Inpatient Medicine: Year in Review

Name: Inpatient Medicine: Year in Review
Uploaded: 2017-10-18T20:11:03+00:00
Duration: PTM36S23
Channel: Kayla Lyons
Description: Inpatient Medicine: Year in Review

Inpatient Medicine: Year in Review
Karen Hauer, MD UCSF August, 2006

Methods Literature review March 2005 - 2006 11 major journals
Am J Med Circulation Annals Internal Med Critical Care Medicine ACP Journal Club JAMA Archives Internal Med Lancet BMJ New Engl J Medicine CMAJ

Selection criteria Relevance for inpatient medicine
Potential to change, inform, or confirm practice Diverse topics, study types

Topics Acute coronary syndromes Insulin in the ICU
Clostridium difficile Contrast nephropathy PE Diagnosing catheter-related infection Medication discrepancies

Case A 75 year old man with diabetes, hypertension, hyperlipidemia, dyspepsia on PPI, and COPD is admitted with chest pain, fever, and cough. Vital signs are pulse 95, BP 145/90, resp 22, 02 sat 97% on room air. On exam JVP is 9 cm, chest clear, cardiac RRR with S4, no edema. BNP is 250. ECG shows NSR with 2 mm ST elevation in V4-6. CXR shows LLL infiltrate.

Question #1 You administer aspirin 325 mg. Do you give Clopidogrel?
Yes, before percutaneous coronary intervention (PCI). Yes, after PCI Yes, if tPA is given No, aspirin is enough

Effect of Clopidogrel Pretreatment before PCI
Negative consequences of platelet activation Coronary artery thrombosis - plaque rupture Thrombotic complications of percutaneous coronary intervention (PCI) What is the optimal timing of clopidogrel treatment in patients with ST elevation MI (STEMI)? Initiated at time of PCI or pretreatment

Effect of Clopidogrel Pretreatment before PCI the PCI Clarity Study Sabatine, N Engl J Med 2005;294:1224 1863 patients with recent STEMI Randomized trial All patients received fibrinolytic, aspirin Clopidogrel 300 mg load, then 75/day or placebo Initiated with fibrinolysis, then PCI at 2-8 days Any patient getting stent received clopidogrel after Outcome: Primary: composite of CV death, MI, or stroke from PCI to 30 days Secondary: MI or stroke before PCI Without load, it takes approx 3-5 days for the antiplt effects of clopidogrel to reach steady state; w/ load, it takes only several hours

Clopidogrel Pretreatment before PCI improved outcomes
Clopidogrel Pre-Rx No pre-Rx Adjusted odds ratio p CV death, MI, stroke post PCI 3.6% 6.2% 0.54 .008 MI or stroke pre PCI 4.0% 0.62 .03 Outcome post PCI: NNT = 39 Trend toward benefit for CV death, MI, stroke individually altho none statistically significant Separated soon after PCI and continued to diverge over time Combining benefits pre and post PCI NNT = 23

Effect of Clopidogrel Pretreatment before PCI the PCI Clarity Study
Clopidogrel pretreatment benefit Regardless of patient characteristics For urgent/elective PCI regardless of timing No difference in bleeding 2.0% vs. 1.9% No increase in bleeding with clopidogrel pretreatment plus GpIIb/IIIa inhibitor Benefit of clopidogrel across a range of pretreatment durations Bleeding - 2% includes major and minor bleeding

Implications of Clopidogrel Pretreatment before PCI
For every 100 patients undergoing PCI Prevent 2 MI’s before PCI Prevent 2 CV deaths, MI or stroke after PCI to 30 days Addition of clopidogrel to ASA in 45,852 patients with acute MI 93% STEMI or BBB 9% reduction in death, MI, or stroke at discharge COMMIT. Lancet 2005;366:1607 COMMIT-half pts received fibrinolytics (urokinase), 5% underwent angiography Benefit of clopidogrel emerged at day 1 despite no loadtaken Taken together, these 2 studies demonstrate benefit of clopidogrel for STEMI

Question #1 You administer aspirin 325 mg. Do you give Clopidogrel?
Yes, before percutaneous coronary intervention (PCI).

