Obstetrics

High risk and low prevalence diseases: Giant cell arteritis

a b s t r a c t

Introduction: Eclampsia is a rare partum and puerperal condition that carries a high rate of morbidity and mortality.

Objective: This review highlights the pearls and pitfalls of the care of patients with eclampsia, including presen- tation, evaluation, and evidence-based management in the emergency department (ED).

Discussion: Eclampsia is a hypertensive disease of pregnancy defined by new onset tonic-clonic, focal, or multifo- cal seizures or unexplained altered mental status in a pregnant or postpartum patient in the absence of other causative etiologies. However, signs and symptoms of preeclampsia and prodromes of eclampsia are often subtle and non-specific, making the Diagnosis difficult. Thus, it should be considered in pregnant and postpartum pa- tients who present to the ED. Laboratory testing including complete blood cell count, renal and liver function panels, electrolytes, glucose, coagulation panel, fibrinogen, lactate dehydrogenase, Uric acid, and urinalysis, as well as imaging to include head computed tomography, can assist, but these evaluations should not delay man- agement. Components of treatment include emergent obstetric specialist consultation, magnesium administra- tion, and blood pressure control in patients with hypertension. definitive treatment of eclampsia requires emergent delivery in pregnant patients. If consultants are not in-house, emergent stabilization and immediate transfer are required.

Conclusions: An understanding of eclampsia can assist emergency clinicians in rapid recognition and timely man- agement of this potentially deadly disease.

Published by Elsevier Inc.

  1. Introduction

This article series addresses high risk and low prevalence diseases that are encountered in the emergency department (ED). Much of the primary literature evaluating these conditions is not emergency medi- cine focused. By their very nature, many of these Disease states and clin- ical presentations have little useful evidence available to guide the emergency physician in diagnosis and management. The format of each article defines the disease or clinical presentation to be reviewed, provides an overview of the extent of what we currently understand, and finally discusses pearls and pitfalls using a question-and-answer format. This article will discuss eclampsia. This condition’s low preva- lence but high morbidity and mortality, as well as its variable atypical Patient presentations and challenging diagnosis, makes it a high risk and low prevalence disease.

* Corresponding author at: 3841 Roger Brooke Dr., Fort Sam Houston, TX 78234, USA.

E-mail address: [email protected] (B. Long).

    1. Epidemiology

Pregnancy-related conditions account for 1.3% of annual ED visits and are responsible for a steeply increasing proportion of morbidity and mortality in women of childbearing age over the last three decades [1-3]. Hypertensive diseases of pregnancy (HDP) represent a broad but non-linear spectrum of partum and puerperal conditions that account for nearly one fifth of maternal deaths worldwide, with preeclampsia and eclampsia being the most severe manifestations of HDP and ac- counting for the largest proportion of these deaths [4]. Eclampsia is rare, occurring in approximately of 0.3% of live births, though there is significant variability in incidence due to factors such as maternal risk factors, economic inequity, and differences in access and quality of ob- stetric care [5-9]. Despite its rarity, eclampsia is associated with serious complications including ischemic and hemorrhagic stroke, coma, heart failure, venous thrombosis, renal failure, disseminated intravascular co- agulation, and fetal demise [9]. Maternal mortality rates range from 5.6% to 14% [10-12]. Additionally, approximately 25% of patients develop long-term sequelae, including cardiovascular-related pathologies

https://doi.org/10.1016/j.ajem.2022.06.004 0735-6757/Published by Elsevier Inc.

(i.e., myocardial infarction, heart failure) [9]. Neonates born to eclamp- tic patients are also at risk of being small for gestational age, hypoxic- ischemic brain injury, and neonatal respiratory distress syndrome [6,9].

Table 1

Diagnostic criteria for hypertensive disorders of pregnancy [13] Condition Diagnostic Criteria Comments

    1. Definition

Eclampsia is a severe manifestation of HDP and is defined by new onset tonic-clonic, focal, or multiFocal seizures or unexplained altered mental status in a pregnant or postpartum patient in the absence of other causative etiologies [13]. The classic understanding of HDP is a linear progression from gestational hypertension to preeclampsia to

Chronic

(pre-gestational) hypertension

Gestational hypertension

BP >140/90 mmHg

BEFORE 20 weeks gestation

BP >140/90 mmHg on two occasions 4 h apart AFTER 20 weeks gestation without associated proteinuria or other features of preeclampsia

Higher risk for

development of preeclampsia and eclampsia.

