Daily Standard of Care For the Critically Ill: An Evidence Based Approach

1. Daily Standard of Care For the Critically Ill: An Evidence Based Approach David Aymond, PGY-II 4/4/13

2. Objectives • Describe Predictive Scoring Systems in the ICU and how they are utilized • Establish who needs VTE prophylaxis in the ICU and the best form of VTE prophylaxis • Describe an evidence based approach to preventing and managing stress ulcers • Describe an evidence based approach to preventing and managing pressure ulcers • Establish who needs enteral nutrition in the ICU and common feeding management issues • Discuss glucose control in a MICU and SICU setting • Discuss prevention strategies for infections • Discuss anti-microbial stewardship recommended by the IDSA for critically ill patients • Provide evidence based approach to analgesia and sedation • Establish accepted sedation scale for LSU-FP • Discuss the possibility of a new ICU note that would be written by the residents as a group and then brought to faculty for approval

3. Purpose of the Lecture • Certain principles should be assessed on all ICU patients. I thought I would explain why, with evidence, these things should be addressed. • Those principles are: • APACHE-II score at admit • VTE prophylaxis • Stress Ulcer prophylaxis • Pressure Ulcer prophylaxis • Nutrition • Glucose control • Line Awareness/Infection Control/Antibiotic principles • Analgesia/Sedation

4. Predictive Scoring Systems in the ICU • Predictive scoring systems have been developed to measure the severity of disease and prognosis of patients in the ICU. These measurements are helpful for clinical decision making, standardizing research, and comparing quality of care across ICUs • Four validated scoring systems exist: Acute Physiologic and Chronic Health Evaluation (APACHE), SAPS, MPM, and SOFA. The APACHE score is widely used in the U.S. • Uses: facilitate evaluation of various interventions by ensuring that patients with similar baseline risks are being compared (VERY useful in ARDS and Sepsis trials); severity scores have also been used to manage hospital resources, assigning pt’s with lower severity scores to less expensive settings/treatments. • Limitations: cannot take into account individual disease mortality, suffers from “Lead time” bias, and must be periodically updated.

5. APACHE • Requires input of many clinical variables (lab values, age, vitals, GCS) from which a severity score is derived. • The APACHE II is the most commonly used scoring system in the U.S. 4 APACHE scoring systems exist: • APACHE II: rest of discussion • APACHE III: this allows for daily updates of clinical information and recalculates estimated mortality on a daily basis. Has greater predictive power than a single projection based upon the first 24 hours of ICU admission. Not widely accepted. • APACHE IV: Observational study of 110,588 consecutive ICU admissions found that APACHE IV predicted mortality more accurately than APACHE II and III and predicted ICU LOS accurately. Not widely accepted. • APACHE II calculator can be accessed on UpToDate, MedCalc, or just by googling (See UpToDate example). It gives a number. • The APACHE II severity score is based upon the worst variables during the initial 24 hours in the ICU.

6. How to Interpret APACHE II Score Also used in: Acute Pancreatitis: score > 8 meaning severe pancreatitis and 18% Mortality, if < 8, 4% mortality. The AGA uses this score to recommend diagnostic and treatment decision making. Sepsis: APACHE II >25 is indication for APC (XIGRIS); a score above 14 increases risk for candidal sepsis.

7. How to Use APACHE II Scoring System • This should be done on all patients in the ICU by inputting the worse values for each variable. This should be done within 24 hrs. A problem with the APACHE II is it can not be done on a daily basis, its only useful on initial admit.

8. Case Example • 43 y/o HIV patient with pyelonephritis admitted to the hospital floor. Her APACHE II score was 41 by the time she was seen the following day (for the second time). This allowed adequate communication between us as the critical care physician and the family. We were able to describe to the family that she had an 85% chance of mortality strictly based on these numbers, not taking into account her disease state (HIV and Sepsis). She had severe sepsis by definition (Mortality rate 50%). The family later decided to withdrawal care for numerous reasons. But, we were able to give them the most accurate information we had as to the chances of her surviving.

