Nursemaid’s Elbow

Posted on January 2, 2023 by David Lewis

Nursemaid’s Elbow

Medical Student Pearl

Erika Maxwell

Memorial University Class of 2023

Reviewed by: Dr. David Lewis

Case

A 10-month-old female is brought into the Emergency Department by her mother with a left arm injury. The infant had a fall from standing and the mother reached out to grab her and caught her left forearm. After the incident, the patient’s mother noticed that the infant was no longer using the arm. The child has no medical history and is not taking any medications. She is vitally stable.

On exam, the child’s left arm is limp and extended at her side. She is using her right arm and hand exclusively, including to grasp for items on the left side of her body (pseudoparalysis). There is no deformity, erythema, edema, or ecchymosis. The arm and hand are neurovascularly intact (strong brachial pulse, pink and warm).

Differential Diagnosis

Nursemaid’s elbow/pulled elbow/radial head subluxation
Elbow fracture
Wrist fracture or soft tissue injury
Shoulder dislocation

Background

A pulled elbow occurs most frequently in young children with the median age for presentation being 2 years [1]. The reason for this is debated in the literature with some sources saying that the annular ligament is weaker in children [2] and others saying that the radial head is smaller [1], both resulting in a less stable joint.

The most common mechanism of injury is axial traction (i.e. pulling on the arm or hand), but falls or rough play may also be responsible [2].

Anatomical Context

The annular ligament holds the radial head in place next to the ulna. When axial traction is applied by pulling the forearm or hand, the radial head may move underneath the annular ligament and trap it in the radiohumeral joint, against the capitellum [1].

Figure 1: The arm on the left displays a normal elbow, whereas on the right the radius is subluxated and trapping the annular ligament against the capitellum [3].

Signs and Symptoms [3]

Pain at elbow
Pseudoparalysis of injured arm
Extension or light flexion of injured arm, often pronated

Diagnosis and Management

A full examination of the upper limb is required. Leave obviously swollen or deformed areas until the end. Palpate the clavicle, humerus, forearm and gently move the joints (shoulder, wrist, and lastly elbow). Pulled elbows rarely result in joint swelling. If this is present an alternative diagnosis should be considered (e.g., supracondylar fracture).

If a pulled elbow is the only likely diagnosis, then it may be reasonable to proceed to a subluxated radial head reduction manoeuvre. However, when the history is not clear (e.g., unwitnessed mechanism involving siblings or a fall), then it is much safer to perform further diagnostic tests prior to manipulation. These include radiograph of the elbow to rule out fracture or elbow ultrasound to rule out joint effusion [4].

Reduction Technique

This is done by supporting the elbow with one hand and using your other hand to move the patient’s arm through the recommended maneuvers. There are 2 different maneuvers to try, and they may be used alone or in combination [1-3,5].

Supinate the child’s forearm with your hand and flex the elbow

Figure 2: Demonstration of the supination/flexion maneuver [5]

Hyperpronate the child’s forearm

Figure 3: Demonstration of the hyperpronation maneuver [5]

Some research has indicated that the hyperpronation maneuver may be more effective and less painful for the patient [2,6], so it may be worth attempting this maneuver first.

If the maneuvers are successful, you may hear a click from the radial head as it moves back into place. The child may briefly cry as the subluxation is reduced. Movement recovery can take anywhere from a few minutes to several hours, but usually occurs within 30 minutes. The greater the delay from injury to presentation and subsequent reduction, the longer it will take for post reduction return to normal movement [2].

If a click is heard or felt during the manoeuvre it can usually be assumed that reduction has occurred. Ideally, it is recommended that the child remain under observation until normal movement returns. However, if delayed, it is reasonable to discharge the child with advice to return.

In any case where an x-ray or ultrasound has not been performed and the child does not rapidly start using their arm post manoeuvre, then imaging is required prior to any further manipulation.

Prognosis

Although a pulled elbow does not result in a permanent injury, it is important to inform the family that their child will be vulnerable to recurrent pulled elbows in the affected arm. Up to 27% of patients with a pulled elbow may experience a recurrence [7-8].

Case continued:

Based on the patient’s history and physical exam, she was diagnosed with a pulled elbow. Using the supination and flexion maneuver followed by the hyperpronation maneuver, an audible click was elicited from the patient’s elbow. Shortly thereafter, she began using the arm again as if no injury had occurred and was discharged home.

Key points:

A pulled elbow is a common upper limb injury in young children presenting to the Emergency Department
Careful assessment may preclude the need for diagnostic imaging however if in any doubt further investigation should be performed prior to manipulation. Many physicians will never forget the time they used a pulled elbow reduction technique in a child with an unexpected supracondylar fracture
HYPERPRONATE and/or SUPINATE & FLEX!
Recurrence is common

References

Aylor, M., Anderson, J., Vanderford, P., Halsey, M., Lai, S., & Braner, D. A. (2014). Reduction of pulled elbow. New England Journal of Medicine, 371(21), e32.
Wolfram, W., Boss, D., & Panetta, M. (2018, December 18). Nursemaid Elbow. Medscape. Retrieved September 6, 2022, from https://emedicine.medscape.com/article/803026-overview#a5
Boston Children’s Hospital. (2021). Nursemaid’s elbow. Retrieved September 6, 2022, from https://www.childrenshospital.org/conditions/nursemaids-elbow
Varga, M., Papp, S., Kassai, T., Bodzay, T., Gáti, N., & Pintér, S. (2021). Two- plane point of care ultrasonography helps in the differential diagnosis of pulled elbow. Injury, 52(1), S21-24.
Kilgore, K., & Henry, K. (2021). Nursemaid’s elbow. Society for Academic Emergency Medicine – Clerkship Directors in Emergency Medicine. Retrieved September 6, 2022, from https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/peds-em-curriculum/nursemaid%27s-elbow
Lewis, D., Argall, J., & Mackway-Jones, K. (2003). Reduction of pulled elbows. Emergency Medicine Journal, 20, 61-62.
Schunk, J. F. (1990). Radial head subluxation: epidemiology and treatment of 87 episodes. Annals of emergency medicine, 19(9), 1019-1023.
Teach, S. J., & Schutzman, S. A. (1996). Prospective study of recurrent radial head subluxation. Archives of pediatrics & adolescent medicine, 150(2), 164-166.

Bicuspid Aortic Valve – An important incidental PoCUS finding?

Posted on December 8, 2022 by David Lewis

Bicuspid Aortic Valve – An important incidental PoCUS finding?

Medical Student Pearl

Khoi Thien Dao

MD Candidate – Class of 2023

Dalhousie Medicine New Brunswick

Reviewed by: Dr. David Lewis

Case:

A 58-year-old male presents to Emergency Department with sudden onset of chest pain that is radiating to the back. He was also having shortness of breath at the same time of chest pain. The patient later reveals that his past medical history only consists of “bicuspid valve”, and he takes no medication. On examination, he was uncomfortable, but no signs of acute distress. His respiratory and cardiac exam were unremarkable for reduced air sound, adventitious sound, heart murmur, or extra heart sound. ECG was normal and initial cardiac markers were within normal range. His chest x-ray is normal.

You are aware that with his medical presentation and a history of bicuspid aortic valve, you need to consider associated concerning diagnosis (aortic root aneurysm and aortic dissection) within the differential (myocardial infarct, congestive heart failure, pneumonia, etc.).

Bicuspid Aortic Valve

Bicuspid aortic valve is one of the most common types of congenital heart disease that affects approximately one percent of population. There is a strong heritable component to the disease. Bicuspid aortic valve occurs when two leaflets fused (commonly right and left coronary leaflets) and form a raphe, a fibrous ridge¹. The fusion of the leaflets can be partial, or complete, with the presence or absence of a raphe¹. Bicuspid aortic valve disease is associated with increasing risks for valve calcification, which lead to aortic stenosis or regurgitation secondary to premature degeneration¹. This congenital heart defect is also a well-known risks factor for aortic dissection and aortic dilatation. Reports have estimated prevalence of aortic dilation in patients with bicuspid aortic valve ranging between 20 to 80 percent, and that the risks of aortic dilation increase with age². Increases risk of aortic dilatation in bicuspid valve disease also leads to a significantly greater risk for aortic dissection^2.3.

The majority of patients with bicuspid aortic valve are asymptomatic with relatively normal valve function and therefore can remain undiagnosed for many years. However, most patients with bicuspid aortic valve will develop complications and eventually require valve surgery within their lifetime. Early diagnosis, while asymptomatic, can enable close follow-up for complications and early intervention with better outcomes. However, asymptomatic individuals are rarely referred for echocardiography.

With increasing use of cardiac PoCUS by Emergency Physicians, there are two scenarios where increased awareness of the appearance of bicuspid aortic valve and its complications may be of benefit.

Known bicuspid aortic valve patients presenting with possible associated complications
Undiagnosed bicuspid aortic valve patients presenting with unrelated symptoms undergoing routine cardiac PoCUS

This clinical pearl provides a review of the clinical approach to bicuspid aortic valve and its associated complications and provides guide to enhancing clinical assessment with PoCUS.

Clinical Approach:

Although bicuspid aortic valve commonly presents as asymptomatic, a detailed focused cardiac history can assess for clinical signs and symptoms related to valve dysfunction and its associated disease, such as reduced exercise capacity, angina, syncope, or exertional dizziness¹. Information about family history with relation to cardiac disease is essential for a clinician’s suspicion of heritable cardiovascular disease. Red flag symptoms that shouldn’t be missed such as chest pain, back pain, hypertensive crisis, etc. should be specifically identified. They are indicators for possible emergent pathologies that should not be missed (for example: acute MI, aortic dissection, ruptured aortic aneurysm, etc.)

Physical examination findings in patients with bicuspid aortic valve include, but not limited to, ejection sound or click at cardiac apex/base, murmurs that have features of crescendo-decrescendo or holosystolic. Clinical signs of congestive heart failure such as dyspnea, abnormal JVP elevation, and peripheral edema may also be present.

Core Cardiac PoCUS:

With cardiac PoCUS, it is important to obtain images from different planes and windows to increase the complexity of the exam and to be able to be confidently interpreting the exam. There are four standard cardiac view that can be obtained: parasternal short axis (PSSA), parasternal long axis (PSLA), subxiphoid (sub-X), and apical 4-chamber view (A4C). Each cardiac view has specific benefits.

Parasternal Long Axis

With the PSLA, the phased-array transducer is placed to the left sternum at 3^rd or 4^th intercostal with transducer orientation pointing toward patient’s right shoulder. Key structures that should be seen are Aortic Valve (AV), Mitral Valve (MV), Left Ventricle (LV), pericardium, Right Ventricle (RV), Left Ventricular Outflow Tract (LVOT), and portion of ascending and descending aorta⁸. It is primarily used to assess left ventricular size and function, aortic and mitral valves, left atrial size⁸. Furthermore, pericardial effusions and left ventricular systolic function can be assessed.

Parasternal Long Axis

Parasternal Short Axis

Using the same transducer position as the PSLA the transducer can be centered to the mitral valve and rotated 90 degrees clockwise to a point where the transducer marker points to patient’s left shoulder to obtain the PSSA. With this orientation, one can assess for global LV function and LV wall motion⁸. Furthermore, with five different imaging planes that can be utilized with this view, aortic valve can be visualized in specific clinical contexts.

Parasternal Short Axis

Apical 4-Chamber

The apical 4-chamber view is generated by placing the transducer at the apex, which is landmarked just inferolateral to left nipple in men and underneath inferolateral of left breast in women. This view helps the clinician to assess RV systolic function and size relative to the LV⁸.

Apical 4-Chamber

Subxiphoid

The subxiphoid view can be visualized by placing a transducer (phased-array or curvilinear) immediately below the xiphoid process with the transducer marker points to patient’s right. The movements of rocking, tilting, and rotation are required to generate an optimal 4-chamber subcostal view. A “7” sign, which consists of visualizing the border between liver and pericardium, the septum, and the RV and LV that looks like number 7. This view allows user to assess RV functions, pericardial effusion, and valve functions⁸. In emergency setting, it can be used for rapid assessments in cardiac arrest, cardiac tamponade, and global LV dysfunction⁸.

From – the PoCUS Atlas

Subxiphoid labelled

7 Sign

PoCUS Views for Aortic Valve Assessment

In assessing the aortic valve, the PSSA and PSLA can be best used to obtain different information, depending on clinical indications. Both views can be used to assess blood flows to assess stenosis or regurgitation. However, the PSLA view includes the aorta where clinician can look for aortic valve prolapse or doming as signs of stenosis and its complications, like aortic dilatation. On the other hand, PSSA are beneficial when assessing the aortic valve anatomy.

Parasternal Long Axis

From PoCUS 101

Parasternal Short Axis

From – the PoCUS Atlas

PoCUS Appearance of Normal Aortic Valve (Tricuspid) vs Bicuspid Aortic Valve

With PSSA view, the normal aortic valve will have three uniformly leaflets that open and form a circular orifice during most of systole. During diastole, it will form a three point stars with slight thickening at central closing point. The normal aortic valve is commonly referred to as the Mercedes Benz sign.

