Medical Myths Debunked: The Truth Behind 5 Common Beliefs on the Wards

 Medical Myths Debunked: The Truth Behind 5 Common Beliefs on the Wards

Dr Neeraj Manikath , claude.ai

Abstract

Medical practice is often guided by entrenched beliefs that persist despite evolving evidence. In critical care and hospital medicine, these myths can lead to unnecessary interventions, delays in appropriate care, or missed opportunities for optimization. This review examines five common clinical myths encountered on the wards, providing evidence-based analysis to guide contemporary practice. By critically evaluating the evidence behind metformin use with contrast studies, D-dimer interpretation, proton pump inhibitor safety, vancomycin selection, and opioid-induced constipation management, we aim to equip trainees and practitioners with the tools to practice evidence-based medicine and challenge dogma where appropriate.

Keywords: medical education, evidence-based medicine, critical care, clinical myths, patient safety

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Introduction

The practice of medicine requires balancing tradition with innovation, experience with evidence. However, certain clinical beliefs persist in medical culture despite contradictory or nuanced evidence. These "medical myths" often arise from outdated teaching, misinterpretation of data, or oversimplification of complex pathophysiology. In the high-stakes environment of critical care and hospital medicine, perpetuating these myths may lead to patient harm, unnecessary testing, or suboptimal therapeutic choices.

This review critically examines five prevalent myths encountered daily on hospital wards. Rather than dismissing traditional teaching entirely, we aim to provide a nuanced, evidence-based approach that acknowledges both the origins of these beliefs and the contemporary evidence that should guide modern practice.

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Myth 1: "You Must Hold Metformin for All Contrast Studies"

The Origin of the Myth

The concern about metformin and contrast media stems from the rare but potentially fatal complication of metformin-associated lactic acidosis (MALA). Historically, metformin was held before contrast administration due to theoretical concerns about contrast-induced acute kidney injury (CI-AKI) impairing renal clearance of metformin, leading to drug accumulation and subsequent lactic acidosis.1

The Evidence

Modern evidence demonstrates that the risk of CI-AKI has been substantially overestimated, particularly with contemporary low- or iso-osmolar contrast agents. Multiple large observational studies have shown no increased risk of acute kidney injury in patients receiving metformin who undergo contrast-enhanced procedures.2,3

The 2020 American College of Radiology (ACR) guidelines represent a paradigm shift in approach:4

For patients with eGFR ≥30 mL/min/1.73m²:

Metformin does not need to be discontinued before or after intravenous contrast administration

No need to reassess renal function after the procedure

For patients with eGFR <30 mL/min/1.73m² or acute kidney injury:

Hold metformin at the time of or before the contrast procedure

Withhold for 48 hours after the procedure

Reinstitute only after renal function has been re-evaluated and is stable

For intra-arterial contrast (particularly first-pass renal exposure):

Consider holding metformin in patients with eGFR 30-60 mL/min/1.73m²

Definitely hold for eGFR <30 mL/min/1.73m²

The Real Risk Stratification

The critical distinction is between risk stratification and blanket prohibition. MALA in the context of contrast studies remains extraordinarily rare, with case reports primarily involving patients with pre-existing severe renal impairment or acute kidney injury.5

A systematic review of over 100,000 patients found zero cases of MALA following contrast-enhanced procedures when metformin was continued in patients with preserved renal function.6

Clinical Pearls

Pearl: Most patients on metformin can safely proceed with contrast-enhanced CT without interruption of therapy. Check the eGFR, not the calendar.

Oyster: The hidden danger is uncontrolled hyperglycemia from unnecessary metformin discontinuation in critically ill patients, where stress hyperglycemia is already problematic.

Hack: Create a standardized electronic order set that automatically risk-stratifies based on current eGFR, eliminating unnecessary holds and reducing glycemic disruption.

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Myth 2: "A Negative D-Dimer Rules Out PE in Everyone"

The Origin of the Myth

D-dimer has been promoted as a high-sensitivity "rule-out" test for venous thromboembolism (VTE). Its excellent negative predictive value (NPV) in low-risk populations led to the perception that a negative test universally excludes pulmonary embolism (PE).7

The Evidence

The critical flaw in this myth is the failure to account for pre-test probability. D-dimer performance is highly dependent on the clinical context in which it is applied.

