post resuscitation cardiac care

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POST resuscitation cardiac arrest careThere is increasing recognition that systematic postcardiac arrest care after return of spontaneous

circulation (ROSC) can improve the likelihood of patient survival with good quality of life. This is

based in part on the publication of results of randomized controlled clinical trials as well as a

description of the postcardiac arrest syndrome.13Postcardiac arrest care has significant potential

to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from

multiorgan failure and brain injury.3,4 This section summarizes our evolving understanding of the

hemodynamic, neurological, and metabolic abnormalities encountered in patients who are initially

resuscitated from cardiac arrest.

The initial objectives of postcardiac arrest care are to

Optimize cardiopulmonary function and vital organ perfusion.

After out-of-hospital cardiac arrest, transport patient to an appropriate hospital with a

comprehensive postcardiac arrest treatment system of care that includes acute coronary

interventions, neurological care, goal-directed critical care, and hypothermia.

Transport the in-hospital postcardiac arrest patient to an appropriate critical-care unit

capable of providing comprehensive postcardiac arrest care.

Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest.

Subsequent objectives of postcardiac arrest care are to

Control body temperature to optimize survival and neurological recovery

Identify and treat acute coronary syndromes (ACS)

Optimize mechanical ventilation to minimize lung injury

Reduce the risk of multiorgan injury and support organ function if required

Objectively assess prognosis for recovery

Assist survivors with rehabilitation services when required

Previous SectionNext SectionSystems of Care for Improving PostCardiac Arrest Outcomes

Postcardiac arrest care is a critical component of advanced life support (Figure). Most deaths occur

during the first 24 hours after cardiac arrest.5,6The best hospital care for patients with ROSC after

cardiac arrest is not completely known, but there is increasing interest in identifying and optimizing

practices that are likely to improve outcomes (Table 1).7 Positive associations have been noted

between the likelihood of survival and the number of cardiac arrest cases treated at any individual
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hospital.8,9Because multiple organ systems are affected after cardiac arrest, successful postcardiac

arrest care will benefit from the development of system-wide plans for proactive treatment of these

patients. For example, restoration of blood pressure and gas exchange does not ensure survival and

functional recovery. Significant cardiovascular dysfunction can develop, requiring support of blood

flow and ventilation, including intravascular volume expansion, vasoactive and inotropic drugs, and

invasive devices. Therapeutic hypothermia and treatment of the underlying cause of cardiac arrestimpacts survival and neurological outcomes. Protocolized hemodynamic optimization and

multidisciplinary early goal-directed therapy protocols have been introduced as part of a bundle of

care to improve survival rather than single interventions.1012 The data suggests that proactive

titration of postcardiac arrest hemodynamics to levels intended to ensure organ perfusion and

oxygenation may improve outcomes. There are multiple specific options for acheiving these goals,

and it is difficult to distinguish between the benefit of protocols or any specific component of care

that is most important.

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FigurePostcardiac arrest care algorithm.

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Table 1Multiple System Approach to PostCardiac Arrest Care

A comprehensive, structured, multidisciplinary system of care should be implemented in a consistent

manner for the treatment of postcardiac arrest patients (Class I, LOE B). Programs should include as

part of structured interventions therapeutic hypothermia; optimization of hemodynamics and gas
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exchange; immediate coronary reperfusion when indicated for restoration of coronary blood flow

with percutaneous coronary intervention (PCI); glycemic control; and neurological diagnosis,

management, and prognostication.

Previous SectionNext Section

Overview of Post

Cardiac Arrest Care

The provider of CPR should ensure an adequate airway and support breathing immediately after

ROSC. Unconscious patients usually require an advanced airway for mechanical support of breathing.

It may be necessary to replace a supraglottic airway used for initial resuscitation with an

endotracheal tube, although the timing of replacement may vary. Methods for securing an advanced

airway are discussed in Part 8.1: Airway Management, but several simple maneuvers deserve

consideration. For example, rescuers and long-term hospital providers should avoid using ties that

pass circumferentially around the patient's neck, potentially obstructing venous return from the

brain. They should also elevate the head of the bed 30 if tolerated to reduce the incidence of

cerebral edema, aspiration, and ventilatory-associated pneumonia. Correct placement of an

advanced airway, particularly during patient transport, should be monitored using waveform

capnography as described in other sections of the 2010 AHA Guidelines for CPR and ECC.

Oxygenation of the patient should be monitored continuously with pulse oximetry.

Although 100% oxygen may have been used during initial resuscitation, providers should titrate

inspired oxygen to the lowest level required to achieve an arterial oxygen saturation of 94%, so as

to avoid potential oxygen toxicity. It is recognized that titration of inspired oxygen may not be

possible immediately after out-of-hospital cardiac arrest until the patient is transported to the

emergency department or, in the case of in-hospital arrest, the intensive care unit (ICU).

Hyperventilation or overbagging the patient is common after cardiac arrest and should be avoided

because of potential adverse hemodynamic effects. Hyperventilation increases intrathoracic pressure

and inversely lowers cardiac output. The decrease in PaCO2 seen with hyperventilation can also

potentially decrease cerebral blood flow directly. Ventilation may be started at 10 to 12 breaths per

minute and titrated to achieve a PETCO2of 35 to 40 mm Hg or a PaCO2of 40 to 45 mm Hg.

