Medical Student Clinical Pearl – Basic ECG Interpretation

Bare Bones Basics of ECG Interpretation from a First Year Medical Student Perspective

Medical Student Clinical Pearl – October 2018

Victoria Kulesza – Med I Class of 2021, Dalhousie Medicine New Brunswick 

Reviewed and Edited by Dr. David Lewis


Physiology

Electrical Events and Corresponding Waves and Lines on a Standard ECG

Basic Interpretation

Common Arrhythmias

Summary

Suggested Resources

References


Physiology

Cardiac cells are electrically polarized in their resting state, with the inside holding a negative charge in comparison to the outside.1,3 Membrane pumps maintain this electrical polarity through the regulation of ions including potassium, sodium, chloride and calcium.1 Depolarization is the key electrical event of the heart that occurs spontaneously in some cells and is initiated by the arrival of an electrical impulse carrying positively charged ions in other cells.1 There are 3 key cells involved in the electrical and mechanical activities that occur within the heart:

 

The sequential depolarization of cells creates a wave of depolarization that transmits across the entire heart, representing a flow of electricity that can be detected by the electrodes placed on the surface of that patient’s body. The waveforms visible on the ECG represent the electrical activity of the myocardial cells, the cells making up the vast majority of the heart.1 At the end of the depolarization process, cardiac cells are repolarized through membrane pumps reversing the flow of ions. Both the depolarization and repolarization are represented as the wave forms on the ECG.1


Electrical Events and Corresponding Waves and Lines on a Standard ECG

P Wave

The heartbeat is initiated in the sinoatrial node located in the posterior wall of the right atrium.4 After the sinus node fires, the atrial myocardium is depolarized in a wave-like fashion causing the atrial contraction. This depolarization and contraction of the atrial myocardial cells results in the first P wave.1 The wave of depolarization does not immediately pass through to the ventricles, the atrioventricular node located at the floor of the right atrium, slows the conduction of the electrical impulse to allow the atria to fully complete their contraction. 1,4 The contraction of the atria forces blood from the atria through the atrio-ventricular valves, known as the tricuspid and mitral valves, into the ventricles.3

PR Interval

This interval is the time that is required for the electrical impulse to travel from the atria, through the AV node, bundle of His, bundle branches and Purkinje fibers to the point where the ventricular myocardium begins its depolarization.5 As blood flows through the AV valves the physiologic pause in electrical conduction is represented on the EKG as the flat line following the initial P wave. The ventricular conduction system is composed of 3 parts including the Bundle of His, Bundle Branches and the Terminal Purkinje Fibers.1 The ventricular depolarization is rapidly transmitted through the Bundle of His which emerges from the AV node and subsequently bifurcates into the left and right bundle branches which carry the impulse down the interventricular septum to their terminating fascicles in multiple Purkinje fibers.1,3 Once this current is delivered to the ventricular myocardium the depolarization causes ventricular contraction visible on the ECG as the QRS complex.1

PR Segment

A straight line between the end of the P wave and the start of the QRS complex reflects the time between the end of atrial depolarization and the start of ventricular depolarization.1

QRS Complex

The QRS complex consists of 3 individual waves in a normal conduction1,3:

  • Q Wave: first deflection downward
  • R Wave: first upward deflection
  • S Wave: first downward deflection subsequent to an upward deflection

A complete QRS complex represents ventricular depolarization as well as the initiation of ventricular contraction.1,3 The use of the term QRS Interval describes the duration of the QRS complex alone indicating the duration of ventricular depolarization specifically.1

ST Segment

A straight line between the end of the QRS complex and the beginning of the T wave known as the ST segment measures the time from the end of ventricular depolarization to the beginning of repolarization.1

T Wave

Following the depolarization of the myocardial cells, there is a short refractory period and subsequent recovery phase identified as the T wave on the ECG.1,3,5 This is phase of ventricular repolarization that begins after the QRS and is completed at the end of the T wave.3,5 Repolarization is a slower process than the depolarization which is illustrated by the broader nature of the T wave in comparison to the QRS.1,5

QT Interval

This interval includes the QRS complex, ST segment as well as the T wave which allows for the measurement of time between the beginning of ventricular depolarization to the end of ventricular repolarization.