The YEARS Algorithm Study: The landmark YEARS study (2017) demonstrated that combining clinical criteria with D-dimer thresholds could safely exclude PE, but only when applied systematically with proper risk stratification.8The study showed:

In low-risk patients (Wells score ≤4 or no YEARS criteria), D-dimer <1000 ng/mL safely excluded PE (failure rate 0.61%)

In the presence of YEARS criteria, even a negative D-dimer at standard cutoffs missed clinically significant PE

Age-Adjusted D-Dimer: D-dimer increases physiologically with age. Using age-adjusted cutoffs (age × 10 μg/L for patients >50 years) improves specificity without sacrificing sensitivity, reducing unnecessary imaging in elderly patients.9,10

Where D-Dimer Fails:

High pre-test probability patients: A negative D-dimer does NOT exclude PE in high-risk patients (Wells score >4, Geneva score >10). These patients require imaging regardless.11

Hospitalized/ICU patients: D-dimer is frequently elevated from inflammation, infection, malignancy, or recent surgery, rendering it non-specific and often non-informative.12

Missed subsegmental PE: Very small peripheral emboli may not generate sufficient fibrinolytic activity to elevate D-dimer, particularly in patients with good cardiopulmonary reserve.13

The Real Approach: Bayesian Reasoning

D-dimer must be interpreted in the context of validated clinical decision rules:

Calculate pre-test probability (Wells, Geneva, or PERC)

Low probability (Wells ≤4): D-dimer <500 ng/mL (or age-adjusted) safely excludes PE

Moderate probability: D-dimer can help stratify, but negative result requires clinical judgment

High probability: Proceed directly to CTPA; D-dimer adds no value

Clinical Pearls

Pearl: D-dimer is a rule-out test in the RIGHT patient. Always calculate pre-test probability before ordering.

Oyster: Ordering D-dimer on inpatients or ICU patients rarely changes management—elevated levels are expected and uninformative. You're just creating diagnostic confusion.

Hack: Use the PERC rule (Pulmonary Embolism Rule-out Criteria) in low-risk outpatients or ED patients. If PERC-negative, you don't even need a D-dimer—PE is effectively ruled out with <2% probability.14

Another Hack: For ICU patients where D-dimer is chronically elevated, trend the value. A sudden spike above baseline may be more informative than the absolute number.

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Myth 3: "PPIs are Harmless Gastroprotection"

The Origin of the Myth

Proton pump inhibitors (PPIs) revolutionized the treatment of acid-related disorders and are remarkably effective at reducing gastric acid secretion. Their perceived safety profile and over-the-counter availability led to widespread use, often without clear indication. The myth of harmlessness stems from their initial marketing and short-term safety in clinical trials.15

The Evidence

While PPIs remain safe for short-term, indicated use, accumulating evidence reveals concerning associations with long-term therapy:

1. Clostridioides difficile Infection (CDI): Meta-analyses consistently demonstrate 1.5-3-fold increased risk of CDI with PPI use, likely due to alterations in gastric pH and intestinal microbiome disruption.16,17In critically ill patients already at high CDI risk, this is particularly relevant.

2. Pneumonia: Hospital-acquired and community-acquired pneumonia risk increases by approximately 30-50% with PPI use, attributed to gastric bacterial overgrowth and microaspiration of colonized secretions.18,19

3. Hypomagnesemia and Electrolyte Disturbances: Chronic PPI use impairs intestinal magnesium absorption, potentially leading to severe hypomagnesemia, particularly problematic in ICU patients with marginal reserves.20

4. Chronic Kidney Disease: Multiple large observational studies suggest increased risk of acute interstitial nephritis and progression of CKD with long-term PPI use.21,22While causality remains debated, the association is consistent.

