptokinase is less preferred for thrombolytic therapy in acute MI if other fibrin-specific agents are available.

Alteplase is a recombinant human tPA that is widely available in the United States [5].  It is fibrin-specific and has FDA-approved indications for STEMI, pulmonary embolism, and acute ischemic stroke [5].  Although alteplase has two FDA-approved dosing strategies for STEMI (90-minute infusion vs 3-hour infusion), the 90-minute infusion (also known “accelerated infusion alteplase”) is more commonly used and recommended by the AHA/ACCF and ESC guidelines due to increased all-cause mortality seen with the 3-hour alteplase infusion (also referred to as “non-accelerated infusion alteplase”) [13,14].  Furthermore, the RAPID I trial demonstrated significantly more rapid, complete and sustained thrombolysis of the infarcted coronary artery with reteplase compared to the non-accelerated infusion alteplase [69].  Accelerated infusion alteplase had a 14% reduction in mortality in comparison to streptokinase plus subcutaneous or intravenous heparin; however, accelerated infusion alteplase was associated with increased risk of bleeding, including a significantly higher report of hemorrhagic strokes [28,29].  The investigators of the Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT-2) trial found no difference in 30-day mortality between accelerated infusion alteplase and tenecteplase in almost 17,000 patients with an acute STEMI who presented within 6 hours of symptom onset [17].

Of the fibrin-specific agents available, reteplase is the only one that is not weight-based, which may allow for easier dosing.  Reteplase is administered as two 10-unit slow IV boluses over 2 minutes that are administered 30 minutes apart [7].  A one-year follow-up of the GUSTO III trial showed no significant differences in mortality between reteplase and accelerated infusion alteplase [70].  However, in the RAPID II trial, reteplase achieved a significantly greater patency (TIMI grade 2 or 3) or complete patency (TIMI grade 3) at 90 minutes compared to accelerated infusion alteplase (83.4% vs 73.3%, p=0.03; 59.9% vs 45.2%, p=0.01, respectively) [71].

Tenecteplase has the shortest administration time and is the most fibrin-specific of the three fibrin-specific agents [6,13,65]. It is administered as one IV bolus over 5 seconds and the selected dose is weight-dependent [6].  For patients 75 years or older, a reduced dose of tenecteplase should be considered [14,26].  In the ASSENT-2 trial, tenecteplase and alteplase had similar reductions in 30-day mortality and rates of intracranial hemorrhage; however, tenecteplase had fewer non-cerebral bleeding and less need for blood transfusions [17].  In comparison to other thrombolytic-based regimens, tenecteplase plus parenteral anticoagulants was associated with a lower risk of all-cause mortality within 30-35 days, as well as major bleeding [29].

Case Resolution:

Further work-up reveals the patient is having a STEMI.  Because the nearest PCI center is more than 2 hours away, you feel that fibrinolysis is indicated.  Screening reveals that the patient has no contraindications to thrombolytic therapy. Your hospital carries alteplase, so you order an accelerated regimen with a 15 mg IV bolus followed by 50 mg (0.75 mg/kg x 80 kg = 60 mg but maximum for this dose is 50 mg) over 30 minutes, followed by 35 mg (0.5 mg/kg x 80 kg = 40 mg but maximum for this dose is 35 mg) over 60 minutes.  You also order aspirin 162 mg orally followed by 81 mg daily, unfractionated heparin (UFH) 4000 units (60 units/kg x 80 kg = 4800 units but maximum for this dose is 4000 units) IV followed by 12 units/kg/hour IV adjusted to aPTT 50-70 seconds (1.5-2 times control at the hospital’s lab), and clopidogrel 300 mg orally followed by 75 mg daily.  You contact the nearest PCI center to arrange transport for diagnostic coronary angiography and subsequent monitoring.  Fortunately, the storm appears to be easing and the patient is tolerating fibrinolysis with stable vital signs.  An ambulance crew will be available to transfer the patient within the next hour.

Take Home Points:

• Thrombolytics (also called fibrinolytics) serve as tissue plasminogen activators (work by converting plasminogen to plasmin), which break the crosslinks between fibrin molecules to destabilize the structural integrity of blood clots.
• Thrombolytics can be useful when treating life-threatening clotting disorders (e.g. acute ischemic stroke, pulmonary embolism, STEMI).
• In general, thrombolytics should be avoided in patients with active hemorrhage or at high risk of hemorrhage in a critical location (e.g. recent spinal or intracranial surgery or trauma).
• Bleeding (internal and external) and hypersensitivity reactions (e.g. angioedema) can occur after thrombolytic administration.
• Non-selective thrombolytics (e.g. urokinase, streptokinase) tend to cause more adverse effects compared to fibrin-selective thrombolytics (e.g. alteplase, tenecteplase, reteplase).
• Thrombolytic therapy for STEMI is recommended if the anticipated time to PCI is greater than 120 minutes from the first medical contact, the patient presents within 12 hours of ischemic symptom onset, and does not have any contraindications to thrombolytic therapy.
• Fibrin-selective thrombolytic agents (e.g. tenecteplase, reteplase, alteplase) are preferred over non-selective agents (e.g. urokinase, streptokinase) for STEMI.
• Patients treated with thrombolytics for STEMI should receive concurrent antiplatelet agents (e.g. aspirin with clopidogrel) and anticoagulants (e.g. enoxaparin, UFH).
• Due to increased risk of bleeding, GP IIb/IIIa inhibitors should not be used with thrombolytics when treating STEMI.

Relevant emDOCs Posts:

http://www.emdocs.net/life-threatening-complications-with-tpa-what-emergency-physicians-should-know/