50% develop preeclampsia, and there is increasing doubt that gestational hypertension and preeclampsia are distinct disorders.**

preeclampsia with severe features to eclampsia in the absence of inter-

vention [13,14]. However, research increasingly supports the notion that HDP may progress in a non-linear fashion [10,15,16]. For example, in one study, 38% of patients who developed acute-onset eclampsia had no signs or symptoms of preeclampsia during their hospital stay [10]. Conversely, other studies have shown that only 1.9% and 3.2% of pa- tients with preeclampsia and preeclampsia with severe features, re- spectively, develop eclampsia in the absence of intervention [15,17]. Nevertheless, patients with HDP are at increased risk of developing eclampsia, and recognition of the conditions in the spectrum of HDP may aid in the diagnosis, prevention, and management of eclampsia [9]. Table 1 outlines the current diagnostic criteria for the spectrum of HDP; however, it is important to recognize the diagnosis of preeclamp-

Preeclampsia BP >140/90 mmHg on two occasions 4 h apart AFTER 20 weeks gestation with associated proteinuria or signs of end-organ dysfunction

-Proteinuria >300 mg in a 24-h Urine collection or spot protein (mg/dL)/creatinine (mg/dL) ratio >= 0.3

-Protein >=2+ on Urine dipstick may be used if quantitative measurement is not

available

1.9% develop eclampsia.

sia is increasingly becoming a clinical one and that emergent obstetric specialist involvement is paramount as soon as these diagnoses are suspected.

According to The American College of Obstetricians and Gynecolo- gists (ACOG), eclampsia can occur during or after the 20th week of preg- nancy and up to 6 weeks postpartum [13]. Two thirds of cases occur during the antepartum period, with the remainder of cases evenly dis- tributed between labor and the postpartum period [18-21]. While the definition includes symptoms and signs past 20 weeks of gestation, eclampsia may occur in those <20 weeks of gestation in patients with renal disease, molar pregnancy, or multiple gestations [21-24].

  1. Discussion
    1. Presentation

While seizures are the defining symptom of eclampsia, the presenta- tion of eclampsia is variable, and many patients present atypically, mak- ing early diagnosis of this condition challenging. Unfortunately, studies have shown that more than one third of eclampsia cases occur acutely and have no signs or symptoms of preeclampsia preceding the seizures. However, up to 83% of eclampsia cases are associated with non-specific prodromal symptoms prior to seizure occurrence [13]. These prodromal symptoms include headache (66-82%), Visual disturbances (27-44%), and upper abdominal pain (25%) [11,13,20,23,25,26]. The headache as- sociated with eclampsia varies in the location and quality of pain, and documented vision disturbances include blurry vision, scotoma, photopsia, diplopia, and transient blindness [21,26-28]. Altered mental

Preeclampsia with severe features

Syndrome of Hemolysis, Elevated Liver enzymes, and Low Platelets (HELLP)

In the absence of proteinuria, new hypertension with any of the following:

-BP >160/110 mmHg

-New thrombocytopenia

laboratory evidence of Liver dysfunction not accounted for by other pathology or intractable right upper quadrant or epigastric abdominal pain

-New or worsening renal insufficiency in the absence of other renal pathology

-Pulmonary edema not accounted for by other pathology

-New intractable headache not accounted for by other pathology

-Visual disturbances In the absence of other causative etiologies:

-Lactate dehydrogenase

>600 IU/L

-Transaminitis 2x Upper limit of normal

-Platelets <100 x 109

3.2% develop eclampsia

A variant of preeclampsia with severe features that is associated with increased morbidity and mortality. Associated with more insidious onset, and nearly 15% present without hypertension or proteinuria. Abdominal pain and nausea/vomiting are often present.

status may also occur prior to and/or after the seizure. Unfortunately, these symptoms cannot be used to rule in or out the diagnosis, and in many situations, history will not be available, as the patient is altered or actively seizing [18,25,26,29]. Seizures associated with eclampsia are typically tonic-clonic and last less than one minute [25].

Similar to patient presentation, physical examination findings in eclampsia are variable. In patients with preeclampsia preceding seizure, common findings include hypertension, edema, clonus, and hyperreflexia [24,28]. Accurate measurement of blood pressure using an appropriately sized cuff is of paramount importance, but the degree of hypertension does not predict eclampsia [24]. Approximately 20% of eclampsia cases occur in the setting of mild hypertension, and blood pressure may be nor- mal in 25% of patients [10,18,21,26].