The clinician should assess vital signs and monitor for recurrent cardiac arrhythmias. Continuous

electrocardiographic (ECG) monitoring should continue after ROSC, during transport, and throughout

ICU care until stability has been achieved. Intravenous (IV) access should be obtained if not already

established and the position and function of any intravenous catheter verified. IV lines should be

promptly established to replace emergent intraosseous access achieved during resuscitation. If the

patient is hypotensive (systolic blood pressure


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therapy in addition to coronary reperfusion (eg, PCI) and other goal-directed postarrest care

therapies.

Overall the most common cause of cardiac arrest is cardiovascular disease and coronary ischemia.14,15

Therefore, a 12-lead ECG should be obtained as soon as possible to detect ST elevation or new or

presumably new left bundle-branch block. When there is high suspicion of acute myocardialinfarction (AMI), local protocols for treatment of AMI and coronary reperfusion should be activated.

Even in the absence of ST elevation, medical or interventional treatments may be considered for

treatment of ACS14,16,17and should not be deferred in the presence of coma or in conjunction with

hypothermia. Concurrent PCI and hypothermia are safe, with good outcomes reported for some

comatose patients who undergo PCI.

Patients who are unconscious or unresponsive after cardiac arrest should be directed to an inpatient

critical-care facility with a comprehensive care plan that includes acute cardiovascular interventions,

use of therapeutic hypothermia, standardized medical goal-directed therapies, and advanced

neurological monitoring and care. Neurological prognosis may be difficult to determine during the

first 72 hours, even for patients who are not undergoing therapeutic hypothermia. This time frame

for prognostication is likely to be extended in patients being cooled.18 Many initially comatose

survivors of cardiac arrest have the potential for full recovery such that they are able to lead normal

lives.1,2,19 Between 20% and 50% or more of survivors of out-of-hospital cardiac arrest who are

comatose on arrival at the hospital may have good one-year neurological outcome.1,2,11Therefore, it

is important to place patients in a hospital critical-care unit where expert care and neurological

evaluation can be performed and where appropriate testing to aid prognosis is available and

performed in a timely manner.

Attention should be directed to treating the precipitating cause of cardiac arrest after ROSC. The

provider should initiate or request studies that will further aid in evaluation of the patient. It is

important to identify and treat any cardiac, electrolyte, toxicological, pulmonary, and neurological

precipitants of arrest. The clinician may find it helpful to review the H's and T's mnemonic to recall

factors that may contribute to cardiac arrest or complicate resuscitation or postresuscitation care:

hypovolemia, hypoxia, hydrogen ion (acidosis of any etiology), hyper-/hypokalemia, moderate to

severe hypothermia, toxins, tamponade (cardiac), tension pneumothorax, and thrombosis of the

coronary or pulmonary vasculature. For further information on treating other causes of cardiac

arrest, see Part 12: Special Resuscitation Situations.

WHO analgesic ladder

Pain ladder
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From Wikipedia, the free encyclopedia

Jump to:navigation,search

"Pain ladder"is a term coined by theWorld Health Organization(WHO) to describe its

guideline for the use of drugs in the management of pain. It was originally applied to the

management ofcancer pain,but is now widely used by medical professionals for themanagement of all types ofpain.

The general principle is to start with first step drugs, and then to climb the ladder if pain is stillpresent. The medications range from household,over-the-counter drugswith minimal side-

effects at the lowest rung, to powerfulopioids.

Contents

[hide]

1 The Ladder 2 See also

3 References

4 External links

The Ladder[edit]

The WHO guidelines[1]

recommend prompt oral administration of drugs when pain occurs,

starting, if the patient is not in severe pain, with non-opioid drugs such asparacetamol

(acetaminophen),dipyrone,non-steroidal anti-inflammatory drugs(NSAIDs) orCOX-2inhibitors.Then, if complete pain relief is not achieved or disease progression necessitates more

aggressive treatment, a mild opioid such ascodeine phosphate,dextropropoxyphene,

dihydrocodeineorTramadolare added to the existing non-opioid regime. If this is or becomesinsufficient, a mild opioid is replaced by a stronger opioid, such asmorphine,diamorphine

(heroin),fentanyl,buprenorphine,oxymorphone,oxycodone,hydromorphone,while continuing

the non-opioid therapy, escalating opioid dose until the patient is pain free or at the maximumpossible relief without intolerable side effects. If the initial presentation is severe pain, this

stepping process should be skipped and a strong opioid should be started immediately in

combination with a non-opioidanalgesic.[2]

Bottom rung of ladder (mild pain): Non opioid +/-adjuvant

Middle rung of ladder (moderate pain): Weak opioid +/- non opioid +/- adjuvant

Highest rung of ladder (severe pain): Strong opioid +/- non opioid +/- adjuvant

The usefulness of the second step (mild opioid) is being debated in the clinical and research

communities. Some authors challenge the pharmacological validity of the step and, pointing totheir higher toxicity and low efficacy, argue that a mild opioid, with the possible exception of