9. VTE Prophylaxis in ICU • Why? A pile of data exist but here is the nuts and bolts: • VTE is major cause of m & m • Most common cause of preventable in hospital death • Prophylaxis lowers mortality and morbidity rates nearly to 0! • Low rate of clinical bleeding with pharmacologic prophylaxis Options for VTE are summarized in the table below:

10. Who to Use VTE Prophylaxis On • Who needs VTE in ICU? • All patients, with the following caveats: • Neurosurgery patients, high bleeding risk, ICDs are effective. LMWH increases bleeding risk. • Renal impairment: LMWH cleared by the kidney and therefore not good option in renal failure, LDUH acceptable. • LMWH has lower incidence of HIT • Neuraxial analgesia increases risk for spinal/epidural hematoma, so go with mechanical prophylaxis Absolutely contraindicated in someone who is bleeding

11. Stress Ulcers • Epidemiology • 15% of all patients in ICU • Can cause perforation, but only 1% Pathophysiology: There are 2 types, Early and Late. Early begins in the proximal regions of the stomach within HOURS of serious illness. *Endoscopy performed in 72 hours shows acute mucosal abnormalities in >75% of pts. 50% of those have evidence of bleeding. Late occur in duodenum. *Recent study of 67 pts with GI bleeding that occurred an average of 14 days after admission, showed the duodenum to be the most common site. Rather early or late stress ulcerations, they both result from the same mechanisms 1. Impaired Mucosal Secretion: the stomach is normally protected by a glycoprotein layer that forms a physical barrier to hydrogen ion diffusion and traps bicarbonate. The bicarbonate neutralizes gastric acid adjacent to the stomach wall. This barrier may be denuded by increased concentrations in bile salts and uremic toxins, which are common in critically ill pts. In addition, the glycoprotein synthesis is decreased when there is poor gut perfusion in shock or sepsis.

12. Stress Ulcers-Pathophysiology (cont) 2. Hypersecretion of Acid: acid secretion increased in head trauma • H. pylori infection may also contribute. A case control study of 149 ICU pts showed that GI bleeding was more common in H. pylori positive patients (36% versus 16%)

13. Stress Ulcers-Why is Prophylaxis Important • GI bleeding due to stress ulceration is associated with increased mortality. In a prospective cohort study of 2,252 pts, mortality was higher among ICU patients with clinically important GI bleeding than among those without (49% vs 9%). Clinically important GI bleeding was defined as overt GI bleeding leading to hemodynamic compromise or requiring blood transfusion.

14. Stress Ulcer Prophylaxis-Risk Factors • Who should be treated depends on the presence of risk factors: • In the aforementioned multicenter prospective cohort study of 2,252 patients, the biggest risk factors for stress ulceration were mechanical ventilation >48 hrs (odds ratio 15.6) and coagulopathy (coagulopathy defined as platelets <50, INR >1.5, PTT 2x normal) (odds ratio 4.3) • Other risk factors have been identified by smaller studies and include major and minor: 1. Major: GI bleeding within a year, GI ulceration within a year, traumatic brain injury, traumatic spinal cord injury, severe burns (>35% of body) 2. Minor: sepsis, ICU admission > 1 week, occult GI bleed lasting >6 days, or high dose glucocorticoid therapy (>250mg Hydrocortisone)

15. Stress Ulcer Prophy-Who Gets It and What? • If any major RF or 2 minor, that is an indication for prophylaxis. • Efficacy of Agents available • The common agents used are H2 blockers, PPIs, Antacids, and Sucralfate. • H2 blockers vsPPIs: a meta-analysis of 13 randomized trials (1,587 pts) found less GI bleeding among those who received PPI (1.3% vs 6.6%). • H2 Blockers vs Antacids: A meta-analysis found the H2 blocker group had a lower rate of overt GI bleeding • H2 Blockers vsSucralfate: A trial randomly assigned 1200 mechanically ventilated pts to receive sucralfate via NG or an H2 blocker (ranitidine). The H2 blocker decreased overt GI bleeding compared to sucralfate (1.7% vs 3.8%). But sucralfate arm had less pneumonias. • Sucralfatevs Antacids: equal Therefore, current recommendations are as follows: • For ICU pts who are able to receive enteral medications and in whom stress ulcer prophylaxis is recommended, an oral H2 Receptor Antagonist (Famotidine (40mg PO daily) or Ranitidine (150mg PO BID)) • For ICU pts who cannot receive enteral medications and in whom stress ulcer prophylaxis is indicated, IV H2 Blocker is preferred (Ranitidine 50mg IV q6 hours OR Famotidine 20mg IV q12)