Clostridium difficile Contrast nephropathy Pulmonary embolism Diagnosing catheter-related infection Medication discrepancies

Case Your patient undergoes successful PCI with stent placement. You also diagnosed pneumonia based on the presentation and initial CXR and started Levofloxacin. His oxygen requirements increase over the first 2 hospital days to the point that he is intubated and admitted to the ICU.

Question #2 Do you initiate intensive insulin therapy in the ICU?
A. No, only in surgical ICU patients. B. Yes. C. Yes, if he is likely to be in the ICU for > 3 days. D. Yes, if glucose at ICU admission is > 300 mg/dl.

Intensive Insulin Therapy in the ICU Van den Berghe, N Engl J Med 2001;345:1359
Benefits of strict glucose control in surgical ICU In-hospital mortality 11% vs. 7%, (p = .01) Greatest benefit with ICU stay > 3-5 days Reduced morbidity Septicemia: 8% vs. 4% (p = .003) Organ failure Does intensive insulin therapy improve prognosis in the medical ICU? Hyperglycemia and insulin resistance are common in the ICU 2001 single institution study in Belgium, 2/3 post cardiac surgery Usual care: maintain glucose , vs (fed on ICU d2); check gluc q 4 hr a.m. gluc avg’s 150 vs. 103 Primary outcome = death during intensive care. Effect was independent of h/o DM No mortality benefit in first 5 days Criticisms: single institution, not blinded, high mortality rate for surgical pts, all pt’s fed

Intensive Insulin Therapy in the Medical ICU Van den Berghe, N Engl J Med 2006;354:449
Prospective, randomized, unblinded trial Intensive: insulin with goal glucose Conventional treatment: insulin drip with goal glucose Primary outcome: in-hospital mortality Secondary outcomes: ICU mortality, organ failure, bacteremia or prolonged antibiotics Role of insulin in MICU has been unknown; patients are sicker than in SICU Patients: expected to need ICU for >= 3 days; enteral feeding as soon as stable 17% had DM Conventional group: start insulin when gluc > 215, taper insulin when gluc < 180 Enteral feeding started as soon as possible after pts hemodynamically stable Other 2ndary outcomes: LOS in ICU and hosp, new renal failure

Intensive insulin therapy and in-hospital mortality
All patients: 40% vs. 37% ; if >= 3 days was 53% vs. 43% 3 days NNT = 10 Predefined subgroup of patients staying in ICU at least 3 days. Excluded patients waiting for floor bed (taking > 2/3 diet p.o., no vital organ support) Small benefits for: creatinine; earlier weaning, earlier discharge from ICU and hosp. no change in infection. Reduced the risk of creatinine elevation, but not need for HD

Intensive insulin therapy and hypoglycemia
Average glucose 150’s with conventional Rx vs. 100’s with intensive insulin More hypoglycemia with intensive insulin, but no adverse clinical events Risk factors: ICU > 3 days, liver failure, dialysis Hypoglycemia was independent risk for death Hypoglycemia = < 40 Hypoglycemia no hemodynamic instability or Sz, most pt’s only had one episode Liver failure = transaminase > 250 Mortality = in-hospital

Intensive insulin therapy in the MICU: implications
Mortality benefit for patients in ICU > 3 days similar to benefit in surgical ICU But. . . Can’t predict length of ICU stay Higher mortality with insulin & ICU < 3 days A reasonable approach Aim for glucose <150 on ICU days 1-3 Consider goal of after day 3 Short ICU stay - may have been due to withdrawal of support, vs hyperglycemia may be adaptive early on in ICU, or insulin may cause stress Maybe early inc gluc is adaptive, or insulin is a metabolic stressor; some can’t respond w/ catechols A reasonable approach while we await more data. Good to avoid marked hyperglycemia. After day 3 - you have started feeds, which would protect agnst hypoglycemia.

Question #2 Do you initiate intensive insulin therapy in the ICU?
C. Yes, if he is likely to be in the ICU for > 3 days.

