Nursemaid’s Elbow

Nursemaid’s Elbow

Medical Student Pearl

 

Erika Maxwell

@ErikaMaxwell

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:

 

  1. A pulled elbow is a common upper limb injury in young children presenting to the Emergency Department
  2. 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
  3. HYPERPRONATE and/or SUPINATE & FLEX!
  4. Recurrence is common

References

  1. 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.
  2. 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
  3. Boston Children’s Hospital. (2021). Nursemaid’s elbow. Retrieved September 6, 2022, from https://www.childrenshospital.org/conditions/nursemaids-elbow
  4. 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.
  5. 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
  6. Lewis, D., Argall, J., & Mackway-Jones, K. (2003). Reduction of pulled elbows. Emergency Medicine Journal, 20, 61-62.
  7. Schunk, J. F. (1990). Radial head subluxation: epidemiology and treatment of 87 episodes. Annals of emergency medicine, 19(9), 1019-1023.
  8. Teach, S. J., & Schutzman, S. A. (1996). Prospective study of recurrent radial head subluxation. Archives of pediatrics & adolescent medicine, 150(2), 164-166.
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Bicuspid Aortic Valve – An important incidental PoCUS finding?

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 dissection2.3.

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.

  1. Known bicuspid aortic valve patients presenting with possible associated complications
  2. 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 3rd or 4th 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 valve5-9

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

  1. Braverman, A. C., & Cheng, A. (2013). The bicuspid aortic valve and associated aortic disease. Valvular heart disease. Philadelphia: Elsevier, 179-218.
  2. Verma, S., & Siu, S. C. (2014). Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med370, 1920-1929.
  3. 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 Surgery31(3), 397-405.
  4. 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 Techniques22(1), 53-55.
  5. 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.
  6. 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. Chest75(4), 434-440.
  7. Shapiro, L. M., Thwaites, B., Westgate, C., & Donaldson, R. (1985). Prevalence and clinical significance of aortic valve prolapse. Heart54(2), 179-183.
  8. Gebhardt, C., Hegazy, A.F., Arntfield, R. (2015). Chapter 16: Valves. Point-of-Care Ultrasound. Philadelphia: Elsevier, 119-125.
  9. Kimura, B. J. (2017). Point-of-care cardiac ultrasound techniques in the physical examination: better at the bedside. Heart103(13), 987-994.
  10. 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). Circulation129(25), 2691-2704.
  11. 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 Echocardiography26(6), 589-596.
  12. 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 cardiology93(8), 1069-1072.
  13. 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. Circulation116(11_supplement), I-264.
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Management of Supraventricular Tachycardia (SVT) in Pregnancy

 

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


References:

  1. 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/
  2. UpToDate – https://www.uptodate.com/contents/supraventricular-arrhythmias-during-pregnancy#H11407709
  3. 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/
  4. 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
  5. 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/
  6. 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

 

 

 

 

 

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

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

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

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

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Delirium vs. Dementia: Different side on the same coin

Delirium vs. Dementia: Different side on the same coin: A Medical Student Pearl

Khoi Dao, Med III

Dalhousie Medicine New Brunswick

Reviewed by Dr. Todd Way

Copyedited by Dr. Mandy Peach

Case:

Mr. D is an 83yo M today presents to Emergency Department through ambulance after a fall. Paramedics report stated that his wife found him pale and heard his complaints of shortness of breath (SoB), chest pain, and feeling weak. She later heard him called for help on the floor and called ambulance. Furthermore, the report also mentioned that he had a fall a week ago. When having a conversation with Mr. D, he stated that everything is fine, that he had no trouble breathing, or chest pain. The only pain that he felt was from his left arm and leg from the fall. He seems to be confused. He stated that he is from Nova Scotia, currently at an airport, and waiting for his friend to pick him up to go to their cabins at New Brunswick.

His initial vitals taken by paramedics was normal except for O2 Sat in 80’s. At the Emergency Department, he received O2 4L in air cannula and his SatO2 quickly brought up to 95%. He was afebrile, blood pressure at normal range, and heart rate was irregularly irregular. There were bruises at his left facial, left upper flank at axillary region, and left arm. There were no signs of basal skull fractures, nor any lacerations on his head. Cranial nerves exam was normal. Upper extremity motor, sensory, and reflex exams were within normal limits. Lower extremity motor found his dorsal flexion and extension on the left side was weaker compared to right side. Patella reflex exam was within normal limits. Respiratory exam was within normal limit. Cardiac exam reveals irregularly irregular pulse, but normal heart sound, no murmur, no extra heartbeat. Abdomen exam was within normal limits.

Past Medical History: hypertension, dyslipidemia, nephrolithiasis, chronic subdural hematoma, infection secondary to left ankle replacement, and Guillain-Barre syndrome (acute inflammatory demyelinating polyneuropathy)

Past Surgical History: bilateral ankle replacements

Initial Investigations:

With his initial presentation, blood work and imaging were ordered. Mr. D’s CBC showed elevated WBC, CRP, with stable Hgb. His ECG showed a new A-Fib.  Chest X-ray found he has consolidation of his left lower lobe, suggestive of pneumonia. Initial CT scan confirmed of left lower lobe consolidation, with multiple new and old rib fractures.

First, establish between Mild Cognitive Impairment (MCI) and Delirium

Dementia, Mild Cognitive Impairment, and delirium are grouped under the umbrella term of neurocognitive disorders, according to DSM-V. However, each of them has their own definitions, underlying pathology, and maybe etiology.

Dementia, or newly named major neurocognitive disorder in DSM-V, is characterized as cognitive decline involving one or more of neurocognitive domains (learning, memory, attention, executive function, perceptual-motor, and social cognition) that is severe enough to interfere with daily function and independence. These daily functioning includes instrumental ADL (iADL) and ADL (Table 1).

To meet the criteria of diagnosing dementia, one must have an evident decline of one or more cognitive domains, either through a collateral history of someone who is close to the patient, or through standardized neuropsychological testing (MMSE, MOCA, …). The decline of cognitive domains should not occur in the context of delirium and are not better explained by another mental disorder.

 Mild cognitive impairment can be considered somewhere between normal cognition and dementia. While it is considered to have deficit of one or more cognitive domains, it does not interfere with daily function activities. Like dementia, the diagnostic criteria require exclusively not in the context of delirium, and that it is not better explained by another mental disorder.

Delirium, on the other hand, is defined of any disturbance of attention and awareness along with cognition (e.g. memory deficit, disorientation, language, visuospatial ability, or perception) over a short period of time (hours to days). It can persist from days to month. Delirium is typically caused by medical conditions, substance intoxications, or medication side effect. Thus, for the diagnostic criteria for delirium to be met, there needs to have evidence from history presentation, physical examination, or laboratory findings of physiological changes that consequently may explain the cognitive disturbances.

Cognition decline as a clinical sign can be challenging for a physician since it is overlapped by neurocognitive disorders. However, there are characteristics that are different between them, which can be shown in Table 2.

Mainly, dementia has a gradual onset, whereas delirium has a more abrupt and acute onset. Attention and orientation are usually impaired in delirium, but generally preserved in dementia in earlier stage.

