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:

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.6

 

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 7

 

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. 8 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. 6

 

Klebsiella spp. and Proteus spp. are other gram negative uropathogens that also produce fimbriae. Klebsiella produce polysaccharide capsules that prevent host defense phagocytosis.6  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. 9

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. 6 Staphylococcus saprophyticus is a gram-positive bacterium that also produces biofilms, as well as a specific epithelial adhesion protein called lipoteichoic acid. 10

 

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. 11 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. 12

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.

 

  1. 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.

 

  1. 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.

 

  1. Harvey S. Urinary tract infection. University of Maryland. Retrieved from: http://www.umm.edu/health/medical/reports/articles/urinary-tract-infection. Updated 2012.

 

  1. Hooton T. Acute uncomplicated cystitis in men. Retrieved from: https://www.uptodate.com/contents/acute-uncomplicated-cystitis-in-men?source=see_link. Updated 2017.

 

  1. 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.

 

  1. 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.

 

  1. 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.

 

  1. Schaffer JN, Pearson MM. Proteus mirabilis and urinary tract infections. Microbiology spectrum. 2015;3(5). http://www.ncbi.nlm.nih.gov/pubmed/26542036.

 

  1. 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.
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SJRHEM Journal Club Report Oct 2017

SJRHEM Journal Club Report Oct 2017

Allyson Cornelis, R1 iFMEM

Hosted by Dr Andrew Lohoar


Abstract:

Idarucizumab for Dabigatran Reversal — Full Cohort Analysis

Charles V. Pollack, Jr., M.D., Paul A. Reilly, Ph.D., Joanne van Ryn, Ph.D., John W. Eikelboom, M.B., B.S., Stephan Glund, Ph.D., Richard A. Bernstein, M.D., Ph.D., Robert Dubiel, Pharm.D., Menno V. Huisman, M.D., Ph.D., Elaine M. Hylek, M.D., Chak-Wah Kam, M.D., Pieter W. Kamphuisen, M.D., Ph.D., Jörg Kreuzer, M.D., Jerrold H. Levy, M.D., Gordon Royle, M.D., Frank W. Sellke, M.D., Joachim Stangier, Ph.D., Thorsten Steiner, M.D., Peter Verhamme, M.D., Bushi Wang, Ph.D., Laura Young, M.D., and Jeffrey I. Weitz, M.D.

N Engl J Med 2017; 377:431-441August 3, 2017DOI: 10.1056/NEJMoa1707278

 

BACKGROUND
Idarucizumab, a monoclonal antibody fragment, was developed to reverse the anticoagulant effect of dabigatran.

METHODS
We performed a multicenter, prospective, open-label study to determine whether 5 g of intravenous idarucizumab would be able to reverse the anticoagulant effect of dabigatran in patients who had uncontrolled bleeding (group A) or were about to undergo an urgent procedure (group B). The primary end point was the maximum percentage reversal of the anticoagulant effect of dabigatran within 4 hours after the administration of idarucizumab, on the basis of the diluted thrombin time or ecarin clotting time. Secondary end points included the restoration of hemostasis and safety measures.

RESULTS
A total of 503 patients were enrolled: 301 in group A, and 202 in group B. The median maximum percentage reversal of dabigatran was 100% (95% confidence interval, 100 to 100), on the basis of either the diluted thrombin time or the ecarin clotting time. In group A, 137 patients (45.5%) presented with gastrointestinal bleeding and 98 (32.6%) presented with intracranial hemorrhage; among the patients who could be assessed, the median time to the cessation of bleeding was 2.5 hours. In group B, the median time to the initiation of the intended procedure was 1.6 hours; periprocedural hemostasis was assessed as normal in 93.4% of the patients, mildly abnormal in 5.1%, and moderately abnormal in 1.5%. At 90 days, thrombotic events had occurred in 6.3% of the patients in group A and in 7.4% in group B, and the mortality rate was 18.8% and 18.9%, respectively. There were no serious adverse safety signals.

CONCLUSIONS
In emergency situations, idarucizumab rapidly, durably, and safely reversed the anticoagulant effect of dabigatran. (Funded by Boehringer Ingelheim; RE-VERSE AD ClinicalTrials.gov number, NCT02104947.)