Case: Question #3 On hospital day 3, your patient has 4 loose stools and subsequent stool testing reveals C. difficile colitis. What risk factors might explain his developing C. difficile infection? Levofloxacin use PPI use Colonization with C. dif in the spore form Your washing your hands with an alcohol-based hand sanitizer

The new Clostridium difficile: what does it mean?
C diff colonization 3% healthy adults 20-40% hospitalized patients Metabolically inactive spore form until gut flora perturbed C diff virulence factors: toxins A and B 2 genes down-regulate toxin production Binary toxin mediates potency of toxins A and B Old pathogen that is emerging with increased virulence. Then converts to vegetative form that replicates, produces toxin

Outbreaks of C diff in health care facilities Loo VG
Outbreaks of C diff in health care facilities Loo VG. N Engl J Med 2005;353:2442. Prospective and case control studies of C diff outbreaks at 12 Quebec hospitals C diff: 2% of all admissions 7% in patients > 90 years Mortality with C diff 25% 30-day mortality Attributable mortality 7% 14% in patients > 90 years 1700 patients in an epidemic at 12 hospitals over 5.5 months Incidence, mortality due to C diff increased with patient age

Case control study: risk factors for C diff
Exposure Odds ratio for C diff Cephalosporins 3.8 Fluoroquinolones 3.9 Not associated with C diff: Other antibiotics Acid blockers, enteral feeding

Severe diarrhea associated with virulent strain
Two genetic mutations increased virulence Binary toxin gene Partial deletion of suppressor gene Severe diarrhea: 22/132 patients (17%) with mutations vs. 0/25 without All isolates susceptible to metronidazole, vancomycin More virulent strain based on genetic analysis - 84% of cases analyzed had these 2 mutations RESISTANT to quinolones

Implications:C diff may be evolving into a more severe disease
4X higher rate of C diff than in past years Prevention and control Barrier precautions Patient isolation Cleaning environment with sporicidal agents Handwashing - soap and water in addition to alcohol-based sanitizers Antibiotic restraint Look for epidemic strain Therefore focus on control, and early ID of outbreaks

Gastric acid suppression and the risk of community-acquired C diff Dial. JAMA. 2005;294:2989
Case control study - United Kingdom population database Not hospitalized in past year Factors associated with community-acquired C diff (adjusted risk) PPI: H2 blocker: 2.0 Only 37% had antibiotics in prior 90 dys Most labs won’t test for the epidemic strain, but it can be suspected based on incidence and severity of disease

Case: Question #3 On hospital day 3, your patient has 4 loose stools and subsequent stool testing reveals C. difficile colitis. What risk factors might explain his developing C. difficile infection? Levofloxacin use PPI use Colonization with C. dif in the spore form Your washing your hands with an alcohol-based hand sanitizer

Case: Question #4 In the ICU, your patient develops worsening hypoxia with stable infiltrates on chest x-ray. You suspect pulmonary embolism (PE), and you want to order a CT to evaluate. What is the best strategy to prevent contrast nephropathy? A. N-acetylcysteine B. Bicarbonate C. IV hydration, & hope he doesn’t develop CHF D. Hydrate, then lasix

Contrast Nephropathy Major causes of renal failure in the hospital
Prerenal, Medications Contrast Consequences of contrast nephropathy Prolonged hospitalization Need for hemodialysis Morbidity and mortality - especially with cardiac disease Oops, should have thought of this before the cardiac cath After cardiac cath, pt’s with ARF have 20% mortality rate

Risk factors for Contrast Nephropathy
Patient: Baseline renal insufficiency DM, CHF Anemia Hypertension, hypotension Age Contrast Amount Type Big risk factors: DM, CRI, hypovolemia High osmolality -> higher risk

Contrast Nephropathy Definition Incidence Pathophysiology
Creatinine increase by 25% or >= 0.5 mg/dl within 48 hrs of contrast Incidence % of all patients receiving contrast Pathophysiology Vasoconstriction -> renal ischemia Direct toxicity

Preventing Contrast Nephropathy: Meta-analysis of 59 trials Pannu, JAMA 2006;295:2765
Hydration NS superior to half NS 1 ml/kg X 6-12 hrs pre-procedure, 6-12 hrs post D5W with 3 amps NaHCO3 better than NS before cardiac cath 3 ml/kg X 1 hr pre-procedure, 6 hrs post Oral hydration works, but IV probably better Merten, JAMA. 2004;291:2328 Mueller, Arch Int Med. 2002;162:329 Unfortunately no large trials, and one comparing hydration to not, but we assume it’s good HCO3:Single center RCT in North Carolina Creatinine >= 1.1 Urine pH measured 1st void after infusion of bolus. No diuretics allowed. 13% vs. 2%