16. Stress Ulcer Prophy-General Principles and Economic Considerations • General Principles: • Enteral nutrition, when possible, alone decreases GI bleeding but is not adequate as a sole measure. This was shown in an observational study performed using data from a randomized trial, enteral nutrition independently reduced overt GI bleeding (RR 0.30) in 1,077 critically ill pts who were mechanically ventilated. Another study of 526 pts in a burn ICU found that the incidence of GI bleeding was lower among pts who received early enteral nutrition alone versus pts who received an H2 blocker alone (3% vs 8%) • H2RAs and PPIs both may increase the rate of nosocomial pneumonia, but there is no difference between the 2. There is no concrete evidence they increase the rate of nosocomial pneumonia. All current recs suggest the agent chosen for prophylaxis should be based on the more definitive medicine-impact on overt GI bleeding- until the relationship between the type of prophylactic agent and the incidence of pneumonia is confirmed. • Economic Considerations: • H2RAs and PPIs are major budget items for our institutions b/c many pts receive them unnecessarily; Treat only those at risk and stop treatment when no longer at risk • Use Enteral rather than IV formulations whenever the gut is functional • use H2RAs over PPIs for most patients (more cost effective with little to no outcome difference)

17. Pressure Ulcers Below is a summary from a JAMA article on pressure ulcers in critical care (JAMA. 2006; 296:974) • Incidence of all acute care settings are anywhere from 0.4% to 38% • Increases risk for infection, pain, and delayed functional recovery • Prolongs hospital stay and associated significant cost of treatment • Now targeted by CMS and other payment agencies • Overall paucity of good clinical trials data in field complicates prevention and management strategies Pathogenesis -Prolonged pressure between a bony prominence and an external surface leads to impaired capillary blood flow and subsequent tissue injury (JAMA. 2003; 289:223). The subsequent ulceration can develop in as little as 2-6 hours. Risk Factors -Numerous; malnutrition and incontinence are 2 of the many

18. Pressure Ulcers-How Do We Fix Them • Current data suggest a one time assessment of risk for a pressure ulcer (termed Braden Scale), a higher score confers a lower risk of ulcer. Then a standard measure is instituted for all at risk patients starting at time of admit. Also, daily skin assessment and documentation by a nurse (wound care or ICU). • Specific Interventions • Minimize immobility by aggressive early physical therapy and ambulate ventilated patients • Patient position: repositioning every 2 hours, but must avoid friction and shear forces during moving (meaning the pt must be completely elevated from touching all surfaces or rolled) • Specialized support surfaces: see table (boring) • OPTIMIZE NUTRITION: full caloric intake with optimum protein balance, THERE IS NO EVIDENCE TO SUPPORT ANY PARTICULAR PROTEIN SUPPLEMENT IN THE ABSENCE OF KNOWN DEFICIENCY • Moisture and incontinence management: BARRIER CREAMS, goal is to keep skin clean and dry • Skin care: dry skin is a risk factor and moisturizers help; vigorous rubbing of the skin harms the patient **I recommend consulting wound care on all patients going into ICU, they are here all day and are getting paid, we do not increase cost by consulting them. Actually its quite the opposite: we make a pile of money off of them.

19. Nutrition Support in the Critically Ill • There are several questions generated when considering feeding: 1. Who should receive nutrition support, what are indications? Define Malnourished? Define who we cant use the gut on? 2. Does early and adequate nutrition actually change outcomes? 3. Is enteral or parenteral feeding better? Is parenteral ever useful? 4. What are the common formulations we feed ICU patients? Which formulations are used in specific pt populations? How do we calculate the rate? 5. What are the potential complications of feeding?

20. Nutrition Support in the Critically Ill: Who Should Receive Nutrition Support • Nutrition support should be provided to the following patients: Only if the pt will not be able to eat for >2 days • If the pt has no contraindication to enteral feeding, begin early enteral feeds (early defined as <48 hours) b/c the potential benefits of early enteral feeding (eg, fewer infections, lower mortality) outweigh its risks. • If the pt is adequately nourished but has contra-indications to enteral feeding, TPN should not be started. Instead D5 containing IVF. This reflects the evidence that early parenteral nutrition increases risk of infection, prolongs mechanical ventilation, increases ICU LOS and hospital LOS. • If malnourished and there is a contraindication to enteral feeding, TPN should be started. It is well recognized that effects of TPN in malnourished pts is unknown, but it is felt that failure to treat the malnourishment will result in a progressive caloric deficit, which increases morbidity. If you expect the pt to eat in 2 days, and they are not malnourished, just start D5 containing IVF If you expect the pt to eat in 2 days, and they are malnourished, still begin enteral *To summarize, all pts should be given enteral nutrition if they cant eat for 2 days; If they can eat in 2 days and are malnourished, still give enteral feeds. If contraindication to enteral feeds, and nourished give D5 containing IVF, if malnourished give TPN.