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48. ASSENT-4 PCI Investigators. Primary versus tenecteplase-facilitated percutaneous coronary intervention in patients with ST-segment elevation acute myocardial infarction (ASSENT-4 PCI): randomised trial. Lancet 2006;367(9510):569-78 doi: 10.1016/s0140-6736(06)68147-6.
49. Pu J, Ding S, Ge H, et al. Efficacy and Safety of a Pharmaco-Invasive Strategy With Half-Dose Alteplase Versus Primary Angioplasty in ST-Segment-Elevation Myocardial Infarction: EARLY-MYO Trial (Early Routine Catheterization After Alteplase Fibrinolysis Versus Primary PCI in Acute ST-Segment-Elevation Myocardial Infarction). Circulation 2017;136(16):1462-73 doi: 10.1161/CIRCULATIONAHA.117.030582.
50. Berwanger O, Lopes RD, Moia DDF, et al. Ticagrelor Versus Clopidogrel in Patients With STEMI Treated With Fibrinolysis: TREAT Trial. J Am Coll Cardiol 2019;73(22):2819-28 doi: 10.1016/j.jacc.2019.03.011.
51. Sabatine MS, Cannon CP, Gibson CM, et al. Addition of clopidogrel to asprin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med 2005;352(12):1179-89.
52. Ross AM, Molhoek P, LUndergan C. A randomized comparison of low-molecular-weight heparin enoxaparin and unfractionated heparin adjunctive to t-PA thrombolysis and aspirin (HART II). Circulation 2001;104:648-52.
53. Baird SH, McBride SJ, Trouton TG, Wilson C. LMWH versus unfractionated heparin following thrombolysis in myocardial infarction. J Am Coll Cardiol 1998;31 (suppl A)(191A).
54. Wallentin L, Dellborg DM, LIndahl B. The low-molecular-10 weight heparin dalteparin as adjuvant therapy in acute myocardial infarction: the ASSENT Plus study. Clin Cardiol 2001;24 (suppl 3):I12-14.
55. ASSENT-3 Investigators. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: the ASSENT-3 randomised trial in acute myocardial infarction. Lancet 2001;358(9282):605-13 doi: 10.1016/s0140-6736(01)05775-0.
56. Antman EM, Morrow DA, McCabe CH, et al. Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction. N Engl J Med 2006;354:1477-88.
57. Topol EJ, GUSTO V Investigators. Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy or combination reduced fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition: the GUSTO V randomised trial. Lancet 2001;357(9272):1905-14.
58. Herrmann HC, Moliterno DJ, Ohman EM, Stebbins AL, Bode C, Betriu A. Facilitation of early percutaneous coronary intervention after reteplase with or without abciximab in acute myocardial infarction: results from the SPEED (GUSTO-4 Pilot) Trial. J Am Coll Cardiol 2000;36(5):1489-96.
59. Antman EM, Gibson CM, De Lemos JA, Giugliano RP, McCabe CH, Coussement P. Combination reperfusion therapy with abciximab and reduced dose reteplase: results from TIMI 14. The Thrombolysis in Myocardial Infarction (TIMI) 14 Investigators. Eur Heart J 2000;21(23):1944-53.
60. Brener SJ, Zeymer U, Adgey AAJ, Vrobel TR, Ellis SG. Eptifibatide and low-dose tissue plasminogen activator in acute myocardial infarction: the integrilin and low-dose thrombolysis in acute myocardial infarction (INTRO AMI) trial. J Am Coll Cardiol 2002;39(3):377-86.
61. Gibson CM, Jennings LK, Murphy SA, Lorenz DP. Association between platelet receptor occupancy after eptifibatide (integrilin) therapy and patency, myocardial perfusion, and ST-segment resolution among patients with ST-segment-elevation myocardial infarction: an INTEGRITI (Integrilin and Tenecteplase in Acute Myocardial Infarction) substudy. Circulation 2004;110(6):679-84.
62. Antman EM, Louwerenburg HW, Baars HF, Wesdorp JCL, Hamer B. Enoxaparin as adjunctive antithrombin therapy for ST-elevation myocardial infarction: results of the ENTIRE-Thrombolysis in Myocardial Infarction (TIMI) 23 Trial. Circulation 2002;105(14):1642-9
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64. GUSTO III Investigators. A comparison of reteplase with alteplase for acute myocardial infarction. N Engl J Med 1997;337:1118-23.
65. Llevadot J, Giugliano RP, Antman EM. Bolus fibrinolytic therapy in acute myocardial infarction. JAMA 2001;286:442-49.
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70. Topol EJ, Ohman EM, Armstrong PW, Wilcox R, Skene AM, Aylward P. Survival outcomes 1 year after reperfusion therapy with either alteplase or reteplase for acute myocardial infarction: results from the global utilization of streptokinase and t-PA for occluded coronary arteries (GUSTO) III trial. Circulation 2000;102:1761-65.
71. Bode C, Smalling RW, Berg G, et al. Randomized Comparison of Coronary Thrombolysis Achieved With Double-Bolus Reteplase (Recombinant Plasminogen Activator) and Front-Loaded, Accelerated Alteplase (Recombinant Tissue Plasminogen Activator) in Patients With Acute Myocardial Infarction. Circulation 1996;94(5):891-98.
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The post Thrombolytic Use for STEMI: What ED Clinicians Should Know appeared first on emDOCs.net - Emergency Medicine Education.

Originally published at Pediatric EM Morsels on February 8, 2019. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Oh, once again, Homer is correct! Physics does matter. As does Anatomy and Physiology with respect to caring for children. We’ve previously discussed how these aspects have significance when evaluating ill and injured children (ex, Thoracic Trauma, Abdominal Trauma), but a recent post on the hazards of children sitting in the front seat of cars has brought to mind another condition that warrants specific consideration Pediatric Cervical Spine Injury. With adults it is relatively straight forward; apply your favorite validated screening tool and if your patient needs imaging, obtain a CT. With children, it isn’t as “simple.” Fortunately, my friend and colleague, Dr. Emily MacNeill has spent some time pondering this and can help us decipher the issue of Pediatric Cervical Spine Injury:

Cervical Spine Injury: Basics

• Fortunately, cervical spine trauma is rare in children! [Gopinathan, 2018; Leonard, 2014]
  • Accounts for only 1-10% of all spinal injuries.
  • Of pediatric spinal injuries, however, the cervical spine is involved in 60-80% of the time.

• The majority of c-spine injuries in children occur between the Skull and C4! [Gopinathan, 2018]
  • Many involve C1 and C2.
  • Atlanto-Axial injuries are more common in children than adults

• Age-related Mechanisms
  • Young infants and Toddlers (Can’t protect themselves)
    • Motor Vehicle Collisions
      • Most common
      • Often related to inappropriate restraint.
    • Falls
  • School age children and Adolescents (Put themselves in harm’s way)
    • Motor Vehicle Collisions
    • Sport-Related Injuries become very prevalent [Babcock, 2018]
      • Higher Risk Sports:
        • Diving
        • Football, Hockey
        • Gymnastics, Cheering
        • Trampoline!
        • Non-motorized vehicle crashes (ex, BMX)
      • Non-organized “Rough Play” around the house is also found to be a risk factor.
  • Non-accidental trauma is also, sadly, a well known mechanism.

Cervical Spine Injury: Anatomy Matters

• Young Child Anatomy & Injury Predisposing Characteristics: [Gopinathan, 2018; Baumann, 2015; Leonard, 2014]
  • Relatively larger head size to body
    • Leads to Higher fulcrum
    • Leads to Higher cervical spine level of injury
  • Elastic / Flexible spinal column
    • The spinal column can be distracted by 5cm without structural injury.
    • Unfortunately, the Spinal Cord cannot!
    • Leads to Spinal Cord Injury Without Radiographic Abnormality (SCIWORA) – so imaging the bones may not be good enough.
  • Poor Musculature – less protection
  • Open Ossification Centers
    • Can make interpretation of images more challenging (just like that elbow film)
      • The Atlas vertebrae has 3 ossification centers that don’t fuse until 7 years of age.
      • The Dens has 2 ossification centers that don’t unite until 5-7 years of age.
    • Can have growth plate injuries!
  • Horizontally oriented vertebral facet joints and Physiologic Wedging of the vertebral bodies – greater incidence of dislocation!