Preventing Contrast Nephropathy: What is the Evidence?
N-acetylcysteine Antioxidant Dose: 600 mg BID X 2 days Early evidence of dramatic benefit: 90% risk reduction vs. placebo (NEJM. 2000;343:180) Subsequent studies mostly favorable but less so Summary Well-tolerated May help Antioxidant: scavenges 02 free radicals, or enhances vasodilatory effects of nitric oxide 22 trials compared N-acetyl to placebo; 12 meta-analyses Start 1 day prior if possible

Preventing Contrast Nephropathy: Hemofiltration
Marenzi. NEJM 2003;349:1333 % Hemodialysis - no benefit (Am J Med 2001) and a second study 114 patients - Coronary interventions Hemofiltration: in ICU, 4-6 hr pre and hr post Problems: Criteria for hemodialysis Logistics of hemofiltration

Preventing Contrast Nephropathy: Summary of the Evidence
Yes Identify high-risk patients Avoid unnecessary contrast Hydration No Hemodialysis Fenoldopam Dopamine Diuretics Maybe Hemofiltration Acetylcysteine Theophylline Severe nephropathy - rare w/ < 100 ml contrast Theophylline - studies conflicting, design heterogeneous

Summary Recommendations
>= 2 risk factors for contrast nephropathy IV hydration before procedure Consider N-acetylcysteine Iso or low-osmolar contrast, minimize amount IV hydration after procedure Of course, monitor for fluid overload Nacetyl: or one study says vit C may work

Case: Question #4 What is the best strategy to prevent contrast nephropathy? Risk factors for contrast nephropathy? yes C. IV hydration

Case: Question #4 In the ICU, your patient develops worsening hypoxia with stable infiltrates on chest x-ray. You suspect pulmonary embolism (PE), but a chest CT is negative for PE. What do you do next? A. D-dimer B. LE doppler ultrasound C. Pulmonary angiography D. Conclude that PE is ruled out

Diagnostic tests for PE in the hospital
D-dimer: unhelpful low specificity in hospitalized or post-op patients, or with cancer Ultrasound: specificity > sensitivity 40% with DVT may have asymptomatic PE Angiography: gold standard, invasive CT: sensitivity for central PE high What about subsegmental PE’s? Sensitivity may be as low as 29% - significance? Angio: also low interobserver agreement for subsegmenal PE (45-66%)

Clinical Validity of a Negative CT with suspected PE: a systematic review Quiroz. JAMA. 2005;293:2012. Meta-analysis of 15 studies using CT to rule out PE 3500 patients, 7 nations Patient follow up 3-12 months After negative CT: Negative likelihood ratio of clot = 0.07 Negative predictive value: 99.1% No benefit to additional studies prior to CT 3 different CT techniques 15 deaths in follow up due to PE

Clinical Validity of a Negative CT with suspected PE? Yes!
Negative predictive value of CT (99%) compares favorably to: V/Q scan: 76-88% Pulmonary angiography: % Visualization of peripheral pulmonary arteries improving with better CT techniques A negative chest CT rules out PE No further testing needed

Case: Question #4 In the ICU, your patient develops worsening hypoxia with stable infiltrates on chest x-ray. You suspect pulmonary embolism (PE), but a chest CT is negative for PE. What do you do next? D. Conclude that PE is ruled out

Case Your patient spikes a temperature to 39 degrees. On exam BP is 140/80, heart rate 100. He has no localizing findings. He has a clean internal jugular line site but you are still concerned about central line infection. How do you make this diagnosis?