21. How Do We Define Malnourished • All studies defined Malnutrition as a premorbid BMI <18.5, >10% weight loss over 6 mos or >5% weight loss in the past month; also can calculate % of ideal body weight • Easier way to define: It is reasonable to assume that malnutrition is impending in any patient who has had little or no nutritional intake for 2 weeks. • Use Pre-albumin, transferrin, and albumin as surrogate markers. Although they are prone to change based on the effects of the critical illness. • Pre-Albumin: <20 decreases acutely in 2 days (t ½ 2 days) • Transferrin: decrease in malnutrition (t ½ 8-10d) • Albumin: <5 decrease with chronic malnutrition (t ½ 20 days)

22. What are the Contraindications to Enteral Feeds • Early enteral nutrition is contraindicated in critically ill patients who are both hemo-dynamically unstable and have not had their intravascular volume fully resuscitated, since those pts are predisposed to bowel ischemia. • Also, bowel obstruction, severe and protracted ileus, major upper gi bleed, intractable vomiting or diarrhea, severe hemodynamic instability, GI ischemia, and high output fistula. **The absence of bowel sounds or flatus following colorectal surgery or surgery for bowel perforation is NOT a contraindication. This has been shown in 5 studies.

23. Does Early and Adequte Nutrition Change Outcomes • Enteral and Parenteral nutrition appear to confer different clinical outcomes in critically ill patients. Parenteral has only shown an increase in infections, and that’s it. Early is defined as feeding in 48 hours. All of the following studies were performed on adequately nourished patients: • Enteral: • Infection: A meta-analysis of 3 randomized trials (133 pts) found a clinically important and statistically significant reduction in infection when enteral nutrition is started early compared to late enteral nutrition or dextrose containing IV fluids (25% vs 41%). In an unpublished update of the meta analysis, seven randomized trials (440 additional patients) were added and the reduction of infectious complications become more statistically significant. • Mortality: In a meta analysis of 8 randomized trials (317 pts) that compared early enteral nutrition to either delays enteral or IV fluids, there was a non statistically significant mortality reduction among the pts who received early enteral nutrition (6% vs 15%). In an unpublished update of the meta-analysis, 14 randomized trials (670 additional pts) were added. The reduction in mortality was almost statistically significant (10% vs 20%). Meaning there is a clinically important and and almost statistically significant reduction in mortality.

24. EnteralvsParenteral • When the 2 forms are analyzed against each other, Enteral has lower infection rates. But, Enteral and Parenteral have no mortality differences when started early. But TPN is associated with longer ICU stay, longer Hospital stay, and prolongs mechanical ventilation. • Enteral with Parenteral supplementation: in a multicenter trial with 4,640 pts who were already receiving enteral nutrition, these pts were randomized to receive supplemental TPN early or late. In both groups, addition of TPN had higher infection rates, longer duration of mechanical ventilation, ICU stay, and hospitilization. There was also increased mortality compared to the enteral nutrition alone.

25. Do We Ever Use Parenteral? • Only if there is a contraindication to enteral feedings and the patient is malnourished

26. What are the Common Formulations Used

27. How Do We Calculate the Rate? • Nutritional goal is 18 kcal of calories/kg per day and 1.5 grams of protein/kg per day. • Look up formulations at hospital and make calculations OR just consult dietary.