**The most recent ACOG guidelines recommend that patients with severe range hyperten- sion (>160/110 mmHg) without proteinuria should be managed similar to those with se- vere preeclampsia [13].

    1. ED evaluation

While eclampsia is a clinical diagnosis, laboratory evaluation is recom- mended to evaluate for complications and alternate or concurrent etio- logic conditions, including complete blood cell count , renal and liver function panels, electrolytes, glucose, coagulation panel, fibrinogen, Lactate dehydrogenase , uric acid, and urinalysis [8,13,21,23,30]. Laboratory testing may reveal thrombocytopenia, elevated creatinine, el- evated aminotransferases, elevated LDH and uric acid, and proteinuria

(Table 1). Patients with new-onset seizure, altered mental status, or focal neurologic deficits should undergo non-contrast head computed tomog- raphy (CT) to evaluate for intracranial hemorrhage or other intracranial pathology. Patients with cardiovascular or respiratory symptoms should undergo electrocardiogram to evaluate for dysrhythmias and right heart strain and chest radiography to assess for other processes such as pulmo- nary edema and pneumonia, among other etiologies [8,13,21,23,30].

    1. ED management

Key components of management include preventing maternal hyp- oxia, treatment of Severe hypertension if present, seizure discontinuation and prevention, and evaluation for emergent delivery if the patient is pregnant. Emergent consultation of an obstetric specialist is recom- mended as soon as the diagnosis of eclampsia is suspected. Delivery of the fetus is the definitive treatment for eclampsia [31]. In the ED setting, foundational emergency care should be provided for stabilization, starting with airway, breathing, and circulation. Assessment and management of respiratory and circulatory compromise and seizure cessation should be optimized while obtaining obstetric consultation. If the airway is not pat- ent, airway protection is recommended with endotracheal intubation. Supplemental oxygen is recommended to prevent hypoxia for both the patient and fetus [23], and adequate Intravenous access is necessary. The patient should also be placed in the Left lateral decubitus position to improve placental blood flow and reduce aspiration risk. While eclampsia is an emergent diagnosis in a seizing pregnant or postpartum patient, mimics must be considered, and thus, immediate assessment of Serum glucose is necessary. Evaluation for trauma, infection, and toxic ingestion is recommended. Additionally, a thorough history and physical examina- tion should be performed to evaluate for an underlying cardiovascular, pulmonary, infectious, or neUrologic emergency (i.e., Elevated intracranial pressure, central nervous system infection, etc.).

The treatment of choice for seizures in pregnancy is magnesium, which demonstrates greater effectiveness compared to other medications in this patient population [32-35]. If the patient is actively seizing, intrave- nous (IV) magnesium sulfate is recommended at a loading dose of 4-6g over 15 min, followed by maintenance infusion of 1-3 g/h, with a goal serum magnesium of 2-3.5 mmol/L (4-5 mEq/L) (Table 2) [21,23,31]. If IV access is not available, magnesium 10 g intramuscular can be ad- ministered (5 g in each buttock). Magnesium is also recommended in pa- tients with preeclampsia for seizure prophylaxis [13]. Magnesium is associated with reduced maternal mortality and risk of Seizure recurrence [36-41]. Absolute contraindications include myasthenia gravis, severe hy- pocalcemia, complete heart block, and myocarditis [13]. Benzodiazepines and phenytoin are less effective than magnesium for seizure prophylaxis in eclampsia but may be used if magnesium is not available or contraindi- cated [13,41]. Up to 10% of patients will have recurrent Seizure activity de- spite an initial bolus of magnesium [42]. If this occurs, a second bolus of magnesium 2 g is recommended over 3-5 min [21]. If further seizures occur, benzodiazepine therapy is recommended [13].

Following magnesium administration and seizure cessation, man- agement of severe hypertension is recommended, as blood pressures over 160/110 mmHg increase the risk of poor outcome [21,43]. Target blood pressure is based on patient baseline blood pressure and mental status, but typically includes a systolic blood pressure (SBP) of 130-150 mmHg and diastolic blood pressure 80-100 mmHg

[14,44,45]. Medications such as labetalol, nicardipine, hydralazine, or ni- fedipine may be used, which will be further discussed in detail [13].