 

http://www.nejm.org/doi/full/10.1056/NEJMoa1707278

 


SJRHEM Journal Club Report

 

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EM Reflections – September 2017

Thanks to Dr Paul Page for leading the discussion

Edited by Dr David Lewis

Top tips from this month’s rounds:

  1. Non-specific Abdo pain – Appendicitis is always high on the differential 

  2. Intoxicated patients are at high risk for Head Injury

  3. Acute Heart Failure has a higher mortality than acute NSTEMI

  4. Enhancing Morbidity and Mortality Rounds Quality


Non-specific Abdo pain – Appendicitis is always high on the differential 

Does a normal white count exclude appendicitis?No – Clinicians should be wary of reliance on either elevated temperature or total WBC count as an indicator of the presence of appendicitis. The ROC curve suggests there is no value of total WBC count or temperature that has sufficient sensitivity and specificity to be of clinical value in the diagnosis of appendicitis. Acad Emerg Med. 2004 Oct;11(10):1021-7.Clinical value of the total white blood cell count and temperature in the evaluation of patients with suspected appendicitis.

Does a normal CRP exclude appendicitis?No – Acad Emerg Med. 2015 Sep;22(9):1015-24. doi: 10.1111/acem.12746. Epub 2015 Aug 20. Accuracy of White Blood Cell Count and C-reactive Protein Levels Related to Duration of Symptoms in Patients Suspected of Acute Appendicitis.

 

A useful review on the diagnosis of appendicitis – JAMA. 2007 Jul 25; 298(4): 438–451. Does This Child Have Appendicitis?

 

Summary of Accuracy of Symptoms

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Summary of Accuracy of Signs

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Finally – Don’t forget Emergency Physicians can learn how to use Point of Care Ultrasound (PoCUS – ?Appendicitis) which can significantly improve diagnostic accuracy in experienced hands. Experience comes with practice.

J Med Radiat Sci. 2016 Mar; 63(1): 59–66. Published online 2016 Jan 20. doi:  10.1002/jmrs.154
Ultrasound of paediatric appendicitis and its secondary sonographic signs: providing a more meaningful finding

See SJRHEM PoCUS Quick Reference

PoCUS – Measurements and Quick Reference

 


Intoxicated patients are at high risk for Head Injury

Intoxicated patients with minor head injury are at significant risk for intracranial injury, with 8% of intoxicated patients in our cohort suffering clinically important intracranial injuries. The Canadian CT Head Rule and National Emergency X-Radiography Utilization Study criteria did not have adequate sensitivity for detecting clinically significant intracranial injuries in a cohort of intoxicated patients.

ACADEMIC EMERGENCY MEDICINE 2013; 20:754–760. Traumatic Intracranial Injury in Intoxicated Patients With Minor Head Trauma

Canadian CT Head Rule not applicable to intoxicated patients (GCS<13)

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CMPA provide useful guidance on the duties expected in the management of intoxicated ED patients.

 

All intoxicated patients, even the so called ‘frequent fliers’ require a full assessment, including history (from 3rd parties if available), full examination (especially neurological), blood glucose level, neurological observations, and this assessment should be carefully documented.

 

Can we defer CT imaging for intoxicated patients presenting with possible brain injury?

This study suggests that deferring CT imaging while monitoring improving clinical status in alcohol-intoxicated patients with AMS and possible ICH is a safe ED practice. This practice follows the individual emergency physician’s comfort in waiting and will vary from one physician to another.

http://www.sciencedirect.com/science/article/pii/S0735675716306805

 

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Acute Heart Failure has a higher mortality than acute NSTEMI

Cardiac markers are routinely used to exclude NSTEMI in patient presenting with chest pain. However the diagnosis of acute heart failure (AHF) is mainly clinical, including CXR, ECG, PoCUS.

Ultrasound B Lines and Heart Failure

 

There is good evidence that BNP can be helpful in ruling out AHF – BMJ 2015;350:h910

Recommended Link – Emergency Medicine Cardiac Research and Education Group

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Emergency Treatment of Acute Congestive Heart Failure

Most recent recommendations from Canadian Cardiovascular Society (2012)

  • 1 – We recommend supplemental oxygen be considered for patients who are hypoxemic; titrated to an oxygen saturation > 90% (Strong Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places relatively higher value on the physiologic studies demonstrating potential harm with the use of excess oxygen in normoxic patients and less value on long-term clinical usage of supplemental oxygen without supportive data.

