Testicular Torsion – EM Reflections January 2022

Authored and Copyedited by Dr. Mandy Peach

Big thanks to Dr. Paul Paul for leading discussion.

All cases are imaginary but highlight important learning points

Case

A 72 yo male presents with acute onset L sided scrotal pain radiating to the groin ongoing 3 hours. In triage he denied any associated trauma. He has no history of scrotal issues. He has vomited once from the pain. He took a leftover morphine tablet he had post knee surgery and that helped temporarily. He denies any fever or diarrhea. He was well prior to the onset of pain.

PMH: OA with R TKA, DLP

Vitals: BP: 157/92 HR 102 RR 20 O2 98% RA T – 36.7

The department is in critical overcapacity, with admitted patients being boarded in hallways. While the nurse is triaging she is interrupted three times with questions from both staff and patients asking when they are to be seen. A testicular exam is not completed at that time.

What is the differential for acute scrotal pain in an adult1?

  • Epididymitis/epididymo-orchitis
  • Fournier’s gangrene
  • Trauma
  • Inguinal hernia
  • Mumps orchitis
  • Testicular cancer
  • Henoch-Schönlein purpura
  • Acute idiopathic scrotal edema
  • Post-vasectomy pain
  • Referred pain
  • Testicular torsion

This patient had no history of trauma, and was otherwise well. He was afebrile and had suspected elevated BP and HR secondary to pain. Tylenol and advil are administered.

2 hours have passed, the patient continues to have ongoing pain and presents back to triage as he has started vomiting again. Repeat vitals are unchanged.

When finally assessed by a physician there is extensive L sided scrotal edema and redness. It is exquisitely tender. The testicle appears to be lying abnormally. You are concerned for torsion.

 

Other than a swollen, red testicle what are other signs/symptoms of torsion2?

  • Acute onset of unilateral testicular pain: the presentation can actually vary; Some present with gradually increasing pain, others fluctuating pain if the testicle is intermittently undergoing torsion and detorsion and some have minimal pain. The patient may describe the pain as radiating to the abdomen, groin or flank.

20% of patients with torsion complain of lower abdominal pain.

 

  • Affected testicle lying high and horizontal: seeing this certainly increases the odds of the patient having torsion, but depending on timing of presentation and swelling it may be difficult to determine the position of the testicle.

 

  • Absent cremasteric reflex: With an intact cremasteric reflex lightly stroking the inner thigh will cause the ipsilateral testicle to retract/elevate3. In torsion, the twisting of the spermatic cord interrupts this reflex. However, the sensitivity of this sign is only 60%

Presence of a normal cremasteric reflex does not rule out torsion

  • Swelling is a sensitive, but not specific sign. It can be found in a number of conditions as listed in the differential above.
  • Nausea/vomiting may be associated, if present there is increased likelihood of torsion (OR 8.87)4 but it is a non-specific sign seen in many presentations. It’s importance is when it is seen in conjunction with the other signs of torsion.

What is Prehn’s sign and what is its utility in assessing for torsion2?

In epididymitis, elevation of the affected testicle can result in relief of scrotal pain. This is Prehn’s sign. If the pain is worsened with this maneuver it is thought to be associated with torsion. This technique is not reliable in differentiating epididymitis from torsion. One study found the majority of patients with torsion, over 90%, had a positive Prehn’s sign.

Combining all these findings into the TWIST score for pediatric patients under the age of 18 years can help guide management in cases where it is unclear5.

High risk with 7 points – PPV 100% for torsion

<5 points – NPV 96%

To avoid missing irreversible ischemia, use this took as a rule  in score only – if a score of 7 consult urology directly to consider surgical intervention without doppler ultrasound2.

This patient is in his 70’s, why would we even consider torsion1?

Torsion typically happens in neonates and postpubertal males, but it can occur in adult males. One retrospective chart review found that 39% of hospitalized males with torsion were age 21 and over. Although rare, it can happen in older adults.

In any male with abdominal pain, regardless of age, consider testicular torsion

This male has pain ongoing for hours, what are the odds the testicle is salvageable2?