28. Glucose control in ICU • Hyperglycemia is associated with poor clinical outcomes in critically ill patients. Over and over again this has been shown. Way too much data exist that shows adverse outcomes in hyperglycemic critically ill pts vseuglycemic critically ill pts to not control on ALL patients. We just need to decide if there needs to be intense control (goal <110) or Normal control (goal <180) • The seminal randomized study treating hyperglycemia in critically ill patients was published by Van den Berghe et al. in 2001 and included 1,548 intubated patients (13% with known diabetes) in a SICU who ere randomly assigned to intensive glycemic control with a target glucose between 80-110mg/dL (n=765), versus a standard care group that was treated with insulin when the blood glucose was >215mg/dL, with a target glucose between 180-200mg/dL (n=783). The study found that the intensive care mortality rate was 42% lower (8% vs 4.6%, p <0.04) in the intensive treatment group, with the benefit reaching statistical significance in pts who remained in the ICU for > 5 days. • The same guy then repeated the same exact study in the MICU. The study did not replicate the mortality benefit seen in the SICU study. Despite no overall mortality benefit, there was reduced morbidity in the intensive treatment group, including less newly acquired AKI, reduced duration of mechanical ventilation, shorter ICU stay, and shorter hospital stay. • In both trials, hypglycemic episodes were increased in the intensive treatment group. Despite this extremely high incidence of hypoglycemia, serious immediate side effects such as seizures and hemodynamic compromise were not reported. However, hypoglycemia was identified as an independent risk factor for death in the MICU group!! Although, this was not observed until 24 hours after the episode. A very large methodological flaw in these studies were in the SICU study, arterial blood was analyzed, in the MICU study, POC glucometers and capillary glucose.

29. Glucose Control in ICU • Brunkhorst et al., did a trial with the same parameters and only found an increased incidence of severe hypoglycemia and serious adverse events. There was no difference in 28 day mortality or mean organ failure. • More recently, the NICE-SUGAR study randomized critically ill (SICU and MICU) pts who were in the ICU for >3 days to an intensive arm and conventional arm in a multinational randomized trial. They found that severe hypoglycemia was more common in the intense control group and that 90 day all cause mortality was increased. The conclusion here was a BG target of 180 mg/dL or less resulted in lower morbidity and mortality compared to a more aggressive glucose control target. • The benefits seen in the SICU study by Van den Berghe were never reproduced. The theory for this is that there was higher mortality in the control group b/c the majority of them were using early PARENTERAL nutrition which increased their mortality from blood stream infections. • To summarize, the current available data suggest MICU and SICU pts who ae in the ICU more than 3-5 days are most likely to benefit from a lower target range, but mortality benefit is lessened or eliminated when hypoglycmic events increase.

30. Current Glucose Recommendations-How to Put It All Together • In critically ill pts admitted to the ICU, all oral anti-hyperglycemic should be stopped. • Insulin should be given and all Insulin should be administered IV, which allows for the rapid reversal of hypoglycemia. Rapides has an insulin infusion protocol that is validated and commonly used in other ICU’s. • Currently, the consensus is to minimize the use of glucose containing IV fluids and only use insulin when needed (sliding scale). No data exists on the use of Lantus in ICU. • Recommended target BG for Diabetic and Non-Diabetic ICU pts • American Diabetes Association <180-200mg/dL • American College of Endocrinology <180mg/dL • Surviving Sepsis Campaign <150mg/dL

31. Infections in ICU • CABSI=Central Venous Catheter Associated Blood Stream Infection • VAP= Ventilator Associated Pneumonia • CAUTI= Catheter Associated UTI • Nosocomial Transmission of MRSA • The following slides on CABSI are based on the paper titled “Guidelines for the Prevention of Intravascular Catheter-related Infections” published by the IDSA based on journal CID 2011:52 (May 1)

32. Infection Preventative StrategiesCABSI • CABSI (NEJM. 2006; 355:2725) (Infect Control Hosp Epidemiology 2008; 29:S22) • Education, Training, and Staffing • Institution wide, standardized education: indications for CVC, proper sterile technique, site maintenance, hub access technique) for all personnel placing and maintaining the CVC (A-I) • Observer to say who broke sterile field, empower to stop procedure • Ensure appropriate nursing, there is a higher observation of CABSI in ICUs where nurses are managing patients with CVCs (A-I) • Selection of Sites • Avoid Femoral site, replace a catheter inserted in a lower extremity site to an upper extremity site as soon as possible (except in Pedi, where femoral is preferred) (category II) • Use a midline catheter or PICC, if CVC contraindicated and duration of IV therapy will exceed 6 days (II) • Evaluate the insertion site daily by palpation through the dressing to discern tenderness and by inspection if transparent dressing is used. Gauze and opaque dressings should not be removed if the pt has no clinical signs of infection. (Category II) • Remover peripheral venous catheters if signs of phlebitis or malfunctioning (B-I) • Avoid the subclavian site in dialysis pts and in advanced CKD, to avoid subclavian vein stenosis • Use US guidance to place CVC to reduce the number of cannulation attempts and mechanical complications. • When adherence to aseptic technique cannot be ensured (i.e. catheters inserted during an emergency), replace the catheter with in 48 hours (B-I) • Hand Hygiene and Aseptic Technique • If you touch a catheter, wash your hands before and after and wear gloves