  • 2 – We recommend CPAP or BIPAP not be used routinely (Strong Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places high weight on RCT data with a demonstrated lack of efficacy and with safety concerns in routine use. Treatment with BIPAP/CPAP might be appropriate for patients with persistent hypoxia and pulmonary edema.

  • 3 – We recommend intravenous diuretics be given as first-line therapy for patients with congestion (Strong Recommendation, Moderate-Quality Evidence).
  • 4 – We recommend for patients requiring intravenous diuretic therapy, furosemide may be dosed intermittently (eg, twice daily) or as a continuous infusion (Strong Recommendation, Moderate-Quality Evidence).
  • 5 – We recommend the following intravenous vasodilators, titrated to systolic BP (SBP) > 100 mm Hg, for relief of dyspnea in hemodynamically stable patients (SBP > 100 mm Hg):
    • i

      Nitroglycerin (Strong Recommendation, Moderate-Quality Evidence);

    • ii

      Nesiritide (Weak Recommendation, High-Quality Evidence);

    • iii

      Nitroprusside (Weak Recommendation, Low-Quality Evidence).

Values and preferences. This recommendation places a high value on the relief of the symptom of dyspnea and less value on the lack of efficacy of vasodilators or diuretics to reduce hospitalization or mortality.

  • 6 – We recommend hemodynamically stable patients do not routinely receive inotropes like dobutamine, dopamine, or milrinone (Strong Recommendation, High-Quality Evidence).

Values and preferences. This recommendation for inotropes place high value on the potential harm demonstrated when systematically studied in clinical trials and less value on potential short term hemodynamic effects of inotropes.

  • 7 – We recommend continuation of chronic β-blocker therapy with AHF, unless the patient is symptomatic from hypotension or bradycardia (Strong Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places higher value on the RCT evidence of efficacy and safety to continue β-blockers, the ability of clinicians to use clinical judgement and lesser value on observational evidence for patients with AHF.

  • 8 – We recommend tolvaptan be considered for patients with symptomatic or severe hyponatremia (< 130 mmol/L) and persistent congestion despite standard therapy, to correct hyponatremia and the related symptoms (Weak Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places higher value on the correction of symptoms and complications related to hyponatremia and lesser value on the lack of efficacy of vasopressin antagonists to reduce HF-related hospitalizations or mortality.

 

Emergency Medicine Cases – Episode 4: Acute Congestive Heart Failure 

In Summary

  • AHF is a serious life-threatening condition in its own right, excluding NSTEMI does not change that. Appropriate management and disposition (almost always admission) is required.
  • Oxygen and intravenous Diuretics are the first-line  treatment
  • Nitrates are recommended in the relief of dyspnea in hemodynamically stable patients (SBP > 100 mm Hg)

 


Enhancing Morbidity and Mortality Rounds Quality

The Ottawa M&M Model

CalderMM-Rounds-Guide-2012

 

 

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Medical Student Clinical Pearl – Reversal of Anticoagulation in the Emergency Department

Reversal of Anticoagulation for Bleeding Complications in the ED


Tess Robart, Med 1

Dalhousie Medicine New Brunswick, Class of 2020

Reviewed by: Dr David Lewis and Liam Walsh (SJRH Pharmacy)


Clinical Question:

Emergency Departments frequently encounter patients on anticoagulant therapy. How are we currently managing anticoagulation reversal in our ED? How do we approach reversal, considering urgency in the face of major bleeding complications or prior to emergency surgery?

Background:

As result of the narrow therapeutic window of many anticoagulants, treatment presents a significant risk for life-threatening bleeds. Major bleeding involving the gastrointestinal, urinary tract, and soft tissue occurs in up to 6.5% of patients on anticoagulant therapy. The incidence of fatal bleeding is approximately 1% each year (1). Standard therapy for the control of coagulopathy related bleeding has traditionally required the use of available blood products, reversal of drug-induced anticoagulation, and recombinant activated factor VII (rFVIIa). The introduction of new direct oral anticoagulants (DOACs), dabigatran, apixaban and rivaroxaban presents the need for a new realm of antidotes and reversal agents.