Tramadol due to its unique action, could be replaced by smaller doses of a strong opioid.[2]
http://en.wikipedia.org/wiki/Pain_ladder#mw-navigationhttp://en.wikipedia.org/wiki/Pain_ladder#mw-navigationhttp://en.wikipedia.org/wiki/Pain_ladder#mw-navigationhttp://en.wikipedia.org/wiki/Pain_ladder#p-searchhttp://en.wikipedia.org/wiki/Pain_ladder#p-searchhttp://en.wikipedia.org/wiki/Pain_ladder#p-searchhttp://en.wikipedia.org/wiki/World_Health_Organizationhttp://en.wikipedia.org/wiki/World_Health_Organizationhttp://en.wikipedia.org/wiki/World_Health_Organizationhttp://en.wikipedia.org/wiki/Cancer_painhttp://en.wikipedia.org/wiki/Cancer_painhttp://en.wikipedia.org/wiki/Cancer_painhttp://en.wikipedia.org/wiki/Painhttp://en.wikipedia.org/wiki/Painhttp://en.wikipedia.org/wiki/Painhttp://en.wikipedia.org/wiki/Over-the-counter_drugshttp://en.wikipedia.org/wiki/Over-the-counter_drugshttp://en.wikipedia.org/wiki/Over-the-counter_drugshttp://en.wikipedia.org/wiki/Opioidshttp://en.wikipedia.org/wiki/Opioidshttp://en.wikipedia.org/wiki/Opioidshttp://en.wikipedia.org/wiki/Pain_ladderhttp://en.wikipedia.org/wiki/Pain_ladderhttp://en.wikipedia.org/wiki/Pain_ladderhttp://en.wikipedia.org/wiki/Pain_ladder#The_Ladderhttp://en.wikipedia.org/wiki/Pain_ladder#The_Ladderhttp://en.wikipedia.org/wiki/Pain_ladder#See_alsohttp://en.wikipedia.org/wiki/Pain_ladder#See_alsohttp://en.wikipedia.org/wiki/Pain_ladder#Referenceshttp://en.wikipedia.org/wiki/Pain_ladder#Referenceshttp://en.wikipedia.org/wiki/Pain_ladder#External_linkshttp://en.wikipedia.org/wiki/Pain_ladder#External_linkshttp://en.wikipedia.org/w/index.php?title=Pain_ladder&action=edit&section=1http://en.wikipedia.org/wiki/Pain_ladder#cite_note-WHO_1996-1http://en.wikipedia.org/wiki/Pain_ladder#cite_note-WHO_1996-1http://en.wikipedia.org/wiki/Pain_ladder#cite_note-WHO_1996-1http://en.wikipedia.org/wiki/Paracetamolhttp://en.wikipedia.org/wiki/Paracetamolhttp://en.wikipedia.org/wiki/Paracetamolhttp://en.wikipedia.org/wiki/Dipyronehttp://en.wikipedia.org/wiki/Dipyronehttp://en.wikipedia.org/wiki/Dipyronehttp://en.wikipedia.org/wiki/Non-steroidal_anti-inflammatory_drughttp://en.wikipedia.org/wiki/Non-steroidal_anti-inflammatory_drughttp://en.wikipedia.org/wiki/Non-steroidal_anti-inflammatory_drughttp://en.wikipedia.org/wiki/COX-2_inhibitorhttp://en.wikipedia.org/wiki/COX-2_inhibitorhttp://en.wikipedia.org/wiki/COX-2_inhibitorhttp://en.wikipedia.org/wiki/COX-2_inhibitorhttp://en.wikipedia.org/wiki/Codeine_phosphatehttp://en.wikipedia.org/wiki/Codeine_phosphatehttp://en.wikipedia.org/wiki/Codeine_phosphatehttp://en.wikipedia.org/wiki/Dextropropoxyphenehttp://en.wikipedia.org/wiki/Dextropropoxyphenehttp://en.wikipedia.org/wiki/Dextropropoxyphenehttp://en.wikipedia.org/wiki/Dihydrocodeinehttp://en.wikipedia.org/wiki/Dihydrocodeinehttp://en.wikipedia.org/wiki/Tramadolhttp://en.wikipedia.org/wiki/Tramadolhttp://en.wikipedia.org/wiki/Tramadolhttp://en.wikipedia.org/wiki/Morphinehttp://en.wikipedia.org/wiki/Morphinehttp://en.wikipedia.org/wiki/Morphinehttp://en.wikipedia.org/wiki/Diamorphinehttp://en.wikipedia.org/wiki/Diamorphinehttp://en.wikipedia.org/wiki/Diamorphinehttp://en.wikipedia.org/wiki/Fentanylhttp://en.wikipedia.org/wiki/Fentanylhttp://en.wikipedia.org/wiki/Fentanylhttp://en.wikipedia.org/wiki/Buprenorphinehttp://en.wikipedia.org/wiki/Buprenorphinehttp://en.wikipedia.org/wiki/Buprenorphinehttp://en.wikipedia.org/wiki/Oxymorphonehttp://en.wikipedia.org/wiki/Oxymorphonehttp://en.wikipedia.org/wiki/Oxymorphonehttp://en.wikipedia.org/wiki/Oxycodonehttp://en.wikipedia.org/wiki/Oxycodonehttp://en.wikipedia.org/wiki/Oxycodonehttp://en.wikipedia.org/wiki/Hydromorphonehttp://en.wikipedia.org/wiki/Hydromorphonehttp://en.wikipedia.org/wiki/Hydromorphonehttp://en.wikipedia.org/wiki/Analgesichttp://en.wikipedia.org/wiki/Analgesichttp://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Adjuvanthttp://en.wikipedia.org/wiki/Adjuvanthttp://en.wikipedia.org/wiki/Adjuvanthttp://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Adjuvanthttp://en.wikipedia.org/wiki/Pain_ladder#cite_note-Schug-2http://en.wikipedia.org/wiki/Analgesichttp://en.wikipedia.org/wiki/Hydromorphonehttp://en.wikipedia.org/wiki/Oxycodonehttp://en.wikipedia.org/wiki/Oxymorphonehttp://en.wikipedia.org/wiki/Buprenorphinehttp://en.wikipedia.org/wiki/Fentanylhttp://en.wikipedia.org/wiki/Diamorphinehttp://en.wikipedia.org/wiki/Morphinehttp://en.wikipedia.org/wiki/Tramadolhttp://en.wikipedia.org/wiki/Dihydrocodeinehttp://en.wikipedia.org/wiki/Dextropropoxyphenehttp://en.wikipedia.org/wiki/Codeine_phosphatehttp://en.wikipedia.org/wiki/COX-2_inhibitorhttp://en.wikipedia.org/wiki/COX-2_inhibitorhttp://en.wikipedia.org/wiki/Non-steroidal_anti-inflammatory_drughttp://en.wikipedia.org/wiki/Dipyronehttp://en.wikipedia.org/wiki/Paracetamolhttp://en.wikipedia.org/wiki/Pain_ladder#cite_note-WHO_1996-1http://en.wikipedia.org/w/index.php?title=Pain_ladder&action=edit&section=1http://en.wikipedia.org/wiki/Pain_ladder#External_linkshttp://en.wikipedia.org/wiki/Pain_ladder#Referenceshttp://en.wikipedia.org/wiki/Pain_ladder#See_alsohttp://en.wikipedia.org/wiki/Pain_ladder#The_Ladderhttp://en.wikipedia.org/wiki/Pain_ladderhttp://en.wikipedia.org/wiki/Opioidshttp://en.wikipedia.org/wiki/Over-the-counter_drugshttp://en.wikipedia.org/wiki/Painhttp://en.wikipedia.org/wiki/Cancer_painhttp://en.wikipedia.org/wiki/World_Health_Organizationhttp://en.wikipedia.org/wiki/Pain_ladder#p-searchhttp://en.wikipedia.org/wiki/Pain_ladder#mw-navigation