Parasternal Short Axis – Normal Tricuspid AV – Mercedes Benz Sign and 3 cusp opening

Pitfall

However, the Mercedes Benz Sign sign can be misleading bicuspid valve disease when three commissure lines are misinterpreted due to the presence of a raphe. A raphe is a fibrous band formed when two leaflets are fused together. It is therefore important to visualize the aortic valve when closed and during opening, to ensure all 3 cusps are mobile. Visualization of The Mercedes Benz sign is not enough on its own to exclude Bicuspid Aortic Valve.

Apparent Mercedes sign when AV closed due to presence of raphe. Fish mouth appearance of the same valve when open confirming bicuspid aortic valve

Bicuspid Aortic Valve

Identification requires optimal valve visualization during opening (systole). Appearance will depend on the degree of cusp fusion. In general a ‘fish mouth’ appearance is typical for bicuspid aortic valve.

Parasternal Short Axis – Fish Mouth Opening – Fusion L & R Coronary Cusps – Bicuspid Aortic Valve

In the parasternal long axis view the aortic valve can form a dome shape during systole, and prolapse during diastole, rather than opening parallel to the aorta. This is called systolic doming. Another sign that can be seen in PSLA view is valve prolapse, when either right or non-coronary aortic valve cusps showed backward bowing towards the left ventricle beyond the attachment of the aortic valve leaflets to the annulus. This can be estimated by drawing a line joining the points of the attachment.

Systolic doming

Diastolic prolapse and systolic doming

PoCUS Appearance of the Complications of Bicuspid Valve Disease

In patients presenting with chest/back pain, shock or severe dyspnea who have either known or newly diagnosed bicuspid valve disease, PoCUS assessment for potential complications can be helpful in guiding subsequent management.

Complications of bicuspid aortic valve include aortic dilatation at root or ascending (above 3.8cm) and aortic dissection ^5-9.

Dilated aortic root, from – sonomojo.com

Aortic root dilatation – Normal maximum = 40mm

Aortic root dilatation with dissection

Valve vegetations or signs of infective endocarditis are among the complications of severe bicuspid valve^5-9

Aortic valve vegetations

General Management of Patients with Bicuspid Valve in the Emergency Department

Management of bicuspid aortic valve disease is dependent on the severity of the disease and associated findings.

For a patient with suspicious diagnosis of bicuspid valve disease, a further evaluation of echocardiography should be arranged, and patient should be monitored for progressive aortic valve dysfunction as well as risk of aortic aneurysm and dissection. Surgical intervention is indicated with evidence of severe aortic stenosis, regurgitation, aneurysm that is > 5.5cm, or dissection¹.

How accurate is PoCUS for Aortic Valve assessment?

Bicuspid aortic valve disease is usually diagnosed with transthoracic echocardiography, when physical examination has revealed cardiac murmurs that prompt for further investigation. However, patients with bicuspid valve disease frequently remain asymptomatic for a prolonged periods. Michelena et al. (2014) suggested that auscultatory abnormalities account for 60 to 70% diagnostic echocardiograms for BAV in community¹⁰.

While there are no published studies on the utility of PoCUS for the diagnosis of bicuspid aortic valve, there are studies on the use of PoCUS as part of the general cardiac exam. Kimura (2017) published a review that reported early detection of cardiac pathology when PoCUS was used as part of the physical exam ⁹. Abe et al. (2013) found that PoCUS operated by expert sonographer to screen for aortic stenosis has a sensitivity of 84% and a specificity of 90% in 130 patients ¹¹. In another study by Kobal et al. (2004), they found that PoCUS has a specificity of 93% and sensitivity of 82% in diagnosing mild regurgitation¹².

There are also limitations of using PoCUS to assess for bicuspid aortic valve disease, or valve disease in general. Obtaining images from ultrasound and interpretation are highly dependent on user’s experiences to assess for the valve⁹. Furthermore, research is needed to investigate the use of PoCUS in lesser valvular pathology.

When a new diagnosis of bicuspid aortic valve is suspected, a formal echocardiogram should be arranged, and follow-up is recommended.

Summary

Bicuspid aortic valve is often asymptomatic and undiagnosed until later in life
Patients with known bicuspid aortic valve disease are closely followed and may require surgical intervention in the event of complications
Diagnosis of bicuspid aortic valve requires careful visualization of valve closing and opening during diastole and systole
The increased use of PoCUS by Emergency Physicians as an adjunct to cardiac examination may result in increased diagnosis of bicuspid aortic valve. These may be related to the presentation or incidental findings
In patients presenting to the Emergency Department with known or newly diagnosed bicuspid aortic valve disease, consider if a complication is related to their presentation
In patient with incidental finding of bicuspid aortic valve disease refer for cardiology follow up

References

Braverman, A. C., & Cheng, A. (2013). The bicuspid aortic valve and associated aortic disease. Valvular heart disease. Philadelphia: Elsevier, 179-218.
Verma, S., & Siu, S. C. (2014). Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med, 370, 1920-1929.
Della Corte, A., Bancone, C., Quarto, C., Dialetto, G., Covino, F. E., Scardone, M., … & Cotrufo, M. (2007). Predictors of ascending aortic dilatation with bicuspid aortic valve: a wide spectrum of disease expression. European Journal of Cardio-Thoracic Surgery, 31(3), 397-405.
Tirrito, S. J., & Kerut, E. K. (2005). How not to miss a bicuspid aortic valve in the echocardiography laboratory. Echocardiography: A Journal of Cardiovascular Ultrasound and Allied Techniques, 22(1), 53-55.
Baumgartner, H., Donal, E., Orwat, S., Schmermund, A., Rosenhek, R., & Maintz, D. (2015). Chapter 10: Aortic valve stenosis. The ESC textbook of cardiovascular imaging. European Society of Cardiology.
Fowles, R. E., Martin, R. P., Abrams, J. M., Schapira, J. N., French, J. W., & Popp, R. L. (1979). Two-dimensional echocardiographic features of bicuspid aortic valve. Chest, 75(4), 434-440.
Shapiro, L. M., Thwaites, B., Westgate, C., & Donaldson, R. (1985). Prevalence and clinical significance of aortic valve prolapse. Heart, 54(2), 179-183.
Gebhardt, C., Hegazy, A.F., Arntfield, R. (2015). Chapter 16: Valves. Point-of-Care Ultrasound. Philadelphia: Elsevier, 119-125.
Kimura, B. J. (2017). Point-of-care cardiac ultrasound techniques in the physical examination: better at the bedside. Heart, 103(13), 987-994.
Michelena, H. I., Prakash, S. K., Della Corte, A., Bissell, M. M., Anavekar, N., Mathieu, P., … & Body, S. C. (2014). Bicuspid aortic valve: identifying knowledge gaps and rising to the challenge from the International Bicuspid Aortic Valve Consortium (BAVCon). Circulation, 129(25), 2691-2704.
Abe, Y., Ito, M., Tanaka, C., Ito, K., Naruko, T., Itoh, A., … & Yoshikawa, J. (2013). A novel and simple method using pocket-sized echocardiography to screen for aortic stenosis. Journal of the American Society of Echocardiography, 26(6), 589-596.
Kobal, S. L., Tolstrup, K., Luo, H., Neuman, Y., Miyamoto, T., Mirocha, J., … & Siegel, R. J. (2004). Usefulness of a hand-carried cardiac ultrasound device to detect clinically significant valvular regurgitation in hospitalized patients. The American journal of cardiology, 93(8), 1069-1072.
Le Polain De Waroux, J. B., Pouleur, A. C., Goffinet, C., Vancraeynest, D., Van Dyck, M., Robert, A., … & Vanoverschelde, J. L. J. (2007). Functional anatomy of aortic regurgitation: accuracy, prediction of surgical repairability, and outcome implications of transesophageal echocardiography. Circulation, 116(11_supplement), I-264.

Management of Supraventricular Tachycardia (SVT) in Pregnancy

Posted on November 30, 2022 by Janeske Vonkeman

Management of Supraventricular Tachycardia (SVT) in Pregnancy

Medical Student Clinical Pearl

Tyson Fitzherbert, DMNB Class of 2024

Reviewed by Dr. Luke Taylor and Dr. David Lewis

Case:

A 30-year-old pregnant (32 weeks) female presents to the emergency department with palpitations and chest discomfort. On ECG they are diagnosed with supraventricular tachycardia, a narrow complex arrythmia – how would you proceed?

Introduction:

Pregnant women have a higher incidence of cardiac arrhythmias. The exact mechanism of increased arrhythmia burden during pregnancy is unclear, but has been attributed to hemodynamic, hormonal, and autonomic changes related to pregnancy. A common arrhythmia in pregnancy is supraventricular tachycardia (SVT). SVT is a dysrhythmia originating at or above the atrioventricular (AV) node and is defined by a narrow complex (QRS < 120 milliseconds) at a rate > 100 beats per minute (bpm). The presentations of SVT in pregnancy are the same as the nonpregnant state and include symptoms of palpitations that may be associated with presyncope, syncope, dyspnea, and/or chest pain. Diagnosis is confirmed by electrocardiogram (ECG).

Figure 1: Rhythm strip demonstrating a regular, narrow-complex tachycardia, or supraventricular tachycardia (SVT).

In general, the approach to the treatment of arrhythmias in pregnancy is similar to that in the nonpregnant patient. However, due to the theoretical or known adverse effects of antiarrhythmic drugs on the fetus, antiarrhythmic drugs are often reserved for the treatment of arrhythmias associated with clinically significant symptoms or hemodynamic compromise. Below is a detailed description of the management of SVT in pregnancy.

Management:

Figure 2: Treatment algorithm for SVT in pregnancy.

General Considerations:

Non‐pharmacological treatment including vagal manoeuvres such as carotid massage and Valsalva manoeuvre are well tolerated and aid in management.
Intravenous adenosine can be used in all three trimesters, including labor.
Electrical cardioversion is an effective treatment method for hemodynamically unstable or drug-refractory patients, which has proven to be safe in all three trimesters, including labor. There are some examples of this leading to pre-term labor in the third trimester.
AV nodal blocking agents and anti-arrhythmic agents may be considered for cardioversion; see table below for effects in pregnancy and breast feeding.

Case Continued:

A modified Valsalva manoeuvre is performed with resolution to sinus rhythm after 2 attempts. The patient is discharged with OBGYN follow-up.

https://sjrhem.ca/modified-valsalva-maneuver-in-the-treatment-of-svt-revert-trial/

Further Reading

The Acute Treatment of Maternal Supraventricular Tachycardias During Pregnancy: A Review of the Literature – https://www.jogc.com/article/S1701-2163(16)34767-3/pdf
Tachycardia in Pregnancy: when to worry? – https://www.rcpjournals.org/content/clinmedicine/21/5/e434

References:

Patti L, Ashurst JV. Supraventricular Tachycardia. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www-ncbi-nlm-nih-gov.ezproxy.library.dal.ca/books/NBK441972/
UpToDate – https://www.uptodate.com/contents/supraventricular-arrhythmias-during-pregnancy#H11407709
Ibetoh CN, Stratulat E, Liu F, Wuni GY, Bahuva R, Shafiq MA, Gattas BS, Gordon DK. Supraventricular Tachycardia in Pregnancy: Gestational and Labor Differences in Treatment. Cureus. 2021 Oct 4;13(10):e18479. doi: 10.7759/cureus.18479. PMID: 34659918; PMCID: PMC8494174. https://www-ncbi-nlm-nih-gov.ezproxy.library.dal.ca/pmc/articles/PMC8494174/
Ramlakhan KP, Kauling RM, Schenkelaars N, et al, Supraventricular arrhythmia in pregnancy, Heart 2022;108:1674-1681. https://heart.bmj.com/content/early/2022/01/26/heartjnl-2021-320451#T2
Goyal A, Hill J, Singhal M. Pharmacological Cardioversion. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www-ncbi-nlm-nih-gov.ezproxy.library.dal.ca/books/NBK470536/
Vaibhav R. Vaidya, Nandini S. Mehra, Alan M. Sugrue, Samuel J. Asirvatham, Chapter 60 – Supraventricular tachycardia in pregnancy, Sex and Cardiac Electrophysiology. https://www-sciencedirect-com.ezproxy.library.dal.ca/science/article/pii/B9780128177280000607

Drop it like it’s Hot – Tetracaine eye drops following corneal abrasion?

Posted on October 7, 2022 by David Lewis

Drop it like it’s Hot- A case presentation and critical appraisal on the use of tetracaine eye drops following corneal abrasion: A Medical Student Pearl

Claudia Cullinan

DMNB, Med 3

Reviewed by Dr. Kavish Chandra

Case:

It’s a sunny July afternoon and you are just starting your shift in the ED when a 25-year-old male presents with sudden onset of severe right eye pain. You bring him into the exam room, and he explains he ran into a tree branch. He is reluctant to open his eye due to the pain and his eye is watering uncontrollably. He also keeps his sunglasses on while you talk because his eye is now extremely sensitive to the bright ED lights.

