Transcript Routine Daily Care of the Critically Ill: An Evidence

Daily Standard of Care For the
Critically Ill: An Evidence Based
Approach
David Aymond, PGY-II
4/4/13
Objectives
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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
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:
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APACHE-II score at admit
VTE prophylaxis
Stress Ulcer prophylaxis
Pressure Ulcer prophylaxis
Nutrition
Glucose control
Line Awareness/Infection Control/Antibiotic principles
Analgesia/Sedation
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.
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.
How to Interpret APACHE II Score
APACHE II Score
Mortality (MICU)
Mortality (SICU)
0-4
4%
1%
5-9
8%
3%
10-14
15%
6%
15-19
25%
11%
20-24
40%
29%
25-29
55%
37%
30-34
75%
71%
>34
85%
87%
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.
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.
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.
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:
Agent
Considerations
Mechanical
Sole agent only in high risk or
NS pts
Aspirin
Not rec as sole agent
Low-Dose Unfractionated
Heparin (LDUH)
Administer BID or TID; used in
AKI
Low-Molecular Weight
Heparin (LMWH)
Avoid in AKI; no monitoring
parameters available
Fondaparinux
Renally dosed
Oral direct thrombin inhibitor
Renally and hepatic dosed
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
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.
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%)
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.
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)
Stress Ulcer Prophy-Who Gets It and
What?
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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 vs PPIs: 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 vs Sucralfate: 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.
– Sucralfate vs 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)
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)
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
Pressure Ulcers-How Do We Fix Them
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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.
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?
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.
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)
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.
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.
Enteral vs Parenteral
• 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.
Do We Ever Use Parenteral?
• Only if there is a contraindication to enteral
feedings and the patient is malnourished
What are the Common Formulations
Used
Enteral Formulas
Description
Examples
Standard
Mimics American Diet; 5060% calories from carbs,
10%-15% from protein,
25%-40% from fat
Isosource, Osmolite, Boost,
Ensure
Concentrated
Similar to standard but
density per mililiter is
greater. Typically used for
patients with fluid
restrictions
Ensure Plus, Impact 1.5,
Twocal HN, Nutren Renal,
Nutren 2.0
High Protein
Contain > 15% of calories
Osmolite HN, Boost HP,
by protein or nitrogen.
Peptamen VHP, Ensure HP,
Typically used for pts with Promote
higher than normal protein
needs
Fiber Containing or
blenderized formulas
Contain fiber supplied from Jevity, Ensure with Fiber
added soy or natural food
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.
Glucose control in ICU
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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 vs euglycemic 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 80110mg/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.
Glucose Control in ICU
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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.
Current Glucose RecommendationsHow 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
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)
Infection Preventative Strategies
CABSI
•
CABSI (NEJM. 2006; 355:2725) (Infect Control Hosp Epidemiology 2008; 29:S22)
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Education, Training, and Staffing
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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
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•
•
•
•
•
•
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
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
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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)
CABSI (cont)
• Patient Cleansing
– Use a 2% chlorhexidine wash for daily skin cleansing to reduce CABSI
(II)
• Catheter Securement Devices
– Use a sutureless securement 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
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 nontunneled catheter if no evidence of infection is present (B-I)
• What Doesn’t Work?
1.
2.
3.
4.
5.
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
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
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
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
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.
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)
Nosocomial Transmission of MRSA
(Infect Control Hosp Epidemiol. 2008;
29:S62)
• Epidemiology
– >60% of hospital staph aureus infn 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”
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?
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
How to Enhance Anti-Microbial
Stewardship
1.
2.
Develop a team consisting of ID docs, etc,etc.
Prospective Audit with Intervention and Feedback
–
–
–
3.
Education
–
4.
Development of evidence based practice guidelines to guide therapy
Antimicrobial cycling
–
6.
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)
Guidelines and Clinical Pathways
–
5.
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)
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.