Previous thought was that 6 hours was the window and that after that the testes is beyond salvage. However, there are longer survival percentages greater than 6-8 hours depending on the history (ie. Intermittent torsion) leading to a range in timelines for irreversible ischemia.  Therefore, regardless of duration of pain, the case should be treated as a surgical emergency.

So, you urgently call urology for consult. They expect to be in house within 20 minutes. They are requesting a formal ultrasound in the meantime. It’s now after midnight so the ultrasound tech has to be called in. Time is ticking, so you grab your ultrasound probe.

What is the evidence for point-of-care ultrasound in testicular torsion?

Sensitivity 88-100%

Specificity 90%2

One chart review of pediatric patients presenting with symptoms suspicious of torsion found point of care scrotal ultrasound performed by pediatric EM physicians was 100% sensitive and 99.1% specific6.

What are the findings concerning for testicular torsion on ultrasound?

Many – it depends on the timing.

From a blood flow perspective

  • Initially as the spermatic cord twists the venous system is most susceptible to obstruction. So if very early, there may be normal appearance of blood flow.
  • As time goes on venous flow may look to still be present, but looks less compared to unaffected testicle.
  • Before, or after, venous flow completely obstructs, arterial flow can show signs of impending obstruction as well with a high resistance pattern on doppler.
  • Finally, there will be no flow present in the testicle and it may shows signs of necrosis.

Obtaining doppler to confirm both venous and arterial flow is imperative when assessing for torsion

Other signs on ultrasound

  • Enlarged, edematous testicle
  • Surrounding fluid within the scrotum
  • Loss of homogenous appearance with hypoechoic areas of infarct
  • Whirlpool sign showing the twisted spermatic cord

Review some images:

Normal appearance testicle7 with flow

Absence of flow (note the affected testicle is also quite edematous)

Normal venous appearance7 – a low flow pattern that stays consistent

Normal arterial appearance7 – notice the peak and gradual trough associated with systole and diastole

High resistance patternconcerning for impeding arterial obstruction

Whirlpool sign9 – notice the yellow coloration of doppler in this image. This is power doppler – it is more sensitive than color doppler for picking up on low flow states10. It is not indicative of direction of flow, just intensity of flow ie. Brighter = more flow.

You see absence of flow on the affected testicle of your patient.

The urologist is in house and you review the images on PoCUS – the patient is brought to the OR.

What if you were rural and transport would be hours? Should you attempt to detort the testicle manually?

The open book maneuver where you ‘open’ or turn the testicle outward to attempt to detort11 is only recommended if there is an anticipated delay of hours to the OR.

The reason? Poor success rate, up to a 1/3 of patients will actually be torting in the opposite direction2.

Bottom line:

  • Suspect testicular torsion in any male, of any age, with abdominal pain.
  • Many classic findings are not reliable to rule out torsion
  • Use bedside ultrasound to assess for color doppler flow, consider using power doppler to detect low states. Findings vary but classically – no flow in the testicle is seen with torsion.
  • Ischemic time is variable, and longer than initially thought, treat every presentation as a surgical emergency regardless of timing of presentation.
  • High suspicion? Don’t wait for formal imaging – call urology.

 

Interested in PoCUS for other scrotal presentations? Review this awesome post by Dr. Rawan AlRashed, PoCUS fellow

Scrotal Pain – Scrotal PoCUS in a nutshell

 

References and further reading:

  1. Eyre, RC. 2022. Acute scrotal pain in adults. UpToDate. Retrieved June 13, 2022 from https://www.uptodate.com/contents/acute-scrotal-pain-in-adults?search=scrotal%20pain%20adult&source=search_result&selectedTitle=1~45&usage_type=default&display_rank=1#H1816144542
  2. Helman, A. Krakowsky, Y. Wolpert, N. Testicular Torsion: A Diagnostic Pathway. Emergency Medicine Cases. July, 2020. https://emergencymedicinecases.com/testicular-torsion. Accessed [June 13, 2022]
  3. Image from https://www.quora.com/What-is-a-cremasteric-reflex
  4. Tali Beni-Israel, Michael Goldman, Shmual Bar Chaim, Eran Kozer. Clinical predictors for testicular torsion as seen in the pediatric ED. The American Journal of Emergency Medicine, Volume 28, Issue 7,2010. Pages 786-789,ISSN 0735 6757,https://doi.org/10.1016/j.ajem.2009.03.025. (https://www.sciencedirect.com/science/article/pii/S0735675709001569)
  5. Barbosa JA, Tiseo BC, Barayan GA, et al. Development and initial validation of a scoring system to diagnose testicular torsion in children. J Urol. 2013;189(5):1859-1864.
  6. Friedman N, Pancer Z, Savic E, Tseng F, Lee MS, Mclean L et al. 2019. Accuracy of point-of-care ultrasound by pediatric emergency physicians for testicular torsion. Journal of Pediatric Urology. VOLUME 15, ISSUE 6, P608.E1-608.E6, DECEMBER 01, 2019DOI:https://doi.org/10.1016/j.jpurol.2019.07.003
  7. Personal ultrasound images from a case of suspected testicular torsion. Deidentified.
  8. Ultrasound of Testicular Torsion. EMRAP. Viewed on https://emergencymedicinecases.com/testicular-torsion/
  9. Patel MS. 2020 Whirlpool sign (testicular torsion). Radiopedia. Accessed June 14, 2022 https://radiopaedia.org/articles/whirlpool-sign-testicular-torsion
  10. Agolah 2022. Power Doppler. Radiopedia. Accessed June 14 2022 https://radiopaedia.org/articles/power-doppler-1?lang=us
  11. Modified from: Cronan KM, Zderic SA. Manual detorsion of the testes. In: Textbook of Pediatric Emergency Procedures, 2nd ed, King C, Henretig FM (Eds), Lippincott Williams & Wilkins, Philadelphia 2008. Assessed June 14, 2022 https://www.uptodate.com/contents/image?imageKey=EM%2F112358

 

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Volume Status Assessment in ED: Beyond the Vitals

Dr. Rawan Alrashed (@rawalrashed)

PEM Physician

PoCUS Fellow

Reviewed and edited by: Dr. David Lewis

Case

A 55 year old man known to have hypertension, diabetes, atrial fibrillation, chronic kidney disease presenting with 1 week H/O fever, SOB, chest pain, cough, fatigability, looking distressed on exam with HR 110, SpO2 of 86% on RA and BP of 87/45. No audible crackles or gallop rhythm, bilateral pitting edema noticed.

So, you are asking yourself should your next step be Fluids or Diuresis ??

Background

Patient presenting to the emergency department as critically ill with shock status presents a challenge in the initial hour to balance their fluid requirements with their volume status to reach an improvement in hemodynamics without causing harm.

Volume status assessment and fluid responsiveness have been investigated using multiple measures ranging from physical examination to laboratory work up to invasive measures. Despite all that, no single or multiple factor have been sensitive or specific enough to guide further fluid management. Currently, PoCUS is progressing widely in aiding the emergency physician to take a decision in assessing patient’s  fluid vs vasopressor vs diuretic needs and guide further resuscitation. PoCUS is noninvasive, readily available, reproducible test that can be augmented with other measures to guide fluid management (1).

 

Pathophysiology

To simplify fluid responsiveness, patients are assessed on accordance of the Frank-Starling curve. Patients will respond to fluid administration if they are on the ascending portion of the Starling curve and no benefit will be added if they are at a plateau where more harm can occur which is difficult to be predict form physical examination solely (2).

 

Figure 1: Frank Starling Law

 

Fluid Challenge

Traditionally volume responsiveness has been assessed by small fluid bolus challenge. A safer alternative to this is passive leg raise (PLR) which is an autotransfusion where you mobilize about 300-500 ml of intravascular volume from the lower limb to the heart by raising the patient legs from 0o to 45o. A Pre-Post assessment of stroke volume within 30-90 sec from PLR can be done to measure the difference where change of 10% consider to be responsive.

This have been shown to have a sensitivity of 77% to 100%, and a specificity of 88% and 99% (1).