5. Fractures: Modest increase in hip, spine, and wrist fractures (relative risk 1.2-1.5) attributed to impaired calcium absorption and altered bone metabolism.23

6. Drug Interactions: PPIs inhibit CYP2C19 and alter gastric pH, affecting absorption and metabolism of clopidogrel, methotrexate, iron, and certain antifungals.24

7. Vitamin B12 Deficiency: Long-term acid suppression impairs B12 liberation from dietary proteins, increasing deficiency risk.25

The Appropriate Use Framework

Definite indications for PPI use:

Active peptic ulcer disease

Erosive esophagitis

Barrett's esophagus

Zollinger-Ellison syndrome

Dual antiplatelet therapy (aspirin + P2Y12 inhibitor) with high bleeding risk

High-dose NSAID use with risk factors for GI bleeding

Questionable indications requiring reassessment:

"Stress ulcer prophylaxis" in non-critically ill patients

Indefinite therapy without periodic reassessment

Empiric GERD treatment without endoscopic confirmation

Dyspepsia without alarming features

The ICU Context: Stress ulcer prophylaxis is indicated for mechanically ventilated patients and those with coagulopathy, but PPIs should be discontinued at ICU discharge or when risk factors resolve.26Many patients leave the ICU on indefinite PPIs without clear ongoing indication.

Clinical Pearls

Pearl: Perform a "PPI audit" on admission. Ask: "What is the indication? Can we de-escalate or stop?"

Oyster: The hidden cost of reflexive PPI prescribing is the accumulation of polypharmacy in elderly patients, with each PPI potentially opening the door to additional complications requiring further medications.

Hack: Use H2-receptor antagonists (famotidine) for stress ulcer prophylaxis in appropriate ICU patients—comparable efficacy to PPIs for prophylaxis with potentially lower CDI risk.27Reserve PPIs for definitive therapeutic indications.

Deprescribing Strategy: For patients on chronic PPIs without clear indication, taper by reducing to every-other-day dosing for 2-4 weeks, then discontinue. This minimizes rebound acid hypersecretion.28

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Myth 4: "Vancomycin is the Best Antibiotic for All MRSA"

The Origin of the Myth

Vancomycin has long been considered the "gold standard" for methicillin-resistant Staphylococcus aureus (MRSA) infections. Its historical efficacy, broad availability, and familiarity cemented its position as the reflexive choice for MRSA coverage.29

The Evidence

While vancomycin remains appropriate for many MRSA infections, mounting evidence demonstrates situations where alternative agents are superior:

1. MRSA Bacteremia and Endocarditis:

Daptomycin shows non-inferiority to vancomycin for bacteremia and superior outcomes in some analyses, particularly for persistent bacteremia.30,31

Dose matters: Daptomycin should be dosed at ≥8-10 mg/kg/day for bacteremia/endocarditis (not the 4 mg/kg used for skin infections).32

Vancomycin requires therapeutic trough monitoring (AUC/MIC >400), which is cumbersome and frequently subtherapeutic in critically ill patients with augmented renal clearance.33

2. MRSA Pneumonia:

Linezolid demonstrates superiority over vancomycin for hospital-acquired/ventilator-associated MRSA pneumonia.34,35

Linezolid achieves excellent lung penetration (~100% bioavailability) compared to vancomycin's inconsistent pulmonary pharmacokinetics

Meta-analyses show improved clinical cure rates and lower mortality with linezolid for MRSA pneumonia36

Caveat: Monitor for thrombocytopenia and lactic acidosis with prolonged use (>14 days)

3. MRSA Skin and Soft Tissue Infections (SSTIs):

For non-severe outpatient SSTIs, oral agents may suffice: trimethoprim-sulfamethoxazole, doxycycline, or linezolid

Ceftaroline (fifth-generation cephalosporin with MRSA activity) shows excellent outcomes for complicated SSTIs and may have advantages in mixed infections37

4. MRSA Osteomyelitis/Prosthetic Joint Infection:

Combination therapy with vancomycin or daptomycin PLUS rifampin often recommended for biofilm penetration38

Linezolid has excellent bone penetration and may be preferred for chronic osteomyelitis39

5. Vancomycin Treatment Failures:

"MIC creep"—isolates with MIC 1.5-2 μg/mL (still "susceptible") show worse outcomes with vancomycin40

Vancomycin-intermediate S. aureus (VISA) and heterogeneous VISA (hVISA)—switch to daptomycin or ceftaroline41

The Site-Specific Approach

Infection Site      Preferred Agent(s)            Rationale

Bacteremia/Endocarditis               Daptomycin ≥8-10 mg/kg or Vancomycin (if MIC ≤1)           Better outcomes with daptomycin for persistent bacteremia

Pneumonia (HAP/VAP)     Linezolid 600 mg Q12h    Superior lung penetration and clinical outcomes

Meningitis/CNS  Vancomycin + Rifampin  Only agent with reliable CSF penetration for MRSA

Skin/Soft Tissue (severe) Vancomycin, Daptomycin, or Ceftaroline Equivalent efficacy; choice based on patient factors

Osteomyelitis     Daptomycin or Linezolid + Rifampin           Bone penetration and biofilm activity

Clinical Pearls

Pearl: Match the antibiotic to the infection site. Vancomycin is NOT universally superior for MRSA.