• As a child matures, the above factors alter changing of the Fulcrum position over time. [Gopinathan, 2018; Baumann, 2015]
  • Infant: ~C2-C3
  • 5 yo: ~C3-C4
  • 10 yo: ~C4-C5
  • Adult: ~C5-C6

• Pediatric patients are often characterized in studies as belonging to one of 3 groups with respect to cervical spine evaluation:
  • < 3 year olds
  • 3 – 8 year olds
  • 9 – 17 year olds

Cervical Spine Injury: Conundrum

• Evaluation of pediatric c-spine is challenging!!
  • Spinal cord injury is rare in children overall.
  • Young children cannot communicate effectively.
  • It is known that children with C-spine injury can, occasionally, be asymptomatic initially. [Gopinathan, 2018; Hale, 2015]
  • Mechanisms and Anatomy change with age.
  • C-Spine clearance “Rules” for Adults do NOT fit all children well. [Gopinathan, 2018; Slaar, 2017; Baumann, 2015]
    • NEXUS – only 1.3% of spine injuries in study were in kids 8 years or younger, but does perform well in 9-17 year olds!
    • Canadian C-Spine Rule – included NO patients <16 years
    • Both have been studied retrospectively and can perform reasonably well for older children.
  • PECARN C-spine Injury Risk Factors have not yet been validated.
    • 8 Risk Factors (when ALL absent, 98% sensitive). [Leonard, 2011]
      • Altered Mental Status
      • Focal Neurologic Findings
      • Substantial Torso Injury
      • Neck Pain
        
      • Torticollis
      • Conditions Predisposing to Cervical Injury
      • Diving
      • High-Risk Motor Vehicle Crash
  • Plain Films are decently sensitive for young children. [Cui, 2016; Nigrovic, 2012]
  • CT imaging images the bones better, but injury in children is often not bony so they add unnecessary radiation to the equation.
  • SCIWORA exists!
  • MRI is costly and often requires sedation.

• Simply put… we are not going to be 100% sensitive… but let’s not be defeatist.
  • Consider High Risk Mechanisms: [Gopinathan, 2018; Baumann, 2015]
    • High Risk Motor Vehicle Collision (fatality, rollover, speed >55mph, ejection, head-on collision)
    • Diving (or axial load) injury
    • Fall > 10 feet
    • Non-Accidental Trauma
  • Consider Patient Specific Risk Factors (ex, Down’s Syndrome and other Musculoskeletal disorders) [Gopinathan, 2018]

Cervical Spine Injury: Proposed Evaluation

• Children < 3 years of age
  • Obtunded? – Obtain CT +/- MRI
  • Alert?
    • If Normal Exam and Low Mechanism
      • Do a thorough exam!
      • Discuss low risk with family.
      • Consider clearing clinically or with plain films [Cui, 2016; Nigrovic, 2012]
    • If Neurologic abnormality – Obtain MRI
    • Obtain CT if: Torticollis, Substantial Torso Injury, High Risk Mechanism, Not Properly Restrained, Predisposing Patient Factors (ex, Down’s Syndrome), or obtaining head CT.

• Children 3 – 8 years of age
  • Obtunded? – Obtain CT +/- MRI
  • Alert?
    • Apply NEXUS (or PECARN).
      • If negative, remove collar.
      • If positive, Neuro symptoms (ex, hands “burning”) or findings? Then MRI!
      • If positive, but no Neuro symptoms / findings, consider Plain Films or LIMITED CT (from skull to C3). [Hannon, 2015; Nigrovic, 2012]

• Children 9 years and older
  • Obtunded? – Obtain CT +/- MRI
  • Alert?
    • Apply NEXUS or Canadian. [Slaar, 2017; Baumann, 2015]
    • If positive, Neuro symptoms (ex, hands “burning”) or findings? Then MRI!
    • If positive, but no Neuro symptoms / findings, consider Plain Films or CT.

Moral of the Morsel

• Anatomy Matters! The spinal column is more flexible than the spinal cord! Don’t overlook SCIWORA and those subtle neurologic symptoms.
• Physics Matters! That fulcrum is really high for the very young, and gradually moves caudally… consider limited CT (skull to C3) for 3-8 year olds who you want to CT.
• Plain films are still en vogue! You can use them to screen low risk patients.
• CTs are of less value in the very young!
• Have a plan! Since there is no validated strategy for clearing children’s c-spine, it is good to have an institutional plan!

References

The post Pediatric Cervical Spine Injury appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Philip Jarrett, MD, MBA (EM Resident Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Avi Ruderman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) // Reviewed by: Anthony DeVivo, DO (EM-Critical Care, Icahn School of Medicine at Mount Sinai Hospital); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case

You are working in the emergency department (ED) of a regional medical center without advanced surgical services. A 48-year-old male arrives by EMS transport with a severe unilateral headache that started one hour prior to arrival. He is vomiting and complaining of neck pain but is otherwise neurologically intact. A non-contrast head computed tomography (CT) demonstrates a diffuse hyperdensity within the sylvian fissure and intraventricular space consistent with subarachnoid hemorrhage (SAH). His blood pressure is 200/120 mm Hg. How would you manage his blood pressure? What preparations would you take prior to transfer?

During your resuscitation, the patient loses consciousness and becomes unresponsive to sternal rub. How does this information affect your transfer preparations? What is your airway approach?

Family arrives and reports that the patient slipped and hit his head on the edge of a kitchen counter around the time of headache onset, but they aren’t entirely sure if the fall was before or after the headache started. The CT read also notes a contusion to the R parietal scalp without clear evidence of skull fracture. How does this information change your management?

Background

SAH is one of the most dangerous conditions we evaluate as emergency physicians, with all-cause mortality rates reported as high as 42% at 30 days.¹ SAH can result from three broad categories of disease, including traumatic vascular catastrophe, non-traumatic aneurysmal rupture and non-traumatic non-aneurysmal hemorrhage (arteriovenous malformations, arterial dissections, central nervous system tumors and others).^2-4 While the majority of SAH cases stem from head trauma, 80% of non-traumatic SAH results from aneurysmal rupture.^5,6 This subset of SAH is referred to in the literature as aneurysmal SAH (aSAH).

Diagnosis

This article will provide a brief summary of the current diagnostic approach for SAH in the ED and will focus most heavily on the ED management and disposition. The standard ED algorithm for the evaluation of SAH begins with a non-contrast head CT, which is most sensitive (98-100%) for patients who present within 6 hours of symptom onset.^7,8 Because the sensitivity of this imaging declines for patients with delayed presentation (>6 hours), a negative CT in the population of delayed presenters is classically followed by lumbar puncture (LP) to assess for xanthochromia.^9,10 Due to the inherent limitations and adverse effects of LP (coagulopathy, patient positioning, time requirement, post-LP headache, etc.), more recent literature has explored CT angiography (CTA) of the brain as an alternative.^11,12

One study found that CT followed by LP was more cost effective than CT followed by CTA or CT followed by observation.¹³ The ACEP clinical policy for acute, non-traumatic headaches lists a level C recommendation for using either a lumbar puncture or a CTA to rule out SAH after a negative CT brain, endorsing the use of shared decision making to address the pros and cons of each modality.¹⁴ However, the AHA/ASA guidelines for the management of aSAH still endorse the use of LP following a negative CT (Class I, Level of Evidence B).¹⁵ CTA can be used to evaluated

The ACEP clinical policy also includes a Level B recommendation for the use of the Ottawa Subarachnoid Hemorrhage Rule for ruling out SAH without a CT scan.¹⁴

Management

Unfortunately, there is no clear benefit for any medical intervention with regards to patient-centered outcomes (as opposed to surgical interventions) based on current data. Most of the following management strategies are based on expert consensus and physiologic theory.