Collateral History:

Initial history taking could be proven to be challenging when patient presents with difficulties with memory or attention. Thus, obtaining a collateral history is pertinent as it is an indicator and a key component to differentiate between dementia and delirium4. Although collateral history is a core clinical skill, it is sometimes overlooked 5. In taking a collateral history, one would need to establish patient’s cognition at their baseline. For instance, questions relate about  a person’s daily activities and whether if they have any difficulties should be explored. Clarification of the onset and progressions of the cognitive changes need to be documented. Furthermore,  other cognitive domains should be also screened, as questions can be seen in Table 2 below 6.

After taking initial history, you thought that Mr. D is confused and could not give a good history of presenting illness, so you decide to call his substitute decision maker (SDM), who happens to be his wife. His wife recalled that he looked pale at lunch, complained of SoB, and when he walked she thought he looked weaker than usual. Then, she heard a called for help and found him on the floor, conscious. He couldn’t get up by himself and so she decided to call an ambulance. His wife mentioned that Mr. D has had some memory loss over half a year, where there were multiple episodes of Mr. D forgetting things. However, a week ago he had a fall walking outside, and she reported that his memory has been progressively worse since the fall. There were several nights when he woke up and asked her what the dates or where he is at. He also appeared to be weak, and, the day before his emergency admission, he complained of chest pain. When asked whether he has any difficulty of performing activity of daily living (ADL), his wife mentioned he had hard time getting dressed. His wife reported he had not seen a specialist for memory decline. She was concerned, however, that his memory was acutely declining over a week compared to the last few months. When asked about EtOH use, he had history of excessively drinking in the past, but currently only one serving per day.

As Mr. D was suspected of delirious that is overlapping of MCI, more investigations were added to investigate the cause of his delirium.

Risk and Precipitating factors of delirium:

Most identified risk factors are involving with underlying brain pathologies (e.g dementia, stroke, or Parkinson)7. With respect to precipitating factors, common examples include, but not limited to, polypharmacy, infection, dehydration, immobility, malnutrition, and the use of bladder catheters (predisposes patient to urinary tract infections)

Differential Diagnoses:

Besides major neurocognitive disorders (e.g. dementia) and mild cognitive impairment that were discussed above, other differential diagnoses should also be considered such as2:

Sundowning – behaviour deterioration seen in evening hours that might be due to impaired circadian regulation or nocturnal factors in the environment

Focal syndromes – includes temporal-parietal, occipital, and frontal dysfunctions

Nonconvulsive status epilepticus – patients often showed non-classical ictal features, but with the following features such as: prominent bilateral facial twitching, unexplained nystagmoid eye movements during obtunded periods, spontaneous hippus, prolonged “postictal state”, automatism, and acute aphasia without structural lesion

Psychiatric illnesses – includes bipolar and depressive disorders with psychotic features

Acute stress disorder – associated with fear, anxiety, and dissociative symptoms, such as depersonalization

Approach to the source of delirium:

As Mr. D was suspected to be delirious, the potential causes can be reflected through laboratory results as well as imaging studies. Sources of cognitive decline can be from systemic illness, isolated organ system dysfunction, drug adverse reactions, intoxications or withdrawal, psychiatric illness, trauma, or neurologic disease2,3. A concise and comprehensive acronym that could be used to establish the source of change in delirium can be used like DIMES8:

Drugs – anticholinergic, anti-emetics, anti-parkinsonian, beta-blockers

Infections – pneumonia, urinary, skin/soft tissue, CNS-related

Metabolics – altered pH, hypo/hyper Na+ or Ca+, acute organ failure, hypoglycemia

Enviromentals – heavy metals,

Structurals – brain injury, CNS pathology, malignancy

Treatment for delirium usually is to manage the underlying cause of the delirium.

Case continues:

                Although Mr. D’s initial imaging investigations found lower lobe consolidation that suggestive of pneumonia, he has a past medical history of chronic subdural hematoma in 2010. A CT head scan was ordered to rule out if there any new bleeding. When the CT head was negative it was most likely his newfound delirium and A-fib were secondary to pneumonia . Blood culture was done, and 2g IV Ceftriaxone was given empirically for his pneumonia. He was transferred to Hospitalist Unit for monitoring for improvement and referred to Geriatric Unit at St. Joseph’s Hospital for further investigation to his MCI.

Key points:

  1. Delirium is characterized as disturbance in attention and in cognition domain over a short period of time that could not be explained by other neurocognitive disorder.
  2. Delirium shared many cognitive declines feature with dementia and MCI. However, features such as acute onset, inattention, and evidence of physiological changes can be used to differentiate
  3. Collateral history is an important clinical tool to identify between delirium and other neurocognitive disorders.
  4. Mnemonics in approaching for delirium can be remembered as DIMES

References:

  1. American Psychiatric Association. (2013). Neurocognitive Disorders. In American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders. https://doi-org.ezproxy.library.dal.ca/10.1176/appi.books.9780890425596.dsm17
  2. Francis J., Young, G.B. (2021). Diagnosis of delirium and confusional states. Retrieved from https://www.uptodate.com/contents/diagnosis-of-delirium-and-confusional-states?search=delirium&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  3. Larson, E.B. (2021). Evaluation of cognitive impairment and dementia. UpToDate. Retrieved from https://www.uptodate.com/contents/evaluation-of-cognitive-impairment-and-dementia?search=delirium%20and%20dementia&source=search_result&selectedTitle=4~150&usage_type=default&display_rank=4
  4. Dyer, A. H., Foley, T., O’Shea, B., & Kennelly, S. P. (2018). Cognitive assessment of older adults in general practice: the collateral history. Irish Journal of Medical Science (1971-), 187(3), 683-687
  5. Fitzpatrick, D., Doyle, K., Finn, G., & Gallagher, P. (2020). The collateral history: an overlooked core clinical skill. European Geriatric Medicine, 11(6), 1003-1007.
  6. Mahdy, R., Amer, M. S., Adly, N. N., & Rasheedy, D. (2021). The Value of Collateral History in Screening for Mild Cognitive Impairment in Elderly with Diabetes Mellitus in Outpatient Clinics. The Egyptian Journal of Geriatrics and Gerontology, 8(1), 21-28.
  7. Fick, D. M., Agostini, J. V., & Inouye, S. K. (2002). Delirium superimposed on dementia: a systematic review. Journal of the American Geriatrics Society, 50(10), 1723-1732.
  8. Melady, D. (2013). Cause of delirium. In Geri-EM. Retrieved from https://geri-em.com/cognitive-impairment/causes-of-delirium/
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A Case of Pyelonephritis

A Case of Pyelonephritis: A Medical Student Clinical Pearl

Natasha Glover

MUN Medicine, CC4

Class of 2022

Reviewed by Dr. Paul VanHoutte

Copyedited by Dr. Mandy Peach

Case

Ms. X, a 23 year old mother of 2 presents to the Emergency Department with a 3 day history of left flank pain and vomiting. She describes the pain as sharp, constant, and worse with touch. Her boyfriend observed her sweating and shivering the night before. She has also experienced a loss of appetite, having been unable to keep any food or liquids “down”. In the ED waiting room, she vomits and describes bright red “streaks” mixed with the vomitus.