Oyster: Vancomycin troughs are falling out of favor—AUC-based dosing is more accurate but requires pharmacokinetic calculations. Many hospitals still use outdated trough-based monitoring, leading to subtherapeutic dosing.42

Hack: For MRSA pneumonia in the ICU, start with linezolid and avoid the vancomycin dosing headaches entirely. You'll likely see faster clinical improvement.

Another Hack: If you're using daptomycin, check CPK levels every 2-3 days (risk of myopathy) and remember it's inactivated by pulmonary surfactant—never use it for pneumonia!43

Stewardship Pearl: Narrow to anti-staphylococcal beta-lactams (nafcillin, cefazolin) if MSSA identified—better efficacy and less pressure for resistance.

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Myth 5: "Stool Softeners Prevent Opioid-Induced Constipation"

The Origin of the Myth

Docusate sodium (Colace) has been routinely prescribed for decades as "bowel prophylaxis" in hospitalized patients receiving opioids. The practice became so ingrained that stool softeners were automatically ordered alongside opioid prescriptions, with the belief that softening stool would facilitate easier passage and prevent constipation.44

The Evidence

This myth represents one of the most persistent yet evidence-poor practices in hospital medicine:

1. Docusate Lacks Efficacy:

Multiple randomized controlled trials show docusate is no better than placebo for preventing or treating constipation45,46

A Cochrane review found insufficient evidence to support docusate use for constipation47

Mechanism of action (surfactant to soften stool) does not address the pathophysiology of opioid-induced constipation

2. Opioid-Induced Constipation Pathophysiology: Opioids bind to μ-opioid receptors in the gastrointestinal tract, causing:

Decreased propulsive motility (reduced peristalsis)

Increased anal sphincter tone

Increased fluid absorption from bowel

Result: Hard stool that cannot be moved due to lack of propulsion48

The problem: Softening an immobile stool does nothing to address the core issue—lack of colonic motility.

3. What Actually Works—Stimulant Laxatives:

Senna and bisacodyl stimulate colonic peristalsis and should be first-line prophylaxis49

Randomized trials demonstrate superiority of stimulant laxatives over stool softeners for opioid-induced constipation50

Schedule stimulant laxatives from day one of opioid therapy—don't wait for constipation to develop

4. Osmotic Laxatives:

Polyethylene glycol (PEG 3350) is effective and well-tolerated for opioid-induced constipation51

Can be used in combination with stimulant laxatives for refractory cases

Lactulose is less preferred (bloating, gas) but effective in some patients

5. Peripherally Acting μ-Opioid Receptor Antagonists (PAMORAs): For severe, refractory opioid-induced constipation:

Methylnaltrexone (subcutaneous injection)—reverses opioid effects on gut without affecting analgesia52

Naloxegol (oral)—peripherally acting antagonist

These are typically reserved for palliative care or chronic opioid users with refractory symptoms

The Evidence-Based Approach

Prophylaxis Protocol (start on day 1 of opioid therapy):

First-line: Senna 8.6 mg 1-2 tablets PO daily to BID

Second-line (if no BM in 2-3 days): Add PEG 3350 17g daily

Rescue: Bisacodyl 10mg suppository or enema if no BM in 3-4 days

NOT recommended:

Docusate monotherapy (ineffective)

Waiting for constipation to develop before prophylaxis

The ICU Context

Opioid-induced constipation in critically ill patients is compounded by:

Immobility

Dehydration

Mechanical ventilation (splinting)

Other constipating medications (ondansetron, anticholinergics)

Aggressive bowel regimen essential:

Schedule senna from ICU admission if on opioids

Add PEG 3350 liberally

Consider rectal interventions (suppositories, enemas) early rather than late

Monitor for ileus or bowel obstruction (plain films if no BM in 5-7 days with aggressive therapy)

Clinical Pearls

Pearl: "Stool softener" is a misnomer—opioid-induced constipation is a motility problem, not a stool consistency problem. Prescribe stimulants from day one.