The patient is visibly in a lot of distress, so you do a quick penlight exam and attempt to assess visual acuity to confirm there is no evidence of penetrating trauma.

At this point you suspect a corneal abrasion, so you move onto a slit lamp and fluorescein examination and add a tetracaine 0.5% (topical anesthetic) to the affected eye. The patient appears more comfortable within seconds. You are able to complete the exam with the patient sitting comfortably in the exam chair. There is no evidence of Seidel sign (streaming fluorescein caused by leaking aqueous humor) and no visible foreign body in the eye. You can visualise a linear yellow lesion along the lateral cornea when viewed with fluorescein under cobalt blue light and you are confident this is a simple corneal abrasion.

Figure 1. Corneal abrasion viewed with cobalt blue light after fluorescein staining. Accessed from DFOptometrists.com

You explain to the patient that he has a corneal abrasion, prescribe him erythromycin 0.5% ophthalmic ointment to be inserted into the affected eye QID for 5 days and encourage him to avoid rubbing his eyes. He can also take PRN ibuprofen if needed. He asks “That one eye drop made my eye feel so much better, can I have a bottle of that to bring home?”

You know he is talking about Tetracaine, and you remember learning about the controversy of using topical anesthetics for the outpatient treatment of corneal abrasions….what do you tell him?

Critical Appraisal : Short-term topical tetracaine is highly efficacious for the treatment of pain caused by corneal abrasions: a double-blind, randomized clinical trial. (2020)

Background:

Corneal abrasions are among the most common ophthalmic presentations to the emergency department (ED). They occur when the corneal epithermal becomes disrupted, such as when tiny foreign bodies land in your eye or when your new puppy accidentally scratches the surface of your eye. Although corneal abrasions typically heal rapidly with minimal risk of complication, they are often VERY painful and can be extremely debilitating. There has been controversy on whether patients should be discharged home with topical anesthetics for short term management of corneal abrasions because of previously described safety concerns regarding toxicity. However, recent literature is beginning to surface suggesting there may be a role for short term topical analgesia following simple corneal abrasion, with appropriate follow up.

Figure 2. Anatomy of the cornea. Accessed form AAFP.org

Clinical Question:

How effective is the home use of topical tetracaine every 30 minutes PRN pain for 24 hours following corneal abrasion?

Reference

Shipman, S., Painter, K., Keuchel, M., & Bogie, C. (2021). Short-Term Topical Tetracaine Is Highly Efficacious for the Treatment of Pain Caused by Corneal Abrasions: A Double-Blind, Randomized Clinical Trial. Annals of Emergency Medicine, 77(3), 338–344. https://doi.org/10.1016/j.annemergmed.2020.08.036

Study Overview:

Population: Patients 18-80 years old presenting to an urban ED in Oklahoma City with suspected acute corneal abrasion.

Intervention: 2mL bottle of Tetracaine 0.5% one drop applied q30 minutes PRN pain for a maximum of 24 hours + antibiotic ophthalmic solution (polymyxin B sulfate/ trimethoprim sulfate) 2 drops to affected eye q4h.

Control: 4 separate 0.5mL ampules of artificial tears (Systane) one drop applied q30 minutes PRN pain for a maximum of 24 hours + antibiotic ophthalmic solution (polymyxin B sulfate/ trimethoprim sulfate) 2 drops to affected eye q4h.

Outcome: Pain rating at 24-48h follow up.

Methods:

Prospective, double blind, randomised control trial of topical tetracaine vs control (artificial tears) in the ED following diagnosis of corneal abrasion in the ED.
Took place in an urban Oklahoma ED from 2015 to 2017.
One hundred and eleven patients were included and were randomly assigned to the treatment or control group.
The patients in both groups had similar baseline characteristics and baseline numeric rating scale (NRS) pain scores (0-10, 10 being the most pain).

Inclusion criteria:

Patients 18 to 80 years old, presenting to the ED with suspected acute corneal abrasion, and gave written informed consent.

Exclusion criteria:

Contact lens wearers, previous corneal surgery or transplant in the affected eye, presented more than 36 hours after their injury, had a grossly contaminated foreign body, had coexisting ocular infection, currently pregnant, retained foreign body, penetrating eye injury, receiving immunosuppression, allergy to study medication, unable to attend follow-up, unable to fluently read and speak English or Spanish, and any injury requiring urgent ophthalmologic evaluation.

Results:

Main outcomes at the 24-48hr follow up appointment:

The overall numeric rating scale (NRS) pain score was significantly lower in the tetracaine group compared to the control group (1 versus 8, P<0.001).
The number of patients found to have a small residual corneal abrasion on their follow up slit-lamp examination was similar between groups (18% in the tetracaine group and 11% in the control group).
There were only two complications in the tetracaine group (versus 6 in the control group), with similar rates of worsening corneal abrasions in both groups. All patients had normal healing after 10 days. No serious adverse outcomes were encountered.

Table 1. Patient baseline demographics and 24-48hr follow up data points.

Group	Tetracaine (n=59)	Control (n=59)
Age, y	35 (28-43)	38 (27-47)
Male patients, No. (%)	36 (61)	34 (58)
Baseline pain rating	7 (6-7.5)	7 (6-8)
24-48hr pain rating	1 (1-2)	8 (7-8)
No. of hydrocodone tablets recorded	1	7
Adverse Events, No (%)	2 (3.6)	6 (11)

Limitations and suggestions for future studies:

Although this was a double-blind study, there are two things that could have made patients aware of their treatment group. First, the control was packaged in 4 ampules and the treatment was packaged in a single bottle. Second, Tetracaine burns when administered to the eye and Systane (control) does not.
The study was slightly underpowered for the primary outcome of efficacy and certainly not powered to determine safety for rare adverse events associated with topical anesthetics. That being said, there are more patients in this trial demonstrating short term safety than previous care reports and series demonstrating tetracaine harm.
There was an extensive exclusion criterion, including patients who wear contacts (which are a common cause of corneal abrasions). By broadening the inclusion criteria, the results could be applied to a greater number of patients.
Patients were required to return for follow up at which time they were required to return their “study drops” so the drops cannot be abused. It would be more feasible to limit the amount of eye drops in the bottle so the patient does not have to return to the ED for bottle disposal.

Our conclusions:

Short term topical tetracaine is an efficacious analgesic for acute corneal abrasions, is associated with less hydrocodone use compared to control, and appears to be safe.

Case

Back to our original question…what do we tell our patient?

Provide him with a limited number of tetracaine drops and administer one drop in affected eye q30 minutes PRN pain for a maximum of 24 hours. Advise him to return to ED if his symptoms persist beyond 48 hours or get worse.

References

McGee, H. T., & Fraunfelder, F. (2007). Toxicities of topical ophthalmic anesthetics. Expert Opinion on Drug Safety, 6(6), 637–640. https://doi.org/10.1517/14740338.6.6.637

Wipperman, J. L., & Dorsch, J. N. (2013). Evaluation and management of corneal abrasions. American Family Physician, 87(2), 114–120.

Yu, C. W., Kirubarajan, A., Yau, M., Armstrong, D., & Johnson, D. E. (2021). Topical pain control for corneal abrasions: A systematic review and meta-analysis. Academic Emergency Medicine, 28(8), 890–908. https://doi.org/10.1111/acem.14222

A Seal Barking… In the ED?? – Croup Management in the Emergency Department

Posted on July 6, 2022 by Mandy Peach

A Seal Barking… In the ED?? – Croup Management in the Emergency Department: A Medical Student Clinical Pearl

Kalpesh Hathi, CC3
MD Candidate, Class of 2023
Dalhousie Medicine New Brunswick

Reviewed by Dr. Jeremy Gross

Copyedited by Dr. Mandy Peach

All case histories are illustrative and not based on any individual.

Case Presentation:

You are the clinical clerk in the ED on a cold Monday, December afternoon. You pick up a chart that describes a 12-month-old baby boy, with a 1-day history of subjective fever of 38.4 C at its highest, respiratory distress, decreased PO intake and mom noting a barking cough.

Vitals: HR: 100 BPM, RR: 45, SpO2: 98% RA, BP: 90/65, Temp: 36.8 C, GCS 15, Wt: 10.2 kg.

You pull out your normal pediatrics vitals chart, and note that aside from a mildly elevated RR, these vitals are within normal limits for this child’s age and the child is afebrile.

What would you want to include in your history and physical?

History:

On history, mom says that the child began having classic URTI symptoms on Sunday (1 day ago) including a cough, rhinorrhea, and increased work of breathing. He also had a temperature of 38.4 C by ear on Sunday. Today, he began having what mom describes as increased work of breathing and a barking seal like cough.

Mom shows you two videos from this morning of the increased work of breathing and the barking-seal like cough:

Example of increased work of breathing (assume this is at home without the monitors attached):

https://www.youtube.com/watch?v=KQTEu1mpRY8&t=3s

As an astute clerk, you look for signs of increased work of breathing including tracheal tug, chest wall indrawing (inter, supra, or subcostal), abdominal breathing, grunting, head bobbing, cyanosis, nasal flaring, pursed lip breathing, and tachypnea.

Example of barking seal-like cough:

https://www.youtube.com/watch?v=UWOrKzgp3Wc

You agree that this sounds classically like a croup presentation.

The rest of the history including pregnancy, family, social, developmental, medications, allergies, and medical is largely unremarkable. The child’s vaccinations are up to date.

Mom is concerned as she feels the child is feeding and drinking less, but they are still having a normal number of wet (~6/day) and dirty (~1/day) diapers.

Physical Exam:

The child appears well in the ED, they are fussy and fighting your exam, they are jumping on the bed and playing with mom, they find comfort in mom, and they are even playing peek-a-boo with the RNs. You currently do not hear the barking seal like cough, nor stridor. They have mild intercostal indrawing, but no other signs of respiratory distress. No cyanosis is present.

Vitals are unchanged from the chart; the RR is still mildly elevated at ~40-45/min.

Resp: Mildly decreased air entry bilaterally, no crackles/wheezes. Mild stridor transmitted from upper respiratory tract upon agitation.

Fluid Status: Moist mucous membranes, fontanelles not bulging or sunken in, skin turgor is normal (no excessive tenting of skin), and when prompted they drink apple juice mixed with water.

You complete a thorough head to toe exam including HEENT, Neuro, Cardio, Abdo, GU, and MSK, aside from some cerumen in the ears and some rhinorrhea, the exam is within normal limits.

Differential Diagnosis [1-3]:

Croup

Bacterial tracheitis

Epiglottitis

COVID-19

Foreign body aspiration

Neoplasm

Hemangioma

Peritonsillar abscess

Retropharyngeal abscess

Acute anaphylaxis reaction

Bronchiolitis

Bronchiolitis and lower respiratory tract infections would present with wheeze rather than stridor [1-3].
Peritonsillar and retropharyngeal abscesses would have a hot potato voice, and potentially a mass on the neck [1-3].
In children <6 months old it is important to consider congenital presentations such as choanal atresia and tracheoesophageal fistula [1-3].
URTI symptoms would not be present in isolated foreign body aspiration but should be considered [1-3].
It is important to differentiate croup from epiglottitis because epiglottitis can lead to rapid deterioration and often requires operating room intubation [1,2]. Drooling suggests epiglottitis whereas cough suggests croup, both have a high sensitivity and specificity for each respective diagnosis [1-3,4].
Bacterial tracheitis the child would look much sicker and more toxic, and this would be represented on vital signs as well [1-3].

Croup:

Croup is a viral illness most commonly caused by parainfluenza virus, it is formally called laryngotracheobronchitis as it is inflammation of upper airway including the larynx, trachea, and bronchi [1,5].

Croup is a common presentation to Canadian emergency departments, most of which will be mild forms of croup, however occasionally hospitalization will be required, and rarely intubation is needed [1,6]

Classically croup will present in children between 6 months – 3 years old, with a 1-2 day history of URTI symptoms followed by a barking cough and stridor [1,7,8]. As this causes inflammation and obstruction of the upper respiratory tract, stridor will be present and often is more pronounced with agitation and at night [1,2]. A low-grade fever may be present, but is not required for the diagnosis, the child will not typically have drooling or dysphagia (if this is present consider epiglottitis) [1-3]. Parents will often be concerned/alarmed by the barking cough sounds.

As with most viral infections, croup is a self-limiting illness and most management is supportive, improvement should be noted within 2-7 days [1,6,7].

The diagnosis of croup is a clinical one of the child meeting the clinical picture outlined above and ruling out other causes with history and physical [1-3]. A radiograph is not needed to diagnose croup however if obtained due to uncertainty, will often show a narrowing of the glottic and subglottic areas in a classic steeple sign [3]. Whereas epiglottitis will show a thumb sign [9].