Indications for Reversal:

Emergency physicians should consider reversal of anticoagulation for patients presenting with bleeding in the case of anticoagulant use, antiplatelet use, trauma, intracranial hemorrhage, stroke, and bleeding of the gastrointestinal tract, deep muscles, retro-ocular region, or joint spaces (2,3). The severity of each hemorrhage should be considered, reversing in cases of shock or if the patient requires blood transfusions because of excessive bleeding (2).

Patients should also undergo reversal of anticoagulation if urgent or emergent surgery is necessary (4).

For most medical conditions requiring anticoagulation, the target international normalized ratio (INR) is 2.0 to 3.0 (5). Notable exceptions to this rule are patients with mechanical heart valves, and antiphospholipid antibody syndrome. These patients require more intense anticoagulation, with target INR values between 2.5-3.5 (5).

The following laboratory assays should be considered, and repeated as clinically indicated (2):

  • PT/INR
  • aPTT
  • TT (thrombin time)
  • Basic Metabolic Panel
  • CBC

Initial assessment should address the following from a patient history (2):

  • How severe is the bleed, and where is it located?
  • Is the patient actively bleeding now?
  • Which agent is the patient receiving?
  • When was the last dose of anticoagulant administered?
  • Could the patient have taken an unintentional or intentional overdose of anticoagulant?
  • Does the patient have any history of renal or hepatic disease?
  • Is the patient taking other medications that would affect hemostasis?
  • Does the patient have any other comorbidities that would contribute to bleeding risk?

See this article for more details on the management of anticoagulation reversal in the face of major bleeding

It is important to note that not all coagulopathies will be anticoagulant drug induced. After all drug-induced causes have been ruled out, it is appropriate to follow previously established protocols (ie. transfusion protocol).


Table 1: Common Anticoagulants and Drug Reversal Considerations 


Table 2: Anticoagulant Reversal Agents (5)

 


Bottom Line: 

 

Anticoagulation leading to clinically significant bleeding is an issue commonly encountered in the emergency department. Therapies designed to combat and reverse anticoagulation are constantly changing in response to new anticoagulant medications. Emergency physicians must be well versed around anticoagulants commonly used, and recognize the antidotes used to treat their overuse in urgent and emergent situations.

 

 


References:

 

  1. Leissinger C.A., Blatt P.M., Hoots W.K., et al. Role of prothrombin complex concentrates in reversing warfarin anticoagulation: A review of the literature. Am J Hematol. 2008;83:137-43.
  2. Garcia D.A., Crowther M. (2017) Management of bleeding in patients receiving direct oral anticoagulants. Retrieved from https://www.uptodate.com/contents/management-of-bleeding-in-patients-receiving-direct-oral-anticoagulants?source=search_result&search=reversal%20of%20anticoagulation&selectedTitle=1~150
  3. UC Davis Health Centre. Reversal of Anticoagulants at UCDMC. Retrieved from Reversal of Anticoagulants at UCDMC – UC Davis Health
  4. Vigue B. Bench-to-bedside review: Optimising emergency reversal of vitamin K antagonists in severe haemorrhage–from theory to practice. Crit Care. 2009;13:209.
  5. Mathew, A. E, Kumar, A. (2010) Focus On: Reversal of Anticoagulation. American College of Emergency Physicians. Retrieved from https://www.acep.org/Clinical—Practice-Management/Focus-On–Reversal-of-Anticoagulation/
  6. Brooks J.C., Noncardiogenic pulmonary edema immediately following rapid protamine administration. Ann Pharmacotherap1999;33(9):927-30.
  7. National Advisory Committee on Blood and Blood Products. Recommendations for Use of Prothrombin Complex Concentrates in Canada. May 16, 2014. http://www.nacblood.ca/resources/guidelines/PCC-Recommendations-Final-2014-05-16.pdf
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RCP – Nar’ pump, mo’ problems

Nar’ pump, mo’ problems, a case on cardiogenic shock

Resident Clinical Pearl (RCP) – June 2017

Mandy Peach, R2 FMEM, Dalhousie University, Saint John, New Brunswick

Reviewed/Edited by Dr. David Lewis and Dr. Kavish Chandra

It’s 11 pm, you’re doing the overnight shift and EMS calls in to report a patient with an ETA of 3 minutes: “80 yo female, found on floor in apartment by husband after reportedly feeling unwell for 2 days. Decreased LOC but arousable and responding appropriately. BP 82/36, HR 120, RR 22, Afebrile, oxygen sat 86% on 6L nasal cannula.”