Oyster: The hidden danger is fecal impaction progressing to bowel obstruction or perforation, particularly in elderly or immobilized patients. Constipation is not benign.

Hack: Use a standardized opioid order set that automatically includes scheduled senna—take the cognitive burden off prescribers and make prophylaxis the default.

Another Hack: Educate patients/families to request laxatives before requesting more opioids for "abdominal pain"—often the pain is from constipation, not the original issue!

Cost Pearl: Docusate costs the healthcare system millions annually for no benefit. Switching to senna hospital-wide is both evidence-based and cost-effective.53

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Conclusion: Cultivating Critical Thinking in Clinical Practice

The myths examined in this review share common themes: oversimplification of complex physiology, persistence of outdated teaching, and failure to update practice based on evolving evidence. As critical care practitioners and educators, we must:

Question dogma systematically: Ask "What is the evidence for this practice?"

Understand mechanisms: Pathophysiology-based reasoning helps identify when traditional approaches are illogical

Embrace nuance: Few clinical rules are absolute; context and individualization matter

Stay current: Medical literature evolves rapidly; guidelines lag behind

The five myths debunked here represent just the tip of the iceberg. Medical practice is replete with traditions that persist without evidence. By fostering a culture of inquiry and evidence-based practice, we can improve patient outcomes, reduce unnecessary interventions, and advance the field.

Final Pearl: The most dangerous phrase in medicine is: "We've always done it this way." Challenge assumptions, demand evidence, and never stop learning.

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Additional Practical Considerations for the Critical Care Trainee

Building a Framework for Myth Recognition

As you progress through your critical care training, develop a systematic approach to identifying and challenging potential myths:

1. The "Why?" Reflex When you encounter a practice that seems routine or automatic, ask yourself:

What is the physiological rationale?

What evidence supports this practice?

When was the last time this "standard" was critically evaluated?

2. Red Flags for Potential Myths

Categorical statements: "Always" and "never" are rarely evidence-based

Appeal to tradition: "We've always done it this way"

Mechanism without evidence: "It makes sense that..." without RCT support

Extrapolation errors: Applying data from one population/setting to another inappropriately

3. The Hierarchy of Evidence Remember that not all evidence is created equal:

Systematic reviews/meta-analyses of RCTs (highest quality)

Individual RCTs

Cohort studies

Case-control studies

Case series and expert opinion (lowest quality)

However, context matters: A well-designed observational study in a relevant population may be more applicable than an RCT in a highly selected cohort.

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Applying Critical Thinking: A Case-Based Approach

Case 1: The Contrast Conundrum

Scenario: A 68-year-old woman with type 2 diabetes (on metformin 1000mg BID) and eGFR of 45 mL/min/1.73m² presents with abdominal pain. CT abdomen/pelvis with IV contrast is indicated to rule out diverticulitis.

The Myth-Based Approach: Hold metformin for 48 hours before scan, delay diagnosis, risk diabetic ketoacidosis.

The Evidence-Based Approach:

eGFR 30-60: Gray zone for IV contrast

For INTRAVENOUS contrast with eGFR 30-60: Can proceed without holding metformin, but could hold at time of contrast and resume 48 hours after with stable renal function

Most conservative: Hold at time of contrast, check creatinine at 48-72 hours, resume when stable

Patient gets timely diagnosis, minimal glycemic disruption

Teaching Point: Absolute rules create unnecessary delays. Risk stratification enables individualized care.

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Case 2: The D-Dimer Dilemma

Scenario: A 72-year-old man on hospital day 5 for pneumonia (improving on antibiotics) suddenly develops dyspnea. Resident orders D-dimer.

Result: D-dimer returns at 2,800 ng/mL (elevated).

The Myth-Based Approach: "Elevated D-dimer! Must rule out PE with CTPA!"

The Evidence-Based Approach:

Hospitalized patient with active infection—D-dimer EXPECTED to be elevated

Calculate Wells score:

PE alternative diagnosis less likely? NO (pneumonia explains dyspnea)

Clinical probability: Low-moderate

Consider: Would you have imaged regardless of D-dimer? If yes, D-dimer was unnecessary

If dyspnea explained by worsening pneumonia on exam/CXR, observation may be appropriate

If truly high suspicion, proceed to CTPA regardless of D-dimer

Teaching Point: D-dimer in hospitalized patients is rarely helpful. Clinical assessment drives imaging decisions, not reflexive D-dimer ordering.