Picture taken from: https://www.pinterest.ca/pin/541980136386136007/

Picture taken from: https://kidshealth.org/Nemours/en/parents/az-croup.html

Workup of the Patient…

You remember some clinical decision aids for croup management… So, you employ the Westley Scoring System for Croup Severity [10]. As our child has a normal LOC, no cyanosis, stridor with agitation, mildly decreased air entry, and moderate retractions. They receive a Westley Score of 4 = moderate croup.

Mild </= 2

Moderate = 3-7

Severe = >/=8

Picture taken from: https://www.uptodate.com/contents/image/print?imageKey=PEDS%2F100744&topicKey=PEDS%2F6004&rank=1~60&source=see_link&search=croup&utdPopup=true

Based on this you pull out a trusted croup decision aid guide [1,11]:

Taken from: https://cps.ca/documents/position/acute-management-of-croup

In summary:

Mild croup, children will be given oral dexamethasone classically the dose is 0.6 mg/kg of body weight, however literature has shown equal effectiveness with 0.3 mg/kg, therefore some practitioners may opt for this lower in patients with moderate or mild croup [1,11,12]. Parents will be educated, and the child will be discharged home [1,11].

Moderate croup, the child will be given the same dose of dexamethasone and will be observed for 4 hours for improvement and sent home if symptoms have improved [1,11].

Severe croup, the child will be given blow-by O2 if cyanosis present, racemic epinephrine 2.25% (0.5 ml in 2.5 ml of normal saline) OR L-epinephrine 1:1000 5 mL, and the same dose of dexamethasone as above [1,11]. They will be observed for 2 hours and either sent home or admitted based on response [1,11].

Of note… previously aerosolized racemic epinephrine or L-epinephrine was given, however to reduce aerosolized treatments during the COVID-19 pandemic some emergency departments have received special authorization to give a puffer with epinephrine which was previously only approved in the US.

Case Conclusion

As our child had moderate croup and weighs 10.2 kg, they were given 0.3 mg/kg of dexamethasone which was 3.6 mg. We also performed a viral swab, which returns negative for COVID-19, but positive for parainfluenza virus, re-enforcing your diagnosis of croup. They were observed in the ED and quickly improved with no more increased work of breathing, and no stridor at rest. As such they were discharged to the care of their parents, and the parents’ received education on supportive management and indications to re-seek medical care. In fact, the SJRH ED has a handy parent information sheet that you give to the mother, which she is very appreciative of.

References:

Ortiz-Alvarez O, Canadian Pediatric Society, Acute Care Committee. Acute management of croup in the emergency department. J Paediatr Child Health. 2017;22(3):166-9. https://cps.ca/documents/position/acute-management-of-croup#ref1
Sizar O, Carr B. Croup. [Updated 2021 Jul 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. https://www.ncbi.nlm.nih.gov/books/NBK431070/
Smith DK, McDermott AJ, Sullivan JF. Croup: Diagnosis and Management. Am Fam Physician. 2018;97(9):575-80. https://www.aafp.org/afp/2018/0501/p575.html
Tibballs J, Watson T. Symptoms and signs differentiating croup and epiglottitis. J Paediatr Child Health. 2011;47(3):77-82. https://pubmed.ncbi.nlm.nih.gov/21091577/
Rihkanen H, Rönkkö E, Nieminen T, et al. Respiratory viruses in laryngeal croup of young children. J Pediatr 2008;152(5):661–5. https://pubmed.ncbi.nlm.nih.gov/18410770/
Rosychuk RJ, Klassen TP, Metes D, Voaklander DC, Senthilselvan A, Rowe BH. Croup presentations to emergency departments in Alberta, Canada: A large population-based study. Pediatr Pulmonol 2010;45(1):83–91. https://pubmed.ncbi.nlm.nih.gov/19953656/

Johnson DW. Croup. BMJ Clin Evid. 2014. https://pubmed.ncbi.nlm.nih.gov/25263284/
Bjornson CL, Johnson DW. Croup in children. CMAJ. 2013;185(15):1317-23. https://www.cmaj.ca/content/185/15/1317
Takata, Fujikawa, Goto. Thumb sign: acute epiglottitis. BMJ Case Rep. 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4904439/
Yang WC, Lee J, Chen CY, Chang YJ, Wu HP. Westley score and clinical factors in predicting the outcome of croup in the pediatric emergency department. Pediatr Pulmonol. 2017;52(10):1329-34. https://pubmed.ncbi.nlm.nih.gov/28556543/
Toward Optimized Practice. Diagnosis and Management of Croup. Clinical Practice Guideline, January 2008. www.topalbertadoctors.org/download/252/croup_guideline.pdf.
Geelhoed GC, Macdonald WB. Oral dexamethasone in the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus 0.6 mg/kg. Pediatr Pulmonol. 1995;20(6):362-8. https://pubmed.ncbi.nlm.nih.gov/8649915

Colovesicular fistula

Posted on March 14, 2022 by Mandy Peach

Approach to diagnosing Colovesicular fistula- A Medical Student Clinical Pearl

Emmanuel Hebert

Med 4, Dalhousie Medicine

Reviewed by Dr. Chris Doiron

Copyedited by Dr. Mandy Peach

Case

54 y/o M presents with a bizarre presenting complaint at 10am Monday morning…

You enter the room to see a man in no apparent distress who tells you that for the past two days something that looks like feces is coming out of his penis. The patient went to the bathroom to urinate Sunday night and noted air coming out of his penis that felt as if he were passing flatus. He then noticed brown foul-smelling liquid upon urinating. There was no blood. He reports no suprapubic fullness, pain with urination, or urgency. He denies any abdominal or pelvic pain. He noted chills Sunday evening which resolved and have not returned after a single dose of acetaminophen 500mg.

Past Medical History:

Hypertension

Adenocarcinoma of rectum- 2019

Radiation Therapy- 2019

Partial Bowel resection with ileostomy and stoma- 2019

Reversion of ileostomy- 2020

Medications: Coversyl Plus

Allergies: Codeine, penicillin

Physical Examination:

Patient is comfortable and appears well. Vitals: HR 85; Temp 36.5; BP: 125/80; O2Sat99% on RA. Abdominal exam is unremarkable. There is no suprapubic or CVA tenderness on palpation. Pelvic exam reveals a penis with no discharge or tenderness.

Initial bloodwork:

WBC: 11×10^9/L
Hgb: 135
Plt: 300×10^9/L
Na: 135
K: 4.0
CRP: 80
Lactate: 1.0
Creatinine: 100
eGFR: N

Urinalysis: Grossly brown with + leukocytes, Nitrite positive and RBCs present

What is the differential diagnosis of pneumaturia?

Recent urinary tract instrumentation, catheterization.
Urinary tract infection with a gas forming organism (emphysematous cystitis).
Emphysematous pyelonephritis (rare) [1]
Colovesicular and enterovesicular Fistula as a result of complicated Diverticulitis, Crohn’s Disease or Carcinoma of the Colon or Bladder

Colovesicular Fistula

Colovesicular and enterovesicular fistulas are defined as connections between the enteric lumen and the bladder. [2] There are many ways that tissue can develop a fistula but in the enteric system there are several common etiologies [3]:

Diverticulitis: 65–79% of cases
Cancer (mostly adenocarcinoma): 10–20%
Crohn’s Disease: 5-7%
Previous radiation, bowel surgery, perforated peptic ulcer, genitourinary coccidioidomycosis, pelvic actinomycosis, and appendicitis make up the remaining cases.

Symptoms of Colovesicular Fistula

Figure 1: Graphic showing the common symptoms of colovesicular fistula

The classic findings of enterovesicular and colovesicular fistulas known as Gouveneur’s Syndrome are suprapubic pain, frequency, dysuria, and tenesmus.

Notwithstanding, pneumaturia, fecaluria and recurrent UTIs are pathognomonic with over 75% of patients presenting with these three findings. [3]

Investigations

Urinalysis (U/A) and culture can be useful on initial presentation to help guide diagnosis. In colovesicular fistula, U/A can reveal white blood cells and feces in the urine. Cultures will typically grow bacteria associated with the enteric system with E. coli being the most common pathogen (81% ). [3] (Note: E. coli is a common pathogen in the setting of an uncomplicated UTI thus E. coli growth does not necessarily mean the patient has a fistula)

It is important to assess for evidence of sepsis in any patient with suspected colovesicular fistula. If the patient displays signs of fever and/or shock, blood and urine cultures and other labs to guide resuscitation and management are indicated. There are no blood tests that help definitively diagnose a colovesicular fistula.

When the clinical suspicion of colovesicular fistula is high, computed tomography (CT) of the abdomen and pelvis with oral/rectal contrast but without IV contrast is indicated. IV contrast is excreted by kidneys and can appear in the bladder confusing the origin of the contrast. Rectal contrast, however, should not appear in the bladder and its presence can help confirm the diagnosis. CT findings indicative of colovesicular fistula include air in the bladder/ureters, visualization of the fistula tract, oral/rectal contrast in the bladder, and bladder thickening adjacent to a thickened loop of bowel. [3]

Point of care ultrasound may identify echogenic material (fecal material), reverberation artifact indicative of gas within the bladder or thickened bowel abutting the bladder though is not generally nor should be considered a modality for the diagnosis of colovesicular fistula.

MRI provides excellent resolution of a fistula tract and potential underlying pathology however, given lack of access and the associated time and financial costs, CT remains the modality of choice for the diagnosis of colovesicular fistula in the emergency department. [3]

Figure 2: CT Abdomen-Pelvis revealing pneumoureter in the left image and the colovesicular tract in the right image.

Management

The definitive management of a colovesicular fistula is surgical repair. Timing is dependent on several factors including hemodynamics at presentation, patient comorbidities, and etiology of the fistula (diverticulitis vs malignancy). In rare cases, conservative management may be considered if the patient is too frail for surgery. Septic patients should be resuscitated as per sepsis guidelines while stable patients should receive broad spectrum antibiotics with ciprofloxacin and metronidazole or amoxicillin-clavulanate being common regimens. Surgical consultation is recommended in all patients after initial resuscitation and imaging. [2]

Back to the case:

CT abdomen-pelvis was performed which showed air in the ureter and bladder as well as a tract connecting the sigmoid colon to the bladder. General Surgery was consulted and Piperacillin/Tazobactam 3.375g IV q6h was started. As the patient was stable, surgery asked that the patient be held in the ED until they could be seen latter in the day.

Two Hours Later

• On reassessment, patient appeared unwell and visibly diaphoretic. He was febrile with a temp of 38.5, a HR of 110 and a BP of 100/70. Repeat labs showed a white count of 14 and a lactate of 2.5.
• Diagnosis of septic shock was made and resuscitation started.
• Surgery was notified who opted to bring the patient to the OR for emergent exploratory laparotomy.

In the OR:

• The bladder was attached to the sigmoid colon via a thick adhesion. The surgeon had difficulty discerning what was bladder and what was intestine.
• Intestine was resected and an ileostomy was placed with stoma.
• Patient tolerated procedure well and was admitted to ICU for monitoring.

Figure 3: Laparoscopic View of bowel adhered to the bladder

Key Takeaways

Most colovesicular fistulas are the result of complicated diverticulitis.
Pneumaturia is highly suggestive for enterovesicular fistula in the absence of recent bladder instrumentation.
CT abdomen/pelvis with oral and rectal contrast without IV contrast is the imaging modality of choice.
Patients can go from stable to septic shock quickly.
The definitive management is surgical [2]

References:

Youssef S. Tanagho, Jonathan M. Mobley, Brian M. Benway, Alana C. Desai, “Gas-Producing Renal Infection Presenting as Pneumaturia: A Case Report”, Case Reports in Medicine, vol. 2013, Article ID 730549, 3 pages, 2013. https://doi.org/10.1155/2013/730549
Granieri, S., Sessa, F., Bonomi, A., Paleino, S., Bruno, F., Chierici, A., Sciannamea, I. M., Germini, A., Campi, R., Talso, M., Facciorusso, A., Deiana, G., Serni, S., & Cotsoglou, C. (2021). Indications and outcomes of enterovesical and colovesical fistulas: systematic review of the literature and meta-analysis of prevalence. BMC surgery, 21(1), 265. https://doi.org/10.1186/s12893-021-01272-6
Tomasz Golabek, Anna Szymanska, Tomasz Szopinski, Jakub Bukowczan, Mariusz Furmanek, Jan Powroznik, Piotr Chlosta, “Enterovesical Fistulae: Aetiology, Imaging, and Management”, Gastroenterology Research and Practice, vol. 2013, Article ID 617967, 8 pages, 2013. https://doi.org/10.1155/2013/617967
Kavanagh, P. Neary, J. D. Dodd, K. M. Sheahan, D. O’Donoghue, and J. M. P. Hyland, “Diagnosis and treatment of enterovesical fistulae,” Colorectal Disease, vol. 7, no. 3, pp. 286–291, 2005.