As with most emergent ED presentations, management begins with an assessment of airway safety and the potential need for endotracheal intubation. When possible, an effort should be made to utilize short-acting sedation and paralytics to retain the neurological exam for consultants. However, institutional norms and provider experience should be considered to ensure that the safest and most efficient approach is utilized, thereby minimizing secondary brain injury from apneic time and hypoxia. When hospital transfer is necessary to obtain neurosurgical consultation, the decision to intubate should be tailored to the patient’s current condition, the capabilities of the transfer team and the transfer route/duration. This decision may be made in conjunction with the receiving center.

Hemodynamics should also be monitored closely in the ED, not only in the context of traumatic SAH for which additional bodily injuries may be identified but also for the potential development of the Cushing triad (hypertension, bradycardia and irregular respirations) indicative of rapidly rising intracranial pressure (ICP) with imminent brainstem compression.¹⁶ Importantly, patients with hypertension and bradycardia, regardless of respiratory status, have a two-fold risk of death from intracranial hemorrhage compared to patients who present with stable vital signs.¹⁶ The definitive treatment for subarachnoid hemorrhage ultimately requires neurosurgical consultation and this should be prioritized as a core component of early management.

When any intracranial hemorrhage (ICH) is suspected, reversal of coagulopathy, in combination with blood pressure (BP) management discussed below, has been shown to provide significant mortality benefit. In a large retrospective cohort study of patients with anticoagulation-associated intracranial hemorrhage, rapid reversal of warfarin anticoagulation to a goal INR < 1.3 within 4 hours of presentation combined with reduction of systolic BP to less than 160 mm Hg resulted in an absolute mortality risk reduction of 7.2%.¹⁷  To this end, any coagulopathy, whether acquired or innate, should be reversed. Specific reversal strategies have been detailed for each class of anticoagulant and coagulopathy in the context of intracranial hemorrhage by multiple sources and is amalgamated by an UpToDate article on the topic.⁶ To review, anticoagulant medications should be held. Warfarin should be reversed with functional coagulation factors via 4-factor prothrombin complex concentrate (PCC) or fresh frozen plasma (FFP), dependent upon institutional availability. Due to the short half-life of these products, vitamin K should also be administered to promote endogenous production of functional coagulation factors. Unfractionated heparin and low molecular weight heparin should be reversed with protamine sulfate. The preferred reversal agent for factor Xa inhibitors and fondaparinux is PCC or andexanet alfa. Lastly, reversal of dabigatran requires the targeted monoclonal antibody idarucizumab or PCC. Regarding antifibrinolytic therapy, at least two large multicenter studies do not support the use of antifibrinolytic agents such as tranexamic acid (TXA) or aminocaproic acid for this purpose.^18,19  While the CRASH-3 trial suggested mild mortality benefit among patients with mild to moderate traumatic brain injury with evidence of ICH on initial CT who received TXA within 3 hours of injury, there were several issues with study design.²⁰  Though the trial also demonstrated pharmacologic safety of TXA, recommendations for the standardized use of TXA within a SAH subgroup are not yet available, and at the time of publication of this article, TXA for SAH is not recommended.

The goal of BP management remains a point of contention in the literature. Numerous studies demonstrate the benefit of aggressive BP reduction for prevention of hematoma expansion and rebleed.^21,22 However, such an approach significantly increases the risk of subsequent cerebral ischemia associated with cerebral vasospasm.^21,22 As a result, there has not yet been convincing evidence to support mortality benefit with specific BP goals. Nonetheless, current recommendations by the Neurocritical Care Society endorse BP reduction to a goal systolic less than 160 mm Hg.²² This is commonly achieved at our center with titratable agents, such as labetalol, nicardipine, or clevidipine.

SAH can result in increased intracranial pressure (ICP) through two mechanisms: hemorrhage into the intracranial cavity and hydrocephalus through obstruction of the ventricular system. As ICP rises, the patient’s cerebral perfusion pressure can become compromised, leading to loss of consciousness.  Unfortunately, most emergency physicians currently lack the capacity to obtain objective, quantitative measurements of ICP in this cohort. Although ultrasound measurement of optic nerve sheath diameter (US-ONSD) is developing traction as a proxy for ICP measurement, the utility of US-ONSD specifically for SAH has been challenged in the literature. Although additional studies are needed, multiple small human studies have shown that US-ONSD is an inconsistent predictor of ICP in patients with SAH and may, in some circumstances, relate inversely to ICP.^23-25 Lumbar puncture opening pressure (LPOP) also has not been extensively evaluated as a method of ICP measurement, but limited data suggests that it is an unreliable modality for ICP measurement.^26,27

Nonetheless, there are several strategies for modulating the intracranial pressure to improve CPP, mostly aimed at reducing ICP. The first is hyperosmolar therapy. Hypertonic saline (HTS) and mannitol pull fluid from the brain parenchyma into blood vessels by increasing the intravascular oncotic pressure.²⁸ However, recent evidence suggests that HTS has a more sustained effect on ICP and a more dramatic improvement of CPP when compared to mannitol.^28-30 A significant complication of aSAH during the following two weeks after injury is cerebral vasospasm and delayed cerebral ischemia. It is believed that avoidance of hypovolemia may be protective. For this reason, we further recommend HTS over mannitol.^29,30 No clear guidelines are available for the dosing strategy but one approach is to give 3.2 mL/kg of 5% hypertonic saline over 10-15 minutes. Concentrations higher than 5% need to be infused via central line. Sodium bicarbonate is an alternative to hypertonic saline with a sodium concentration of 8.4%.³¹  To convert to a different concentration, multiply the sodium dose in mL by 5, then divide by the new concentration [for example, 320 mL of 5% saline would be 533 mL of 3% saline (320 * 5 / 3), or 190 mL of sodium bicarbonate (320 * 5 / 8.4)]. Additional doses can be administered every four hours so long as the serum sodium remains less than 155 mEq/L.

In addition to maintaining euvolemia, oral nimodipine at a dose of 60 mg PO every 4 hours should be administered to prevent vasospasm and delayed cerebral ischemia.¹⁵ Nimodipine should be held in the setting of hypotension or when there is concern for inadequate CPP (such as with altered mental status in the absence of an intracranial pressure monitor), given the lack of evidence nimodipine’s CPP effects. Furthermore, patients who develop decreasing levels of consciousness may be experiencing reduced CPP or cerebral vasospasm.^15,32 In this scenario, antihypertensive medications should be held. Interestingly, this population has shown mortality benefit with vasopressor support using norepinephrine or phenylephrine that bolsters CPP, though this decision is best made in collaboration with consultants.³²

Adjunctive strategies to decrease the ICP include elevating the head of the bed to 30-45 degrees.^33,34 Raising the head of the bed decreases hydrostatic pressure and is a reasonable adjunct. Hyperventilation can significantly decrease ICP in the acute setting but must be used judiciously given evidence that prolonged hypocarbia reduces CPP.¹⁵  Hyperventilation induces cerebral vasoconstriction which may be deleterious to the goal of preventing vasospasm and should be avoided unless herniation appears imminent.