You hear the vitals, and many differentials run through your mind – PE, sepsis, hemorrhage, tamponade. Your main concerns are: this person needs more airway support and they are in shock, and when you think shock you think ‘fluids’.

EMS rolls in with your patient and she looks awful – pale, mottled extremities and drowsy. She is being re-assessed, RT is present to switch to a face mask, IV access is being established and you’re about to pound her with fluids when you are handed her ECG:

1https://lifeinthefastlane.com/ecg-library/basics/inferior-stemi/

This lady clearly is having an inferior STEMI – there is marked ST elevation in II, III and aVF with early Q wave formation.

 

Take home point #1: In any Inferior STEMI, you must suspect RV involvement

Look for ST elevation in V1 and depression in V2, or ST elevation in lead III > lead II. If these are present – get a 15 lead ECG.1

On closer look at our patient’s ECG there is ST elevation in V1-V2 and the elevation in lead III is indeed larger than lead II. You order the 15 lead.

2 https://lifeinthefastlane.com/ecg-library/right-ventricular-infarction/

Look for ST elevation in right sided leads V3-V6, but the money is on V4R – ST elevation in this lead has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% for RV infarction2. Our patient does have RV infarction seen by ST elevation in V4R.

 

Take home point #2: RV involvement is associated with increased risk of cardiogenic shock and death with a mortality of 50% within the first 48 hours3. If there is RV involvement, giving nitroglycerin for chest pain is CONTRAINDICATED

Due to a poorly functioning RV, patients are pre-load sensitive2. If you decrease the pre-load then they have even less to pump, further worsening the hypotension.

So we have diagnosed this lady with cardiogenic shock secondary to AMI (the most common cause of cardiac related shock) and we determined she has RV involvement. We know we can’t give her nitroglycerin. Let’s reassess her status – the basic ABC’s.

Airway & Breathing – the RT has since advanced her to a non-rebreather with a sat level in the high 80’s. You suggest trying Optiflow or BiPAP as a temporizing measure – this lady is going to need to be intubated.

 

Take home point #3: Positive pressure ventilation requires a stable, cooperative patient – which is often not the case in cardiogenic shock

Positive pressure can decrease pre-load and potentially worsen hypotension3. It is a temporizing measure only. The majority will require endotracheal intubation to maintain their saturation as their work of breathing is a large expenditure of energy.

You successfully complete a RSI and the saturation improves to 94-98%.

Circulation – Repeat BP is 82/36. You complete a cardiac point-of-care-ultrasound (PoCUS) and see poor contractility, but no pericardial effusion or large clots suggesting chordae or papillary rupture. IVC is > 50% collapsible.

 

Take home point #4: On PoCUS, heart failure caused by acute ischemia will show a large RV and small LV secondary to low filling pressures, which is best seen on the apical 4 chamber view3

Your patient continues to be hypotensive – you give a small 500 cc bolus; you don’t want to overload a poorly pumping heart with fluid it can’t handle. However you anticipate that this will not be enough to improve her BP, and as she continues to be hypotensive her myocardial ischemia worsens, which subsequently worsens her pump dysfunction in a vicious cycle. She needs pressure support.

 

Take home point #5: Cardiogenic shock requires vasopressor support

If systolic BP > 90: Start with dobutamine for inotropy. Double up on agents – likely will need to add a vasoconstrictor. Dopamine is usually the next to add.

If systolic BP < 90: Can still use dobutamine, but need to add norepinephrine for vasoconstriction. Dopamine alone will worsen BP as it is a vasodilator.

3Tintinalli’s Comprehensive Guide to Emergency Medicine.

You start dobutamine and dopamine peripherally with the intention of obtaining central venous assess once stabilized.