QUICK TIPS on STEMI equivalents

Posted on March 7, 2022 by Mandy Peach

QUICK TIPS on STEMI equivalents – A Medical Student Clinical Pearl

Ilya Abelev

MD Candidate, Class of 2022

Dalhousie Medical School New Brunswick

Reviewed by Dr. Jay Mekwan

Copyedited by Dr. Mandy Peach

Why recognize STEMI’s?²

STEMI’s indicate an infarction pattern on ECG, and can guide emergency physicians to identify patients who would benefit from emergent catheterization and revascularization.

What is a STEMI?

(S-T Segment Elevation Myocardial Infarction)

A patient presents with clinical symptoms consistent with an acute coronary syndrome together with S-T segment elevation (STE) on ECG or a new LBBB.

What is a STEMI equivalent?

A STEMI equivalent is an ECG pattern suggestive of ischemia that should trigger emergency physicians to consult specialists such as interventional cardiologists for revascularization interventions – similar to a STEMI.

MI Definition¹

• ≥ 2.5 mm STE in V2-V3 for males < 40 years*
• ≥ 2 mm STE in V2- V3 for males ≥ 40 years*
• ≥ 1.5 mm STE in V2-V3 for females regardless of age*
• ≥ 1 mm STE all other leads

• New J-point elevation ≥ 1 mm from prior ECG should be considered ischemic
• The J-point is defined as the junction between the QRS termination and the ST-segment onset, and the ST-segment should be measured against the isoelectric TP segment (assuming a stable baseline)³

J point in a) normal; b) c) J point elevation; d) J point depression; e) with J wave (Osborn wave)

Osborn wave: Characteristically seen in hypothermia (typically T < 30C), but they are not pathognomonic (4)

Mnemonic for Stemi Equivalents – PTSD (5)

Posterior MI
T wave Abnormalities
Sgarbossa Criteria
Diffuse ST depression with ST elevation in AVR

Posterior MI (1,6)

“Posterior MIs are easily missed because of the absence of any ST elevation. Posterior involvement is estimated to occur in 15-21% of all acute myocardial infarctions and in isolation ~3% of the time, typically due to occlusion of the left circumflex or right coronary arteries.”

More Information(7)

“As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.”

Posterior MI is suggested by the following changes in V1-3:

Horizontal ST depression
Tall, broad R waves (>30ms)
Upright T waves
Dominant R wave (R/S ratio > 1) in V2” (7)

Image illustrating reciprocal changes in V2 and how a ST depression in V2 can appear like a STEMI when flipped (reciprocal)

Where to expect reciprocal changes?

PAILS (8)

Posterior MI – anterior reciprocal changes
Anterior MI – inferior reciprocal changes
Inferior MI – lateral reciprocal changes

Lateral MI <-> inferior or septal reciprocal changes*** exception to mnemonic
Septal MI – posterior reciprocal changes

T wave abnormalities

de Winter T-waves (9,10)

Key 12-Lead Features

“J-Point depression with up-sloping ST segments.
Tall, prominent, symmetric T waves in the precordial leads.
Upsloping ST segment depression > 1mm at the J-point in the precordial leads.
Absence of ST elevation in the precordial leads.
ST segment elevation (0.5mm-1mm) in aVR.
“Normal” STEMI morphology may precede or follow the DeWinter pattern.”

Wellens Syndrome(11)

Rhinehart et al (2002) describe the following Diagnostic criteria(12) for Wellens syndrome:

• “Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
• ECG pattern present in pain-free state
• Isoelectric or minimally-elevated ST segment (< 1mm)
• No precordial Q waves
• Preserved precordial R wave progression
• Recent history of angina
• Normal or slightly elevated serum cardiac markers”

“There are two patterns of T-wave abnormality in Wellens syndrome:

Type A/1 – Biphasic, with initial positivity and terminal negativity (25% of cases)
Type B/2 – Deeply and symmetrically inverted (75% of cases)”

Sgarbossa Criteria(13,14)

In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG can be difficult
Abnormal depolarisation should be followed by abnormal repolarisation, manifesting as ST-segment and T-wave deviations that do not necessarily indicate acute ischaemia (“appropriate discordance”)

Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)

Concordant ST depression > 1 mm in V1-V3 (score 3)

Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

“These criteria are specific, but not sensitive (36%) for myocardial infarction. A total score of ≥ 3 is reported to have a specificity of 90% for diagnosing myocardial infarction.”(13)

Diffuse ST depression with ST elevation in AVR(1)

“STE ≥ 1 mm in aVR or V1 with STD ≥ 1 mm in ≥ 6 leads can suggest left main coronary artery insufficiency, proximal LAD insufficiency, or triple vessel disease, especially if accompanied by pathologic Q-waves, hemodynamic compromise, and/or refractory symptoms.”

• Widespread deep ST depression involving V2-6, I, II, aVL
• ST elevation in aVR > V1

Examples of STEMI Equivalents(16): Resource to test knowledge of STEMI equivalents

Conclusion:

Definition of MI varies by age and sex
Use PTSD mnemonic to remember the STEMI equivalents.
a. Use PAILS to remember appropriate location of reciprocal changes
Initiate appropriate consultation to revascularize/ stent for both STEMI and STEMI equivalents

References

Daniel Kreider; Jeremy Berberian. STEMI Equivalents: Can’t-Miss Patterns EMRA [Internet]. [cited 2022 Feb 19]. Available from: https://www.emra.org/emresident/article/stemi-equivalents/
Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Fourth Universal Definition of Myocardial Infarction (2018). Circulation. 2018 Nov 13;138(20):e618–51.
J point ECG Interval • LITFL • ECG Library Basics [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/j-point-ecg-library/
Slovis C, Jenkins R. Conditions not primarily affecting the heart. BMJ. 2002;
STEMI Equivalents for ECGs – YouTube [Internet]. [cited 2022 Feb 19]. Available from: https://www.youtube.com/watch?v=lH19cYBdvaQ
van Gorselen EOF, Verheugt FWA, Meursing BTJ, Oude Ophuis AJM. Posterior myocardial infarction: the dark side of the moon. Neth Heart J. 2007;
Posterior Myocardial Infarction • LITFL • ECG Library Diagnosis [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/posterior-myocardial-infarction-ecg-library/
Tiny Tips: STEMI? Don’t forget your PAILS! – CanadiEM [Internet]. [cited 2022 Feb 19]. Available from: https://canadiem.org/chest-pain-pails/
de Winter RJ, Verouden NJW, Wellens HJJ, Wilde AAM. A New ECG Sign of Proximal LAD Occlusion. N Engl J Med. 2008;
DeWinter’s T-Waves [Internet]. [cited 2022 Feb 19]. Available from: https://handbook.bcehs.ca/clinical-practice-guidelines/pr-clinical-procedure-guide/pr16-12-lead-ecgs/stemis-equivalents-imposters/stemi-equivalents/dewinters-t-waves/
Wellens Syndrome: A Historical Literature Review – Dr. Jason West [Internet]. [cited 2022 Feb 19]. Available from: https://jacobiem.org/wellens-syndrome-a-historical-literature-review-dr-jason-west/
Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002;
Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified sgarbossa rule. Ann Emerg Med. 2012;
Sgarbossa Criteria • LITFL • ECG Library Diagnosis [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/sgarbossa-criteria-ecg-library/
Sgarbossa Criteria – MEDZCOOL – YouTube [Internet]. [cited 2022 Feb 19]. Available from: https://www.youtube.com/watch?v=oLFJy1e9WWI&t=135s
STEMI Equivalents — Maimonides Emergency Medicine Residency [Internet]. [cited 2022 Feb 19]. Available from: https://www.maimonidesem.org/blog/stemi-equivalents-1

A Case of Pneumomediastinum

Posted on January 26, 2022 by Mandy Peach

A Case of Pneumomediastinum: A Medical Student Clinical Pearl

Reviewed by Dr. Maria Kovalik

Copyedited by Dr. Mandy Peach

Nick Ellingwood, Med II

Dalhousie Medicine New Brunswick (DMNB)

Case

A 16 year-old male presented to the emergency department complaining of shortness of breath which started 3 days prior. He stated that he was unable to take a deep breath. The patient described a sore throat with a productive cough. The patient also revealed that he was having some generalized chest tightness which did not radiate and was non-pleuritic. The patient was also experiencing some diarrhea as well as nausea when he eats. The patient denied any abdominal pain, vomiting, dysphagia, or fever. He had no past medical or surgical history and taking no medications.

On Examination:

Vitals: Temp=36.7^oC, HR=126, RR=24, BP=100/62, O₂ Sat=95% The patient was sitting comfortably but did appear to be dyspneic. He was of normal body habitus.

On examination, upon palpation there was crepitus in the lower neck, supraclavicular region, and shoulder region on both sides. There was diffused crackles upon auscultation over the anterior and posterior chest wall. Good air entry into the base of both lungs and no wheezing. There was a normal S1 and S2 with no additional heart sounds or murmurs. Abdomen was soft and non-tender with normal bowel sounds.

A nasopharyngeal swap, chest X-ray, cervical X-ray, CBC, electrolytes, creatinine, urea, random glucose were ordered.

Figure 1. Chest X-ray showing extensive subcutaneous emphysema along the chest wall and lower neck and a pneumomediastinum. There is bilateral perihilar opacities but no pneumothorax or pleural effusion.

Figure 2. Cervical X-rays showing subcutaneous emphysema in the supraclavicular and lower neck regions as well as the retropharyngeal region extending beyond the angle of the mandible.

Etiologies of Pneumomediastinum^1,2:

Acute asthma exacerbations
Covid-19 or other lower respiratory infections
Injury to thoracic cavity or airways from surgery, trauma, inhalation of drugs, or Valsalva maneuvers
Perforated esophagus (Boerhaave syndrome)

Case Continued:

A CT chest was ordered to evaluate the extent of the pneumomediastinum and subcutaneous emphysema and rule out severe etiologies such as esophageal and bronchi rupture which were not present. The nasopharyngeal swap came back negative for Covid-19 but positive for another coronavirus. The bloodwork showed leukocytosis (25×10⁹/L) but was otherwise unremarkable. The diagnosis of pneumomediastinum secondary to coronavirus infection was made.

Pathophysiology:

As seen in Figure 3, a pneumomediastinum can result from air escaping from small alveolar ruptures into the surrounding bronchovascular sheath. Air then travels along a pressure gradient through the bronchovascular sheath to the hilum and builds up in the mediastinum.³ From there, air can freely move subcutaneously to the chest wall, upper limbs, and neck. Less commonly, air will directly escape into the mediastinum from a more central structure such as the upper respiratory tract or the esophagus.

Figure 3. Pathophysiology of pneumomediastinum and subsequent subcutaneous emphysema.

https://www.uptodate.com/contents/image/print?imageKey=PEDS%2F111129&topicKey=6352&search=pneumomediastinum&rank=1~111&source=see_link

Additional Exam Findings:

Hamman’s sign is described as a crunching or rasping sound heard over the precordium that is synchronous with systole and tends to be best heard with the patient in the left lateral decubitus position. This sign can be positive in up to 50% of patients with pneumomediastinum and is specific for pneumomediastinum or pneumopericardium^4,5.

PoCUS Findings:

Firstly, in a pneumomediastinum the visualization of the cardiac structures is commonly obstructed by the presence of an “air gap” which is characterized by diffused A-lines anterior to the heart when in the parasternal and apical views. This can also be present in pneumothorax; however, the key difference is that in a pneumothorax the cardiac structures will be visualize during diastole when the heart dilates and pushes the pleural air to the side. In a pneumomediastinum, the air gap will vary with the respiratory cycle (not the cardiac cycle such as in a pneumothorax) because during inspiration the lungs will expand and push the air in the mediastinum cranially allowing the cardiac structures to be visualized⁶.

There are other clinical tools that can be used to differentiate a pneumomediastinum and a pneumopericardium like ECG changes. However, they can also be easily differentiated using PoCUS because the cardiac structures can’t be visualized in the subxiphoid view in a pneumopericardium. In contrast, the absence of air between the diaphragm, pericardium and myocardium allows the cardiac structure to be visualized in the setting of a pneumomediastinum as seen in Figure 4⁷.

Figure 4. PoCUS images showing a pneumomediastinum where box A (subxiphoid view) shows cardiac structures. The parasternal long (B), parasternal short (C), and apical (D) views all show diffuse A-lines suggesting the presence of the air superficial to the heart. These findings would suggest a pneumomediastinum⁷.