The definitive treatment for aSAH is aneurysm coiling or clipping, given that 30% of patients with untreated aSAH will rebleed in the first month following initial hemorrhage.³⁵  Coiling is accomplished through endovascular means and boasts superior outcomes, while clipping is a surgical procedure available to patients that do not qualify for coiling.^{15, 35} Patients with SAH should be transferred to facilities capable of providing these therapies even if an aneurysm isn’t initially found, as repeat angiography will often be performed several days later. All patients should be admitted to a neurological intensive care unit for frequent neurological examination, close hemodynamic monitoring and titration of any infused agents.¹⁵

While several grading scales for aSAH have been published, they have limited utility in predicting clinical outcomes and do not change management in the ED.³⁶ The most important clinical predictors of poor outcome include patient age, volume of blood seen on CT scan and GCS score.^36,37 The formal scoring systems are largely designed to predict post-surgical complications. As a result, it is our opinion that there is little role for these grading scales in the ED and are not discussed here.

There are scenarios in which it is unclear whether the patient’s SAH represents an aneurysmal or post-traumatic etiology. While no specific blood pressure targets or hyperosmolar therapies have been recommended for traumatic SAH, it is our practice that all SAH be treated as aneurysmal until proven otherwise, so as not to deny benefit to the aSAH cohort.

Case Conclusion

When our case begins, the patient is hypertensive with an intact mental status. Titratable IV blood pressure agents such as labetalol, nicardipine or clevidipine should be started with a goal of lowering the systolic blood pressure to less than 160 mm Hg so long as the patient maintains consciousness. Additionally, 60 mg of nimodipine should be administered orally every 4 hours.

When the patient loses consciousness, we should be concerned that his cerebral perfusion pressure is compromised. At this point, we need to stop any antihypertensives and, if needed, use vasopressors to support his CPP. IV HTS can be administered while raising the head of the bed to 45 degrees. A repeat head CT should be obtained to evaluate for hydrocephalus and the patient will need either an external ventricular drain or a bolt to monitor his intracranial pressure.

So long as the story is unclear whether the patient had a traumatic injury prior to the headache, it is safest to treat the patient as if he presented with an aneurysmal SAH with the therapies described above.

Takeaway points

• Maintaining cerebral perfusion pressure is the priority in subarachnoid hemorrhage.
• In conscious patients, target a systolic blood pressure of 140 – 160 mm Hg and administer nimodipine.
• In unconscious patients, support CPP with vasopressors in consultation with neurosurgery.
• To treat elevated ICP, use hypertonic saline. The dose is 3.2 mL/kg of 5% hypertonic saline.