 

Figure 2: Passive Leg raising technique (uptodate)

 

Volume Status Assessment

PoCUS have been used in volume status assessment and fluid responsiveness using multiple surrogates which can be classified as follows for simplification:

  1. Cardiac PoCUS: core and advanced.
  2. Stroke volume Assessment: VTI of LVOT/Carotid artery.
  3. Vascular Assessment: IVC, IJV.
  4. Venous Congestion: Hepatic, portal, & intra-renal doppler.
  5. Lung PoCUS.

 

1) Cardiac PoCUS

The target of Cardiac PoCUS is to assess for possible causes of hypotension and shock status using the RUSH or SHoC protocol (3).

 

Figure 3: SHoC Protocol (3).

 

2) Cardiac Output Assessment

Two measures can be used to assess fluid responsiveness: the left ventricular outlet tract (LVOT) and the carotid artery where you assess the velocity time integral (VTI) representing the column of blood passing through the vessel through time. This can be used as surrogate of fluid responsiveness before and after the PLR where a change of 10-15% consider as fluid responsive (4).

 

a. LVOT measurements

Cardiac output variation of greater than 14% has a high positive predictive value for the patient being fluid responsive while values less than 10% are associated with a high negative predictive value (1)

Cardiac output (mL/min) = Stroke Volume (mL/cycle) x Heart Rate (bpm)

Stroke Volume= LVOT area    x    LVOT VTI

 

PoCUS Technique (4)

  • Using the cardiac phased array probe to get apical 5 chamber view and parasternal long axis view.
  • Apical five chamber view, with visualization of the LVOT (A).
  • Pulsed wave Doppler interrogation of the LVOT. The interrogation window is placed just above the aortic valve, and the line of interrogation is positioned parallel to the long-axis of the LVOT itself (B).
  • Measuring the area under the curve of the LVOT Doppler waveform to derive the velocity time integral (C) .
  • Diameter of the LVOT, measured from a parasternal long-axis view (D)

Figure 4: Stroke volume measurement at the LVOT.

 

 

b. Common Carotid Artery

Two measurement are applied to the carotid artery: the carotid blood flow and the corrected carotid flow time index. These measure are recently established in the field of cardiac output assessment and accuracy is still under debate with further studies needed.

 

  • The carotid blood flow is the integral of blood volume that is ejected through the carotid artery with each cardiac cycle. An increase of carotid blood flow by 20% after PLR is indicative of fluid responsiveness with a sensitivity of 94% and specificity of 86% (6).

 

  • The corrected carotid flow time index  (CFTI) representing the flow time between the onset of systole and the closure of the aortic valve as the duration of the full cardiac cycle. A change in the CFTI of 25% following PLR was found to have high specificity but a low sensitivity accordingly a cutoff values of 10% to 15% are more typical, still further studies are needed to specify the accurate cut off value (4).

 

PoCUS Technique (4,5)

a. The linear transducer is placed at approximately at the level of the thyroid cartilage, with the orientation marker pointed toward the patient’s head (A).

b. The Carotid artery identified in long-axis and the bulb before the bifurcation visualized and the doppler is applied within 2–3 cm proximal to the carotid bulb, interrogation line (green) has also been angled to make it more parallel to the long-axis of the artery.

c. The Doppler angle correction cursor is placed parallel to the direction of blood flow with insonation angles <60° .

d. Carotid artery Doppler waveform with measurement of the systolic flow time (SFT) and total cycle time (CCT).

e. Calculate the corrected flow time index using the following formula (Figure-5):

                                           CFTI=SFT/√CCT

f. Calculate the carotid blood flow using velocity time integral tracing and carotid diameter (Intima to intima)  then apply it in this formula (Figure-6):

                                     blood flow=π×(carotid diameter)2/4×VTI×heart rate

 

Figure-5: Corrected Carotid Flow Time Index Measurement (4).

 

Figure-6: Carotid Blood Flow measurement (5).

 

 

 

3) Vascular Assessment

a. Inferior vena cava (IVC)

Measurements of IVC diameter and respiratory variation with the collapsibility index as a predictor of fluid responsiveness was found to be having pooled sensitivity and specificity of 63% and 73% respectively (7).  