 

Basic Interpretation

The most effective way to ensure clinically significant abnormalities are not missed on ECG is to develop a consistent order of analysis. One suggested order is as follows:

 

A. Determine Rate:

  1. Sinus Tachycardia = >100 BPM
  2. Sinus Bradycardia = <60 BPM
  3. Three Ways to Determine Rate:
    • Identify an R wave that falls on or near one of the heavy lines of the ECG strip, count the number of large squares between this first R wave and the beginning of the subsequent wave. Divide 300 by the number of large squares between the R waves to determine the number of cardiac cycles per minute. Counting the number of small squares between R waves and dividing 1500 by this number would identify with greater accuracy the heart rate.1
    • Identify the series of small pink indicators above the rhythm strip that identify 3 second intervals and count the number of cycles between two 3 second intervals – multiply this number by 10 to identify the number of beats per minute.1
    • In the event of an irregular heartbeat identify the number of QRS complexes and multiply this number by 6. Each started ECG paper reads at 25mm/s therefore 1 ECG represents 10 seconds of activity.2

Thaler 2015

 

B. Intervals:

Identify the length of the PR and QT Intervals as well as the width of the QRS complexes

Normal Interval Lengths5:

  1. PR = 0.12 – 0.20 sec
  2. QT = varies with overall heart rate
  3. QRS = 0.05 – 0.10 sec

 

 

 

 

 

 

 

C. Rhythm5:

  1. P waves present and normal?
  2. QRS complexes wide or narrow? General pattern – regular, regularly irregular or irregularly irregular?
    1. Wide = >0.12 sec
    2. Narrow = <0.12 sec
  3. Relationship between P waves and QRS complexes
  4. Overall rhythm regular or irregular?

 

D. Axis

  1. The ECG electrodes record the average direction of flow of electrical current within the heart.
  2. Lead I is the zero reference point, any axis lying below is deemed positive while those lying above are deemed negative.
  3. When the wave of depolarization begins, any lead that views this wave as moving towards it will record this as a positive deflection on the ECG paper.
  4. Assessment of P Wave Axis:
    • Atrial depolarization begins at the sinus node in the right atrium and follows a right to left and inferior direction. This depolarization of the right to left atria should demonstrate a positive deflection in leads aVL, I, II and aVF.
  5. Assessment of QRS Complex Axis:
    • As the wave of depolarization moves through the interventricular septum the current moves in a left to right direction. This wave may not be visible on the ECG but when apparent appears as a negative deflection in leads I, aVL (V5 and V6). As a result of the increased size of the left ventricle in comparison to the right, the remainder of the QRS complex vector of flow is directed leftward and is demonstrated as the positively deflected R wave in most left lateral and inferior leads. The aVR lead will record a deep negative deflection based on the direction of flow being away from this lead.

 


 

Common Arrhythmias1

1. Sinus Tachycardia

  • HR >100 bpm
  • Can be normal or pathologic, strenuous exercise can cause HR above 100.

 

2. Sinus Bradycardia

  • HR <60 bpm
  • Can be normal or pathologic, many well-conditioned athletes maintain a resting HR below 60.

 

3. Paroxysmal Supraventricular Tachycardia

  • HR 150-250 bpm
  • Narrow complex QRS
  • Very common, sudden onset, sudden termination.
  • Clinical Symptoms: palpitations, shortness of breath, dizziness. Possibly induced by alcohol, caffeine or extreme excitement.

 

4. Atrial Flutter

  • P waves 250-350 bpm
  • Atrial depolarization occurs so rapidly that discrete P waves are indiscernible.
  • Leads II and III demonstrate a prominent saw-tooth
  • AV node cannot handle the number of atrial impulses therefore there is an unequal number of P waves to QRS complexes – some electrical impulses from the sinus node bump into a refractory node and go no further, this is called AV Block. 2:1 block is most common while 3:1 and 4:1 are also frequently observed.
  • Clinical Symptoms: shortness of breath, angina type discomfort.

 

 

5. Atrial Fibrillation

  • AV Node may receive >500 impulses per minute
  • More common than atrial flutter, most commonly sustained arrhythmia.
  • No true P waves are discernible, AV node allows occasional impulses to pass through to the ventricles, creating an irregularly irregular ventricular rate often in the range of 120-180 bpm.
  • Clinical Symptoms: some patients experience no symptoms, others experience shortness of breath, chest pain, palpitations and dizziness.