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Not all pain yields completely to classic analgesics, and drugs that are not traditionally

considered analgesics, but which reduce pain in some cases, such assteroidsorbisphosphonates,

may be employed concurrently with analgesics at any stage.Tricyclic antidepressants,class Iantiarrhythmics,oranticonvulsantsare the drugs of choice forneuropathic pain.Up to 90 percent

of cancer patients, immediately preceding death, use suchadjuvants.Many adjuvants carry a

significant risk of serious complications.

[2

PHYSIOTHERAPY FOR PT ON VENTILATOR WITH

BASAL PNEUMONIA

PREVENTION OF PNEUMONIA AFTER OPERATION

Before undergoing elective surgical procedures, patients should be instructed about taking deep breaths and

ambulating postoperatively (unless there is a medical contraindication to doing so). Such instruction is especially

important in patients who are at high risk for pneumonia after operation. This group includes patients scheduled for

abdominal aortic aneurysm repair or thoracic procedures, those older than 60 years, those undergoing general

anesthesia, those whose functional status is poor, those with greater than 10% weight loss, those on long-term

steroid therapy, those with COPD, smokers, those with abnormally low or high BUN levels, and those receiving more

than 4 units of blood preoperatively.2,62

Patients who are also at high risk but are not candidates for preoperative

respiratory instruction include those undergoing emergency surgical intervention, those with impaired sensoria, and

those with a history of cerebrovascular accident with residual neurologic deficit (although, depending on the type of

deficit, this patient population may benefit from preoperative teaching as well).

Incentive spirometry is valuable for preventing pneumonia after operation and is a cost-effective adjunct to early

ambulation. It benefits a wide range of patients but is especially effective in moderate-risk and high-risk patients, who

should receive extra attention in ensuring compliance with this simple intervention. Although chest physiotherapy has

been proposed as a means of potentially decreasing postoperative pneumonia, a meta-analysis of 14 published

studies assessing the usefulness of this modality after upper abdominal procedures did not support its routine use.63

Like many other infections in critically ill patients, VAP is often preventable. Well-designed studies have found

numerous interventions to be effective in lowering the incidence of VAP.64

Some of these interventions are as simple

as positioning the patient appropriately or educating health care workers about risk factors for VAP.
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Hand HygieneAppropriate hand hygiene is a simple but underused method of preventing nosocomial infection.

Lack of attention to hand hygiene has been a persistent problem worldwide for decades, and

physicians often have the poorest compliance. The alcohol foams and gels currently available are

more effective than hand washing in killing the bacteria present on the hands and take

substantially less time to use, improving compliance with hand hygiene in the ICU.65

Such

preparations now represent the hand hygiene method of choice in most cases and should be

readily available throughout the ICU. Hands that are visibly dirty or are soiled with blood or body

fluids should still be washed with antimicrobial soap and water, however. Appropriate hand

hygiene practices should be followed both before and after contact with a patient who has an

endotracheal tube or tracheostomy in place, regardless of whether gloves are worn. In addition,

hand decontamination is required before and after contact with any respiratory device that is used

on a mechanically ventilated patient.65

Gloves should be worn for handling respiratory secretions or objects contaminated with such

secretions. They should be changed between contacts with different patients, after handling respiratory secretions. In

addition, gloves should be changed between contacts with a contaminated body site and the respiratory tract or any

portion of the ventilator circuit on the same patient. Gowns are also recommended when soiling with respiratory

secretions is anticipated; they should be removed after the soiling occurs and before any contact with other ICU

patients.