Treatment:

Pneumomediastinum normally follows a benign course and is self-limiting
Some patients undergo bronchoscopy or esophagogram to rule out airway or esophageal injury
Admission is recommended to observe for complications because pneumopericardium and pneumorachis can arise^8,9
Supplemental oxygen is given to help promote gas reabsorption
Simple analgesics are used for pain management as needed

Case Conclusion:

The patient was on 4L/min of oxygen while in hospital, and his symptoms significantly improved. Repeat chest X-ray showed improvement in pneumomediastinum and subcutaneous emphysema and he was discharge after 3 days. A chest X-ray 10 days later showed minimal subcutaneous emphysema, and the patient had no symptoms.

Clinical Pearls:

Pneumomediastinum is rare but something to keep in your differential for chest pain and SOB especially in young thin males
There are some life-threatening etiologies of pneumomediastinum that must be ruled out
There are some specific PoCUS findings for pneumomediastinum that can help with your diagnosis
The treatment for pneumomediastinum is rest, simple analgesics, and oxygen

References:

1: Ojha S, Gaskin J. Spontaneous pneumomediastinum. BMJ Case Rep. 2018;2018:bcr2017222965. Published 2018 Feb 11. doi:10.1136/bcr-2017-222965

2: Spontaneous pneumomediastinum in children and adolescents – UpToDate [Internet]. [cited 2021 Dec 17]. Available from: https://www.uptodate.com/contents/spontaneous-pneumomediastinum-in-children-and-adolescents?search=pneumomediastinum&source=search_result&selectedTitle=1~111&usage_type=default&display_rank=1

3: Ivan Macia, Juan Moya, Ricard Ramos, Ricard Morera, Ignacio Escobar, Josep Saumench, Valerio Perna, Francisco Rivas, Spontaneous pneumomediastinum: 41 cases, European Journal of Cardio-Thoracic Surgery, Volume 31, Issue 6, June 2007, Pages 1110–1114

4: Sahni S, Verma S, Grullon J, Esquire A, Patel P, Talwar A. Spontaneous pneumomediastinum: time for consensus. N Am J Med Sci. 2013 Aug;5(8):460-4. doi: 10.4103/1947-2714.117296. PMID: 24083220; PMCID: PMC3784922.

5: Alexandre AR, Marto NF, Raimundo PHamman’s crunch: a forgotten clue to the diagnosis of spontaneous pneumomediastinumCase Reports 2018;2018:bcr-2018-225099.

6: Ng L, Saul T, Lewiss RE. Sonographic evidence of spontaneous pneumomediastinum. Am J Emerg Med. 2013 Feb;31(2):462.e3-4. doi: 10.1016/j.ajem.2012.08.019. Epub 2012 Nov 15. PMID: 23158605.

7: Zachariah, S., Gharahbaghian, L., Perera, P., & Joshi, N. (2015). Spontaneous pneumomediastinum on bedside ultrasound: case report and review of the literature. The western journal of emergency medicine, 16(2), 321–324. https://doi.org/10.5811/westjem.2015.1.24514

8: Vanzo V, Bugin S, Snijders D, Bottecchia L, Storer V, Barbato A. Pneumomediastinum and pneumopericardium in an 11-year-old rugby player: a case report. J Athl Train. 2013 Mar-Apr;48(2):277-81. doi: 10.4085/1062-6050-48.1.11. Epub 2013 Feb 20. PMID: 23672393; PMCID: PMC3600931.

9: Belotti EA, Rizzi M, Rodoni-Cassis P, Ragazzi M, Zanolari-Caledrerari M, Bianchetti MG. Air within the spinal canal in spontaneous pneumomediastinum. Chest. 2010 May;137(5):1197-200. doi: 10.1378/chest.09-0514. PMID: 20442120.

It’s Not Over Till It’s Over – ECMO Resuscitation in the ED

Posted on November 30, 2021 by Mandy Peach

It’s Not Over Till It’s Over – ECMO Resuscitation in the ED: A Medical Student Clinical Pearl

Ryan Buyting

Med III, Class of 2022

Dalhousie Medicine New Brunswick (DMNB)

Reviewed by Dr. Luke Taylor

Copyedited by Dr. Mandy Peach

Extracorporeal Membrane Oxygenation (ECMO), also sometimes referred to as extracorporeal life support (ECLS), employs components from traditional cardiopulmonary bypass machines to augment a patient’s heart and/or lung capacity for a prolonged duration of days to weeks. Importantly, ECMO is not a treatment but a bridge to native heart/lung recovery or durable organ replacement. ¹

ECMO has been a hot topic of discussion over the past year based on its role in supporting patients with severe COVID-19 infections. The Extracorporeal Life Support Organization (ELSO), the World Health Organization and the Surviving Sepsis Campaign (SSC) Guidelines recommend considering ECMO, in specialized centers, for patients with COVID-19 who develop severe acute respiratory distress syndrome (ARDS). ² Many of these cases made use of veno-venous ECMO, which exclusively provides pulmonary bypass for severe respiratory failure.

This article will focus on veno-arterial ECMO (which provides both cardiac and pulmonary bypass) and seeks to provide readers with an overview of the following:

What is an Extracorporeal Cardiopulmonary Resuscitation (ECPR) code?
Which patients should be considered for acute ECMO initiation?
What care will patients need in the ED post-circuit initiation?
What is the evidence for the use of ECPR?

Calling an ECPR Code and Patient Selection

An ECPR code essentially mobilizes the cannulation team to initiate an ECMO circuit in a previously high-functioning patient. The goal is to restore end-organ perfusion, buying time to investigate the underlying causative pathology, with hopes of improving long-term survival and neurological outcomes. Emergency physicians should consider calling an ECPR code for severe cardiac and/or pulmonary failure deemed refractory to conventional therapies. ³ Patients in cardiac arrest are potential candidates for ECPR if they meet the following:

reversible cause of arrest
witnessed arrest with bystander CPR
total chest compression time < 60 minutes
no known preexisting terminal illnesses

Review the reversible causes of cardiac arrest or see the image below outlining the “Hs and Ts” mnemonic.

Figure 1: The Hs and Ts / Reversible Causes of Cardiac Arrest ⁴

The timing at which an ECPR code should be initiated is (at present) left to physician discretion, but often depends on the availability of the cannulation team. ECMO as an option for a given patient should be anticipated and considered early amid a code to allow the team and equipment to be assembled. Most often the procedure is performed by a cardiac surgeon, however there is growing interest and involvement from vascular, general, and trauma surgeons. ⁵

The initiation of ECMO is divided into 3 stages:

(1) vascular access,

(2) insertion of ECMO cannulas and connection to the circuit once the patient is determined to be an ECMO candidate,

(3) pump initiation.

In emergent situations, unilateral peripheral cannulation is the preferred and most expedient method. ⁶ This approach also allows for the continuation of high-quality CPR while access is obtained. Either through surgical exposure or under ultrasound guidance, a venous drainage cannula is placed in the femoral vein. Blood is returned from the machine through a similarly placed cannula in the adjacent femoral artery. Several alternative circuits are possible in extenuating circumstances depending upon patient injuries or characteristics. ¹

Figure 2: Veno-arterial peripheral ECMO via unilateral femoral-arterial and femoral-venous cannulation. ⁷

Post-Circuit Initiation Critical Care

After the circuit has been initiated, the lines should be closely examined; the venous drainage blood should be dark red and the arterial return blood should be bright red. Given the proximity of the vessels and the fact that these procedures are often done with ongoing CPR, this confirmation of placement is crucial.

Next, it is important to reassess the patient’s rhythm; if the patient is in VFIB, defibrillation should be repeated after a few minutes on circuit as it is important to have an ejecting left ventricle on ECMO to prevent distention. ⁸

At this point, the team should obtain a right radial arterial line (for accurate measurement of the MAP) and an ABG (to assess for adequate oxygenation and the need for setting adjustments). Vasopressors and/or inotropes should be initiated as required to meet a target MAP of 60-80mmHg. If LV distention (as assessed based on arterial line pulsatility >10mmHg or POCUS) is not improved with these medications on board, an LV vent (such as an Impella or intra-aortic balloon pump) may be needed. ⁸

Important next steps in the process include the initiation of therapeutic hypothermia, planning for the placement of a distal perfusion catheter to prevent leg ischemia, and, based on the etiology of the arrest, any other appropriate treatment (such as transfer to the cardiac catheterization laboratory for acute coronary syndrome).

Current Evidence for ECPR

No randomized trials concerning the use of ECPR have been published to date. Sonneville and Schmidt recently summarized the four most robust observational studies comparing the use of ECPR versus conventional CPR in patients with out-of-hospital cardiac arrest. ⁹ They describe a large study that reported similar low survival rates between 525 patients managed with ECPR and 12,666 patients with conventional CPR, with no significant effect of ECPR on outcomes after adjusting for confounders. ¹⁰ However, more recently, after instituting very strict patient selection criteria, Bartos et al. reported a relative risk reduction of 29% for death or poor neurological outcome (95% CI, 18%–41%) for patients receiving between 20 and 59 minutes of CPR and 19% (95% CI, 10%–27%) for patients receiving more than 60 minutes of CPR. ¹¹ This group has since published the University of Minnesota ECPR Protocol here. ¹²

Until results from randomized trials become available, it is likely that difficult continuation decisions will need to be made on a case-by-case basis at physician discretion. Protocols requiring objective data input such as specific time periods, lactate level and oxygenation status upon arrival, may help ease this burden in the meantime, if only marginally.

References

Badulak JH, Shinar Z. Extracorporeal Membrane Oxygenation in the Emergency Department. Emerg Med Clin North Am. 2020;38(4):945-959. doi:10.1016/j.emc.2020.06.015
Ramanathan K, Shekar K, Ling RR, et al. Extracorporeal membrane oxygenation for COVID-19: a systematic review and meta-analysis. Crit Care. 2021;25(1):211. doi:10.1186/s13054-021-03634-1
Extracorporeal Life Support Organization (ELSO). Guidelines. Accessed August 29, 2021. https://www.elso.org/Portals/0/ELSO%20Guidelines%20General%20All%20ECLS%20Version%201_4.pdf
@lightssirensaction. Hs and Ts. Accessed August 28, 2021. https://www.instagram.com/p/CA4MMdVBy8V/
McCallister D, Pilon L, Forrester J, et al. Clinical and Administrative Steps to the ECMO Program Development. IntechOpen; 2019. doi:10.5772/intechopen.84838
Stoecklein H, Slack S, Tonna JE, Youngquist ST. ECMO & ECPR. JEMS. Published December 2, 2017. Accessed August 28, 2021. https://www.jems.com/patient-care/ecmo-ecpr/
Lawler PR, Silver DA, Scirica BM, Couper GS, Weinhouse GL, Camp PC. Extracorporeal Membrane Oxygenation in Adults With Cardiogenic Shock. Circulation. 2015;131(7):676-680. doi:10.1161/CIRCULATIONAHA.114.006647
Cevasco M, Takayama H, Ando M, Garan AR, Naka Y, Takeda K. Left ventricular distension and venting strategies for patients on venoarterial extracorporeal membrane oxygenation. J Thorac Dis. 2019;11(4):1676-1683. doi:10.21037/jtd.2019.03.29
Sonneville R, Schmidt M. Extracorporeal Cardiopulmonary Resuscitation for Adults With Refractory Out-of-Hospital Cardiac Arrest. Circulation. 2020;141(11):887-890. doi:10.1161/CIRCULATIONAHA.119.044969
Bougouin W, Dumas F, Lamhaut L, et al. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. Eur Heart J. 2020;41(21):1961-1971. doi:10.1093/eurheartj/ehz753
Bartos JA, Grunau B, Carlson C, et al. Improved Survival With Extracorporeal Cardiopulmonary Resuscitation Despite Progressive Metabolic Derangement Associated With Prolonged Resuscitation. Circulation. 2020;141(11):877-886. doi:10.1161/CIRCULATIONAHA.119.042173
Yannopoulos D, Bartos JA, Martin C, et al. Minnesota Resuscitation Consortium’s Advanced Perfusion and Reperfusion Cardiac Life Support Strategy for Out‐of‐Hospital Refractory Ventricular Fibrillation. J Am Heart Assoc. 5(6):e003732. doi:10.1161/JAHA.116.003732

Bell’s Palsy or Stroke?

Posted on October 26, 2021 by Mandy Peach

Bell’s Palsy or Stroke? A Medical Student Clinical Pearl

Alicia Synette, Med III

Class of 2022 MUN

Reviewed by Dr. Jeremy Gross

Copyedited by Dr. Mandy Peach

Case

A 48M presented to the Emergency Department with right sided facial droop and altered facial sensation for two days.

He woke up one morning and described the right side of his face as feeling “saggy”. At this time, he assumed that he had slept funny. The facial droop progressed that day until it became noticeable by his wife. Two days later, he decided to go to the ER when his symptoms did not resolve. At this time, he described altered sensation at the right side of the face and tongue, which he compared to the feeling of local anesthetic after dental work. His smile was “crooked”, he was unable to purse his lips, and he could not completely close his right eye. The affected eye was also red and irritated. Taste and hearing were unchanged. Review of systems was otherwise unremarkable.