  1. Pearls and pitfalls
    1. Why is eclampsia missed, and what is a simplified means of identifying eclampsia?

One study of obstetric clinicians found a misdiagnosis rate of 31% for patients with preeclampsia, which was associated with a higher rate of complications, re-hospitalization, and patient cost [46]. Misdiagnosis of eclampsia and other conditions in the spectrum of HDP is likely second- ary to their often variable and subtle presentations. Prodromal symp- toms are present in the majority of patients but are non-specific and include headache, visual disturbances, and Gastrointestinal symptoms [26]. The non-specific nature of these prodromal symptoms may cause them to be ignored by patients or misattributed to other more benign causes by healthcare clinicians, leading to late presentation, diagnostic delay, or misdiagnosis. Elevations in blood pressure that may otherwise be considered a reactive response to discomfort should trigger an eval- uation in pregnant women and those in the postpartum period. Aside from the development of seizures, there is no correlation of physical ex- amination findings, laboratory abnormalities, or symptoms that can de- finitively rule in or rule out eclampsia. Thus, eclampsia should be considered in pregnant and postpartum women presenting to the ED, especially in patients with symptoms such as headache, confusion/al- tered mental status, vision changes, and hypertension. Identification of maternal risk factors may aid in risk stratification, but the absence of risk factors does not exclude eclampsia as a potential diagnosis (Table 3).

    1. What is the utility and limitations of the ED evaluation including laboratory assessment and imaging?

Because the diagnosis of eclampsia is clinical, the primary utility of maternal laboratory and imaging testing in the ED is to evaluate for other etiologic conditions and evidence of end-organ damage, including CBC, renal and liver function panels, electrolytes, glucose, coagulation panel, fibrinogen, LDH, uric acid, and urinalysis. Testing should not delay consultation with obstetrics and the initiation of management for patients with suspected eclampsia. While the diagnostic criteria does allow for the absence of protein in the urine, proteinuria identified by dipstick urinalysis should be interpreted with caution, as it is 55% sensitive and 84% specific for >300 mg/ 24-h urine protein, the diagnos- tic criterion for proteinuria in HDP [14]. In addition to the maternal testing, when possible, a fetal ultrasound and non-stress test should be performed to evaluate for fetal distress, growth restriction, and oligohydamnios [8].

Imaging to include head CT non-contrast has an integral role in the evaluation of patients with Severe headache, new seizure, focal neurol- ogic deficit, or altered mental status. This may reveal reversible cerebral vasoconstriction syndrome, cerebral venous thrombosis, posterior re- versible encephalopathy syndrome (PRES), subarachnoid hemorrhage, or other Intracranial Hemorrhage , which can impact ED manage- ment [47-49]. Of note, up to 90% of patients with eclampsia will demon- strate features of PRES on neuroimaging [48,49].

Table 2

Magnesium dosing considerations for eclampsia [8,31]

Dose

IV

IM

Serum Cr > 1.2 mg/dL or GFR < 60 mL/min

Refractory to initial bolus

Refractory to 2nd bolus

Mg not available or contraindicated

Initial Bolus

Maintenance

4-6 g over 15-20 min

2 g/h

10 g (5 g each buttock)

5 g every 4 h

4-6 g over 15-20 min

1 g/h

2 g over 3-5 min

Benzodiazepine (lorazepam 4 mg IV)

Benzodiazepine

Drip

Table 3

Maternal risk factors for eclampsia [9,13]

High-risk

Table 5

Patient monitoring during magnesium administration [14] Parameter Frequency

      • Previous preeclampsia/eclampsia
      • Multifetal gestation

Respiratory rate, heart rate,

and blood pressure

Every 30 min

Moderate-risk

      • First pregnancy
      • Maternal age > 35 years
      • Family history of preeclampsia
      • Body mass index >30
    1. What mistakes can be made with magnesium administration? How is magnesium toxicity managed?

Magnesium is a safe and effective medication in patients with preeclampsia and eclampsia, and maternal toxicity is rare with Close monitoring (Table 4). However, most emergency clinicians are unaccus- tomed to the management of a magnesium IV infusion and the poten- tially serious complications that may occur if the patient is not closely monitored. Adverse effects of magnesium infusion, which are rarely life-threatening, include flushing, headaches, nystagmus, hypothermia, acute kidney injury, Urinary retention, and constipation [16,42]. These effects are typically seen at magnesium levels of 3.8-5 mmol/L and are mild and self-limited in most patients [16]. Life-threatening complica- tions are possible with magnesium toxicity, which highlights the impor- tance of close monitoring of patients on magnesium infusion. While increasing serum magnesium concentrations correlate with the severity of magnesium toxicity, the decision to continue magnesium infusion should be based on physical examination findings rather than a serum magnesium level [16]. The first physical examination finding of magne- sium toxicity is loss of deep tendon reflexes. A physical examination with testing of deep tendon reflexes should be performed and docu- mented upon completion of the loading dose of magnesium and every two hours while on a magnesium infusion (Table 5) [13,14,31]. At ther- apeutic magnesium levels of 2-3.5 mmol/L, deep tendon reflexes may be diminished but are rarely absent, and the presence of deep tendon reflexes is highly sensitive for non-toxic serum magnesium levels [13,16]. Urine output should be measured and recorded hourly, and