2 weeks prior to her visit, she describes having dysuria and suprapubic pressure. She has a history of frequent UTIs, so she took an old bottle of unfinished amoxicillin from a previous diagnosis of cystitis and took the remaining 3 pills over the course of the 3 days. Reports that dysuria and pressure subsided afterwards.

 

PMHx:
Frequent UTIs

 

Medications:
No prescription medications

 

Social:

Smokes marijuana daily

No EtOH consumption

No other recreational drug use

1 month ago became sexually active with a new partner, reports that partner was tested prior to beginning their sexual relationship

 

Physical Exam:

HR 112 BP 132/88 T 37.8 RR 18 SpO2 97%

Appears in mild discomfort. No respiratory distress. Oriented to person, place, and time. Dry oral mucosa. Skin tenting. No facial edema.

Mild tachycardia, otherwise normal cardiac exam. Equal breath sounds to the bases, no adventitious sounds. Abdomen was non-distended, soft, moderate tenderness in the LUQ and LLQ, no rebound tenderness, no masses, no evidence of hepatosplenomegaly. Tenderness at the left flank.

Peripheral pulses present, equal, capillary refill <2s . No peripheral edema.

 

Differential Diagnosis:

  1. Pyelonephritis
  2. Renal colic
  3. Ectopic pregnancy
  4. Gonorrhea/chlamydia infection
  5. Nephrotic syndrome
  6. Splenic flexure syndrome

 

Urinalysis:

Leukocyte esterase 25

Blood casts 50

Protein 20

HCG negative

Culture: E.coli positive (reported after 24 hours in lab)

 

Labs:

Sodium 140

Potassium 4.2

Chloride 108

Creatinine 274

Hgb 135

HCT 0.450
LKC 23.7

PLT 281

CRP 506.3

Lipase 8

Bedside renal U/S unable to detect any hydronephrosis.

A CT is ordered to rule out infected renal stone.

Left kidney is markedly larger than the right kidney. Stranding around the left kidney. No evidence of obstruction, hydronephrosis or hydroureter.

Assessment:

This patient is mildly hypovolemic. She also has a new AKI, likely pre-renal as the result of NSAID use and volume depletion. She has a left sided pyelonephritis given her recent history of cystitis (likely suboptimally treated by the use of old remaining antibiotics for a previous UTI), left flank pain with costovertebral tenderness and various abnormal lab findings

Imaging rules out obstructive causes and other complicating factors. As a result, she requires fluid resuscitation, pain management, nausea/vomiting management, IV antibiotics, and admission to the hospitalist unit.

 

Let’s Break it Down; Assessment of Acute Kidney Injury:

Pathogenesis of Pyelonephritis:

 

The majority of pyelonephritis cases are the result of lower genitourinary infections that travel up through the ureters and into the kidneys. Other sources of infection occur through hematogenous spread, which is most often seen in chronically ill and immunocompromised patients. Additionally, metastatic manifestations of fungal and staphylococcus may spread distantly from the skin. Escherichia coli is the most common pathogen observed in cases of pyelonephritis.

 

Treatment of pyelonephritis is highly dependent on whether or not it is classified as a complicated UTI or an uncomplicated UTI.

 

Complications:

 

-Higher mortality among elderly, immunocompromised patients, and those who develop septic shock

-A small number of individuals, particularly those with structural abnormalities, complex renal obstructions, congenital anomalies, develop chronic pyelonephritis. Chronic pyelonephritis is characterized by nonspecific symptoms as well as histologic findings of lymphoplasmacytic infiltrates, thyroidization, tubulointerstitial scarring, glomerulosclerosis, and fibrosis.  It accounts for approximately 20% of end-stage kidney disease.

Figure 2: Chronic pyelonephritis with focal and segmental glomerulosclerosis with periglomerular fibrosis (Jones silver stain) from the National Kidney Foundation

Management for Ms. X:

Ceftriaxone 1mg IV q24h because she was systemically unwell
Fluid resuscitation with normal saline
Pain management with acetaminophen 975 PO QID and morphine 5mg SC q3h PRN
Nausea and vomiting management with ondansetron (Zofran) 8mg IV q8h PRN
Admit to hospitalist for further monitoring and management

 

References:
1. Hooton, T., Gupta K. Acute complicated urinary tract infection (including pyelonephritis) in
adults. UpToDate. https://www.uptodate.com/contents/acute-complicated-urinary
-tract-infection-including-pyelonephritis-in-adults. Published 2021. Accessed July 14,
2021.
2. Buonaiuto VA, Marquez I, De Toro I, et al. Clinical and epidemiological features and
prognosis of complicated pyelonephritis: a prospective observational single
hospital-based study. BMC Infect Dis. 2014;14(1):639. doi:10.1186/s12879-014-0639-4
3. Fogo AB, Lusco MA, Najafian B, Alpers CE. AJKD Atlas of Renal Pathology: Chronic
Pyelonephritis. Am J Kidney Dis. 2016;68(4):e23-e25. doi:10.1053/j.ajkd.2016.08.001
4. Khanna R. Clinical presentation &amp; management of glomerular diseases: hematuria,
nephritic &amp; nephrotic syndrome. Mo Med. 2011;108(1):33-36.
http://www.ncbi.nlm.nih.gov/pubmed/21462608. Accessed July 14, 2021.
6. NB Provincial Health Authorities Anti-Infective Stewardship Committee. Treatment of adult
urinary tract infections. 2021. doi:10.1002/14651858.CD003237.pub2
7. Rahman M, Shad F, Smith MC. Acute kidney injury: A guide to diagnosis and management.
Am Fam Physician. 1970;86(7):631-639. https://www.aafp.org/afp/2012/1001/
p631.html. Accessed July 14, 2021.
8. Scheid DC. Diagnosis and Management of Acute Pyelonephritis in Adults. Vol 71.
American Academy of Family Physicians; 1970. https://www.aafp.org/afp/
2005/0301/p933.html. Accessed July 12, 2021.

 

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Murmurs for the Learners: An approach to pediatric heart murmurs

Murmurs for the Learners: An approach to pediatric heart murmurs – A Medical Student Clinical Pearl

Luke MacLeod, Med IV

DMNB Class of 2022

Reviewed by Dr. Tushar Pishe

Copyedited by Dr. Mandy Peach

Case:

You are a senior medical student working in the emergency department and are asked to see Charlie, a 3-year-old boy who had a fall.  He is accompanied by his uncle Kevin, who gives you the history.  About one hour ago, Charlie was climbing onto a chair when he fell off and hit his head.  The chair was only a few feet off the ground and the floor was covered with a rug.  Charlie cried for several minutes after the fall, but there was no loss of consciousness or vomiting following the event.

Kevin tells you that Charlie is a healthy boy with no known medical issues or surgical history. There have been no concerns with his growth or development thus far.  He has no allergies, does not take any medications, and is up to date on his immunizations.  Kevin is unable to tell you much about Charlie’s family history.  He recently adopted Charlie, whose biological parents are no longer involved.

On exam, you observe an active and responsive 3-year-old.  He is afebrile with stable vital signs.  He has normal colour and shows no signs of respiratory distress.  There is a small bump on the top of his head, but no other injuries are noted.  His neurological exam reveals no focal neurological deficits.  To complete the exam, you feel his abdomen, which is soft and non-tender with no organomegaly, and auscultate his heart and lungs.  His lungs are clear with no crackles or wheeze. On auscultation of the heart, you detect a soft, non-radiating systolic murmur that seems to go away with inspiration.