In the meantime, cardiac labs and portable CXR are pending, you treat this patient as any other STEMI in terms of dual anti-platelet and anti-coagulation loading.

 

Take home point #6: Do not give beta blockers

Do not give beta blockers in RV infarcts as high risk of bradycardia and AV block due to ischemia of the AV nodal artery3.

You consult cardiology to activate the cath lab.

 

Take home point #7: Early revascularization in ischemic related cardiogenic shock is key

Early revascularization has a long term mortality benefit, preferably if done within 6 hours4.  Catheterization or CABG is the preferred method over thrombolytic therapy.

You consult cardiology to activate the cath lab.

Back to our patient –

This lady did go on to the cath lab and had stenting of her RCA, however her infarct likely occurred > 48 hours before presentation. Unfortunately, despite aggressive vasopressor therapy and revascularization, she coded immediately after the procedure and resuscitation attempts were unsuccessful, emphasizing the poor prognosis associated with ischemia related cardiogenic shock.

 

Bottom line for cardiogenic shock: fluid bolus 500 cc 0.9% NaCl, vasopressor support and RSI. Early revascularization is key – catheterization is preferred. Despite these interventions, the diagnosis portends a poor prognosis.

 

References

  1. Inferior STEMI – Life in the Fast Lane https://lifeinthefastlane.com/ecg-library/basics/inferior-stemi/
  2. Right Ventricular Infarction – Life in the Fast Lane https://lifeinthefastlane.com/ecg-library/right-ventricular-infarction/
  3. Tintinalli, JE. (2016). Cardiogenic Shock (8th ed.) Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (pages 349-352). New York: McGraw-Hill.
  4. Cardiogenic Shock – Literature Summary – Life in the Fast Lane https://lifeinthefastlane.com/ccc/cardiogenic-shock-literature-summaries/

 

This post was copyedited by Kavish Chandra @kavishpchandra

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SHoC blog from @CanadiEM

Social media site @CanadiEM recently featured the @CJEMonline @IFEM2 #SHoC Consensus Protocol, featuring authors from @SJRHEM among others.

So why do we need another ultrasound protocol in emergency medicine? RUSHing from the original FAST scan, playing the ACES, FOCUSing on the CAUSE and meeting our FATE, it may seem SHoCking that many of these scanning protocols are not based on disease incidence or data on their impact, but rather on expert opinion. The Sonography in Hypotension (SHoC) protocols were developed by an international group of critical care and emergency physicians, using a Delphi consensus process, based upon the actual incidence of sonographic pathology detected in previously published international prospective studies [Milne; Gaspari]. The protocols are formulated to help the clinician utilize ultrasound to confirm or exclude common causes, and guides them to consider core, supplementary and additional views, depending upon the likely cause specific to the case.

Why would I take the time to scan the aorta of a 22 year old female with hypotension, when looking for pelvic free fluid might be more appropriate? Why would I not look for lung sliding, or B lines in a breathless shocked patient? Consideration of the shock category by addressing the “4 Fs” (fluid, form, function, and filling) will provide a sense of the best initial therapy and should help guide other investigations. Differentiating cardiogenic shock (a poorly contracting, enlarged heart, widespread lung B lines, and an engorged IVC) in an elderly hypotensive breathless patient, from sepsis (a vigorously contracting, normally sized or small heart, focal or no B lines, and an empty IVC) will change the initial resuscitation plan dramatically. Differentiating cardiac tamponade from tension pneumothorax in apparent obstructive shock or cardiac arrest will lead to dramatically differing interventions.

SHoC guides the clinician towards the more likely positive findings found in hypotensive patients and during cardiac arrest, while providing flexibility to tailor other windows to the questions the clinician needs to answer. One side does not fit all. That is hardly SHoCing news. Prospective validation of ultrasound protocols is necessary, and I look forward to future analysis of the effectiveness of these protocols.

References

Scalea TM, Rodriguez A, Chiu WC, et al. Focused Assessment with Sonography for Trauma (FAST): results from an inter- national consensus conference. J Trauma 1999;46:466-72.

Labovitz AJ, Noble VE, Bierig M, Goldstein SA, Jones R, Kort S, Porter TR, Spencer KT, Tayal VS, Wei K. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. Journal of the American Society of Echocardiography. 2010 Dec 31;23(12):1225-30.