Question #5 Remove the catheter, culture the tip
Draw blood cultures peripheral and through the catheter Draw 2 peripheral blood cultures Any diagnostic approach is fine as long as I don’t need to replace the central line

Catheter-related bloodstream infection
High morbidity and mortality 12-27% mortality Prolong hospital stay by 1 week Clinical presentation - nonspecific Fever, +/- hypotension No other source Line site usually clean Increased risk with catheter > 7 days

Diagnosing intravascular device-related bloodstream infection
Remove the catheter Qualitative or quantitative tip culture or Keep the catheter Blood cultures through the catheter Catheter and peripheral blood cultures Differential time to positivity > 2 hours Paired quantitative cultures: 3-5 X higher concentration of organisms from catheter

Meta-analysis: Methods of diagnosing intravascular device-related bloodstream infection Safdar. Ann Intern Med. 2005;142;451. Highest sensitivity Qualitative cultures: catheter tip (90%) or through catheter (87%) Paired quantitative blood cultures (87%) Differential time to positivity (85%) Highest specificity Paired quantitative blood cultures (98%) Quantitative blood culture through catheter (90%) 51 studies

Summary: diagnostic tests for catheter-related bloodstream infection
Best test: Paired quantitative blood cultures Differential time to positivity also accurate and more widely available Only test when catheter infection suspected Positive predictive value of tests much higher with high clinical suspicion Avoids overuse of antibiotics 51 studies

Question #5 B. Draw blood cultures peripheral and through the catheter

Case Under your excellent care, your patient is ready to return home from the hospital. His medications on discharge are coumadin, atenolol, benazepril, atorvastatin, and omeprazole. As you handoff his care to his primary care doctor, what are the risks of a medication problem?

Question #6 None - you explained the regimen to him yourself
He has close primary care followup so he should be fine until his clinic appointment You are fine because of your system to meet the JHACO Patient Safety Goal to obtain and document the patient’s medications on admission, and discharge The risk is real and a medication discrepancy would increase his risk of readmission

JHACO National Patient Safety Goal #8: medication reconciliation
process during a transition in care comparing what medications the patient has been taking previously with the medications about to be provided Hospital admission and discharge: important transitions in care Discharge medication list must be communicated to the next provider of care (not just the patient)

Post Hospital Medication Discrepancies Coleman. Arch Intern Med
What are the prevalence and contributing factors associated with medication discrepancies - prehospital -> discharge -> meds actually taken after discharge What are risk factors for medication discrepancies? Are medication discrepancies associated with readmission?

Post Hospital Medication Discrepancies: study population
375 Adults >= 65 years old Admitted with common conditions likely to require discharge to skilled nursing facility CHF, COPD, CAD, DM, stroke, PVD, arrhythmia Back conditions, hip fracture Discrepancies = what was patient told vs. what was planned All community living adults

Categorizing Medication Discrepancies
Medication Discrepancy Tool (MDT) Meds assessed by NP hours after discharge to home Discrepancies Systems-based: doctor or system Patient-based: intentional or non-intentional Did they try to take it correctly? All community living adults

Medication Discrepancies
14% of patients 38% of those had > 1 discrepancy Average # meds: 9 with discrepancy vs. 7 without (p < .001) Common offenders (50% of discrepancies) Anticoagulants Diuretics, ACE inhibitors Lipid-lowering agents PPIs All community living adults

Causes of Medication Discrepancies
System (49%) Bad instructions Conflicting instructions Duplication Patient (51%) Nonintentional nonadherence (34%) $$ Intentional nonadherence Bad instructions - illegible, incomplete

Implications of Medication Discrepancies
30-day readmission rates higher with medication discrepancies (14% vs. 6%, p =.04) Transitions of care are a high risk time Medication reconciliation in the hospital won’t solve the problem Multiple interventions needed Post discharge follow up reconciliation Systems improvements Patient education

Question #6 D. The risk is real and a medication discrepancy would increase his risk of readmission

Take Home Points Acute coronary syndromes: clopidogrel plus ASA before PCI improves outcomes Insulin in the medical ICU: tight glucose control improves survival with ICU stay > 3 days Clostridium difficile: increasingly virulent, increasingly common in the hospital and community All community living adults

Take Home Points Contrast nephropathy: IV hydration for high risk patients PE: negative spiral CT rules out clinically important PE Diagnosing catheter-related infection: diagnose with paired catheter and peripheral quantitative cultures, or differential time to positivity Medication discrepancies: common after hospital discharge due to nonintentional non-adherence or systems problems All community living adults

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