You are reassured from the history and exam that Charlie’s head injury was very minor and that no further investigations or interventions are necessary, but you wonder about the significance of his heart murmur.

 

What is a heart murmur?

 

A heart murmur is an additional sound, often described as whooshing or blowing noise, heard between heart beats that is generated by turbulent blood flow in or near the heart.1,2  Heart murmurs are very common, with up to 90% of children having one either during infancy or later in childhood.  However, less than 1% of these murmurs are due to congenital heart disease.3  If the heart murmur is related to a serious underlying condition, the child may have signs or symptoms such as cyanosis, cough, shortness of breath, or light-headedness.1  Most murmurs are asymptomatic, but the absence of symptoms does not always mean that the murmur is benign.3 In some cases a murmur may be the only sign of an underlying heart condition.4

 

How to describe a murmur

 

Before picking up your stethoscope, you’ll want to make sure you have clean ear canals so you can pick up subtle murmurs.  The characteristics use to describe a murmur can be remembered with the pneumonic Q-TIP ROLS (note: this is not a recommendation to clean your ears with cotton swabs).

 

Quality

The quality of a murmur can be described as harsh, blowing, musical, rumbling, or vibrating.3

 

Timing

Timing describes when the murmur occurs in the cardiac cycle.  A systolic murmur occurs between S1 and S2.  These can be further categorized into four sub-types:

  • Early systolic: heard with or immediately after S1 and ends about halfway through systole.
  • Mid-systolic/systolic ejection murmur: heard midway between S1 and S2. Increases then decreases in volume (crescendo-decrescendo).
  • Mid-to-late systolic: heard about halfway through systole and ends before S2
  • Holosystolic/pansystolic: heard throughout systole.

Click here to listen to a holosystolic murmur: https://www.youtube.com/watch?v=MzORJbyHTT0

 

A diastolic murmur occurs between S2 and S1.  These can be further categorized into three sub-types:

  • Early diastolic: a high-pitched murmur heard with or immediately after S2.
  • Mid-diastolic: heard soon after S2 and ends before S1.
  • Late diastolic/presystolic: heard just before S1.

 

A continuous murmur is heard throughout the cardiac cycle.3

 

Intensity

A grading system from 1-6 is used to describe a murmur’s intensity, with higher values representing greater volumes.3  The following table details what each grade indicates:5

Pitch

A murmur can have low, medium, or high pitch.  High pitch murmurs are best detected using the diaphragm of the stethoscope, while low pitch murmurs are easier to hear using the bell.3

 

Radiation

This is the furthest point from the location (see below) where the murmur can still be detected.3

 

Other sounds

S3: heard in early diastole (shortly after S2).  S3 can be present in hyperdynamic states or with a large VSD.  This sound is best heard with the bell over the apex (for blood flow to the left ventricle) or the lower left sternal border (for blood flow to the right ventricle). When an S3 is present, the heart beat cadence is often described using the word “Kentucky” where “Ken” is S1, “tuc” is S2, and “ky” is S3.5

 

S4: heard late in diastole (just before S1) when there is turbulent blood flow into a stiff ventricle, such as in hypertrophic cardiomyopathy, myocardial dysfunction, semilunar valve stenosis, or tachycardia-induced cardiomyopathy.  S4 is best heard with the bell and is a pathologic exam finding.  When an S4 is present, the heart beat cadence is often described using the word “Tennessee,” where “Ten” is S4, “nes” is S1, and “see” is S2.5

 

Click below to listen to S3 and S4 heart sounds

https://www.youtube.com/watch?v=o8eqYHCy7dw

 

Ejection clicks

These are high pitch sounds that are often generated by abnormal heart valves.  The affected valve is determined based on the location, timing, and nature of the click as shown in the table below:5

Pericardial friction rub

A coarse grinding sound heard with pericarditis. This is best heard along the left sternal border.5

 

Location

This is the point where the murmur is most easily heard.3

 

Shape

Shape describes a murmur’s volume pattern. A few examples are shown below:6

What are the characteristics of benign and pathological murmurs?

 

Some red flag characteristics of pathologic murmurs are listed below.4,7

  • Holosystolic
  • Diastolic
  • Grade 3 or higher
  • Harsh quality
  • Systolic click
  • Max intensity at upper left sternal border
  • Abnormal S2
  • Greater intensity with standing

 

Characteristics of benign murmurs can be remembered using The Seven S’s.4,8

  • Systolic
  • Soft
  • Short (not holosystolic)
  • Small (non-radiating)
  • Sweet (not harsh)
  • Single (no clicks or gallops)
  • Sensitive (changes with position or respiration)

 

Click below to listen to an innocent heart murmur

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

 

Here are some examples to practice differentiating innocent from pathological murmurs:

https://teachingheartauscultation.com/pediatric-murmur-recognition-program-intro

 

What are some of the more common pediatric heart murmurs?

 

Innocent9

  • Classic vibratory parasternal-precordial stills murmur
  • Pulmonary ejection murmur
  • Systolic murmur of pulmonary flow in neonates
  • Venous hum
  • Carotid bruit

 

Pathologic4

  • Ventricular septal defect
  • Atrial septal defect (example: https://www.youtube.com/watch?v=W8gg2S-mvSQ)
  • Patent ductus arteriosus
  • Teratology of Fallot
  • Pulmonary stenosis
  • Coarctation of the aorta
  • Aortic stenosis
  • Transposition of the great arteries

 

Next steps

 

In patients with a heart murmur and an abnormal chest X-ray or ECG, an echocardiogram is indicated.  The echocardiogram is the gold standard test to diagnose congenital heart defects.  While the chest X-ray and ECG are low cost tests and can help rule out other diagnoses, they are not particularly useful in identifying the cause of a heart murmur. 3

An innocent heart murmur in an asymptomatic patient with an otherwise normal exam does not require referral to cardiology.  However, the patient should be followed by their family physician to monitor the murmur.

Patients who are symptomatic, have a pathologic murmur, and/or have other concerning exam findings should be referred to a pediatric cardiologist.10

 

Case Conclusion

 

Charlie’s heart murmur lacked any of the red flag characteristics.  It was soft (grade 2) systolic murmur that did not radiate and changed with inspiration, which are all reassuring signs.  He was also asymptomatic and had an otherwise normal exam.

You explain to Kevin that Charlie looks well and that there are no signs of serious head trauma.  You mention that you did notice a heart murmur that is likely benign.  Charlie does not need to see a specialist, but you recommend that he have a follow up appointment with his family doctor in the next few weeks to monitor the heart murmur.