PATIENT POSITIONINGAspiration of upper airway secretions occurs in healthy adults as well as in ill ones. It is, however, a matter of much

greater concern in critically ill patients with decreased host defenses, who are at increased risk for VAP. Maneuvers

to reduce aspiration of gastric contents therefore have the potential to decrease the incidence of VAP. Because the

supine position is associated with an increased risk of aspiration (especially if the patient is receiving tube feedings

via a nasoenteric tube), placing the patient in a semirecumbent positionvia the simple expedient of raising the head

of the bed to an angle of 30 to 45 or greateris recommended as a means of possibly preventing VAP (if not

medically contraindicated).

A prospective, randomized trial involving 86 patients in two ICUs (neither of them surgical) was stopped at the first

interim analysis because of the significant difference in the incidence of VAP between semirecumbent patients and

supine patients.66

The incidence of both clinically suspected VAP and microbiologically proven VAP was drastically

reduced in patients positioned with the head of the bed at a 45 angle (from 34% to 8% and from 23% to 5%,

respectively). Enteral feeding was also independently associated with the risk of VAP: supine patients receiving

enteral feedings had a 50% chance of acquiring VAP. A subsequent prospective, randomized trial of 109 patients

found that a target backrest elevation of 45 was not achieved 85% of the time, and the actual treatment position

(28) did not prevent the development of VAP compared with the standard position (10).67

The supine position has been identified as an independent risk factor for VAP in other observational studies of ICU

patients as well. In addition, patients who require transport from the ICU are at substantially higher risk for VAP than

Figure 1

Recommended

Approach to

Antibiotic

Treatment
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those who do not (24.2% versus 4.4%).68

It is possible that the VAP rate is increased because patients requiring

transport are sicker at baseline, but it is also possible that the rate is higher in this group partly because patients are

supine for much or all of their transport time.

Because static bed rest is known to increase the risk of pulmonary (and nonpulmonary) complications, it has been

theorized that postural oscillation and rotation may prevent VAP. Specialized kinetic beds are available that provide

continuous movement and are capable of reducing pulmonary complications in surgical patients. A study of 106 blunt

trauma patients in a surgical ICU demonstrated a significant decrease in VAP in patients randomly selected to

undergo continuous postural oscillation.69

A study of 65 surgical patients immobilized because of head injury or

traction showed a nonstatistical trend toward a decreased risk of pneumonia in patients treated with kinetic beds .70

Finally, a study of 69 liver transplant patients randomly assigned to either continuous lateral rotation or a conventional

bed found that the incidence of lower respiratory tract infections was decreased in the study group, as was the length

of time to the development of infection; however, the duration of mechanical ventilation and length of stay were

unchanged.71

Overall, there appears to be a trend toward decreased VAP in surgical patients treated with kinetic beds. In addition,

various accompanying nonpulmonary complications can also be prevented by this treatment (e.g., decubitus ulcers).

Accordingly, kinetic beds should be used in surgical patients who are expected to have a prolonged ICU course.

Choice of Feeding RouteAlthough elevation of the head of the bed reduces aspiration, it does not prevent gastroesophageal reflux. Because

gastric overdistention is also associated with an increased risk of aspiration, there has been considerable interest in

identifying a route of feeding that is associated with a decreased incidence of VAP. This issue is directly relevant to

the postoperative setting, in which many patients, as a consequence of the surgical procedure, experience ileus,

which is often exacerbated by narcotics given for pain relief. The generally appropriate reluctance to feed a patient

with a large gastric residuum in the ICU setting should be balanced against the desire to provide adequate nutrition

as soon as is practicable after an operation, as well as against the multiple advantages of enteral feeding over

parenteral feeding. Accordingly, the timing for initiating feedings postoperatively must be individualized on the basis

of each patient's situation and condition. In addition, whereas feeding a supine patient greatly increases the risk of

VAP, there is no documented benefit to postpyloric feeding or to using smaller nasogastric tube s72

and no clear

recommendations can be made regarding how best to feed a postoperative patient enterally.

Minimization of Endotracheal IntubationExtended mechanical ventilation is a major risk factor for VAP; it follows, then, that decreasing or eliminating the need

for an endotracheal tube has the potential to lower the incidence of VAP. There are two major strategies by which this

goal can be accomplished: (1) earlier extubation (i.e., removing an endotracheal tube when it is no longer needed)

and (2) noninvasive ventilation (i.e., continuing ventilatory support without the presence of an endotracheal tube). In

addition, the route of intubation (oral versus nasal) can influence the development of pneumonia.73

Although the optimal mode of weaning has not been definitively determined, it is clear that many patients are kept

intubated even when they no longer require mechanical ventilation. The use of a weaning protocol, a sedation
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protocol, or both has been shown to reduce the duration of mechanical ventilation. In addition, daily interruption of

sedation until a patient is awake has been demonstrated to decrease the number of ventilator days in a medical ICU

population.74

Importantly, a randomized, controlled trial of 336 patients demonstrated that the combination of a

spontaneous awakening trial and a spontaneous breathing trial led to decreased time on the ventilator and ICU length

of stay as well as decreased mortality for 1 year compared with a spontaneous breathing trial with sedation per usual

care.75This approach has not been extensively studied in the surgical ICU, where the issue is complicated by the

greater need for postoperative narcotics. Regardless of the technique or protocol employed, patients should be

assessed daily to determine whether ventilatory support is still necessary. Extubated patients have a substantially

lower incidence of postoperative pneumonia than patients with an endotracheal tube in place.