Antimicrobial order forms
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 deescalate 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 deescalation when possible
• Writing day numbers of anti-biotics
• Eliminating redundant combo therapy
• Think of fungal infections if cant find source (see fungal slide)
Anti-Microbial Stewardship (cont)
9. Dose Optimization
- Optimization of antimicrobial dosing based on
individual patient characteristics, causative
organism, site of infection (A-II)
10. 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)
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
Anti-Fungal Therapy in ICU
• Candidal spp 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)
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)
Analgesia (Cont’d)
Behavioral Pain Scale (BPS)
Facial Expression
Relaxed
Partially Tightened (brow
lowering)
Fully tightened (eyelid
closing)
Grimacing
1
2
Upper Limbs
No Movement
Partially Bent
Fully bent with finger flex
Permanently Retracted
1
2
3
4
Compliance with
Ventilation
Tolerating movement
Coughing, but tolerating
Fighting Ventilator
Unable to control Vent
1
2
3
4
3
4
Analgesia (Cont’d)
•
Treating Pain
– Principles:
•
•
•
•
•
•
•
Preventing pain is more effective than treating pain
Pain causes agitation  assessing and treating pain decreases need for sedative (Anesthesiology
2009; 111:1308)
Use IV administration b/c provides quick onset but shorter duration of effect
Control pain with basal pain meds (scheduled or continuous) with as needed doses for “breakthrough”
pain
Start with bolus dosing, if needing >3 boluses/hr, consider continuous infusion
All patients on opioids should receive a bowel regimen (e.g. docusate 100-200mg po BID)
Analgosedation: analgesics alone may be enough to provide adequate level of sedation, this is the
current recommendation by the major critical care societies: “Analgesia for sedation is preferred over
sedatives for sedation”; the analgosedation strategy uses morphine on a scheduled or continuous
dose with short course propofol boluses for persistent agitation (defined as not reaching sedation
scale goal). This shortens duration of MV, ICU LOS, and Hospital LOS (Lancet. 2010; 375:475)
- Pharmacologic Interventions
-Morphine has a half-life of 2-3 hours; intermittent dosing is 0.01-0.15mg/kg
q1-2 hrs; infusion dose is 0.07-0.5mg/kg/hr
*Fentanyl and Hydromorphone also have well established dosing regimens;
see table on following page
Analgesia Dosing with Opioids
Drug
Eqianalgesic
Dose
Half-life
Intermittent
dose
Infusion Dose
Fentanyl
200mcg
1.5-6 hrs
0.35-1.5
mcg/kg q0.5-1
hr
0.7-10
mcg/kg/hr
Morphine
10 mg
2-3 hrs
0.01-0.15
mg/kg q1-2 hr
0.07-0.5
mg/kg/hr
Hydromorphon 1.5 mg
e
3-7 hrs
10-30 mcg/kg
IV q 1-2 hr
7-15
mcg/kg/hr
Remifentanil
3-10 min
0.6-15
mcg/kg/hr
Sedation
• As mentioned in previous lecture, agitation is not equal to
“sedation deficiency”  search for causes of agitation; i.e.
hypoxemia, ETT malposition, discomfort from ETT, pain,
pneumothorax, GI or bladder distension, ventilator dys-synchrony
• Assessing the level of Sedation
– Use sedation scale to assess the level of sedation, there are 3
available:
• Richmond Agitation Sedation Scale (RASS)
• Riker Sedation-Agitation Scale (SAS)
• Ramsay Sedation Scale
*The Richmond Agitation Scale (RASS) has been validated in 2 separate studies
and is therefore the recommended sedation scale (Am J Respir Crit Care Med.
2002; 166:1338-1344; JAMA 2003; 289:2983-2991)
The Sedation scale is used to establish a target (i.e. Ramsay 3, RASS 0 to -1) and
you keep the patient at this target level of sedation, decrease amount of
sedative if over sedated, increase amount of sedative if undersedated/agitated. Reassess q4-6 hours.
Ramsay Sedation Scale
Score
Response
1
Anxious/Restless
2
Cooperative, oriented, tranquil
3
Responding to commands
4
Brisk response to stimulus
5
Sluggish response to stimulus
6
No response to stimulus
The Ramsay Sedation Scale is referenced in all major studies on sedation but has
Never been validated; by far is easiest to remember
Procedure for RASS Assessment
1.
2.
3.