 

 

References:

  1. Heart Pulse Sound Wave Icon Stock Vector – Illustration of blood, healthcare: 91331428. Accessed November 19, 2021. https://www.dreamstime.com/stock-illustration-heart-pulse-sound-wave-icon-background-image91331428
  2. Heart Murmur | NHLBI, NIH. Accessed November 18, 2021. https://www.nhlbi.nih.gov/health-topics/heart-murmur
  3. Heart murmurs: MedlinePlus Medical Encyclopedia. Accessed November 18, 2021. https://medlineplus.gov/ency/article/003266.htm
  4. Pediatric Heart Murmurs: Evaluation and management in primary care. Accessed November 18, 2021. https://oce-ovid-com.ezproxy.library.dal.ca/article/00006205-201103000-00006/HTML
  5. Frank JE, Jacobe KM. Evaluation and Management of Heart Murmurs in Children. Am Fam Physician. 2011;84(7):793-800.
  6. Approach to the infant or child with a cardiac murmur – UpToDate. Accessed November 18, 2021. https://www.uptodate.com/contents/approach-to-the-infant-or-child-with-a-cardiac-murmur?search=heart%20murmurs&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  7. Physical Examination – Textbook of Cardiology. Accessed November 18, 2021. https://www.textbookofcardiology.org/wiki/Physical_Examination
  8. Pediatric Heart Murmur Recognition Program intro. Teaching Heart Auscultation to Health Professionals. Accessed November 19, 2021. https://teachingheartauscultation.com/pediatric-murmur-recognition-program-intro
  9. Bronzetti G, Corzani A. The Seven “S” Murmurs: an alliteration about innocent murmurs in cardiac auscultation. Clin Pediatr (Phila). 2010;49(7):713. doi:10.1177/0009922810365101
  10. Begic E, Begic Z. Accidental Heart Murmurs. Med Arch. 2017;71(4):284-287. doi:10.5455/medarh.2017.71.284-287
  11. McConnell ME, Adkins SB, Hannon DW. Heart murmurs in pediatric patients: When do you refer? Am Fam Physician. 1999;60(2):558-565.

 

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A Case of Smoke Inhalation Injury

A Case of Smoke Inhalation Injury – A Medical Student Clinical Pearl

Emmanuel Hebert

MD Candidate, Class of 2022

Dalhousie Medicine New Brunswick

Reviewed by Dr. Matthew Greer

Copyedited by Dr. Mandy Peach

Case

 A 54-year-old Male presents to the emergency room via EMS. He woke up at nighttime to his house on fire. He says he woke up coughing due to the smoke and was able to crawl out of the house while ablaze and called EMS. He was then transported to the hospital. He also reports that his voice is more rough than usual and that he has pain on his back.

Past Medical History: Unremarkable

Medications: No prescriptions medications.

Physical Examination: Patient is seen wearing a non-rebreather mask with an oxygen rate of 12L/min. He appears well and is in no acute distress. He has singed scalp hair and appears flushed. The patient’s vitals are HR-110, BP-125/80, Temp-36.5, O2 sat- 99%. Patient weighs 130 kg. His back appears very red but there are no open lacerations or blisters. There is good air entry bilaterally with no adventitious sounds or wheeze.  There is soot in the mouth as far back as can be visualized. The oropharynx is dry and mucous contains soot.

Figure 1: First degree burns on the back.

 

Initial bloodwork:

  • WBC: 10×10^9/L
  • Hgb: 135
  • Plt: 300×10^9/L
  • Na: 135
  • K: 4
  • Glu: 6
  • Carboxyhemoglobin: 5%
  • EtOH: Neg

 

What is the differential diagnosis of dysphonia?

-Acute laryngitis

-Functional dysphonia

-Tracheal Injury

-Injury to recurrent laryngeal nerve

-Caustic ingestion, smoke inhalation injury, blister chemical agents

-Neck masses (benign and malignant) [5,7]

 

Smoke Inhalation Upper Respiratory Tract Injury

 

Definition: Inhalation injury refers to damage to the respiratory tract or lung tissue from heat, smoke, or chemical irritants carried into the airway during inspiration [1].

Damage to the airway can be broken into three different affected zones with their own clinical consequences:

 

Upper Airway

  • The leading injury in the upper airway (above the vocal cords) is thermal injury due to heat exchange in the oro- and nasopharynx.
  • Injuries occurring early include erythema, ulcerations, and edema.
  • It is for this reason that aggressive fluid resuscitation should be avoided as the edema resulting from the heat transfer, can be compounded with fluid resuscitation, resulting in a further compromised airway. [2]

 

Tracheobronchial

  • Injuries to the tracheobronchial system occurs due to the chemical makeup of the smoke. When smoke stimulates the vasomotor and sensory nerve endings, neuropeptides get released which cause bronchoconstriction and vasodilation. Due to this inflammatory response, a loss of plasma proteins and fluid from the intravascular space into the alveoli and bronchioles ensues. This causes alveolar collapse and causes a VQ mismatch resulting in hypoxia. [3]

 

Parenchymal Injury

  • Injuries to the parenchyma occur because of the above mechanism resulting in alveolar collapse, which then cause increased transvascular fluid flux, a decrease in surfactant, and a loss of hypoxic vasoconstriction and therefore impaired oxygenation. [3]

Figure 2. Mechanisms of smoke inhalation injury in tracheobronchial area [4]

 

Management

Patients with smoke inhalation injuries are also at risk for carbon monoxide poisoning. It is for this reason that carboxyhemoglobin is used to assess degree of carbon monoxide toxicity. The treatment for this is 100% oxygen via non-rebreather. Another treatment that can be used is hyperbaric therapy. Choice of hyperbaric therapy should be made in consultation with a hyperbaric specialist and patient must be stable prior to transport. [3]

One of the earliest decisions to make in the management of patients with suspected smoke inhalation injuries is whether to secure the airway. In patient whom the airway is non-patent or there is an obstruction, the decision is easy to either attempt intubation via endotracheal tube or secure a surgical airway. The decision is less straight forward when the patient does not seem to be having any difficulties with ventilation and oxygenation. In the case of smoke inhalation injury, early intubation can be lifesaving. [6] This is due to the delayed fashion of bronchoconstriction in addition to the thermal changes that result from heat/smoke inhalation. Clinical judgement must be used however, to avoid intubating everyone prematurely. There are several red flag symptoms that physicians can use to assess whether a patient with smoke inhalation injury requires prophylactic intubation. [5]

 

Indications for early intubation:

  • Signs of airway obstruction: hoarseness, stridor, accessory respiratory muscle use, sternal retraction
  • Extent of the burn (TBSA burn > 40-50%)
  • Extensive and deep facial burns
  • Burns inside the mouth
  • Significant edema or risk for edema
  • Difficulty swallowing
  • Signs of respiratory compromise: inability to clear secretions, respiratory fatigue, poor oxygenation or ventilation
  • Decreased level of consciousness where airway protective reflexes are impaired
  • Anticipated patient transfer of large burn with airway issue without qualified personnel to intubate en route

 

Back to the case:

Due to our patient having progressive hoarseness, as well as soot throughout his oropharynx, the decision was made to secure his airway before it became too difficult to do so. A discussion was had with the patient about the risks and benefits to intubation and sedation while the inflammatory response could take its course and he consented to the procedure. Using rapid sequence intubation, rocuronium, a paralytic was used at a dose of 1mg/kg=130mg and propofol was used as a sedative at 1mg/kg=130mg. Fentanyl was used for analgesia at a dose of 1mcg/kg= 130mcg.

Due to the complexity of intubating a patient with possible impending upper airway collapse, it is important to have the best person available for intubation with one pass and ENT should be consulted so that a surgical airway can be obtained. One should also consider awake intubation due to high risk of upper airway occlusion. With this patient, a video laryngoscope was used to place the endotracheal tube.