PMH: T2DM, HTN, hyperlipidemia

Medications: Ramipril, Fenofibrate, Janumet, Rosuvastatin, ASA, Lantus, Humalog

On exam, he appeared well, he was afebrile, and vital signs were stable. Pupils were equal and reactive to light. Conjunctival injection was present at the right eye with increased tearing. Mild facial droop was apparent. The right eyelid was droopy and he was unable to keep it closed against resistance. Facial movements on the right side were also weak (smile, purse lips, puff cheeks, close eyes tight), however, weakness of the forehead muscles could not be appreciated when asked to raise his eyebrows. Sensation to light touch was altered at V1. Pinprick touch was normal. There was no deviation of the tongue. He had 5/5 strength and normal sensation bilaterally at the extremities. Normal rapid alternating movements and normal heel to shin test. Normal hearing bilaterally and no hyperacusis.

Accessed from grepmed – https://www.grepmed.com/

Differential Diagnosis for Facial Nerve Palsy

Table 1: differential diagnosis for facial nerve palsy.⁶

Investigations

Lab results were unremarkable aside from an elevated random blood glucose. HbA1C level from one month prior to the ER visit was 11.1%.

CBC – LKC 8.2, Hgb 137, PLT 213

Electrolytes – Na 140, K 3.9, Cl 103

Glucose (random) 9.9

Urea 5.4, Ca+ 2.45, Mg 0.87, TSH 1.33

CT head showed no evidence of mass lesion, hemorrhage, hydrocephalus, subacute or chronic infarct.

Bell’s Palsy

Bell’s palsy is an isolated CNVII (facial nerve) paresis/paralysis as a result of acute inflammation and/or edema of the nerve. The onset is typically acute and progresses within hours, and while the cause is unknown, it is thought that the most likely etiology is viral (HSV, CMV, EBV).⁵

The facial nerve innervates the facial muscles, therefore, CNVII palsy presents with sudden onset unilateral facial paralysis, which can include:¹

Eyebrow sagging.
Inability to close the eye.
Disappearance of the nasolabial fold.
Drooping at the affected corner of the mouth, which is drawn to the unaffected side.²

CNVII also innervates the lacrimal glands, salivary glands, stapedius muscle, and taste fibres on the tongue, therefore, other associated features can include:¹

Decreased tearing.
Hyperacusis
Loss of taste sensation on the anterior 2/3 of the tongue. ²

Figure 1: Anatomy of the facial nerve.⁶

Risk Factors⁵

Pregnancy
Severe pre-eclampsia
Obesity
Hypertension
Diabetes
Upper respiratory illnesses

House-Brackmann Classification

The House-Brackmann classification seen below is used to determine severity of facial nerve dysfunction and has prognostic value. The lower the grade, the more likely a patient is to make a full recovery.⁷

Table 2: House-Brackmann classification of facial nerve dysfunction.³

Diagnosis

Diagnosis of Bell’s Palsy is considered a clinical diagnosis so there is no gold standard test, however, other causes of facial nerve palsies tend to have associated features and can be ruled out clinically. Most significantly, it is important to rule out life-threatening central lesions, such as ischemic/hemorrhagic stroke.⁴

Central vs. Peripheral Lesions

Central lesions – result in forehead sparing, as the facial nerve is innervated by ipsilateral and contralateral fibres from the motor cortex. Patients with forehead sparing need a head CT to rule out a central cause such as a stroke or mass!⁵

Peripheral lesions – the lesion is below the nucleus, and all the fibres innervating the facial nerve will be affected. Results in no forehead sparing.⁵

Figure 2: facial nerve lesion vs. supranuclear lesion with forehead sparing.⁶

Other pertinent findings on history can include: rashes, arthralgias, or fevers, exposure to ticks (Lyme disease), and vesicular eruption (Ramsay Hunt Syndrome). In addition to a full cranial nerve and peripheral nerve exam, physical examination should involve assessment of the ear, tympanic membrane, and parotid gland for signs of AOM, cholesteatoma, or parotid tumor.⁶

Further investigations⁶

Lyme serology: if clinical suspicion for Lyme disease
Head CT: gradual onset of symptoms or forehead sparing
Neurology referral: bilateral palsies or no improvement

Treatment

Corticosteroids +/- antiviral is the choice of treatment for Bell’s Palsy. Studies have demonstrated that antivirals alone have no benefit, but in combination with corticosteroids there is a significantly increased benefit compared to corticosteroids alone. Patients should be started on corticosteroids within 72 hours of presentation for a course of at least 7 days. Physicians can also discuss with patients the potential benefit of adding an anti-viral.⁸

Eye care is an important consideration in these patients as a proportion will have incomplete eye closure, putting them at risk of corneal injury. Artificial tears during the day are recommended as well as taping the eyelid closed to prevent excessive dryness or trauma.⁹

With treatment, patients will see improvement within weeks and most experience full recovery within 3-4 months.⁵

Case Conclusion

Our patient was started on valacyclovir 100mg TID x7 days and prednisone 60mg daily x 7 days for suspected Bell’s Palsy. Despite a normal CT, which helped to rule out central causes of facial paresis (stroke, subdural hematoma, brain tumor), the potential forehead sparing of the patient’s presentation presented concern for stroke. He was referred to Stroke Prevention Clinic and was seen the following day.

Neurology assessed the patient and appreciated that there was mild weakness in the forehead noted as a “reduction of wrinkles”, therefore, the diagnosis of Bell’s Palsy was confirmed. It was recommended that he continue the valacyclovir and prednisone course. It was also recommended that he patch the eye in the evenings and continue to use lubricating eye drops in the affected eye to prevent exposure keratitis.

Key Points

Bell’s palsy results in unilateral facial nerve paresis/paralysis, without forehead sparing
Associated symptoms may include: decreased tearing, hyperacusis, loss of taste
No investigations are required; however, patients with true forehead sparing need a head CT as this finding is suggestive of a central lesion
Patients with systemic symptoms, gradual onset, or bilateral symptoms should have further work-up
Most cases will resolve in 3-4 months with treatment
Treatment with corticosteroids +/- an antiviral for 7 days should be initiated within 72 hours of symptom onset

References

Baugh, R., et al. 2013. Clinical Practice Guideline. Otolaryngology–Head and Neck Surgery, 149(3_suppl), pp.S1-S27. Retrieved from: https://journals.sagepub.com/doi/10.1177/0194599813505967?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
2021. CRACKCast E105 – Brain and Cranial Nerve Disorders – CanadiEM. Retrieved from: https://canadiem.org/crackcast-e105-brain-cranial-nerve-disorders/
House, J. and Brackmann, D., 1985. Facial Nerve Grading System. Otolaryngology–Head and Neck Surgery, 93(2), pp.146-147. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/3921901/
McCaul, J., Cascarini, L., Godden, D., Coombes, D., Brennan, P. and Kerawala, C., 2014. Evidence based management of Bell’s palsy. British Journal of Oral and Maxillofacial Surgery, 52(5), pp.387-391. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/24685475/
org.au. 2021. RACGP – A general practice approach to Bell’s palsy. Retrieved from: https://www.racgp.org.au/afp/2016/november/a-general-practice-approach-to-bell%E2%80%99s-palsy/#1
Tiemstra JD, Khatkhate N. Bell’s palsy: diagnosis and management. Am Fam Physician. 2007 Oct 1;76(7):997-1002. PMID: 17956069. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/17956069/
Yoo, M., et al. 2020. Evaluation of Factors Associated With Favorable Outcomes in Adults With Bell Palsy. JAMA Otolaryngology–Head & Neck Surgery, 146(3), p.256. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/31971554/
Hato, N., et al. Efficacy of early treatment of Bell’s palsy with oral acyclovir and prednisolone. Otol Neurotol. 2003 Nov;24(6):948-51. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/14600480/
Ronthal, M. Greenstein, P. 2021. Bell’s palsy: Treatment and prognosis in adults. Retrieved from Uptodate October 26, 2021 from https://www.uptodate.com/contents/bells-palsy-pathogenesis-clinical-features-and-diagnosis-in-adults?search=bells%20palsy%20management&topicRef=5286&source=see_link

Vertigo Makes the World Go Round – A Case of BPPV

Posted on October 26, 2021 by Mandy Peach

Vertigo Makes the World Go Round – A Case of BPPV: Medical Student Clinical Pearl

Johnathan Rose, Med III

Class of 2022

Dalhousie Medical School New Brunswick (DMNB)

Reviewed by Dr. Maria Kovalik

Copyedited by Dr. Mandy Peach

Case:

A 73-year-old female presented to the emergency department via EMS with a three-day history of dizziness and associated nausea. On further questioning she stated that the dizziness began suddenly when she awoke three days prior. It felt like her environment was spinning and was made worse with movements. Episodes lasted about 30-60 seconds and would resolve if she stayed still. Her mobility was impaired due to feeling unsteady on her feet. She felt nauseous when dizzy but had no emesis; Gravol provided mild relief. She denied any headaches, vision/hearing changes, chest pain, shortness of breath, bowel/bladder changes, recent infections, muscle weakness, paresthesia, or constitutional symptoms.

She was an otherwise healthy 73-year-old with no past medical or surgical history. She was taking no medications. She did not smoke, drink alcohol, or use any recreational drugs.

Physical Exam:

The patient’s vital signs were all within normal limits and stable. Upon inspection, she appeared her stated age, was well kempt, and was laying very still with her eyes closed. She was alert and oriented x3. Her cranial nerve exam II-XII was normal. She had 5/5 strength in upper and lower limbs bilaterally. Tympanic membranes were normal bilaterally.

Upon sitting up, she had mixed horizontal and torsional nystagmus in her eyes bilaterally, as well as when she laid back down (Figure 1). When performing the Dix-Hallpike manoeuvre, she had mixed horizontal and torsional nystagmus when her head was tilted both left and right.

From: https://icrcat.com/en/nystagmus/

Figure 1. Types of Nystagmus. Diagram showing the 3 major forms of nystagmus: horizontal, vertical, and rotary.

What is vertigo?

There are four main types of dizziness: vertigo, light-headedness, presyncope, and disequilibrium. Vertigo is the most common, accounting for 54% of presentations¹. Vertigo is the sensation of dizziness or illusory movement. Some people may perceive it as the environment moving while others perceive self-motion. It is often caused because of asymmetry in the vestibular system or dysfunction of the labyrinth, vestibular nerve, or central vestibular structures located in the brainstem². Vertigo is a symptom, not a diagnosis, and the causes can be broken into two broad categories: central and peripheral³.

Does this patient have a central or peripheral cause of vertigo?

The history alone from a patient presenting with vertigo is able to correctly reveal the diagnosis in ¾ patients¹. Therefore, it is necessary to ask questions that will help differentiate the causes of vertigo, as further investigations may not be helpful in doing so (Table 1).

Table 1. Distinguishing features between central and peripheral causes of vertigo^{1, 4}.

	Peripheral	Central
Onset	Sudden	Gradual
Intensity	Severe	Mild
Duration	Seconds	Continuous
Nystagmus	Horizontal and torsional; can be inhibited by fixation of gaze	Purely vertical, horizontal, or torsional; cannot be inhibited by fixation of gaze
Associated neuro findings	Rare	Common
Tinnitus	Common	Rare
Nausea/Vomitting	Frequent, severe	Infrequent, mild

Physical exam for differentiating between central and peripheral vertigo should include a HINTS exam

Interpretation of the HINTS

“A benign HINTS exam is defined as abnormal HIT + direction-fixed horizontal nystagmus + absent skew.

A dangerous HINTS exam is defined as any one of:

Normal/untestable HIT
or direction-changing horizontal nystagmus present/untestable
or skew deviation present/untestable

(Untestable refers to those patients with obvious oculomotor pathology or lethargy in whom the tests were unable to be completed).

The acronym INFARCT can be used to remember what constitutes a dangerous HINTS exam:

Impulse Normal

Fast-phase Alternating

Refixation on Cover Test.”⁸

Based on her history and physical exam findings, it is likely that our patient has peripheral vertigo.

What is the differential diagnosis for central vertigo¹?

Multiple sclerosis
Migraine
Transient ischemic attack or stroke
Brain tumor

What is the differential diagnosis for peripheral vertigo¹?

Benign positional paroxysmal vertigo (BPPV)
Ménière’s disease
Vestibular neuronitis
Acute labyrinthitis
Otosclerosis

What type of peripheral vertigo does our patient have?

The most common causes of peripheral vertigo are BPPV, Ménière’s disease, and vestibular neuronitis⁵. Table 2 illustrates some of the features that can be used to distinguish the causes of peripheral vertigo.

Table 2. Distinguishing features between common causes of peripheral vertigo⁵.