 

6. Premature Ventricular Contractions

  • Most common ventricular arrhythmia.
  • Retrograde P wave or no P wave prior to the QRS.
  • Wide QRS of at least 0.12 seconds in majority of the leads often followed by a compensatory pause before the subsequent beat.
  • Often occur randomly and rarely require treatment unless an isolated PVC is noted in the setting of acute MI as it may trigger ventricular tachycardia or ventricular fibrillation.
  • When to worry:
    • Frequent PVCs
    • Consecutive runs, 3+ in a row
    • Multiform – demonstrating variation in the site of origin
    • Occurring on the T wave – “R-on-T” phenomenon
    • PVC in the setting of an acute MI

 

 

7. Ventricular Tachycardia

  • Rate 120-200 bpm
  • Wide complex QRS
  • A run of 3+ consecutive PVCs.
  • Prolonged ventricular tachycardia is an emergency requiring immediate treatment to prevent cardiac arrest.
  • May be uniform or polymorphic, uniform being more closely associated with healed infarctions and polymorphic waveforms more commonly associated with acute coronary events.

 

8. Ventricular Fibrillation

  • Spasmodic tracings or coarse ventricular fibrillation or fine ventricular fibrillation without any true QRS complexes.
  • Heart generates no cardiac output, CPR and defibrillation are required immediately.
  • Most common arrhythmia in adults who experience sudden death.
  • Common predisposing factors:
    • Myocardial ischemia/infarction
    • Heart failure
    • Electrolyte disturbances
    • Hypoxemia or hypercapnia
    • Hypotension or shock
    • Overdoses of stimulants especially when used in combination with others

 


 

Summary

 


 

 


 

Suggested Resources

Teaching Medicine – Rhythm Strip Interpretation Practice

ECG Guide Mobile Smartphone App

  • Available through itunes app store

The Only EKG Book You’ll Ever Need

  • PDF available online through Dalhousie Library

 

References

  1. Thaler, M. S. (2015). The Only EKG Book You’ll Ever Need (9th ed.). Lippincott, Williams & Wilkins.
  2. Andrade, J. (2013). ECG Guide [Mobile application software]. Retrieved from http://itunes.apple.com
  3. Dubin, D. (2000). Rapid interpretation of EKG’s: An interactive course (6th ed.). Tampa, Fla.: Cover Pub.
  4. McKinley, M. P., OLoughlin, V. D., Harris, R. T., & Pennefather-O’Brien, E. E. (2015). Human anatomy (4th ed.). New York, NY: McGraw-Hill Education.
  5. Khan, M. (2008). Rapid ECG interpretation (3rd ed., Contemporary cardiology (Totowa, N.J). Totowa, N.J.: Human Press.
  6. Thomas, V. (n.d.). Premature Ventricular Contractions Treatment Cape Town. Retrieved from https://cardiorhythm.co.za/premature-ventricular-contractions/
  7. https://inside.fammed.wisc.edu/medstudent/pcc/ecg/axis.html
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Medical Student Clinical Pearl – PoCUS and Clavicle Fractures

Using PoCUS to diagnose clavicular fractures

Medical Student Pearl – May 2018

Danielle Rioux – Med III Class of 2019, Dalhousie Medicine New Brunswick 

Reviewed by Dr. Mandy Peach and Dr. David Lewis

Case: A 70 year-old man presented to the emergency department with pain in his left shoulder and clavicular region following a skiing accident. He slipped and fell on his left lateral shoulder while he was on skis at the ski hill. He has visible swelling in his left shoulder and clavicular region, and was not able to move his left arm.

On exam: The patient was in no sign of distress. He was standing and holding his left arm adducted close to his body, supporting his left arm with his right hand. There was swelling and ecchymosis in the left clavicle, mid-shaft region, with focal tenderness. On palpation, there was crepitation, tenderness, swelling, and warmth in this region. He was unable to move his left shoulder due to pain. His neurovascular exam on his left arm was normal. Auscultation of his lungs revealed normal air-entry, bilaterally and no adventitious sounds.

Point of Care Ultrasound (PoCUS): We used a linear, high-frequency transducer and placed it in the longitudinal plane on the normal right clavicle (see Image 1.), and the fractured left clavicle (see Image 2.). Image 3 shows the fractured clavicle in the transverse plane.

 

Image 1. PoCUS of normal right clavicle along the long axis of the clavicle (arrows depict the hyperechoic superficial cortex with deep acoustic shadowing).