Figure 3: Video laryngoscopy of an airway with smoke inhalation injury

 

During the intubation, it was seen that the tissue surrounding the airway was quite edematous with black soot present as well. This was an impending airway collapse! The endotracheal tube was placed, and the patient was monitored in the ICU overnight. As expected, edema ensued and oropharynx, tongue became edematous. The patient was stabilized on propofol drip over the next 2 days and was extubated on the third day post intubation.

 

Key Takeaways

  • Early identification of smoke inhalation injury is critical to survival.
  • The longer delay of intubation is, the harder it becomes. Consider awake intubation.
  • Red flag symptoms: Respiratory distress, respiratory depression, or altered mental status, Progressive hoarseness, Supraglottic or laryngeal edema/inflammation on bronchoscopy or NPL, Full thickness burns to face or perioral region, Circumferential neck burns, Major burns over 40-60% of body surface
  • Early intubation=lower mortality

 

References:

 

  1. Woodson CL. Diagnosis and treatment of inhalation injury. In: Total Burn

Care, 4 ed, Herndon DN (Ed), 2009.

  1. Sheridan RL. Fire-Related Inhalation Injury. N Engl J Med 2016; 375:1905.
  2. Rehberg S, Maybauer MO, Enkhbaatar P, et al. Pathophysiology, management and treatment of smoke inhalation injury. Expert Rev Respir Med 2009; 3:283.
  3. Herndon, D. N. (2018). 16. In Total burn care (pp. 174–183). essay, Elsevier.
  4. ABLS Provider Manual. (2019). Ameriburn.org
  5. Cioffi WG, Mason AD Jr, et al. The risk of pneumonia in thermally injured patients requiring ventilatory support. J Burn Care Rehabil 1995; 16:262.
  6. Reiter R, Hoffmann TK, Pickhard A, Brosch S. Hoarseness-causes and treatments. Dtsch Arztebl Int. 2015;112(19):329-337. doi:10.3238/arztebl.2015.0329

 

 

 

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Approach to Medical Abortion Complications in the ED

Approach to Medical Abortion Complications in the ED – A Medical Student Clinical Pearl

Victoria Mercer

MD Candidate | Class of 2023
Dalhousie Medicine New Brunswick

Case:

A 28 year old female presents to the ED with cramping abdominal pain and heavy vaginal bleeding ongoing for 4 days. She has soaked through 4 regular pads in the last 2 hours, an increase from her ongoing bleeding. She also describes an increase in lower abdominal pain and some lightheadedness. Taking her medical history you discover she was 9 weeks pregnant and had a medical abortion approximately 4 days ago.

Vitals: HR 101, BP 101/65, RR 19, SpO2 98%, T 37.5°C

Brief Review of Medical Abortion

Medical abortions account for approximately 40% of abortions and is both an effective and safe method of terminating pregnancies that are <11 weeks(1). Serious complications are rare but must be recognized by the emergency physician to prevent morbidity and mortality.

Standard regimen of medical abortions includes administration of 200mg oral Mifepristone, a progesterone receptor antagonist, followed by 800mg of Misoprostol, a synthetic prostaglandin, 24-48 hours later (1). Mifepristone disrupts pregnancy growth and misoprostol induces uterine contractions to aid in the expulsion of the pregnancy contents (2).

Expectations vs complications

Bleeding

Bleeding and cramping generally begin 1-4 hours after ingestion of misoprostol however the heaviest bleeding generally occurs 3-8 hours post ingestion as the pregnancy tissue is expelled from the uterus (2). Duration of bleeding is generally 11 to 17 days (1,2). Heavy bleeding is defined as soaking through 2 pads per hour for at least 2 hours, upon which patients should be counselled to seek medical assistance (1,2).

Differential diagnosis of post medical abortion hemorrhage: Uterine atony (40-50%), retained products of conception (POC), placenta previa or accreta, coagulopathies

Cramping & Pain

Over 90% of patients following mifepristone-misoprostol will experience cramping (3). This may be moderate pain that responds to oral analgesics such as acetaminophen, ibuprofen or in some cases, an opioid (3). When pain is not improving or controlled by oral medication, this could be concerning (2,3).

Differential of refractory pain: incomplete abortion, ectopic pregnancy, infection

Fever

Temperatures above 38.0 °C for several hours despite antipyretics is abnormal and should warrant investigation for infection. Most cases of postabortion infections are due to endogenous flora or pre-existing infections. If retained POC is identified via ultrasound, broad spectrum antibiotics should be administered and obstetric and gynecology should be consulted for surgical management (2).

Pearl:

Post-abortion triad includes pain, low-grade fever and bleeding. Most often caused by RPOC(4).

Approach to Patient in ED After a Medical Abortion

 

 

Case Continued:

Pelvic examination findings include a soft and enlarged uterus. No cervical lacerations are identified. On ultrasound you notice increase heterogenicity within the endometrial cavity and a thickened endometrial wall. You suspect the cause for her post-abortion hemorrhage is due to RPOC.

You begin a bimanual uterine massage and initiate methylergonovine administration. After 3 repeat doses, the bleeding begins to subside. Vital signs remain stable and OB/GYN is consulted for further management.

 

References

  1. First-trimester pregnancy termination: Medication abortion – UpToDate [Internet]. [cited 2021 Nov 8]. Available from: https://www.uptodate.com/contents/first-trimester-pregnancy-termination-medication-abortion?search=medical%20abortion&source=search_result&selectedTitle=1~72&usage_type=default&display_rank=1#H2018734958
  2. Orlowski MH, Soares WE, Kerrigan KL, Zerden ML. Management of Postabortion Complications for the Emergency Medicine Clinician. Annals of Emergency Medicine. 2021. 77(2):221-232. doi.org/10.1016/j.annemergmed.2020.09.008
  3. Kruse B, Poppema S, Creinin MD, Paul M. Management of side effects and complications in medical abortion. American Journal of Obstetrics and Gynecology. 2001. 183(2):S65–75.
  4. Abortion Complications Clinical Presentation: History, Physical, Causes [Internet]. [cited 2021 Nov 9]. Available from: https://emedicine.medscape.com/article/795001-clinical#b4
  5. Yahya B. Retained products of conception [Internet]. [cited 2021 Nov 9]. Available from: https://radiopaedia.org/articles/retained-products-of-conception
  6. Kerns J, Steinauer, J. Management of postabortion hemorrhage. Contraception (Stoneham). 2013. 87(3): 331-342. 10.1016/j.contraception.2012.10.024

 

 

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Allergic Acute Coronary Syndrome (Kounis Syndrome)

Allergic Acute Coronary Syndrome (Kounis Syndrome) – A Medical Student Clinical Pearl

Amar Bhardwaj CC3

Dalhousie Medicine New Brunswick

Class of 2022

Reviewed and edited by Dr. Kavish Chandra

Copyedited by Dr. Mandy Peach

 

Case presentation

A 52-year-old female presents to the ED with sudden onset left sided chest with radiation to her left arm shortly after eating.  The patient is diaphoretic and has been experiencing exertional dyspnea since her meal.  Patient also noted they developed an itchy red rash on their face and torso. There was no evidence of angioedema or other classical clinical signs or symptoms of anaphylaxis.