Hernandez C, Shuler K, Hannan H, Sonyika C, Likourezos A, Marshall J. C.A.U.S.E.: cardiac arrest ultra-sound exam – a better approach to managing patients in primary non-arrhythmogenic cardiac arrest. Resuscitation 2008;76:198–206

Atkinson PR, McAuley DJ, Kendall RJ, et al. Abdominal and Cardiac Evaluation with Sonography in Shock (ACES): an approach by emergency physicians for the use of ultrasound in patients with undifferentiated hypotension. Emerg Med J 2009;26:87–91

Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in Shock in the evaluation of the critically lll. Emerg Med Clin North Am 2010;28:29 – 56

Jensen MB, Sloth E, Larsen KM, Schmidt MB: Transthoracic echocardiography for cardiopulmonary monitoring in intensive care. Eur J Anaesthesiol. 2004, 21: 700-707.

Gaspari R, Weekes A, Adhikari S, Noble VE, Nomura JT, Theodoro D, Woo M, Atkinson P, Blehar D, Brown SM, Caffery T. Emergency department point-of-care ultrasound in out-of-hospital and in-ED cardiac arrest. Resuscitation. 2016 Dec 31;109:33-9.

Milne J, Atkinson P, Lewis D, et al. (April 08, 2016) Sonography in Hypotension and Cardiac Arrest (SHoC): Rates of Abnormal Findings in Undifferentiated Hypotension and During Cardiac Arrest as a Basis for Consensus on a Hierarchical Point of Care Ultrasound Protocol. Cureus 8(4): e564. doi:10.7759/cureus.564

Sonography in Hypotension and Cardiac Arrest: The SHoC Consensus Statement

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CAEP Definition of an Emergency Physician and the Importance of Emergency Medicine Certification

CAEP Definition of an Emergency Physician

An emergency physician is a physician who is engaged in the practice of emergency medicine and demonstrates the specific set of required competencies that define this field of medical practice. The accepted route to demonstration of competence in medicine in Canada is through certification by a recognized certifying body.*

CAEP recognizes that historically many of its members are physicians who have practiced emergency medicine without formal training and certification. Many have been, and continue to be key contributors to developing emergency medicine and staffing emergency departments in Canada. CAEP acknowledges the contributions of these valued physicians and recognizes them as emergency physicians. It is CAEP’s vision going forward that physicians entering emergency practise will demonstrate their competencies by obtaining certification.

* Recognized certifying bodies in Canada are:
The Royal College of Physicians & Surgeons of Canada
The College of Family Physicians of Canada
(Emergency Physicians with equivalent non-Canadian training and certification are also recognized in Canada eg The American Board of Emergency Medicine)

CAEP Statement on the Importance of Emergency Medicine Certification in Canada

It is CAEP’s vision, that by 2020 all emergency physicians in Canada will be certified in emergency medicine by a recognized certifying body.*

Toward that vision, provincial governments and Faculties of Medicine must urgently allocate resources to increase the numbers of emergency medicine postgraduate positions in recognized training programs so the Colleges are able to address the gap in human resources and training. Furthermore, physicians who have historically practiced emergency medicine without certification must be supported in their efforts to become certified. CAEP is committed to facilitate this process by cataloguing and nationally coordinating practice- and practitioner-friendly educational continuing professional development programs designed to assist non-certified physicians to be successful in their efforts.

* Recognized certifying bodies in Canada are:
The Royal College of Physicians & Surgeons of Canada
The College of Family Physicians of Canada
(Emergency physicians with equivalent non-Canadian training and certification are also recognized in Canada eg The American Board of Emergency Medicine)

We have also published on this topic, highlighting the need for more resident positions in New Brunswick and PEI. Read our paper here.

 

Read more from CAEP here.

 

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SJRHEM at Interprofessional Health Research Day 2017

iHR day is a collaboration between Horizon Health – Saint John Zone, the University of New Brunswick – Saint John Campus, the New Brunswick Community College – Saint John Campus and Dalhousie Medicine New Brunswick.