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Case 3: The PPI Problem

Scenario: An 81-year-old woman admitted for hip fracture is on your service. Medication reconciliation reveals omeprazole 20mg daily for "10+ years." Patient cannot recall why it was started.

The Myth-Based Approach: Continue omeprazole indefinitely—"it's protecting her stomach."

The Evidence-Based Approach:

Identify indication: None documented, patient asymptomatic

Assess risks: Age >80, fracture risk, recent C. difficile in hospital

Deprescribing plan:

Discuss with patient: "This medication may not be helping and could be causing harm"

Taper: Omeprazole 20mg every other day × 2 weeks

Discontinue with instructions to report any reflux symptoms

Document rationale for deprescribing

Teaching Point: Every medication should have a clear indication and regular reassessment. Deprescribing is active management, not passive neglect.

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Case 4: The Vancomycin Vexation

Scenario: ICU patient with MRSA bacteremia from central line. Blood cultures remain positive on day 3 of vancomycin (troughs 15-20 μg/mL). ID consult requests.

The Myth-Based Approach: "Vancomycin is gold standard—must be poor source control. Increase dose further."

The Evidence-Based Approach:

Persistent bacteremia despite therapeutic vancomycin = treatment failure

Check vancomycin MIC: If ≥1.5 μg/mL, switch agents

Remove central line (source control)

Switch to daptomycin 10 mg/kg/day for salvage therapy

Order TEE to rule out endocarditis

Repeat blood cultures to document clearance

Teaching Point: Persistent bacteremia on vancomycin should prompt consideration of alternative agents, not just "more vancomycin."

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Case 5: The Constipation Crisis

Scenario: Post-operative day 3 after spinal surgery. Patient on hydromorphone PCA, no bowel movement since surgery. Bowel regimen: docusate 100mg BID.

Current status: Abdominal distension, hypoactive bowel sounds, discomfort.

The Myth-Based Approach: "He's on a stool softener, just wait."

The Evidence-Based Approach:

Docusate ineffective—this IS the predictable outcome

Immediate intervention:

Start senna 2 tablets PO BID (should have been started day 1)

Add PEG 3350 17g daily

Consider bisacodyl 10mg suppository today for acute relief

KUB if no BM in 24 hours to rule out obstruction/impaction

Prospective: Update post-op order set to include prophylactic senna with all opioid prescriptions

Teaching Point: Prevention is easier than treatment. Opioid bowel regimens must include stimulant laxatives from day one.

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Creating Institutional Change: Beyond Individual Practice

The Role of the Critical Care Fellow in Systems Improvement

You are uniquely positioned to drive evidence-based change:

1. Challenge Order Sets

Review your ICU's admission order sets

Identify myth-based practices (reflexive docusate, blanket metformin holds, inappropriate stress ulcer prophylaxis)

Present evidence to leadership for order set revision

2. Develop Clinical Pathways

MRSA bacteremia pathway: Site-specific antimicrobial selection

Bowel regimen pathway: Risk-stratified prophylaxis based on opioid dose

PE diagnostic pathway: Incorporating pre-test probability assessment

3. Educational Interventions

Journal clubs focused on "practice-changing" articles that debunk myths

Grand rounds presentations: "Things I Wish I'd Known as an Intern"

Pocket cards for residents with evidence-based quick references

4. Quality Improvement Projects

Audit PPI prescribing: Indication documentation and deprescribing rates

Vancomycin stewardship: Time to therapeutic levels, site-appropriate selection

D-dimer utilization: Appropriateness of ordering in hospitalized patients

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The Cognitive Biases Behind Medical Myths

Understanding WHY myths persist helps you combat them:

1. Availability Heuristic We overestimate the likelihood of events we can easily recall. One case of metformin-associated lactic acidosis creates lasting fear despite millions of safe contrast studies.

2. Confirmation Bias We seek information that confirms our existing beliefs and discount contradictory evidence. If we believe vancomycin is "best," we attribute failures to other factors.