 

 

Clip 1. PoCUS of normal right clavicle along the short axis of the clavicle. The transducer is moving from the lateral to medial, note the visible hyperechoic curved superficial cortex and the subclavian vessels at the end of the clip. 

 

Image 2. PoCUS of normal right clavicle along the short axis of the clavicle (arrows depict the hyperechoic superficial cortex with deep acoustic shadowing).

 

 

Image 3. PoCUS of a fracture in the left clavicle along the long axis of the clavicle

 

 

Clip 2. PoCUS of a fracture of the left clavicle, viewed in the long axis of the clavicle. Compare this view with image 1.

 

 

 

Clip 3. PoCUS of a fracture in the left clavicle viewed in the short axis of the clavicle. Compare this view with Clip 1. Note the fracture through the visible cortex and the displacement that becomes apparent halfway through the clip.

 

Radiographic findings: Radiographic findings of the left clavicle reveal a mid-shaft spiral clavicular fracture.  (Image 4).

Image 4. Radiographic image of fractured left clavicle.

 

Take home point: Research has shown that Ultrasonography is a sensitive diagnostic tool in the evaluation of fractures (Chapman & Black, 2003; Eckert et al., 2014; Chen et al., 2016).

This case provides an example of how PoCUS can be used to diagnose clavicle fractures in the emergency department. In a rural or office setting where radiography is not always available, PoCUS can be used to triage patients efficiently into groups of those with a fracture and those with a low likelihood of a fracture. This would enable more efficient medical referrals while improving cost-effectiveness and patient care.

 

References:

Chapman, D. & Black, K. 2003. Diagnostic musculoskeletal ultrasound for emergency physicians. Ultrasound, 25(10):60

Eckert, K., Janssen, N., Ackermann, O., Schweiger, B., Radeloff, E. & Liedgens, P. 2014 Ultrasound diagnosis of supracondylar fractures in children. Eur J Trauma Emerg Surg., 40:159–168

Chen, K.C., Chor-Ming, A., Chong, C.F. & Wang, T.L. 2016. An overview of point-of-care ultrasound for soft tissue and musculoskeletal applications in the emergency department, Journal of Intensive Care, 4:55

 

This post was copyedited by Dr. Mandy Peach

 

 

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Medical Student Clinical Pearl – Urinary Tract Infections

Urinary Tract Infections


Rob Hanlon, Med 1

Dalhousie Medicine New Brunswick, Class of 2021

Reviewed by: Dr David Lewis

 


 

Urinary tract infections (UTIs) are common in both the inpatient and outpatient settings. As such, it is important to understand the etiology, pathogenesis, and treatment of such infections. This post will focus primarily on uncomplicated UTIs, bacteriology and pathogenesis, treatment options with consideration for drug resistance.

Types of UTIs: 

The term UTI encompasses different infections. These include asymptomatic bacteriuria, acute uncomplicated cystitis, recurrent cystitis, complicated UTI, catheter-associated asymptomatic bacteriuria, catheter-associated UTI, prostatitis, and pyelonephritis. 1 There are two broad classifications: uncomplicated and complicated.

Uncomplicated UTIs refer to infections occurring in individuals with normal urinary tracts; meaning they have no structural or neurological issues, such as neurogenic bladder. These are differentiated into lower (bladder and urethra) and upper (ureters and kidneys) urinary tract infections; cystitis and pyelonephritis respectively. 2 Typical symptoms of cystitis include dysuria, urinary frequency and urgency, suprapubic pain, and hematuria. Symptoms of pyelonephritis include fever, chills, flank pain, costovertebral angle tenderness, and nausea/vomiting. 3

Risk factors of uncomplicated UTIs include being female (proximity of urethral opening to anus), frequent sexual intercourse, history of recurrent UTIs, use of spermicide-coated condoms, diaphragms, obesity, and diabetes. 3 Menopause also increases the risk for UTIs as the decrease in estrogen causes the walls of the urinary tract to thin, which decreases resistances to bacteria. 4 Uncomplicated UTIs do occur in men; albeit, less frequently than women. Risk factors in men include anal intercourse (fecal bacteria), lack of circumcision, and benign prostatic hyperplasia. 5

 

Complicated UTIs refer to infections that are typically more severe and difficult to treat. This type of infection can be seen in people with structural abnormalities impairing the flow of urine, catheter use or other foreign bodies, renal transplantation, and kidney/bladder dysfunction.4

 