The day featured oral and poster presentations by health researchers from these four institutions, an outstanding keynote speaker, and a great opportunity to discuss health research with your colleagues. More information here


SJRHEM Research had 8 research abstract accepted to this event:

 

 

Initial validation of the core components in the SHoC-Hypotension Protocol. What rates of ultrasound findings are reported in emergency department patients with undifferentiated hypotension? Results from the first Sonography in Hypotension and Cardiac Arrest in the Emergency Department (SHOC-ED1) Study; an international randomized controlled trial.

Combination of easily measurable real time variables to predict ED crowding

ULTRASIM: ULtrasound in TRAuma SIMulation. Does the use of ultrasound improve diagnosis during simulated trauma scenarios?

Does point of care ultrasonography improve diagnostic accuracy in emergency department patients with undifferentiated hypotension? The First Sonography in Hypotension and Cardiac Arrest in the Emergency Department (SHOC-ED1) Study; an international randomized controlled trial.

Does point of care ultrasound improve resuscitation markers in emergency department patients with undifferentiated hypotension? The first Sonography in Hypotension and Cardiac Arrest in the Emergency Department (SHOC-ED 1) Study; an international randomized controlled trial.

Combatting sedentary lifestyles; can exercise prescriptions in the Emergency Department lead to a behavioural change in patients?

Determining ED staff documentation practice, awareness, and knowledge of intimate partner violence questioning and documentation tools

To choose or not to choose: evaluating the effect of a Choosing Wisely knowledge translation initiative in rural and urban EM physicians

 

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Interprofessional Health Research Day 2017 – Devon McLean

ULTRASIM: ULtrasound in TRAuma SIMulation. Does the use of ultrasound improve diagnosis during simulated trauma scenarios?

Point of care ultrasound (US) is a key adjunct in the management of trauma patients, in the form of the extended focussed assessment with sonography in trauma (E-FAST) scan. This study assessed the impact of adding an edus2 ultrasound simulator on the diagnostic capabilities of resident and attending physicians participating in simulated trauma scenarios.

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Interprofessional Health Research Day 2017 – Fiona Milne and Kalen Leech-Porter

Combatting sedentary lifestyles; can exercise prescriptions in the Emergency Department lead to a behavioural change in patients?

Patients with chronic diseases such as COPD, coronary artery disease, depression and anxiety are known to benefit from exercise. They also frequently visit the emergency department (ED). Despite the large therapeutic window and evidence supporting its role in disease management, there are few studies examining prescribing exercise in the ED. We asked: Is exercise prescription in the ED feasible and effective?

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Interprofessional Health Research Day 2017 – Janeske Vonkeman

Determining ED staff documentation practice, awareness, and knowledge of intimate partner violence questioning and documentation tools

Domestic violence (DV) rates in smaller cities have been reported to be some of the highest in Canada. It is highly likely that emergency department staff will come across victims of intimate partner violence (IPV) in their daily practice. The purpose of this study is to better understand current practices for detecting IPV, staff awareness and knowledge surrounding IPV, available screening tools, and barriers to questioning about IPV. in the emergency department (ED). Finally, we will determine whether ED staff would be willing to implement a brief 3-question IPV screening tool, the Partner Violence Screen (PVS) in their daily practice.

 

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Welcome Block 10

Dr. A. Sundaram

March 8- April 3

PGY1 Ophthalmology
“I go by Aish. I am a first year Ophthalmology resident. I am originally from Alberta and did my undergrad in medical sciences and business at University of Western Ontario. I subsequently did my medical school at University of Alberta.”


Dr. F. MacKay

March 8- April 3

PGY1 FM

“Hi there. My name is Fraser. I live across the street. I am an alumni of Dal, U of T, Holland College, and the mean streets of many a Canadian city. I am a Family Medicine Resident. For now, when not developing my Doctoring skills, I am busy training my daughters to be astronauts and/or circus acrobats.”


Dr. D. Rollo

March 8- April 3

PGY1 FM

“Born, raised and refined in Western Canada. Home grown in Okotoks AB then borrowed a degree in biochemistry from UBC in Kelowna before I finally landed on Vancouver Island to learn medicine. From West to East, quite the jump and quite the adventure!”


Clinical Clerks

Sean Casey

March 6 – March 26

3rd DMNB

 

 

 

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