PoCUS Technique (8)

  • Use the curvilinear or phased array probe.
  • placed in the sub-xiphoid space with the transducer flat against the abdomen identifying RA and gradually fanning the probe until the intrahepatic IVC can be identified.
  • The probe is then rotated 90 degrees with the marker toward patient head to obtain the IVC in long axis view.
  • IVC diameter is measured 2 cm inferior to the cavo-atrial junction or about 1 cm inferior to the branching of the hepatic veins (Figure 7).
  • M-mode can be used to track IVC collapse during inspiration in spontaneously breathing patients.

Figure-7: IVC and measurement of respiratory variation (Collapsibility Index)

 

Measurements:

Collapsibility Index (Caval Index)

The collapsibility index=(maximal vessel diameter – minimal vessel diameter)÷maximal vessel diameter

It has been demonstrated that venous collapsibility may be inversely proportional to CVP: a 1 mmHg change in central venous pressure correlates to about 3.3% change in IVC collapsibility (9).

 

IVC diameter (cm) CI (%) CVP (mmHg)
<1.5 100% <0-5 Volume depleted
1.5-2.5 >50% <10 Less predictive of responsiveness
1.5-2.5 <50 >10
>2.5 0% >20 Volume overload

 

Important to note that sole interpretation of the IVC for volume assessment was found to be poorly correlating and thus should be used in conjunction with  other measures and integrated on patient presentation (9).

 

b. Internal Jugular Vein (IJV)

Internal jugular vein is used for the assessment of the central venous pressure in comparable way to IVC. A small study of non-ventilated patients who were simultaneously undergoing CVP monitoring, a mean IJV diameter of 7 mm correlated with a CVP of 10 mmHg (8). 

Collapsibility index of the IJV with change of 39% consider the patient as volume depleted but this carries a limitation of the intrabdominal/ intrathoracic pressure effects (4).

PoCUS Technique

  • Use the linear Probe
  • Identify the IJV in transverse plane then rotate the probe 90o toward the patient head.
  • Image of IJV is obtained where it narrows into a paintbrush appearance (Figure 8).
  • The height where the IJV tapers correlates with jugular venous distension.
  • The IJV diameter is measured using M-mode through several respiratory cycles, and the end expiratory diameter is used as the final measurement.

Figure-8: Internal Jugular vein

 

4)Venous Congestion (VEXUS):

This includes assessment of the Hepatic/Portal/Intrarenal veins wave forms which has been correlated to the level of venous congestion thus estimating the end organ volume effects.

Hepatic Vein Doppler mainly reflects the right atrium filling pattern, portal and intrarenal venous Doppler provide additional information about right atrial filling pressure and its correlation with congestive organ injury (10).

 

PoCUS Technique (9)

Hepatic Vein Doppler

  • The probe is placed over the liver in the subcostal position to visualize the middle hepatic vein. Pulsed-wave Doppler is used 2-4 cm from where the hepatic vein drains into the IVC.

Findings: The waveform of the hepatic vein is reversed with higher velocities seen in diastole in states of volume overload. In severe volume overload, retrograde flow is seen in systole (Figure 9)

 

Figure-9: Hepatic vein doppler different wave forms (11).

 

Portal Vein Doppler

  • Moving towards the portal vein, the transducer is placed in the right mid-axillary line

Findings: Flow through the portal vein is normally monophasic, but in the presence of hypervolemia, pulsatility will be present. This can be quantified using the pulsatility index where a pulsatility index greater than 50% indicates severe volume overload.

 

Figure 10: Portal vein doppler wave forms (11).

 

Intra-renal Doppler

  • The curvilinear transducer is placed on the posterior axillary line

Findings: A normal Doppler waveform is continuous. With increasing venous congestion, there is a decrease in the systolic component of the wave with progression to biphasic (systolic/diastolic phases), and with severe renal congestion, there is complete absence of systolic flow showing only diastolic phase.

 

Figure 11: Intra-renal doppler wave forms (11).

 

Figure-12: the change in the venous doppler according to progression of venous congestion (10).

 

Figure -13: VExUS grading system for venous congestion using IVC and different venous doppler wave form for categorization.

 

5)Lung Ultrasound 

A meta-analysis showed that LUS is 88% sensitive and 90% specific for acutely decompensated heart failure and was more sensitive at detecting pulmonary edema than CXR (8).