Ddx	Duration	Provoking Factors	Special features	Physical exam findings
Labyrinthitis	Seconds – Minutes	Change in position	Hearing loss and tinnitus	Hearing loss
Vestibular neuronitis	Seconds – Minutes	URTI	Imbalance	Normal hearing
BPPV	Seconds – Minutes	Change in position	Positional	Positive Dix-Hallpike
Ménière’s disease	Hours	Spontaneous	Hearing loss and tinnitus	Hearing loss

Taking into account both the history and physical exam, our patient has clear case of BPPV. She had a sudden onset of dizziness that is worse with changes in position and lasts 30-60 seconds before resolving if still. She had associated nausea and no other neurological signs. This, along with a positive Dix-Hallpike, is enough to secure the diagnosis.

BPPV Pathophysiology

BPPV is caused by canalithiasis, often calcium carbonate crystals, within the semicircular canals (Figure 2). The semicircular canals normally function to detect angular movements of the head. However, these heavy stones can cause inappropriate movement of the endolymph within the canals during times of linear accelerations, such as with gravity. Ultimately, this causes the improper sensation of spinning when the head shifts with respect to gravity⁶.

From: https://balanceanddizziness.org/disorders/vestibular-disorders/bppv/

Figure 2. Mechanism of BPPV. Calcium crystals normally found within the utricular cavity are displaced and fall into the semicircular canals. Once displaced, they then cause the erroneous sensation of spinning when the head moves⁶.

Treatment

Although episodes of dizziness last seconds to minutes, the symptoms may persist for up to two weeks, and will often resolve spontaneously⁶. Symptoms may recur after remission⁵.

Treatment options are limited for those with BPPV. Medications are often not helpful, and treatment with vestibular suppressant medications such as antihistamines and/or benzodiazepines should be avoided⁷. For those who find the symptoms to be too distressing, the Epley maneuver may be performed to try and dislodge the otoliths from the semicircular canals (Figure 3)⁶. This maneuver has roughly a 77% success rate in the literature, but anecdotally seems to be less while also making patients more nauseous⁵.

Figure 3. Epley Maneuver. Steps involved in trying to reposition the calcium debris within the semicircular canals to migrate toward the common crus and exit into the utricular cavity⁶.

Our Case

Our patient ended up having BPPV that would likely resolve on its own within 2 weeks. No further diagnostic workup was required. Treatment options were limited; she was disappointed when she learned we had no medications that would provide her relief of her spinning world. The Epley maneuver was offered with the premise that it may or may not help relieve symptoms but will likely make her more nauseous, which she declined.

Clinical Pearls

Vertigo is a symptom, not a diagnosis.
A detailed history is required to elicit features of central or peripheral causes of vertigo.
Serious causes of central vertigo need to be considered.
Physical examination should include a neurological, cardiovascular, eye, and ear exam.
Rule out orthostatic hypotension by seeing if the patient feels dizzy when they sit up as well as when they lay down.
Treatment with vestibular suppressant medications such as antihistamines and/or benzodiazepines should be avoided⁷.
The Epley maneuver may be useful in some patients but will likely increase their nausea.

References

Labuguen RH. Initial Evaluation of Vertigo. Am Fam Physician. 2006;73(2):244-251.
Evaluation of the patient with vertigo. https://www.uptodate.com/contents/evaluation-of-the-patient-with-vertigo?search=vertigo&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H1
Baumgartner B, Taylor RS. Peripheral Vertigo. StatPearls. 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430797/
Chang AK. Dizziness and vertigo. In: Mahadevan SV, Garmel GM, editors. An Introduction to Clinical Emergency Medicine. 2nd ed. Cambridge: Cambridge University Press; 2012. p. 289–300.
Dommaraju S, Perea E. An approach to vertigo in general practice. Australian Family Physician. 2016;45(4):190-194.
Benign paroxysmal positional vertigo. https://www.uptodate.com/contents/benign-paroxysmal-positional-vertigo?search=vertigo&source=search_result&selectedTitle=5~150&usage_type=default&display_rank=5#H4
Stanton M, Freeman AM. Vertigo. StatPearls. 2021. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482356/
MacKay, J. HINTS exam in Acute Vestibular Syndrome. 2016. Retrieved Oct 26, 2021 from https://sjrhem.ca/resident-clinical-pearl-hints-exam-in-acute-vestibular-syndrome/

A Case of Post-traumatic Delayed Facial Nerve Palsy in a Child

Posted on October 8, 2021 by Mandy Peach

A Case of Post-traumatic Delayed Facial Nerve Palsy in a Child – A Medical Student Clinical Pearl

Jacqueline Mincer, BSc, MSc

Dalhousie Medicine New Brunswick Class of 2022, Med III

Reviewed by: Dr. Erin Slaunwhite

Copyedited by: Dr. Mandy Peach

History of Presenting Illness:

A 10-year-old girl presented to the emergency department (ED) one week after a bike accident with left-sided hemifacial palsy. The patient was biking down a hill without a helmet when she fell onto her left side. Emergency medical services (EMS) brought the patient to the ED with a Glasgow Coma Scale (GCS) score of 15. The patient denied loss of consciousness, nausea, vomiting or headache. Small amounts of blood were noted around her left tragus; however, the patient denied any hearing impairments at the time. She was otherwise healthy with no prior surgeries, no allergies, and no medications.

CT head, CT cervical spine, and shoulder XR were ordered. Imaging revealed a transverse fracture through the distal third of the clavicle with 100% displacement (Figure 1). CT head and cervical spine were both reported as normal, with no significant post-traumatic abnormalities detected.

Figure 1: L clavicle fracture

The clavicle fracture was treated non-operatively. The patient was discharged home with a sling to immobilize the shoulder and was provided with an outpatient follow-up appointment with orthopedics.

Four days after the accident, left-sided facial changes were first noticed and had been progressively worsening. The patient complained of left-sided numbness, photosensitivity, difficulty blinking, and lip palsy (Figures 2a, 2b). There was ongoing bloody drainage and intermittent hearing difficulties from the left ear.

Figure 2: L sided facial nerve palsy*:

2a) incomplete closure of the left eye

2b) limited ability to open mouth/smile on the left side; decreased movement of the upper left eyebrow

*photos taken with consent of patient and parent

ANATOMY REVIEW:

To build a complete differential diagnosis, let’s first review the anatomy of the facial nerve as it enters and exits the skull:

The facial nerve is the 7^th paired cranial nerve.
It arises in the pons and travels through the temporal bone via the internal acoustic meatus then travels through the “Z” shaped facial canal exiting the skull via the stylomastoid foramen (Figure 5).
Upon exiting the skull, the facial nerve runs anteriorly to the outer ear and gives rise to the posterior auricular nerve branch. The main motor root of the facial nerve passes through the parotid gland, ultimately splitting into 5 terminal branches: the temporal, zygomatic, buccal, marginal mandibular and cervical branches (Figure 6).

Figure 5: Pathway of facial nerve through skull.

Dalhousie Medicine neuroanatomy lab manual.

Figure 6. Branches of the facial nerve (VII)

The facial nerve is a mixed nerve, containing motor, sensory and parasympathetic fibers.(1)

Motor: innervates muscles of facial expression.
Sensory: taste sensation from anterior 2/3 of the tongue (via chorda tympani, a branch of the mandibular nerve, V3).
Parasympathetic: supplies glands of the head and neck
- Lacrimal gland (tearing), sublingual and submandibular glands (salivary).

IMPORTANT FEATURES ON HISTORY AND PHSYICAL EXAM:

History:

Onset and progression (gradual onset more suggestive of mass lesion)
Recent rashes, arthralgias, fevers or other illnesses
Tick exposure, recent trauma, or prior history of peripheral nerve palsy

Exam:

Head & Neck: inspect external ear, ear canal, tympanic membrane, oropharynx. Palpate parotid gland.
Neurologic exam: cranial nerve exam (Figure 8) and full neuro exam. Differentiate between upper motor neuron and lower motor neuron lesions by assessing forehead involvement. Forehead paralysis on affected side is suggestive of a lower motor neuron (peripheral) lesion. While no forehead paralysis on the affected side is suggestive of an upper motor neuron (central) lesion. This is due to bilateral innervation of the forehead from the central nervous system.
Skin: inspect for lesions suggestive of herpes zoster, Lyme disease or dysmorphic features

https://www.reviewofoptometry.com/article/the-neurologic-exam-stepbystep

Figure 8: Cranial nerve function and testing

DIFFERENTIAL DIAGNOSIS:

Pediatric facial nerve palsy can be congenital, acquired, or idiopathic.

Congenital: secondary to delivery trauma, genetic causes, or may make up one feature of a broader syndromic malformation.(2)

Acquired: resulting from infection or damage/trauma to nearby structures.

Infectious pathogens include Borrelia Burgdorferi, Herpes Varicella-Zoster (most common), Epstein-Barr virus, Haemophilus influenza, Tuberculosis, CMV, Adenovirus, Rubella, Mumps, Mycoplasma pneumoniae, and HIV.
Disease to neighbouring structures (Figure 7) include Otitis media, Cholesteatoma, Mastoiditis, and Meningitis.

https://www.statpearls.com/ArticleLibrary/viewarticle/49275

Figure 7: neighbouring structures to facial nerve

Trauma/injury to the facial nerve from temporal bone fractures (at the basilar level)
Iatrogenic paralysis (surgical complication) from procedures involving the parotid gland, middle ear or mastoid.

Less common, acquired etiologies:

Inflammatory: vasculitis, HSP, or Kawasaki disease.
Neoplasm: schwannoma, hemangioma, bone tumor (rhabdomyosarcoma, histiocytosis), leukemia, parotid gland tumors.

Idiopathic: In approximately 50% of cases, the etiology remains unknown. Idiopathic facial paralysis is commonly referred to as “Bell’s Palsy”

INVESTIGATIONS, PROGNOSIS, TREATMENT:

Investigations, prognosis and treatment are all highly dependent on the overall clinical picture, including underlying etiology and severity of palsy.(3)

Investigations:

Imaging is warranted in patients who present with atypical signs, such as involvement of neighbouring cranial nerves, chronic otitis media, acute mastoiditis, temporal bone trauma, suspected malignancy, slow onset (>3 weeks), or no improvement at 6 months.
In “typical” incomplete facial palsy with good recovery, imaging may not be necessary.
Consider serologic testing to rule out Lyme disease if warranted.
Consider EEG, neuroimaging, lumbar puncture based on history and physical exam. (3)

Prognosis:

Prognosis will vary depending on cause and mechanism of injury.
Most children with Bell’s palsy recover well and regain most if not all of their function. (3)

Treatment:

If applicable, treat the underlying disorder (e.g. Lyme disease, acute otitis media).
Bell’s Palsy:
- Early treatment (within 3 days of symptom onset) with oral glucocorticoids. (2)
- Prednisone 1-2mg/kg daily (up to 60-80mg) x 5 days, then a five-day taper by 10mg per day. (3)
Congenital or permanent acquired facial palsy: consider surgical consult
All patients will require supportive care:
- Artificial tears to protect the cornea of the affected eye.
- Taping of the eyelid shut overnight in patients unable to completely close the eye.

Case Conclusion:

The ED physician consulted the on-call radiologist and neurosurgeon. The CT-head from the day of the accident was revisited, detecting a 4cm basilar skull fracture to the left temporal bone (Figure 10).

Figure 10: Basal skull fracture

Delayed hearing loss and bloody drainage from the left ear was suggestive of a trauma-induced tympanic membrane perforation.

Inflammation from the basilar skull fracture and/or ruptured tympanic membrane likely explains compression of the facial nerve. In this case, the delayed presentation of left-sided facial palsy is a reassuring prognosis. It points towards inflammatory compression of the nerve as opposed to complete laceration of the nerve at the time of trauma.

She was discharged home with a two-day prescription for Dexamethasone 10mg PO once daily. A plan was made for a repeat CT head in 6-8 weeks as well as outpatient follow up with orthopedic surgery, neurosurgery, and pediatric neurology.

Take Home Points:

o Facial nerve palsy in children can be classified as congenital, acquired or idiopathic in nature.
o The case presented here was an acquired facial nerve palsy, following a traumatic basilar skull fracture.
o Investigations, prognosis and treatment are highly dependent on underlying etiology and severity
o If known, it is important to treat the underlying etiology.
o Consider glucocorticoids at early onset (within 3 days of presentation) as well as supportive management (artificial tears, eyelid taping).

References:
1. The Facial Nerve (CN VII) – Course – Functions – TeachMeAnatomy [Internet]. [cited 2021 Jun 14]. Available from: https://teachmeanatomy.info/head/cranial-nerves/facial-nerve/
2. Ciorba A, Corazzi V, Conz V, Bianchini C, Aimoni C. Facial nerve paralysis in children. World J Clin Cases. 2015 Dec 16;3(12):973–9.
3. Facial nerve palsy in children – UpToDate [Internet]. [cited 2021 Jun 14]. Available from: https://www.uptodate.com/contents/facial-nerve-palsy-in-children?search=-%09Facial%20nerve%20grading%20(House-Brackman&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H4519763