urine output should be at least 100 mL/4 h [13]. This is critically impor-

Urine output Hourly

Deep tendon reflexes At end of loading dose and then every two hours

while on magnesium infusion

If signs of magnesium toxicity occur, the magnesium infusion should be stopped immediately. If evidence of cardiopulmonary compromise is present, calcium should be given as an antidote for magnesium toxicity. This can be provided as a 1 g bolus of Calcium gluconate over 2-5 min and can be repeated every 5 min as necessary [16,51]. Normal saline and Loop diuretics can also be administered to enhance renal clearance of magnesium [51]. In severe cases and in patients with severely im- paired kidney function, hemodialysis may be necessary for magnesium clearance [51].

Table 6

Blood pressure medication regimens and considerations [8,14,30,31,44,53]

Medication Initial Dose Considerations

Labetalol 20 mg IV – If no response, repeat dose in 20 min

  • If suboptimal/no response within 10 min of second dose, give third dose of 40 mg IV
  • If suboptimal/no response within 10 min of third dose, give fourth dose of 80 mg IV
  • Maximum Cumulative dose is 220-300 mg
  • Once control is obtained, start infusion at 1-2 mg/kg/h
  • 200 mg PO can be administered if IV access is unavailable
  • side effects: bronchoconstriction, heart block, Sleep disturbances, bradycardia, orthostatic hypotension, fatigue
  • Avoid in patients with asthma or congestive heart failure or heart rate < 60 bpm

tant, as urinary retention can be seen in magnesium toxicity, and de- creased urine production may signal impairment of renal function, both an adverse effect of magnesium administration and the primary

means of magnesium elimination in the body. Because 90% of magne-

Nicardipine Start at 3-5 mg/h continuous

drip; titrate by 2.5 mg/h every 5-15 min until blood pressure controlled (maximum 15 mg/h), then reduce infusion

– Side effects: tachycardia,

flushing, headache

sium is eliminated through the urine, dose adjustments should be made in patients with existing renal disease and those who develop renal injury in the course of treatment [50]. Respiratory depression, car- diac Conduction abnormalities, and refractory hypotension are associ- ated with severe toxicity and magnesium levels of 5-7.5 mmol/L. [16]

Table 4

Serum magnesium levels and correlating symptoms [16,41]

Hydralazine 5-20 mg IV – Repeat dose in 20 min if no response

  • If no response after 3 doses, consider another agent
  • Maximum cumulative dose is 20-30 mg
  • If response is achieved, repeat bolus every 3 h
  • Side effects: Labile blood pressures, headache, lightheadedness, flushing, nausea, palpitations, reflex

Serum Magnesium Concentration (mmol/L)

2-3.5

(therapeutic)

Symptoms

Flushing, headaches, nystagmus, acute kidney injury, urinary retention, constipation (all self-limited)

tachycardia

Nifedipine 10 mg PO – Repeat BP in 20 min; if BP

>=160/110 mmHg, readminister 20 mg PO

    • Side effects: reflex tachycardia, headache, hypotension
    • Use with caution with patients

>3.5 Loss of patellar reflexes

>5 Respiratory arrest, cardiac conduction abnormalities, refractory hypotension

>12.5 Cardiac arrest

receiving magnesium sulfate (theoretical risk of Neuromuscular blockade and hypotension when combined)

Table 7

Eclampsia pearls

  • Eclampsia is a severe manifestation of HDP and is defined by new onset

tonic-clonic, focal, or multifocal seizures or unexplained altered mental status in a pregnant or postpartum patient in the absence of other causative etiolo- gies.