The patient is otherwise healthy and has a family ischemic heart disease.

Her vitals are BP 160/90, temperature 36.4, HR: 152, RR: 20, Sats:98% O2 on room air. The cardiovascular and respiratory exam are otherwise normal. The ECG shows sinus tachycardia without evidence of other abnormalities.

 

Image source: Burns, Ed. “Sinus Tachycardia • LITFL • ECG Library Diagnosis.” Life in the Fast Lane • LITFL, 7 Feb. 2021, litfl.com/sinus-tachycardia-ecg-library/.

Her hsTnT is 8 and the repeat marker is unchanged and the diagnosis of Kounis syndrome is considered.

 

Kounis syndrome

Kounis syndrome is defined as a concurrent acute coronary syndrome (ACS) in the setting of mast cell activation, which can be spontaneous or secondary to an allergic reaction (Lerner et al. 2017).  Kounis syndrome can be triggered by food, insect stings, drugs, environmental exposure and underlying medical conditions (Rodrigues et al. 2013). Allergen induced mast cell activation and release of inflammatory mediators leads to vasospasms, intimal thickening, and upregulation of proinflammatory cytokines that affect the coronary arteries and potential for occlusion progressing to an acute MI. The epidemiology remains scarce, and thus the prevalence is not entirely known as it is often missed or under diagnosed (Kounis, 2013; Kounis 2016).

Patients with Kounis syndrome can present with dyspnea, angioedema, pruritis, urticaria, gastrointestinal distress and hemodynamic instability. Airway compromise is of high importance in severe anaphylactic reactions with the potential to progress to anaphylactic shock. Along with an anaphylactic response, the coronary arterial effect can accelerate plaque rupture and cause symptoms indistinguishable from ACS.

Kounis Syndrome can be classified into three types (Kounis 2013)

Type I:

Acute coronary syndrome with normal or near-normal coronary arteries.

Type II:

Pre-existing atherosclerotic disease with syndrome causing coronary artery spasm, plaque rupture or erosion leading to acute MI.

Type III:

Coronary artery stent thrombosis with evidence of aspirated thrombus specimens containing eosinophils and mast cells respectively.

 

Presentation

Patients with this Kounis syndrome typically present with anaphylactic signs and symptoms accompanied with chest pain and associated signs and symptoms of acute coronary syndrome.  Table 1 depicts pertinent signs and symptoms that may point you in the right direction.

Table 1. Clinical and laboratory findings in Kounis syndrome (Adapted from Kounis 2016)

 

Kounis syndrome is a clinical diagnosis.

Management

There are no guidelines addressing the management of Kounis syndrome. However, treatment needs to address any hemodynamic instability as well as the cardiac and allergic concerns. Involvement of cardiology and allergy specialists can be helpful.

Concurrent management of anaphylaxis does not generally interfere with management of ACS however careful analysis of the risks and benefits of epinephrine administration to treat anaphylaxis without exacerbating cardiac ischemia. Case reports describe the successful treatment of Kounis syndrome patients with intramuscular epinephrine (Lerner et al. 2017). Other agents that have shown to aid symptomatically in allergic responses are H1 and H2 blockers as well as systemic corticosteroids for prevention of potential delayed phase reactions.

ACS management may be guided by cardiology and does not differ from traditional management with the exception that aspirin may be omitted due to its potential role propagating anaphylaxis (Lerner et. 2017). Other anti-platelets can be administered however beta-blockers are avoided as analgesics like morphine (further histamine release; Lerner et al. 2017). The timing and role of cardiac catheterization will be guided by cardiology and may involve intracoronary vasodilator infusion or thrombus evacuation (Carr and Helman, 2016).

Summary

In a patient presenting with ACS and severe allergic reaction/anaphylaxis, consider Kounis syndrome. There are no guidelines to assist in the management but the key aspects of managing ACS and anaphylaxis are critical in treating Kounis syndrome as well early consultation with cardiology and allergy.

References:
Carr, D. Helman A. Anaphylaxis and Anaphylactic Shock. Emergency Medicine Cases. February, 2016. https://emergencymedicinecases.com/anaphylaxis-anaphylactic-shock.

Kounis, N. G. (2016). Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management. Clinical Chemistry and Laboratory Medicine (CCLM), 54(10), 1545-1559
Kounis, N. G. (2013). Coronary hypersensitivity disorder: the Kounis syndrome. Clinical therapeutics, 35(5), 563-571.

Lerner M, Pal RS, Borici-Mazi R. Kounis syndrome and systemic mastocytosis in a 52-year-old man having surgery. CMAJ. 2017 Feb 6;189(5):E208-E211. doi: 10.1503/cmaj.151314. Epub 2016 Aug 2. PMID: 27486207; PMCID: PMC5289872.

Mattu, A. Demeester, S. Cardiology Corner: Kounis Syndrome. EMRAP. June, 2021. https://www.emrap.org/episode/emrap2021june1/cardiology

Rodrigues MC, Coelho D, Granja C. Drugs that may provoke Kounis syndrome. Braz J Anesthesiol. 2013 Sep-Oct;63(5):426-8. doi: 10.1016/j.bjan.2013.04.006. PMID: 24263049.

 

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Paediatric Supracondylar Fractures

Paediatric Supracondylar Fractures – A Medical Student Clinical Pearl

 

Reviewed by Dr. Joanna Middleton

Copyedited by Dr. Mandy Peach

Christine Crain (She/Her), CC3
Dalhousie Medicine MD Candidate, Class of 2022

Relevant Case:

On a Saturday, a three-year-old presented to the emergency department with his mother. He’d been playing in the backyard with his older sister who was on their swing. Unfortunately, the boy walked in front of the swing and was hit by his sister. He fell onto an outstretched hand and immediately began to cry and hold his elbow.

Problem:

There are two kinds of Supracondylar fracture; extension, which accounts for up to 95% of these fractures; and the far less common flexion fracture which occurs almost exclusively in older adults.

When a paediatric patient falls into an outstretched hand, the olecranon engages with the fossa, then acts as a fulcrum hyperextending the elbow, punching the olecranon through the relatively thin and weak supracondylar region of the humerus.

Figure 1: Case courtesy of Dr Samir Benoudina, Radiopaedia.org, rID: 39938

The Gartland classification (Fig.1) of supracondylar humeral fractures are based on the degree and direction of any displacement where Type 1 fractures imply little (1b) to no displacement (1a). Type 2 fractures displace the anterior humeral line (Fig.2) but leaves the posterior cortex intact; while type 3 fractures are completely displaced.

Figure 2: The anterior humeral line should pass through the middle third of the humeral capitulum. Case courtesy of Dr Samir Benoudina, Radiopaedia.org, rID: 41167.

Since these fractures commonly occur in children, learners especially need to be aware of the ossification centers within the elbow to be certain that they’re recognized as normal anatomy and not additional fractures. The age of the child should help you to estimate, with the help of a handy mnemonic, which ossifications centers should be visible on radiograph:

Figure 3: Case courtesy of Leonardo Lustosa, Radiopaedia.org, rID: 80555

In our case, with a three-year-old male, we would expect to see the Capitellum and Radial Head, but no other centers. We know any “fragments” in these areas are not additional fractures.