33. CABSI (cont) • Maximal Sterile Barrier Precautions • Use cap, mask, sterile gown, sterile gloves, and sterile full body drape for the insertion of CVCs, PICCs, or guidewire exchange (B-I) • Use a sterile sleeve on the ultrasound to protect aseptic technique (B-I) • Skin Preparation • Prepare clean skin with a >0.5% chlorhexidine preparation with alcohol before CVC and Art line insertion and during dressing changes (A-I) • Antiseptics should be allowed to dry before proceeding (B-I) • Catheter Site Dressing Regimens • Use either sterile gauze or sterile transparent dressing to cover the catheter site (A-I) • If the site is bleeding or oozing, use a gauze dressing until this is resolved (II) • Replace catheter site dressing if the dressing becomes damp, loosened, or visible soiled (B-I) • DO NOT submerge in water, showering can be permitted if site is protected with impermeable dressing • Replace gauze dressings on CVC q2 days • Replace transparent dressings q7 days • Monitor cath sites visually when changing the dressing or by palpation through an intact dressing on a regular basis. If pts have TTP at site, fever without a source should have dressing removed to allow thorough exam of the site (B-I)

34. CABSI (cont) • Patient Cleansing • Use a 2% chlorhexidine wash for daily skin cleansing to reduce CABSI (II) • Catheter Securement Devices • Use a suturelesssecurement device (II) • Antimicrobial Impregnated Catheters • Only if CABSI present after all other measures • Systemic Abx Prophylaxis • NEVER • Antibiotic/Antiseptic Ointments • NEVER, unless hemodialysis port • Antibiotic Lock Prophylaxis, Antimicrobial Catheter Flush and Catheter Lock Prophylaxis • Only if long term cath who have a h/o multiple CABSI

35. CABSI (cont) • Replacement of CVCs, Including PICCs and Hemodialysis Catheters • Do not remove CVCs or PICCS on the basis of fever alone (II) • Do not use guidewire exchanges to prevent infection or if there is suspected infection (B-I) • Use a guidewire exchange to replace a malfunctioning non-tunneled catheter if no evidence of infection is present (B-I) • What Doesn’t Work? • Antimicrobial ointment at CVC insertion site (except dialysis) • Placement of PICCs rather than CVC (infection rate is same) • Systemic AB prophy • Routine BC drawing • Routine catheter replacement

36. CABSI • How do we use all that info: • Institute our current educational requirements to place CVCs, appoint “boss” of each procedure to stop if aseptic technique broken, help nurses if busy by assessing dressing sites • Avoid Femoral site, use only IJ or Subclavian with U/S guidance • If CVC placed in ER and we are not sure of aseptic technique (i.e. trauma case) change the catheter over a guidewire within 48 hours • Wash our hands before and after • Full sterile clothing for all involved, that includes guidewire exchanges • Only use Chlorhexidine prep for procedures and let it dry • Do not need antibiotic impregnated wheel • Cover the site with sterile gauze or sterile transparent dressing; change that dressing if its soiled, loose, or damp; If site is bleeding or oozing, use gauze until resolved • Replace gauze q2 days and transparent q7 days

37. VAP • Ventilator Associated Pneumonia (VAP). Data below from Infect Control Hosp Epidemiol. 2008;29:S31) • This is defined as pulmonary parenchymal invasion by a microorganism in a patient receiving mechanical ventilation for more than 48 hrs. • Pathogenesis: Inoculation of the formerly sterile lower respiratory tract by aspiration of oral secretions, colonization of the respiratory tract with pathogenic organisms, and the use of contaminated respiratory equipment/medications (breathing treatments). • Rates are 10/1,000 ventilator days and is associated with 10% mortality; VAP results in prolonged mechanical ventilation, increased hospital stay, and increased cost