  • Eclampsia should be considered in pregnant and postpartum patients pre- senting to the ED, even in the absence of the Classic symptoms of preeclamp- sia. Symptoms of preeclampsia and prodromes of eclampsia are often subtle and non-specific.
  • Laboratory testing and imaging can assist, but they should not delay diagnosis

and management of eclampsia.

  • Management focuses on emergent obstetric specialist consultation, magne- sium administration, and reduction of blood pressure in patients with hyper- tension.
  • Monitor patients on magnesium infusion closely to identify early signs and symptoms of toxicity. Reduce magnesium dose in patients with renal dys- function.
  • Consider maternal medical history when selecting a blood pressure agent, as some may exacerbate underlying conditions. Do not use ACE-I or ARB medi- cations in pregnant patients. Labetalol, hydralazine, nicardipine, and nifedi- pine may be used.
  • For patients who do not improve with seizure control and blood pressure management and display continued altered mental status or seizure, non– convulsive status epilepticus, central nervous infection, PRES, ICH, and other intracranial pathologies should be considered. In these patients, neurologic consultation and neuroimaging are recommended.
    1. How should blood pressure be managed?

In addition to seizure prophylaxis, management of blood pressure is paramount in patients with preeclampsia and eclampsia. Pharmacologic therapy is necessary in patients with SBP >=160 mmHg and DBP

>=110 mmHg [13]. There are several safe and effective regimens for man- aging hypertension in pregnancy, including labetalol, hydralazine, nicardipine, and nifedipine (Table 6). A large meta-analysis found no difference in efficacy or safety between hydralazine and labetalol or hy- dralazine and calcium channel blockers [52]. Of note, angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers should be avoided in pregnant patients, as these medications have ter- atogenic effects including fetal renal agenesis and dysfunction [14].

    1. How should patients refractory to standard treatment be managed?

While patients with eclampsia typically improve with seizure and blood pressure management, clinicians must consider other conditions and treatment options if the patient does not improve within 10-20 min following blood pressure and seizure control. Non-convulsive sta- tus epilepticus, central nervous infection, PRES, ICH, and other intracra- nial pathologies should be considered in those with continued altered mental status or seizure, and neurologic consultation and neuroimag- ing, if not obtained previously, are recommended. recurrent seizures in the patient receiving a magnesium infusion should be treated with a second bolus of magnesium [13]. Benzodiazepines such as lorazepam 4 mg IV can also be administered [54-57]. If seizures continue despite these interventions, phenytoin, levetiracetam, ketamine, or propofol can be administered. Endotracheal intubation is likely necessary at this stage as well [ 54-57].

Table 7 lists pearls for the ED evaluation and management of eclampsia.

  1. Conclusions

Eclampsia is a hypertensive disease of pregnancy defined by new onset tonic-clonic, focal, or multifocal seizures or unexplained altered mental status in a pregnant or postpartum patient in the absence of other causative etiologies. The diagnosis is not always clear, as signs and symptoms of preeclampsia and prodromes of eclampsia can be

subtle and non-specific. Emergency clinicians must consider these con- ditions in pregnant and postpartum patients who present to the ED. Laboratory testing including CBC, renal and liver function panels, elec- trolytes, glucose, coagulation panel, fibrinogen, LDH, uric acid, and uri- nalysis, as well as imaging to include non-contrast head CT, can assist. However, laboratory and imaging should not delay management and stabilization. Management includes emergent obstetric specialist con- sultation, magnesium administration, and reduction of blood pressure in patients with hypertension.

CRediT authorship contribution statement

Marina Boushra: Writing – review & editing, Writing – original draft, Visualization. Sreeja M. Natesan: Writing – review & editing, Writing – original draft, Visualization, Supervision. Alex Koyfman: Writing – review & editing, Supervision, Conceptualization. Brit Long: Writing – review & editing, Writing – original draft, Visualization, Supervision, Conceptualization.

Declaration of Competing Interest

None.

Acknowledgements

SN, MB, BL, and AK conceived the idea for this manuscript and con- tributed substantially to the writing and editing of the review. This man- uscript did not utilize any grants, and it has not been presented in abstract form. This clinical review has not been published, it is not under consideration for publication elsewhere, its publication is approved by all authors and tacitly or explicitly by the responsible authorities where the work was carried out, and that, if accepted, it will not be published elsewhere in the same form, in English or in any other language, includ- ing electronically without the written consent of the copyright-holder. This review does not reflect the views or opinions of the U.S. govern- ment, Department of Defense, U.S. Army, U.S. Air Force, or SAUSHEC EM Residency Program.

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