The presence of an endotracheal tube in itself, independent of the need for mechanical ventilation, also appears to be

a risk factor for VAP. The tube hinders both airway reflexes and coughing, allowing secretions that accumulate above

the tube to enter the airways over time and serve as a nidus of infection. This problem is eliminated in patients who

are ventilated noninvasively with bilevel positive airway pressure (BiPAP). Multiple studies have found noninvasive

ventilation to be associated with lower pneumonia rates and mortalities than conventional ventilation. However, these

studies were done in medical ICUs, predominantly on patients with COPD exacerbations, and it is unclear whether

similar results are achievable in patients with postoperative respiratory failure.

Reintubation is also an independent risk factor for the development of VAP.76

However, fear of the potential adverse

consequences of reintubation should not prevent an awake patient who passes a spontaneous breathing trial from

being extubated. Many postoperative patients who are extubated and have unexpected ventilatory problems can be

managed without reintubation on BiPAP. In addition, although it is unclear what the correct percentage of extubation

attempts that require reintubation would be, it is clear that the number is not zero. The decision to extubate is, in a

way, comparable to the decision to perform an appendectomy. If every patient on whom an appendectomy is done

has appendicitis, it is likely that too few operations are being done and that some patients are being allowed to

experience a ruptured appendix needlessly. Similarly, if every patient who is extubated postoperatively does well, it islikely that too few extubations are being done and that some patients are being kept intubated inappropriately and

thus experiencing preventable morbidity.

Nasal intubation increases the risk of sinusitis, which, even though only 10% of patients with opacified sinuses have

recoverable bacteria, is associated with an increased incidence of VAP.77

It is not clear whether sinusitis causes VAP

or merely represents a marker of patients who are at higher risk for pneumonia. In either case, given the association

between nasotracheal intubation and increased infection rate and mortality, nasotracheal intubation should not be

considered a first-line method of obtaining airway control.

Ventilator ManagementAlthough, in theory, ventilator tubing, suction catheters, and humidification systems could all play a role in the

development of pneumonia, none of them have been convincingly shown to have an impact on VAP rates.

Condensate in the ventilator tubing can become contaminated, but multiple randomized trials have demonstrated that

routinely changing ventilator circuits in patients with respiratory failure does not lower the VAP rate.78

Circuits should

be changed when they are visibly soiled with vomit or blood or are malfunctioning. In addition, condensate should

periodically be drained and discarded.
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Heat moisture exchangers (HMEs) are frequently used instead of heated water humidification systems because

HMEs are relatively inexpensive and require neither electricity nor active heating elements. HMEs minimize the

formation of condensate within ventilator circuits, thereby, in theory, potentially decreasing VAP rates. One study

found HMEs to yield lower infection rates than humidification systems,79

but at present, there is no clear consensus in

favor of either type of device. Either an open single-use catheter system or a closed multiuse catheter system may be

used for suctioning. Although open systems are associated with increased environmental contamination, current

evidence suggests that the incidence of VAP is not significantly affected by the type of suctioning system used.80

In

addition, when closed systems are used, routine changing of inline suction catheters does not reduce the incidence of

VAP,81

nor is there convincing evidence that more frequent suctioning prevents VAP.

Ventilator WeaningGiven that the rate of VAP increases with increasing duration of mechanical ventilation, it is imperative to provide all

attempts at ventilator weaning in the ICU as a VAP preventive strategy. Daily interruption of sedation, that is,

spontaneous awakening trials, and daily spontaneous breathing trials are therefore recommended.75

,82

It has been

documented that a wake up and breathe protocol that pairs daily spontaneous awakening trials (i.e., interruption of

sedatives) with daily spontaneous breathing trials results in better outcomes for mechanically ventilated patients in

the ICU.

Prevention of Oropharyngeal ColonizationOropharyngeal colonization can be decreased by means of either antiseptic therapy or a comprehensive oral hygiene

program. Oral chlorhexidine gluconate (0.12%), given before and after cardiac procedures, has proved effective in

preventing postoperative pneumonia.83

In a prospective, randomized, blinded trial, patients receiving a chlorhexidine

rinse, which has documented activity against both aerobes and anaerobes, experienced a 69% decrease in the

incidence of postoperative pneumonia. This decrease was not associated with a change in antibiotic resistance

patterns after operation and was accompanied by a reduction in postoperative antibiotic use. Similar results were

demonstrated in a study in the surgical ICU that demonstrated that an oral care protocol combining tooth brushing

and twice-daily application of chlorhexidine gluconate decreased the VAP rate from 5.2 per 1,000 ventilator days to

2.4 per 1,000 ventilator days.84

These results are consistent with a recent meta-analysis demonstrating that topical

chlorhexidine is beneficial in preventing VAP, with the most significant benefit present in cardiac surgery patients .85

An additional randomized trial with 2% chlorhexidine solution four times daily versus normal saline (n = 207)

confirmed a VAP reduction (7 versus 21 per 1,000 ventilator days,p= .04), and a meta-analysis of two studies using

2% chlorhexidine revealed an overall relative risk of VAP for patients in the chlorhexidine group of 0.53 (95% CI 0.31

to 0.90;p= .02).86

Interestingly, the addition of electric tooth brushing to oral care with 0.12% chlorhexidine was not

effective for VAP prevention.87

Drainage of Subglottic SecretionsSecretions that pool above an inflated endotracheal cuff may be a source of aspirated material that results in VAP.