38. How to Lower Rates of VAP • There are 2 groups of specific interventions shown to lower VAP rates • Interventions to Minimize Duration of Mechanical Ventilation (see previous lecture on mechanical ventilation for more details) • Utilize NIPPV when possible • Daily readiness testing for extubation • Use of weaning protocols • Daily sedation interruption • Interventions to Minimize Microaspiration and Lower Respiratory Tract Contamination • HOB >30 degrees at all times • Maintain ETT cuff pressure of 20 cm H20 • Daily oral care with chlorhexidine mouthwash (Peridex) • AVOID UNPLANNED EXTUBATION AND REINTUBATION If pt gets VAP, see Sanfords Guide to Antimicrobial Therapy for treatment recommendations

39. CAUTI • Catheter Associated UTI (CAUTI) • There is an over whelming number of ICU pts who have foley catheters. Do they all need one? • UTIs are the most common hospital acquired infection, and 80% are in catheterized patients • Risk factors for CAUTI: old age, woman, length of use, and failure to maintain a closed drainage system.

40. CAUTI: How to Prevent • This is data from a large study published in Infection Control Hospital Epidemiology. 2008; 29;S41 • The following are the suggested ways to decrease the number of catheters placed and UTIs • Define indications for foley; utilize bladder scanners and straight cath techniques if no indication for long term OR if urinary retention • Promote timely removal by making it part of the daily review on rounds by physicians • When accessed for urine studies, instruct nurse to use proper hand hygiene prior to system manipulation • Things that do NOT help in decreasing the rates of UTI and should not be done • Routine use of antimicrobial or silver impregnated catheters • Routine urine culture of asymptomatic patients • Routine treatment of asymptomatic bacteriuria (how do you know in pinecrest patients?) • Routine systemic antibiotics for prophylaxis • Routine change of catheter on a set schedule • Continuous bladder irrigation with an antimicrobial (as a preventative measure)

41. Nosocomial Transmission of MRSA(Infect Control Hosp Epidemiol. 2008; 29:S62) • Epidemiology • >60% of hospital staph aureusinfn are MRSA • MRSA infection associated with higher mortality, longer length of stay, and higher cost of care compared to MSSA infn • Why do the nasal swabs for MRSA? • Colonized pts are at a 29% increased risk of developing active MRSA infection within 18 mos • Colonized patients infect their environment, then healthcare workers spread this infected environment to all other patients via unclean hands • If pt is MRSA nasal swab positive, the CDC recommends: “contact precautions indicated for these patients: private room (cohort if not available), gown and gloves to enter room, removal of gown and gloves before exiting room, and strict hand hygiene before and after patient contact”

42. Current Recommendations to Decrease MRSA Rates • Daily cleaning of MRSA infected patients equipment, with very close attention to high touch areas (bed rails, commodes, door handles, carts) • Dedicate “MRSA Equipment” when possible (i.e stethoscopes, beds, vents, etc) • The aforementioned journal article showed a decrease in MRSA infections and transmission when pts were bathed daily in chlorhexidine. This was later validated by a separate study that showed the same thing. Should this be an institutional protocol for RRMC?

43. IDSA Guidelines to Enhance Antimicrobial Stewardship (CID 2007) • Anti-Microbial stewardship refers to “an activity that leads to appropriate selection, dose, route and duration of anti-microbial therapy”. Why does the IDSA feel this topic is important? All information is from IDSA guideline • Many studies have demonstrated worse outcomes if there is a delay in antibiotic administration (30 min- 4 hrs) • Anti-microbial stewardship has been shown to limit the emergence and transmission of anti-microbial resistance. Also, has been shown to reduce health care costs without adversely impacting quality of care • Effective anti-microbial stewardship has consistently demonstrated a decrease in use (22%-36%) with annual savings ranging from $200,000 to $900,000 (A-II) in both larger academic hospitals and smaller community hospitals • The following recommendations are from acute care hospitals, most of the studies have focused on adults in the ICU