Bacteriology and Pathogenicity:

 

It is important to note that recently the urinary tract has been found to be colonized by a normal microbiome, similar in concept to the gut and vaginal lumens. The urinary tract has traditionally been thought to be a sterile lumen. Changes in the bacterial make-up may contribute to a disease state in the urinary tract.6 There is more research needed to fully appreciate how changes to the normal bacteria contribute to disease and specifically to UTIs. There is ongoing research to determine how the microorganisms become pathological and if the normal flora can be a source of a pathological process.6 There is research indicating possible alternative treatments such as probiotics and dietary modifications that can impact urinary tract diseases.6 The impact of antibiotics on the normal urinary tract bacteria is also a current research topic.6 Clinically, the presence of UTI symptoms would indicate that there is a pathological process present and, when indicated, antibiotics as first-line treatments are still recommended.

There are two mechanism by which bacteria enter the urinary tract, these are ascending infections and haematogenous infections. The ascending mechanism occurs when perineal/fecal bacteria enter the urethra and travel up towards the bladder/kidneys. The haematogenous route occurs when bacteria from the blood enter the kidneys.7

 

Bacteria causing UTIs are termed uropathogens. The common UTI causing organisms are gram negative Klebsiella spp., Escherichia coli, and Proteus spp., and gram positive Enterococci spp. and Staphylococcus saprophyticus. E. coli being the most common uropathogen; seen in 80% of cases. More opportunistic organisms can be isolated in complicated UTIs, such as Pseudomonas spp. and fungal Candida spp.4 8

 

Uropathogenic E. coli (UPEC) strains contain virulence factors that allow them to colonize the urinary tract. Fimbriae are filamentous cell surface extensions that allow the bacteria to adhere to the uroepithelium and promote invasion into the tissue. Other surface molecules include flagella that allow the bacteria to mobilize up the urinary tract. 9 UPEC also produce toxins such as haemolysin, which damage epithelial cells and induce inflammatory responses (causing UTI symptoms). Factors allowing adherence of UPEC to uroepitehlium are paramount, as urine could wash away the bacteria. Other virulence factors allow the bacteria to thrive and grow. 7

 

Klebsiella spp. and Proteus spp. are other gram negative uropathogens that also produce fimbriae. Klebsiella produce polysaccharide capsules that prevent host defense phagocytosis.7  It also produces an enzyme called urease, produced by Proteus spp. as well, which hydrolyzes urea into ammonia and CO2. The bacteria use ammonia as a source of nitrogen for metabolism. The enzymatic process also increases the pH of the urinary tract and leads to the formation of renal stones. 10

Proteus

 

Pseudomonas aeruginosa is a gram-negative commonly associated with nosocomial acquired UTIs, especially when catheters are in place. Its major virulence factor is the production of biofilms, which protect it from host defenses and many antimicrobials. 7 Staphylococcus saprophyticus is a gram-positive bacterium that also produces biofilms, as well as a specific epithelial adhesion protein called lipoteichoic acid. 11

 

Although some of these uropathogens have similar virulence mechanisms, it is important to understand the different types of pathogens and their virulence factors because different antimicrobials target specific parts of the bacteria and the bacteria can be resistant to specific treatment options.

 

Treatment with Consideration for Antimicrobial Resistance

Multiple factors must be considered when choosing treatment options for UTIs in order to determine the risk of increased drug resistance. Patients are considered to be at a higher risk of drug resistance if, within the last three months, they have been found to have a multidrug resistant strain in their urine, they have been admitted to a hospital or other care facility, used broad-spectrum antibiotics, or have a travel history to areas known for resistant strains. 3

 

For low risk patients, treatments for uncomplicated cystitis include nitrofurantoin, trimethoprim-sulfamethoxazole, and fosfomycin. Choosing which drug depends on the individual’s allergies, local rates of resistance, and availability. If the patient has used one of these drugs within the last three months, the remaining two drugs are possible options. 3 If first-line treatments are not an option, then an oral beta-lactam, such as amoxicillin-clavulanate is appropriate. If allergic to this, then a fluoroquinolone such as ciprofloxacin can be used.3

 

Table 1: Drugs and dosages for empiric treatment of uncomplicated cystitis. 3

 

 

For higher risk patients, a urine culture and antimicrobial susceptibility testing should be ordered. First-line treatments (see above) can be used as empiric treatments until test results are obtained. However, if the patient is unable to take these treatments, test results should be obtained prior initiating treatment. 3