References

1. Ingall T, Asplund K, Mähönen M, Bonita R. A multinational comparison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study. Stroke. 2000 May;31(5):1054-61. doi: 10.1161/01.str.31.5.1054. PMID: 10797165.
2. Schwartz T, Solomon R. Perimesenphalic Nonaneurysmal Subarachnoid Hemorrhage: Review of the Literature. Neurosurgery. 1996;39(3):433-440. doi:10.1097/00006123-199609000-00001
3. Bikmaz K, Erdem E, Krisht A. Arteriovenous fistula originating from proximal part of the anterior cerebral artery. Clin Neurol Neurosurg. 2007 Sep;109(7):589-91. doi: 10.1016/j.clineuro.2007.04.002. Epub 2007 Jun 4. PMID: 17544573.
4. Rogers LR. Cerebrovascular complications in cancer patients. Oncology (Williston Park). 1994 Jun;8(6):23-30; discussion 31-2, 37. PMID: 8074980.
5. Edlow JA. Diagnosis of subarachnoid hemorrhage. Neurocrit Care. 2005;2(2):99-109. doi: 10.1385/NCC:2:2:099. PMID: 16159051.
6. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med. 2000 Jan 6;342(1):29-36. doi: 10.1056/NEJM200001063420106. PMID: 10620647.
7. Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ 2011;343:d4277.
8. Backes D, Rinkel GJ, Kemperman H, et al. Time-dependent test characteristics of head computed tomography in patients suspected of nontraumatic subarachnoid hemorrhage. Stroke 2012;43(8):2115–9.
9. Backes D, Rinkel GJ, Kemperman H, Linn FH, Vergouwen MD. Time-dependent test characteristics of head computed tomography in patients suspected of nontraumatic subarachnoid hemorrhage. Stroke. 2012 Aug;43(8):2115-9. doi: 10.1161/STROKEAHA.112.658880. Epub 2012 Jul 19. PMID: 22821609.
10. Edlow JA, Panagos PD, Godwin SA, Thomas TL, Decker WW; American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. 2008 Oct;52(4):407-36. doi: 10.1016/j.annemergmed.2008.07.001. PMID: 18809105.
11. Holdgate A, Cuthbert K. Perils and pitfalls of lumbar puncture in the emergency department. Emerg Med (Fremantle). 2001 Sep;13(3):351-8. doi: 10.1046/j.1035-6851.2001.00239.x. PMID: 11554868.
12. McCormack RF, Hutson A. Can computed tomography angiography of the brain replace lumbar puncture in the evaluation of acute-onset headache after a negative noncontrast cranial computed tomography scan? Emerg Med. 2010 Apr;17(4):444-51.
13. Malhotra A, Wu X, Kalra V, Schindler J, Forman H. Cost‐effectiveness Analysis of Follow‐up Strategies for Thunderclap Headache Patients With Negative Noncontrast CT. Acad Emerg Med. 2016;23(3):243–250. doi:10.1111/acem.12891.
14. Godwin S, Cherkas D, Panagos P, et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of Emergency Medicine. 2019;74(4):e41–e74. doi:10.1016/j.annemergmed.2019.07.009.
15. Connolly S, Rabinstein A, Carhuapoma R, et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage. Stroke. 2012;43(6):1711–1737. doi:10.1161/STR.0b013e3182587839.
16. Bhandarkar P, Munivenkatappa A, Roy N, et al. On-admission blood pressure and pulse rate in trauma patients and their correlation with mortality: Cushing’s phenomenon revisited. Int J Crit Illn Inj Sci. 2017 Jan-Mar;7(1):14-17. doi: 10.4103/2229-5151.201950. PMID: 28382254; PMCID: PMC5364763.
17. Kuramatsu JB, Gerner ST, Schellinger PD, et al. Anticoagulant reversal, blood pressure levels, and anticoagulant resumption in patients with anticoagulation-related intracerebral hemorrhage. JAMA. 2015 Feb 24;313(8):824-36. doi: 10.1001/jama.2015.0846. PMID: 25710659.
18. Baharoglu M, Germans M, Rinkel G, et al. Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. Cochrane Db Syst Rev. 2013;8(8):CD001245. doi:10.1002/14651858.CD001245.pub2.
19. Post R, Germans M, et al. Ultra-early tranexamic acid after subarachnoid haemorrhage (ULTRA): a randomized controlled trial. The Lancet. 2021:397(10269):112-118. doi:10.1016/S0140-6736(20)32518-6
20. CRASH-3 trial collaborators. Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial. Lancet. 2019 Nov 9;394(10210):1713-1723. doi: 10.1016/S0140-6736(19)32233-0. Epub 2019 Oct 14. Erratum in: Lancet. 2019 Nov 9;394(10210):1712. PMID: 31623894; PMCID: PMC6853170.
21. Wijdicks EF, Vermeulen M, Murray GD, et al. The effects of treating hypertension following aneurysmal subarachnoid hemorrhage. Clin Neurol Neurosurg. 1990;92(2):111-7. doi: 10.1016/0303-8467(90)90085-j. PMID: 2163791.
22. Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al; Neurocritical Care Society. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011 Sep;15(2):211-40. doi: 10.1007/s12028-011-9605-9. PMID: 21773873.
23. Zoerle T, Caccioppola A, D’Angelo E, et al. Optic Nerve Sheath Diameter is not Related to Intracranial Pressure in Subarachnoid Hemorrhage Patients. Neurocrit Care. 2020 Oct;33(2):491-498. doi: 10.1007/s12028-020-00970-y. PMID: 32314244.
24. Bäuerle J, Niesen WD, Egger K, et al. Enlarged Optic Nerve Sheath in Aneurysmal Subarachnoid Hemorrhage despite Normal Intracranial Pressure. J Neuroimaging. 2016 Mar-Apr;26(2):194-6. doi: 10.1111/jon.12287. Epub 2015 Aug 17. PMID: 26278326.
25. Caffery TS, Perret JN, Musso MW, Jones GN. Optic nerve sheath diameter and lumbar puncture opening pressure in nontrauma patients suspected of elevated intracranial pressure. Am J Emerg Med. 2014 Dec;32(12):1513-5. doi: 10.1016/j.ajem.2014.09.014. Epub 2014 Sep 18. PMID: 25284485.
26. Cartwright C, Igbaseimokumo U. Lumbar puncture opening pressure is not a reliable measure of intracranial pressure in children. J Child Neurol. 2015 Feb;30(2):170-3. doi: 10.1177/0883073814533006. Epub 2014 May 5. PMID: 24799366.
27. Bergsneider M, Yang I, Hu X, et a. Relationship between valve opening pressure, body position, and intracranial pressure in normal pressure hydrocephalus: paradigm for selection of programmable valve pressure setting. Neurosurgery. 2004 Oct;55(4):851-8; discussion 858-9. doi: 10.1227/01.neu.0000137631.42164.b8. PMID: 15458593.
28. Huang XC, Yang LL. [Comparison clinical efficacy of 3% hypertonic saline solution with 20% mannitol in treatment of intracranial hypertension in patients with aneurysmal subarachnoid hemorrhage]. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2015 Jul;44(4):389-95. Chinese. PMID: 26555416.
29. Shi J, Tan L, Ye J, Hu L. Hypertonic saline and mannitol in patients with traumatic brain injury: A systematic and meta-analysis. Medicine (Baltimore). 2020 Aug 28;99(35):e21655. doi: 10.1097/MD.0000000000021655. PMID: 32871879; PMCID: PMC7458171.
30. Cook A, Jones M, Hawryluk G, et al. Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients. Neurocritical Care. 2020;32(3):647–666. doi:10.1007/s12028-020-00959-7.
31. Bourdeaux CP, Brown JM. Randomized controlled trial comparing the effect of 8.4% sodium bicarbonate and 5% sodium chloride on raised intracranial pressure after traumatic brain injury. Neurocrit Care. 2011 Aug;15(1):42-5. doi: 10.1007/s12028-011-9512-0. PMID: 21298358.
32. Williams G, Maroufy V, Rasmy L, et al. Vasopressor treatment and mortality following nontraumatic subarachnoid hemorrhage: a nationwide electronic health record analysis. Neurosurg Focus. 2020 May 1;48(5):E4. doi: 10.3171/2020.2.FOCUS191002. PMID: 32357322.
33. Findlay JM. Current management of aneurysmal subarachnoid hemorrhage guidelines from the Canadian Neurosurgical Society. Can J Neurol Sci. 1997 May;24(2):161-70. PMID: 9164696.
34. Winkelman C. Effect of backrest position on intracranial and cerebral perfusion pressures in traumatically brain-injured adults. Am J Crit Care. 2000 Nov;9(6):373-80; quiz 381-2. PMID: 11072552.
35. Lindgren A, Vergouwen MD, van der Schaaf I, et al. Endovascular coiling versus neurosurgical clipping for people with aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev. 2018 Aug 15;8(8):CD003085. doi: 10.1002/14651858.CD003085.pub3. PMID: 30110521; PMCID: PMC6513627.
36. Hijdra A, van Gijn J, Nagelkerke NJ, et al. Prediction of delayed cerebral ischemia, rebleeding, and outcome after aneurysmal subarachnoid hemorrhage. Stroke. 1988 Oct;19(10):1250-6. doi: 10.1161/01.str.19.10.1250. PMID: 3176085.
37. Singer RJ, Ogilvy CS, Rordorf G. Subarachnoid hemorrhage grading scales. Biller J, ed. UpToDate. Waltham, MA: UpToDate Inc.

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Today on the emDOCs cast with Brit Long, MD (@long_brit), we cover two more oncologic emergencies, including tumor lysis syndrome and neutropenic fever.

Episode 43: Oncologic Emergencies Part 2

Hyperleukocytosis/Leukostasis

– Occurs with WBC greater than 50,000 (classically greater than 100,000).

– Leukostasis occurs in the setting of hyperleukocytosis with symptoms and is an emergency. It is seen with acute

– May occur with myeloid leukemia (20% of patients) or chronic myeloid leukemia with blast crisis most commonly, but it can occur with other malignances.

– Symptoms are due to white cells plugging microvasculature and/or tissue hypoxemia with cytokine damage, often resulting in respiratory (30% of patients) and neurologic (40%) symptoms.

– If untreated, mortality at one week reaches 40%.

– Pulmonary symptoms include dyspnea and hypoxia. Arterial pO₂ levels may be falsely decreased due to the elevated WBCs utilizing O₂.

– Neurologic signs/symptoms include vision changes, headache, dizziness, tinnitus, ataxia, confusion, and coma. Patients with hyperleukocytosis have increased risk of intracranial hemorrhage for at least one week after treatment.

– Close to 80% of patients will display fever, so provide antibiotics. Myocardial ischemia, limb ischemia, and renal disease may also be present.

– Labs: High WBC (often above 100,000), falsely elevated platelets, and hyperkalemia. DIC is present in 40%.

– Management involves lowering the WBC count by cytoreduction (induction chemotherapy or leukopheresis), so hematology/oncology must be emergently consulted. Adequate fluid resuscitation is vital to maintain perfusion to end organs. Only chemotherapy has been shown to reduce mortality, as opposed to leukopheresis.  Hydroxyurea (50-100 mg/kg/day) is also an option for asymptomatic hyperleukocytosis patients. DIC and tumor lysis syndrome are major risks during the treatment of leukostasis.

Neutropenic Fever

– Neutropenic fever is a commonly treated condition in the ED and an oncologic emergency. The cytotoxic medications used to treat malignancy have several effects on the body besides killing the cancer: the medications affect myelopoiesis (or production of blood/immune cells) and destroy the integrity of the gastrointestinal mucosa, allowing microbe translocation.