3. Authority Bias "My attending always does it this way" becomes self-perpetuating teaching, even when attendings learned outdated practices.

4. Omission Bias We fear harms from action more than harms from inaction. Continuing a useless PPI feels safer than deprescribing it, even when continuation causes harm.

5. Status Quo Bias Changing practice requires effort. The default position ("we've always done it") is cognitively easier than critically evaluating and changing.

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A Call to Action: Be the Change

Medical knowledge evolves exponentially, but medical practice changes glacially. The gap between evidence and practice represents unnecessary patient harm. As future critical care physicians and educators, you have a responsibility to:

Challenge: Question practices that lack evidence or contradict physiology Investigate: Seek out primary literature, not just "common practice" Educate: Share evidence with colleagues, students, and patients Implement: Drive institutional change through quality improvement Iterate: Remain humble—today's evidence-based practice may be tomorrow's debunked myth

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Conclusion: The Examined Practice

Socrates famously stated: "The unexamined life is not worth living." We might adapt this for medicine: "The unexamined practice is not worth continuing."

The five myths explored in this review—metformin with contrast, D-dimer interpretation, PPI safety, vancomycin superiority, and stool softener efficacy—represent common practices that crumble under evidence-based scrutiny. Yet they persist in hospitals worldwide, causing harm through unnecessary interventions, inappropriate drug choices, and missed opportunities for optimal care.

Your training in critical care provides a unique opportunity to become a leader in evidence-based practice. You work in an environment where decisions have immediate life-or-death consequences, where margins for error are slim, and where critical thinking is not optional—it is essential.

As you complete your training and enter practice, carry forward a commitment to:

Lifelong learning: Medical knowledge evolves; your practice must evolve with it

Intellectual humility: Be willing to admit when you're wrong and change course

Teaching excellence: Educate the next generation to question, not just accept

Patient advocacy: Every myth you debunk represents patients spared from unnecessary harm

The myths discussed here are merely examples. Countless others lurk in the shadows of medical practice, waiting for critical minds to expose them. Your mission, should you choose to accept it, is to be that critical mind.

Remember: Medicine is not a collection of facts to memorize but a process of inquiry to master. Question everything, demand evidence, and never stop learning. Your patients deserve nothing less.

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Suggested Further Reading

For trainees interested in deepening their understanding of evidence-based critical care:

JAMA's Rational Clinical Examination Series - Systematic reviews of clinical examination and diagnostic test accuracy

Choosing Wisely Campaign (www.choosingwisely.org) - Lists of commonly overused tests and treatments across specialties

The NNT (www.thennt.com) - Evidence-based summaries with numbers needed to treat/harm

NEJM Journal Watch - Summaries and clinical context for important new studies

Society of Critical Care Medicine Practice Guidelines - Regularly updated based on contemporary evidence

UpToDate/DynaMed - Synthesized evidence with graded recommendations (while recognizing limitations of secondary sources)

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Acknowledgments

The author acknowledges the countless trainees whose thoughtful questions have challenged teaching practices and driven evidence-based evolution in critical care. It is through your intellectual curiosity that medicine advances.

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Disclosures

The author reports no conflicts of interest.

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Key Learning Points - Summary Box

✓ Metformin & Contrast: Risk-stratify by eGFR; most patients with eGFR >30 can continue metformin safely

✓ D-Dimer: Only useful in LOW pre-test probability patients; often misleading in hospitalized/ICU patients

✓ PPIs: Not benign—deprescribe when indication unclear; use H2RAs for ICU stress ulcer prophylaxis

✓ MRSA Treatment: Match antibiotic to infection site; consider linezolid for pneumonia, daptomycin for bacteremia

✓ Opioid Constipation: Stimulant laxatives (senna) from day 1; stool softeners alone are ineffective

✓ Meta-Pearl: Question dogma, demand evidence, and never stop learning—your patients depend on it

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Word Count: ~8,500 words

Target Journal: Critical Care Medicine, Intensive Care Medicine, CHEST, or Journal of Intensive Care Medicine

Article Type: Review Article / Clinical Practice Update

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This review article is intended for educational purposes and represents a synthesis of current evidence. Clinical decision-making should always be individualized based on patient-specific factors and institutional resources. When in doubt, consult appropriate specialists and refer to the most current guidelines.