Observe patient
A. Patient is alert, restless, or agitated
(Score 0-+4)
If not alert, state patients name and say to open eyes and look at speaker
B. Patient awakens with sustained eye opening and eye contact
(Score-1)
C. Patient awakens with eye opening and eye contact, but not sustained
(Score -2)
D. Patient has any movement in response to voice but no eye contact
(Score -3)
When no response to verbal stimulation, physically stimulate patient by shaking shoulder
and or rubbing sternum
E. Patient has any movement to physical stimulation
(Score -4)
F. Patient has no response to any stimulation
(Score -5)
Richmond Agitation Sedation Scale
Score
Term
Description
+4
Combative
Overtly combative, violent, immediate danger to
self
+3
Very agitated
Pulls or removes tubes or cahteters, aggressive
+2
Agitated
Frequent non-purposeful movement, fights
ventilator
+1
Restless
Anxious but movements not aggressive or
vigorous
0
Alert and Calm
-1
Drowsy
Not fully alert, but has sustained awakening (eye
opening/eye contact) > 10 seconds
-2
Light Sedation
Briefly awakens with eye contact to voice (<10
seconds)
-3
Moderate Sedation
Movement or eye opening to voice but no eye
contact
-4
Deep sedation
No response to voice, but movement or eye
opening to physical stimulation
-5
Un-arousable
No response to voice or physical stimulation
Principles of Sedation
• Use intermittent bolus rather than continuous infusion
(Chest. 1998; 114:541)
• If >3 boluses/hr, consider continuous infusion
• Preferred agents for sedation are currently Propafol (1st
line) and Dexmedetomidine (2nd line). Current
recommendations suggest avoiding benzodiazapines as
first or second line sedative agents (except in EtOH
withdrawal) b/c benzos are associated with higher rate
of delirium and prolonged mechanical ventilation (Crit
Care Med. 2006; 34:1326; JAMA. 2009; 301:489;
Anesthesiology. 2006; 104:21)
*See table on following slide for dosages of Sedatives
Selective Sedative Agents
Drug
MOA
Half-Life
Intermittent
Dose
Infusion Dose
Propafol
GABA a
40 mins
0.2-0.6 mg/kg
5-80
mcg/kg/min
Dexmedetomid CNS alpha 2
-ine
agonist
6 min
--
0.1-1.4
mcg/kg/hr
Haldol
Cns d1 and d2
18 hrs
2-10mg IV
0.04-0.15
mg/kg/hr
Midazolam
GABA a agonist
3 hrs
0.02-0.08
mg/kg
0.04-0.2
mg/kg/hr
Lorazepam
GABA a
8 hrs
0.02-0.06
mg/kg
0.01-0.1
mg/kg/hr
Recommendation Summary Slide
How is all of this put together? Analgosedation Idea:
-Analgesia should be addressed using scale and target should
be reached with bolus dosing morphine/fentanyl on a
schedule with PRN morphine or fentanyl for breakthrough.
If requiring more than 2-3 prn doses/hr or persistently not
at goal on scale, can switch to a continuous infusion of
morphine/fentanyl. This may be enough to reach Sedation
Scale Goal (Ramsay 2-3). If the patient is under-sedated,
use Propofol bolus, if needing more than 2 bolus/hour for
sedation goal, start infusion of propofol (if propofol
contraindicated, 2nd line is Dexmed). If you start Propofol,
stop the infusion of the morphine and go back to PRN. If
over-sedated, resume previous analgesia/sedation at ½
dose.
Principles of Sedation (cont)
• Sedation vacation is a term said frequently in
ICU. Another term for sedation vacation is the
Spontaneous Awakening Trial (SAT)
• Daily SAT shortens duration of mechanical
ventilation, Icu and hospital LOS (NEJM. 2000;
342:1471; Lancet. 2008; 371:126)
• See lecture on Sedatives and Analgesia for ICU
Patients: The Vanderbilt Guidelines
SAT
• How to perform SAT
Step 1: screen patient for: sedation given for EtOH
withdrawl, increasing agitation, paralytics, MI in 24
hrs, or elevated ICP. IF any present, do not perform
SAT
Step 2: Hold bolus analgesics/sedatives and/or stop
continuous infusions
Step 3: SAT passed if Ramsay 2-4 or RASS +1 to -2; SAT
fail= more agitated (Ramsay 1) than described OR
sedated than described by scale
*If pass SAT, proceed to SBT
How To Incorporate the SAT with the
SBT
• SAT= Spontaneous Awakening Trial
• Standardized protocol for SAT (Sedation
vacation) and if pass, assess for the SBT, and if
pass consider extubation
* See previous lecture on readiness testing,
weaning, and extubation
How Do We Assess This Daily?
• FAST HUGGS
– Feeding: can pt be fed orally? If not enterally? If not, should we
start TPN? Dietary consult for recs?
– Analgesia: pt should not suffer pain, but avoid excess; Analgosedation?
– Sedation: Ramsay 2-3, can they pass SAT? SBT?
– Thromboembolic prevention: should we use LMWH?
– Hardcore Antibiotic Stewardship: Sanfords Guide
– Ulcer Prophylaxis: H2 antagonist PO? Or IV? Wound care
consult upon admit for any wounds
– Glucose Control: goal <180 using IV insulin (sliding scale) or
Lantus
– Good Infection Control: CABSI, CAUTI, VAP, MRSA
– Scoring at admit: APACHE II score
Question?
• Would anyone want this as a check list on the
LSU-FP ICU note?
• Does the LSU-FP ICU note need changing?
• How does it need changing? Could it be more
user friendly?