– The absolute neutrophil count (ANC) reaches its nadir of <500 at 12-14 days after chemotherapy.

– Fever is often the earliest, and sometimes only, manifestation of infection in these patients due to the muted inflammatory response. Many patients with cough and pneumonia will not show an infiltrate on chest Xray, which depends on the body’s neutrophil response to infection, while those with cellulitis may have more subtle erythema.

– Diagnosis per Infectious Diseases Society of America:

• A single oral temperature >38.3°COR a sustained temperature >38.0°C for 1 h, and
• an absolute neutrophil count (ANC) <500 cells/μLOR <1000 cells/μL with an expected decrease to <500 cells/μL. ANC is calculated by: (% neutrophils + % bands) × white blood cell (WBC) count (cells/μL).

– Notice this is an oral temperature, but if the patient has mucositis, then use tympanic membrane or axillary thermometry.  Classically rectal temperatures are avoided due to risk of local mucosal trauma and bleeding.

– 20-30% of fevers in neutropenic patients are due to infection. Bacteria are the most common infectious cause, and the species is usually part of the endogenous flora (up to 80). Gram-positive bacteria became most common (60% of cases), specifically S. epidermidis . Gram-negative infections are typically more serious.   Fungal pathogens are more common in high-risk patients with prolonged antibiotic use and increasing number of treatment cycles. Most viral pathogens affect those high-risk patients and are due to reactivation (70%), rather than primary infection.

– High-risk patients are those presenting with shock or are critically ill, ANC levels < 500, ANC levels that are low for > 7 days, or other organ dysfunction (liver/kidney).

– Several risk scores for stratification include the MASCC risk index and the CISNE score.

– MASCC: Use in neutropenic patients with fever at least 100.4°F (38ºC). Do not use in patients with acute leukemia undergoing induction chemotherapy or allogeneic hematopoietic stem cell transplant conditioning, per IDSA guidelines. Patients with scores > 21 have low risk for adverse events, but those with scores, < 21 are high risk.

– CISNE: For use in adult outpatients ≥18 years old with solid tumor, fever ≥38°C (100.4°F) over 1 hour, and neutropenia (500 cells/mm³or fewer, or 1,000 cells/mm³ with expected decrease to 500). It should not be used in patients who are obviously unwell, defined by the original study authors as any of the following: acute organ failure (renal, cardiac, and respiratory), decompensation of chronic organ insufficiency, septic shock and hypotension (systolic BP <90 mmHg), known severe infection, or other serious complications that would themselves require admission. Low risk is 0, intermediate is 1-2, and high risk is 3 or more.

– Management of these patients revolves around early recognition of neutropenic fever. CBC and blood cultures with lactate, urinalysis, renal function panel, liver function panel, chest x-ray, and ECG are also recommended.

– Guidelines quote 60 minutes as the timeframe within which patients should be given bug juice after recognition. If antibiotics are delayed, mortality rates can reach 70%.

– Empiric treatment within sixty minutes is aimed at treating the most likely and virulent pathogens. Broad-spectrum coverage includes gram-positive and negative bacteria. IDSA guidelines state those high-risk patients should start with cefepime 2g, meropenem 1g, or piperacillin-tazobactam 4.5g. Ceftazidime 2g monotherapy has increasing resistance among gram-negative bacteria and does not adequately cover gram-positive bacteria.  Vancomycin should only be added in the setting of the following: skin/soft tissue/central line infections, pneumonia, mucositis, or hemodynamic shock. If necrotizing mucositis, intraabdominal/pelvic infection, sinusitis, or perirectal cellulitis is present, then add anaerobic coverage.  Monotherapy against Pseudomonas, as opposed to dual coverage, has equivalent outcomes with less adverse events. If penicillin allergic, use ciprofloxacin plus clindamycin or aztreonam plus vancomycin.  An empiric antifungal agent should be added if fungal infection is suspected, after 4-7 days in high-risk patients with no change in temperature, and if reassessment/clinical studies have not demonstrated a cause of infection.

– For central lines, there is a great deal of controversy surrounding the removal of these lines if they are suspected as the source. There is a grade 1B recommendation for removal of the central line for S. aureus, P. aeruginosa, or Candida. A pocket infection or deep infection along the central line track or port is also cause for removal. Speak with the oncologist and admitting physician regarding line removal.

– Low risk patients based on clinical decision making and/or clinical scoring may be appropriate for discharge. This decision should be made with oncology, with rapid follow-up. Success rates in outpatient treatment are approach 80%, with 20% needing readmission. Those at risk for failing outpatient treatment includes age > 70 years, poor performance status at home, severe mucositis, and neutropenia less than 100.  Regimens include ciprofloxacin plus amoxicillin/clavulanic acid, with ciprofloxacin and clindamycin another option for penicillin-allergic patients.

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APPLY NOW: Essentials of Emergency Medicine Education Fellowship 2022

The Essentials of Emergency Medicine (EEM) conference is in May 2022, but opportunities start NOW. This conference is one of the largest live EM educational conferences in the world with over 2,000 attendees. The conference organizers are offering an amazing opportunity for EM residents anywhere in the U.S./Canada to serve as an EEM Fellow for the next EEM conference May 10-12, 2022.

EEM Education Fellowship

emDOCs and EEM have partnered to offer one mini-fellowship position to eligible residents anywhere in the U.S./Canada. Those selected to participate will receive:

• FREE conference registration
• FREE 4-night hotel stay at the Hilton Union Square, San Francisco, CA
• A travel stipend of US $500

As part of the EEM staff, fellows will get a rare opportunity to experience the behind-the-scenes work associated with developing and producing one of the world’s largest and best EM educational conferences. Fellow responsibilities will include online chat moderation, social media management, CME preparation, research projects, and more. A common theme voiced by previous EEM fellows has been the opportunity to interact directly and develop meaningful relationships with the renowned, fun, and master clinician-educators in the EEM faculty.

Quotes from prior EEM 2021 Fellows

“This conference broadened my worldview with regards to what a career in medical education can look like. Namely, it is not confined to traditional academia, program leadership, or research; it can be about creating excellent educational experiences and cultivating a community of people who are passionate about delivering the best clinical care possible.  This fellowship gives you the opportunity to work with a group of dynamic individuals who are excited about teaching and emergency medicine. I would do it again in a heartbeat.” –Kristen Ng, MD

“I absolutely loved my experience as an EEM fellow. The content itself is amazing, and I think distilling pearls in real time really helps solidify learning. Not only, being able to see the work put in by the conference organizers and behind the scenes coordination was an invaluable experience for medical education.” –Kelly Wong, MD

Contest: Clinical Post

Application Process

Submit a clinical post idea to the editors of emdocs.net at editors@emdocs.net on anything clinically relevant to EM providers. Once the topic is approved, the post should present a case, background, discussion, summary, and references. The clinical post should be 2000 words or less. Cover a new topic not yet discussed on emdocs.net   

Examples of prior clinical posts include: 

1. Electrical cardioversion in the ED: who crashes and how to improve
2. Lactated Ringers versus Normal Saline: Myths and Pearls in the ED

All applicants must be in good standing at an accredited Emergency Medicine program in the United States or Canada, and be available to attend all 3 conference days in San Francisco (May 10-12, 2022). Applicants should complete a brief online application and upload material through the online forms below. The application process is open now.