 

For complicated UTIs, such as catheter infections, treatment depends on the severity of the illness. Urine culture and susceptibility testing should be performed. In the case of a catheter infection, it should be removed and a sample from the catheter should be cultured. 12 If the catheterized patient requires treatment prior to obtaining test results, treatment should cover gram-negative bacilli. Third-generation cephalosporins can be used in this case. Critically ill patients should be put on broad spectrum antibiotics such as carbapenems and vancomycin, in order to cover pseudomonas and methicillin-resistant Staphylococcus aureus infections respectively. 13

Local (New Brunswick, Canada) Information on Antimicrobial Treatment of UTIs can be found here:

NB Antibiotic Guidelines and Resources

 

 

This is not an exhaustive description of infection types, treatments, or resistance mechanisms. This post focused on uncomplicated UTIs and their treatments because they are commonly seen in the clinical setting. An in-depth patient history is crucial for understanding the possible causes of a UTI and for developing a differential diagnosis. These should be included alongside test results when evaluating treatment options.

 

 


References:

 

  1. Kalpana Gupta, Larissa Grigoryan, Barbara Trautner. Urinary tract infection. Annals of Internal Medicine. 2017;167(7). https://search.proquest.com/docview/1975585404.
  2. Ana L Flores-Mireles, Jennifer N Walker, Michael Caparon, Scott J Hultgren. Urinary tract infections: Epidemiology, mechanisms of infection and treatment options. Nature Reviews. Microbiology. 2015;13(5):269. http://www.ncbi.nlm.nih.gov/pubmed/25853778. doi: 10.1038/nrmicro3432.
  3. Hooton T, Gupta K. Acute uncomplicated cystitis in women. Retrieved from: https://www.uptodate.com/contents/acute-uncomplicated-cystitis-in-women?source=see_link. Updated 2017.
  4. Harvey S. Urinary tract infection. University of Maryland. Retrieved from: http://www.umm.edu/health/medical/reports/articles/urinary-tract-infection. Updated 2012.
  5. Hooton T. Acute uncomplicated cystitis in men. Retrieved from: https://www.uptodate.com/contents/acute-uncomplicated-cystitis-in-men?source=see_link. Updated 2017.
  6. Aragón IM, Herrera-Imbroda B, Queipo-Ortuño MI, et al. The urinary tract microbiome in health and disease. European Urology Focus. 2016. doi: 10.1016/j.euf.2016.11.001.
  7. Walsh C, Collyns T. The pathophysiology of urinary tract infections. Surgery (Oxford). https://www.sciencedirect.com/science/article/pii/S0263931917300716. doi: 10.1016/j.mpsur.2017.03.007.
  8. Beyene G, Tsegaye W. Bacterial uropathogens in urinary tract infection and antibiotic susceptibility pattern in jimma university specialized hospital, southwest ethiopia. Ethiopian journal of health sciences. 2011;21(2):141. http://www.ncbi.nlm.nih.gov/pubmed/22434993. doi: 10.4314/ejhs.v21i2.69055.
  9. Bien J, Sokolova O, Bozko P. Role of uropathogenic escherichia coli virulence factors in development of urinary tract infection and kidney damage. International journal of nephrology. 2012;2012:681473. http://www.ncbi.nlm.nih.gov/pubmed/22506110. doi: 10.1155/2012/681473.
  10. Schaffer JN, Pearson MM. Proteus mirabilis and urinary tract infections. Microbiology spectrum. 2015;3(5). http://www.ncbi.nlm.nih.gov/pubmed/26542036.
  11. Raul Raz, Raul Colodner, Calvin M. Kunin. Who are you: Staphylococcus saprophyticus? Clinical Infectious Diseases. 2005;40(6):896-898. http://www.jstor.org/stable/4463165. doi: 10.1086/428353.
  12. Fekete T. Catheter-associated urinary tract infection. Retrieved from: https://www.uptodate.com/contents/catheter-associated-urinary-tract-infection-in-adults?source=see_link#H123172989. Updated 2016.
  13. Hooton T, Gupta K. Acute complicated urinary tract infection (including pyelonephritis) in adults. Retrieved from: https://www.uptodate.com/contents/acute-complicated-urinary-tract-infection-including-pyelonephritis-in-adults?source=see_link#H12414288. Updated 2017.
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