44. How to Enhance Anti-Microbial Stewardship 1. Develop a team consisting of ID docs, etc,etc. 2. Prospective Audit with Intervention and Feedback • Audit of antimicrobial use with direct interaction and feedback to the prescriber, can result in reduced inappropriate use of antimicrobials (A-I) • Formulary Restriction • Formulary restriction can lead to immediate and significant reductions in anti-microbial use and cost (A-II) 3. Education • Education is considered to be an essential element of any program designed to influence prescribing behavior and can provide a foundation of knowledge that will enhance and increase the acceptance of stewardship strategies (A-III). However, education alone, without active intervention, is only marginally effective and has no sustained impact (B-II) 4. Guidelines and Clinical Pathways • Development of evidence based practice guidelines to guide therapy 5. Antimicrobial cycling • There are insufficient data to recommend the routine use of antimicrobial cycling as a means of preventing or reducing antimicrobial resistance over a prolonger period of time (C-II). Substituting one antimicrobial for another may transiently decrease selection pressure and reduce resistance to the restricted agent. Unless the bug has been eliminated from the bacterial population, however, reintroduction of the original antimicrobial is again likely to select for the expression of the resistance in the exposed bacterium. 6. Antimicrobial order forms

45. Anti-Microbial Stewardship (cont) 7. Combination therapy • There are insufficient data to recommend the routine use of combination therapy to prevent the emergence of resistance (C-II). Combination therapy does have a role in certain clinical contexts, including use for empirical therapy for critically ill patients at risk of infection with Multi drug resistant pathogens, to increase the breadth of coverage and the likelihood of adequate initial therapy (A-II) 8. De-escalation of therapy: De-escalating anti-biotics is important b/c we know the largest risk factor for anti-microbial resistance is high rates of previous exposure to broad spectrum antibiotics, especially in patients with high rates of co-morbid conditions (Pinecrest). It is essential to de-escalate antibiotics as the clinical situation evolves. How do we de-escalate? • Stopping anti-biotics when we are sure there is no infection • Tailoring anti-biotics once infecting organism known (i.e should not say “weve already started Vanc and Zosyn for HCAP, so should finish the course”) • Daily assessment of antibiotic use on rounds with daily recommendations for de-escalation when possible • Writing day numbers of anti-biotics • Eliminating redundant combo therapy • Think of fungal infections if cant find source (see fungal slide)

46. Anti-Microbial Stewardship (cont) • Dose Optimization - Optimization of antimicrobial dosing based on individual patient characteristics, causative organism, site of infection (A-II) • Parenteral to Oral Conversion - Switch to oral antimicrobials with excellent bioavailabilty when the patients condition allows can decrease LOS and health care costs (A-I)

47. What Does Our Program Do With These Recommendations • Use the resources available to us by our pharmacy and open communication with the ID physicians available (Dr. McLemore) • Have a team on alpha, consisting of 3rd year and staff, who review anti-microbial use on all ICU patients during rounds • That team make recommendations to all alpha residents from Sanfords Guide to Antimicrobial Therapy each day on rounds. Also, provide that pocket guide to each resident • Follow formulary restrictions provided by our pharmacy, they are based in evidence and our local resistance patterns • Assess daily the possibility of de-escalation and parenteral to oral conversion

48. Anti-Fungal Therapy in ICU • Candidalspp are far and away the most common fungal infections in the ICU, with aspergillus and zygomycoses occurring in SEVERELY IMMUNOCOMPROMISED patients • There are some patients who are at a much higher risk for fungal infections and MAY benefit from empiric anti-fungal therapy when presenting with Sepsis. Those risk factors for candida blood stream infection are: • TPN • GI Surgery or bowel disruption • Neutropenia/high dose steroids/hematologic malignancy/bone marrow transplant • Previous exposure to broad spectrum antibiotics • High APACHE score (>8)

49. Current Guidelines for Analgesia and Sedation in the Critically Ill • Pain/Analgesia • Pain assessment and control is associated with shorter duration of MV, ICU LOS, and VAP (anesthesiology, 2009; 111:1308) • Assessment is best utilized by establishing a target for patient comfort and use a pain scale to determine if pain is at target • Interactive patients: Numerical Rating Scale or Wong-Baker Visual Scale (face scale) • Non-Interactive patients: • Behavioral Pain Scale (BPS)=12 point scale; 0 points=no pain; 12 points=severe pain. Validated by a study published in Crit Care Med. 2001; 29:258. • Surrogate raters/family members=ask a family member “are they in pain”, this was done and published, the outcome of the trial showed that family members were 80% sensitive and 67% specific assessing pain (Crit Care Med.2000; 28:1347)

50. Analgesia (Cont’d)Behavioral Pain Scale (BPS)