Judging Criteria

Your blog post (≤2000 words) submission will be judged on:

1. Relevance: How relevant is this submission to EM education and/or clinical practice?
2. Innovation: How creative and innovative is this submission?
3. Design: How well is the information presented?
4. Content: How well did this candidate present the material with respect to clarity, conciseness, accuracy, references?

Important Dates

Deadline for submission: January 15, 2022

Fellowship winner announced: January 31, 2022

Application Materials:

1. Your post-graduate year of training
2. Your EM residency program name, program director’s name and his/her email
3. Your email address
4. Your blog post (acceptable formats include Microsoft word, PDF, Google Docs)

Questions? Email us at editors@emDocs.net  

Go to the Application Submission Site

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#1: CAPITAL CHILL RCT – Extreme Hypothermia in OHCA

Spoon Feed
There was no benefit in 180-day mortality or neurological outcome in adults with out-of-hospital cardiac arrest (OHCA) when cooling to 31°C vs 34°C.

Why does this matter?
Therapeutic hypothermia is not better than normothermia, per the TTM trial. A range of temperatures, from 32-36°C, is acceptable according to the AHA and others. The authors note a pilot study and some animal studies that suggest the extreme hypothermia, 28-32°C may offer greater neuroprotection. Is this right?

How low can you go?
This was a single center RCT with 367 adults who were comatose after OHCA and were randomized to 31°C or 34°C. There was no difference in 180-day composite mortality and neurological outcome between the two temperatures; 48.4% at 31°C vs 45.4% at 34°C, RR 1.07 (95%CI, 0.86-1.33). No secondary outcomes were different, except ICU length of stay was longer in the 31°C group. There was no increase in adverse events in the cooler group. Take home: There is no benefit in going colder than 32°C.

Source
Effect of Moderate vs Mild Therapeutic Hypothermia on Mortality and Neurologic Outcomes in Comatose Survivors of Out-of-Hospital Cardiac Arrest: The CAPITAL CHILL Randomized Clinical Trial. JAMA. 2021 Oct 19;326(15):1494-1503. doi: 10.1001/jama.2021.15703.

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#2: Intradermal Sterile Water for Back Pain?

Spoon Feed
For acute non-specific low back pain (LBP), intradermal sterile water injection (ISWI) + IV NSAID reduced pain and improved patient satisfaction vs IV NSAID alone.

Why does this matter?
Nonspecific low back pain can be quite unsatisfying to treat in the ED. Is there a way that we can decrease the patient’s pain with more than a shot of ketorolac? The authors investigate a new, simple procedure to decrease pain and increase patient satisfaction by injecting sterile water in the region of maximal pain.

Are you sure they are using just water?!
This was a prospective RCT with 112 patients equally split into 2 groups; everyone received an IV NSAID, but the intervention group received the ISWI. As for the details of the procedure, they used a 26-gauge, 0.5 inch insulin syringe to inject 0.1cc sterile water in a square pattern (each side was 3cm) around the area of maximal pain. Each injection created a small skin wheal, similar to a TB skin test. See image below from the article for reference. At 10 min post-ISWI, the patient’s pain was significantly improved, and the pain relief persisted for 24 hours (still statistically significant). Interestingly, the authors note that this procedure has been shown effective for other painful conditions of the back, such as kidney stones and LBP from labor. Finally, the authors state that other studies have shown less reduction in pain if the procedure was performed with sterile saline!

As for ED patient satisfaction? The ISWI group was highly satisfied 88% of the time, compared to the control group, which was highly satisfied only 16% of the time.

After reading this article, I feel like I don’t actually understand anything about pain. Although I still have a hard time accepting the results of this well-done study, this is a potentially practice-changing paper for me. Since this is an essentially risk-free intervention (with the exception of brief pain) with potential significant benefit, I will offer the ISWI procedure to nearly all my ED patients with acute lower back pain.

Pro tip: Many EDs stock vials of 10cc of sterile water that you can order. This is more practical than using a 1000cc bottle of sterile water and throwing away the unused 999.6cc.

Source
The effectiveness of intradermal sterile water injection for low back pain in the emergency department: A prospective, randomized controlled study. Am J Emerg Med. 2021 Apr;42:103-109. doi: 10.1016/j.ajem.2021.01.038. Epub 2021 Jan 20.

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#3: Steroids for Pediatric Retropharyngeal and Parapharyngeal Abscesses

 Spoon Feed
Corticosteroid use for pediatric patients with retropharyngeal abscesses (RPAs) or parapharyngeal abscesses (PPAs) was associated with lower rate of surgical drainage, less frequent opioid use, and reduced hospital costs.

Why does this matter?
RPAs and PPAs are rare but potentially life-threatening diagnoses. They are most often diagnosed in children, and the incidence of these diseases has been increasing over the past 20 years. RPAs and PPAs can be treated with medical management alone (antibiotics, hydration, and analgesia) or in combination with surgical drainage. Would the addition of corticosteroids to medical management provide any benefit and possibly reduce the need for surgical drainage?

More meds = less scalpel?

Design: This was a multicenter, retrospective study of children aged 2 months to 8 years admitted to a PHIS participating hospital from January 2016 to December 2019 with a diagnosis of RPA or PPA. Children with complex chronic conditions or neck trauma were excluded. Included in the study were 2,259 patients with 1,677 (74.2%) in the non-corticosteroid group and 582 (25.8%) in the corticosteroid group.

Results: The primary outcome of surgical drainage occurred less often in the corticosteroid group compared to the non-corticosteroid group (22.2% vs 51.5%; P < .001). However, more patients who received corticosteroids had delayed surgery compared to the patients who did not receive corticosteroids (59.7% vs 29.4%; P < .001). Patients in the corticosteroid group had less frequent opioid medication use (45.2% vs 54.4%; P < .001), reduced length of stay (median 4 hours shorter; P = .02), and lower overall hospital costs (RR: 0.92; 95% CI: 0.88–0.97; P < .001). Patients in the corticosteroid group were 2.2-times more likely to have return ED visit within one week (95% CI: 1.24–4.05, P=.009) but rates of 30-day hospital readmission did not differ between the groups.

Limitations: The study had several limitations including its observational design, significant heterogeneity regarding corticosteroid and antibiotic use, and several potential confounders. In addition, information about the patient’s exam and diagnostic results (imaging findings) was not available.

Implications: This study suggests that including corticosteroids for medical management of RPAs and PPAs is associated with reduced need for surgical drainage, less opioid use, and lower hospital costs. I would like to see more data on corticosteroids (specifically an RCT), but based on this study, l will be giving my patients with RPAs and PPAs corticosteroids in the future.

Source
Corticosteroids in the Treatment of Pediatric Retropharyngeal and Parapharyngeal Abscesses. Pediatrics. 2021 Nov;148(5):e2020037010. doi: 10.1542/peds.2020-037010. Epub 2021 Oct 25.

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