Specially designed endotracheal tubes are available that have a separate opening above the cuff of the tube to allow

either continuous or intermittent suctioning and drainage of secretions that accumulate in the subglottic space.
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A meta-analysis of five prospective, randomized trials evaluating the role of subglottic secretion drainage in 896

patients demonstrated that subglottic secretion drainage shortened the duration of mechanical ventilation and ICU

stay and delayed the onset of pneumonia by 6.8 days and suggested that this could be an effective strategy in

patients intubated for more than 72 hours.76

Subsequent to the publication of this meta-analysis, however, the largest

randomized trial of subglottic secretion drainage was performed in 714 cardiac surgery patients.88

No statistically

significant decrease in overall VAP rates was noted with continuous aspiration of subglottic secretions, although there

was a decrease in hospital antibiotic use in the experimental group. For patients who required mechanical ventilation

for more than 48 hours, VAP rates, ICU length of stay, and hospital antibiotic use were all decreased in patients

treated with continuous aspiration of subglottic secretion, although this was not associated with an improvement in

mortality.

In addition, a randomized trial of 280 patients in a medical-surgical ICU combining subglottic secretion drainage with

an endotracheal tube with a polyurethane cuff demonstrated a decrease in both early and late VAP compared with a

conventional endotracheal tube with a polyvinyl cuff without subglottic secretion drainage.89

Most recently, a

prospective trial at four French centers randomized adult patients intubated with a tracheal tube allowing drainage of

subglottic secretions to undergo intermittent subglottic secretion drainage (SSD) (n= 169) or not (n= 164). VAP,

diagnosed by quantitative culture of distal airways, occurred in 14.8% of SSD patients versus 25.6% of control

patients (p= .02, relative risk reduction 42.2%, 95% CI 10.4 to 63.1) but had no impact on the duration of mechanical

ventilation or ICU mortality.90

At present, use of subglottic secretion drainage is hindered by logistical difficulties. These specialized tubes require

routine maintenance in the ICU to ensure that the suction lumen remains patent. In addition, any decision to place the

tubes in patients undergoing surgery must also be made preoperatively and communicated to the anesthesiologist or

emergency department physician before the patient is intubated.

Silver-coated Endotracheal Tubes

There are significant data on preventing catheter-related bloodstream infection with antiseptic or antibiotic-

impregnated catheters; however, until recently, there were no data as to whether a similar approach would be

beneficial in preventing VAP.

Silver has broad-spectrum antimicrobial activity and has been used topically to prevent infections after thermal injury.

Both animal and in vitro studies demonstrate that silver-coated endotracheal tubes are effective in decreasing

bacterial colonization and adherence compared with standard tubes.91

Based on the antimicrobial efficacy of silver

and an extensive clinical history without significant toxicity, a recent prospective, randomized trial compared the

efficacy of silver-coated endotracheal tubes with that of conventional endotracheal tubes for the prevention of VAP in

patients requiring mechanical ventilation for more than 24 hours (NASCENT trial).92

A total of 766 patients received

endotracheal tubes coated on the inner and outer lumen with silver, whereas 743 patients were randomized to

receive control endotracheal tubes. Patients who had emergency surgery or trauma made up 10% of the enrolled

patient population, and over 30% of patients had their endotracheal tube placed in the operating room. Patients who

received the silver-coated tubes had decreased incidence of VAP (7.5% versus 4.8%) and delayed occurrence of

VAP. No statistically significant differences were noted in the duration of ICU or hospital stay or mortality. It should be

noted that one controversial aspect of the study is the fact that 30% of positive BALs recovered organisms not
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typically considered to be pathogenic, and when the data were analyzed without these organisms, the p value

between the silver-coated endotracheal tubes and control tubes increased to .06.93

Despite this, an accompanying editorial to this trial suggested that silver-coated endotracheal tubes should probably

be used in trauma patients, in light of the fact that the benefit seen with the tubes occurred during the first 10 days of

mechanical ventilation and that they would most likely be effective in a high-risk patient population.94 In addition, a

cost-effectiveness analysis concluded that despite the increased cost of routinely placing silver-coated endotracheal

tubes, their efficacy more than outweighed the cost, and they could potentially be a cost-saving strategy for

preventing VAP.95

Pharmacologic ApproachesWidely varying study results and significant infection control concerns have made SDD an extremely controversial

practice. The term is actually a misnomer in that successful SDD protocols employ a combination of systemic

antibiotics and nonabsorbable antibiotics given both orally and via a nasogastric tube. This is an important point:

meta-analyses of SDD studies generally show that SDD is not effective if systemic antibiotics are not included.96