Another meta-analysis determined the sensitivity and specificity of ultrasound for detection of pleural effusions as 93% and 96% respectively. The sensitivity approaches 100% with pleural effusions >100 mL in volume (8).

PoCUS Technique

  • Use the linear or curvilinear probe.
  • In longitudinal plane, along the midclavicular, midaxillary line then the posterior-lateral point.

Findings:

  • B-lines are hyperechoic vertical lines extending from the pleura down to the bottom of the US image (Figure 14). Two or fewer B-lines in each section is considered normal
  • Pleural effusion can be identified with presence of V-sign (extension of vertebral line proximal to the diaphragm (Figure-15) .  

 

Figure 14: B-Lines

Figure 15: Pleural effusion

 

 

 

 

 

 

 

 

 

 

Case Conclusion

Patient was found to have reduced LV function with Dilated IVC and CI of 15%, VExUS grade 2. Assessment of COP after PLR didn’t show a proper change thus patient was started on diuretic and respiratory support with consideration of inotropic support. 

Conclusion

The table below (8) shows a summary of the evidence related to the different used marker for volume assessment from physical exam to the use of PoCUS. Thus, it is imperative that we do not rely on one single tool, but rather integrate both pertinent physical examination and POCUS findings for better probability of coming to the right decision.

 

 

References

  1. Pourmand A, Pyle M, Yamane D, Sumon K, Frasure SE. The utility of point-of-care ultrasound in the assessment of volume status in acute and critically ill patients. World J Emerg Med. 2019;10(4):232-238. doi:10.5847/wjem.j.1920-8642.2019.04.007.
  2. Praveen P., Shanmugam L., Prasath, P. A review of role of lung ultrasound and clinical congestion score in acute left ventricular failure. International Journal of Advances in Medicine. 2020;7. 720. 10.18203/2349-3933.ijam20201130.
  3. Atkinson P, Bowra J, Milne J, et al. International Federation for Emergency Medicine Consensus Statement: Sonography in hypotension and cardiac arrest (SHoC): An international consensus on the use of point of care ultrasound for undifferentiated hypotension and during cardiac arrest – CORRIGENDUM. CJEM. 2017;19(4):327. doi:10.1017/cem.2017.31.
  4. Millington SJ, Wiskar K, Hobbs H, Koenig S. Risks and Benefits of Fluid Administration as Assessed by Ultrasound. Chest. 2021;160(6):2196-2208. doi:10.1016/j.chest.2021.06.041.
  5. Ma IWY, Caplin JD, Azad A, et al. Correlation of carotid blood flow and corrected carotid flow time with invasive cardiac output measurements. Crit Ultrasound J. 2017;9(1):10. doi:10.1186/s13089-017-0065-0.
  6. Marik PE LA, Young A, Andrews L. The use of bioreactance and carotid Doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients. Chest. 2013;143(2):364-370. doi:10.1378/chest.12-1274.
  7. Long E, Oakley E, Duke T, Babl FE. Does Respiratory Variation in Inferior Vena Cava Diameter Predict Fluid Responsiveness: A Systematic Review and Meta-Analysis. Shock (Augusta, Ga). 2017;47(5):550-559.
  8. Kearney, D., Reisinger, N., & Lohani, S. (2022). Integrative Volume Status Assessment. POCUS Journal7(Kidney), 65–77.
  9. Argaiz Eduardo R, Koratal A., Reisinger N. Comprehensive Assessment of Fluid Status by Point-of-Care Ultrasonography. Kidney360
  10. Galindo P, Gasca C, Argaiz ER, Koratala A. Point of care venous Doppler ultrasound: Exploring the missing piece of bedside hemodynamic assessment. World J Crit Care Med. 2021;10(6):310-322. Published 2021 Nov 9. doi:10.5492/wjccm.v10.i6.310.
  11. Dinh, V. (n.d.). Vexus ultrasound score – fluid overload and venous congestion assessment. POCUS 101. Retrieved March 29, 2022, from https://www.pocus101.com/vexus-ultrasound-score-fluid-overload-and-venous-congestion-assessment/. 

 

 

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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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