Most commonly in supracondylar fractures, there are other signs we look for that may indicate injury to the cartilage and forming bone:

  • Sail Sign shows a joint effusion under the Anterior fat pad (Fig. 4)
  • Posterior Fat Pad sign is the same, only on the posterior aspect of the elbow (Fig. 4)
  • And, as noted above, the Anterior Humeral Line should intersect the middle third of the Capitellum (Fig. 2)

Figure 4: Showing both Anterior and Posterior fat pad sign. Case courtesy of Assoc Prof Frank Gaillard, Radiopaedia.org, rID: 13527

Finally, given the number of vascular/neural structures that pass through the elbow, what complications are there to be aware of? As with all fractures, there is a risk of non/malunion, this is a relatively low risk however and is beyond the scope of this pearl.

Vascular complications include Volkmann’s contracture which can occur with injury to the brachial artery. This can result in a volar compartment syndrome leading to fibrosis and contracture of flexor muscles.

Finally, injury to any of the nerves that travel to innervate the hand/forearm can occur. Innervation through the Radial, Median (as well as the Anterior Interosseous nerve), and Ulnar nerves can be verified by a few quick and easy maneuvers as seen in Figure 5.

Figure 5: Innervation of the hand for the purposes of nerve injury screening.

Case Resolutions:

Inspection prior to radiographs showed intact sensation, brisk capillary refill with strong distal pulses, and ongoing ability to move joints below the injury. He was sent for radiographs which reported a supracondylar fracture. We casted his elbow and sent him for follow up to the Ortho fracture clinic the following week.

Conclusion

While learners may initially think ossification centers of the elbow are fracture fragments, using CRITOE they will be able to rule out joint involvement. This will allow you to move more quickly onto other radiographic signs of fracture.

References

  1. https://radiopaedia.org/articles/supracondylar-humeral-fracture-2
  2. https://radiopaedia.org/articles/gartland-classification-of-supracondylar-humeral-fractures
  3. https://radiopaedia.org/articles/anterior-humeral-line
  4. https://radiopaedia.org/articles/elbow-ossification-mnemonic
  5. https://radiopaedia.org/articles/sail-sign-elbow-1
  6. https://www.orthobullets.com/pediatrics/4007/supracondylar-fracture–pediatric

 

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Polymyalgia Rheumatica

Polymyalgia Rheumatica – A Medical Student Clinical Pearl

Alexis Lamontagne

MD Candidate, Class of 2022

DMNB, Dalhousie University

Case:

A 73 y/o M presents with a 1 week history of proximal muscle aches and stiffness including his hips, shoulders and neck. He describes the stiffness as worse in the morning, recently he has had trouble getting out of bed at all. He finds that the stiffness is relieved and regains function as he begins to move around. He also notes increased stiffness after periods of immobility. It has become progressively worse over the past week which lead to seeking medical help in the emergency department.

There are no other associated symptoms including jaw claudication, headache, weight loss, fevers, chills, night-sweats, vision changes, paresthesias, or preceding cold or illness.

The patient has no significant past medical history. His only regular medication is omeprazole. He does not smoke, consumes 4 alcoholic drinks per day, and uses no other recreational drugs. He lives at home with his wife and they are both retired.

While asking about whether there are any rheumatological conditions that run in the family you learn that his older brother has Polymyalgia Rheumatica (PMR).

 

Polymyalgia Rheumatica:

The clinical syndrome of PMR should be considered in those aged over 50 presenting with pain and stiffness of the neck, shoulders and hips that is typically worst in the early hours of the morning or on waking, and tends to improve over the course of the day. Inflammatory markers (ESR/CRP) are typically elevated and anaemia may be present due to inflammation. Symptoms of PMR should resolve rapidly with low-dose glucocorticoids.

Differential:

Although weight loss, fever and synovitis/tenosynovitis have all been described in PMR, they should raise suspicion of :

  • malignancy,
  • deep-seated or disseminated infection (such as endocarditis or osteomyelitis),
  • inflammatory arthritides such as rheumatoid arthritis (RA), spondyloarthropathy, or crystal arthropathy.

 

Investigations:

Bloodwork reveals a normal CBC and an elevated CRP at 108.

 

Treatment:

Prednisone is initiated at 15mg PO daily. If the initial dose of 15mg does not demonstrate clinical improvement in one week, this can be increased to 20mg or a maximum dose of 25mg.

Once symptoms are controlled for 2 to 4 weeks the dose of prednisone can be tapered. Prednisone can be reduced by 2.5mg every 2 to 4 weeks until 10 mg daily is reached. The dose can then be further tapered by 1 mg per month until cessation or symptoms flare. There is no consensus regarding an optimal tapering regime.

Should a flare occur during the taper, a CRP should be measured and prednisone increased to the lowest dose that relieves symptoms. If a patient relapses several times during the taper, dose reductions can be lengthened to six to eight weeks. If a relapse occurs after the cessation of glucocorticoid use, a CRP should be obtained and prednisone can be initiated at the original dose which managed symptoms.

CRP should be measured again 2 months after the initiation of glucocorticoid therapy and 3 to 6 months thereafter during the course of treatment. Monitoring for symptoms of PMR and Giant Cell Arteritis (GCA) should also take place throughout treatment.

 

Pathophysiology:

The cause of polymyalgia rheumatica (PMR) is unknown.

The strongest risk factor for PMR is increasing age. It is unheard of in those under 50 years old and incidence increases with each decade, peaking around 75 years. Proposed mechanisms include ageing of the immune system (immunosenescence), ageing of the tissues, and ageing of neurohumoral regulatory systems. Based on the clustering of cases in space and time, it has been proposed that PMR may be triggered by infection. This could lead to persistent inflammation on a background of chronic low-grade inflammation secondary to decline in adaptive immunity and a compensatory increase in innate immune mechanisms. (Mackie 2013)

 

Relationship to Giant Cell Arteritis:

There is a well-known association between PMR and giant cell arteritis (GCA). Many patients with GCA also have polymyalgic symptoms and some patients with PMR subsequently develop GCA (Mackie 2010). There is some discussion as to whether PMR and GCA are separate disease entities or two conditions on a single pathophysiological spectrum. For the practising clinician it is important to realise that PMR and GCA are treated with different doses of glucocorticoids and that treatment of GCA is a medical emergency, whereas the immediate priority with PMR is to exclude other conditions before starting treatment. All patients with PMR should be assessed for signs and symptoms of GCA at diagnosis and screened for underlying GCA at follow-up visits. These symptoms include constitutional symptoms, headache, jaw claudication, ocular involvement, large vessel involvement, and anemia.

 

Conclusion:

With a prescription for prednisone, a follow up was arranged with the patient’s family doctor in one week. The patient was advised that the family doctor would taper his prednisone, monitor CRP, and screen for symptoms of PMR and GCA. Additionally, monitoring for the adverse effects of glucocorticoids, including osteoporosis, glucose intolerance, and hypertension would take place.

 

References:

Mackie SL. Polymyalgia rheumatica: pathogenesis and management. Clin Med (Lond). 2013;13(4):398-400.

Mackie SL. Et al. Can the prognosis of polymyalgia rheumatica be predicted at disease onset? Results from a 5-year prospective study. Rheumatology (Oxford). 2010 Apr; 49(4):716-22.

 

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