,97

Multiple recent meta-analyses examining the effect of SDD show decreased mortality in patients receiving SDD.98100

A 2007 meta-analysis of 3,331 patients who received SDD including both parenteral and enteral antibiotics

demonstrated a 26% decrease in overall mortality.99

A follow-up meta-analysis from the same group examining 9,473

patients demonstrated a marked decrease in gram-negative respiratory tract infections with an odds ratio of 0.11

(95% CI 0.06 to 0.20) and a small decrease in gram-positive respiratory tract infections with an odds ratio of 0.52

(95% CI 0.34 to 0.78).101

These findings were consistent with a Cochrane meta-analysis that included 36 trials

involving 6,922 patients.100

In a subgroup analysis of 17 trials of 4,295 patients receiving both topical and systemic

antibiotics, SDD decreased mortality with an odds ratio of 0.78 (95% CI 0.68 to 0.89), and respiratory infection was

markedly decreased with an odds ratio of 0.35 (95% CI 0.29 to 0.41).

There is significant concern, however, that even if SDD is effective in ICUs with low endemic rates of vancomycin-

resistant enterococcus, MRSA, and multidrug-resistant gram-negative bacteria (as is common in Europe), it might

lead to enhanced selection of these and other resistant organisms in ICUs where they are endemic (as is common in

the United States).102

A recent study in 13 ICUs demonstrated that even though SDD was effective,103

intestinal

colonization with gram-negative bacteria resistant to ceftazidime, tobramycin, or ciprofloxacin increased from 5, 7,

and 7%, respectively, prior to the institution of SDD or selective oropharyngeal decontamination to 15, 13, and 13%,

respectively, after treatment.96

Furthermore, resistance levels in the respiratory tract were not more than 6% for all

three antibiotics prior to the study but were greater than 10% for all three after initiating SDD. In addition, a study in a

surgical ICU in Austria demonstrated an increase in oxacillin resistance in S. aureusisolates from 17 to 81% over a

5-year period where SDD was practiced.97

A 6-year study of 360 trauma patients receiving SDD also reported a

moderate increase in the development of resistant organisms.104

Owing to infection control concerns, SDD is not widely accepted in the United States. It is noteworthy that routine use

of SDD to prevent VAP is not recommended in most guidelines for preventing pneumonia or sepsis.21

,58

,104
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Another pharmacologic approach that has been proposed as a means of preventing VAP is avoidance of drugs that

raise stomach pH, on the assumption that these agents may lead to bacterial overgrowth and, eventually, to VAP.

The available data, however, indicate that this assumption is incorrect. A prospective, randomized trial involving

1,200 patients in 16 ICUs that compared the H2receptor antagonist ranitidine with sucralfate found no difference in

the VAP rate between the ranitidine group and the sucralfate group .105

Notably, the rate of clinically important GI

bleeding was higher in the sucralfate group. On the basis of this definitive study, drugs that raise stomach pH should

not be avoided for infection control reasons.

Education of Health Care WorkersObviously, to implement interventions that prevent VAP, health care workers must be aware that such interventions

exist. Although ICU directors clearly play a major role in the overall direction of care, direct daily care of patients

undergoing mechanical ventilation is provided by respiratory therapists and nurses, and these professionals stand to

benefit most from educational efforts.

Multiple recent publications attest to the efficacy of educational programs in preventing VAP.106108

In one of these, aprogram was initiated that was directed toward respiratory care practitioners and nurses in five ICUs at a single

academic center.106

Initially, 114 respiratory therapists and 146 nurses took a 20-question pretest to determine their

level of knowledge about methods of preventing VAP. They then received a 10-page self-study module that provided

information about VAP and outlined prevention strategies. Both immediately after the intervention and 6 months later,

participants took a posttest that was identical to the original test. Test scores improved at both time points,

demonstrating that the information taught was both learned and retained.

In the 12 months before implementation of the education program, 191 episodes of VAP were identified (12.6 per

1,000 ventilator days). In the 12 months following completion of the program, however, only 81 episodes of VAP (5.7

per 1,000 ventilator days) were identified [seeFigure 2]. The greatest success in VAP prevention was achieved in the

surgical/trauma/burn ICU, where VAP rates decreased from 18.1 to 6.6 per 1,000 ventilator days. These results

highlight the importance of disseminating information on VAP prevention to the health care workers who are providing

the day-to-day care for patients at risk for VAP.

VAP BundlesPneumonia in the postoperative setting cannot be eliminated, but its incidence can be

substantially decreased by following evidence-based prevention guidelines. Unfortunately,

compliance with such guidelines is far from uniform.

Although multiple interventions have been demonstrated to prevent VAP, it is logical to assume

that a strategy that stresses compliance with multiple evidence-based practices would be superior to a strategy

focusing on a single intervention. This has led to the increasingly common practice of using bundles to prevent VAP.

A recent review of VAP bundles analyzed four publications that included at least three components of the Institute for

Healthcare Improvement (IHI) ventilator bundle (head of the bed elevation, sedation holiday, daily assessment of

readiness to extubate, peptic ulcer disease prophylaxis, and deep vein thrombosis prophylaxis) .109

Each article

examining VAP bundles included a mix of surgical and medical patients. Each successfully brought down VAP rates.

Figure 2 Influence

of an Education

Program
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post resuscitation cardiac care

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