Jones & Bartlett Learning Medicine Blog

Perioperative statin therapy has long been felt to confer cardiac protection during both cardiac surgery and major noncardiac surgery.  Until recently the data have been scarce to definitively make claims in support of this belief.  In 2004, Durazzo et al. conducted the first randomized trial examining the use of Perioperative statins in major noncardiac surgery.  They compared the use of atorvastatin 20 mg daily compared against placebo initiated 2 weeks prior to elective major vascular surgery and continued for 45 days post-operatively.  The investigators found that statins were associated with a 70% relative risk reduction of the combined end-point of death, nonfatal MI, unstable angina, or stroke. [1] Prior to this in 1999, Christenson had demonstrated cardioprotective effects of statins during coronary artery bypass grafting surgery. [2]

Statins are thought to be beneficial for a myriad reasons:

• They lower lipids and have additional pleiotropic effects.
• The cardioprotective effects of statins during the perioperative period is more likely related to their pleiotropic effects than their lipid-lowering effects.
• Statins inhibit the action of HMG-CoA Reductase which is the rate-limiting step in cholesterol synthesis, but effective lipid lowering takes months.
• Perioperative studies have demonstrated that statins confer a cardioprotective benefit when started even 1-2 weeks in advance of major surgery.
• These pleiotropic effects of statins include suppression of endothelial nitric oxide which promotes coronary vasodilation.
• Statins also reduce lipopolysaccharide-induced tissue factor release, decrease plasminogen activator inhibitor levels, and increase tissue plasminogen activator; the combination of which reduces coronary thrombosis.
• Statins also have anti-inflammatory properties which may provide more plaque stability. [3]

Acid suppression has long been associated with an increased risk of developing Clostridium difficile infection (CDI), having recurrent Clostridium difficile infection, and now has been shown to increase the complication rate and mortality from Clostridium difficile infection.  This risk applies to both H2-blockers and proton pump inhibitors (PPI), but the risk appears to be significantly higher for proton pump inhibitors.

Several prior studies and meta-analyses have demonstrated an increased risk of Clostridium difficile infection with proton pump inhibitor therapy.[1,2,3]    Howell et al. performed a case-cohort study investigating over 101,000 patient discharges at a tertiary medical care center over a five-year period.  They discovered a three-fold increased incidence of nosocomial CDI in patients receiving daily PPI therapy compared with controls not receiving any acid suppression therapy.  The risk of CDI was two-fold in patients receiving daily H2-blocker therapy and 4.5-fold increased risk for patients receiving twice daily PPI therapy.[1]  The meta-analysis performed by Deshpande et al. reviewed 30 observational studies between 1990 and 2010 and concluded that PPI therapy is associated with a two-fold increased the risk for CDI.[3]

In addition, we know that PPI use increases the risk of recurrent CDI.  A retrospective, cohort study by Linsky et al. analyzed 1166 inpatients at a single center over a five year period and determined that use of PPI within 14 days of CDI diagnosis increased the rate of recurrent CDI after appropriate treatment by 42% compared with those patients not receiving PPI therapy.[4]

Pneumothoraces are a common problem in the ER and the ICU.  The traditional screening test for a pneumothorax in the hospital is the chest radiograph; however, chest radiographs are not very sensitive in the setting of trauma and in ventilated patients.  A recent study of 225 trauma patients demonstrated that an AP chest x-ray had only 20.9% sensitivity for detecting a pneumothorax versus a CT scan of the chest.[1] A chest CT scan is the gold standard for the diagnosis of a pneumothorax, but a CT scan is extremely expensive and exposes a patient to about 7 mSv radiation (the equivalent of 70 chest x-rays).  Another modality that is gaining traction as the principal diagnostic modality to evaluate for post-traumatic pneumothoraces is a transthoracic ultrasound.  Thoracic ultrasound look for the presence or absence of lung sliding, comet tail artifacts, A line, a lung point, and a “Seashore sign” or “Bar code sign” on M Mode sonography to determine whether a pneumothorax is present.  A transthoracic ultrasound takes only a few minutes to perform and is performed as a part of the E-FAST exam right in the trauma bay of the ER.  It costs nothing, is associated with no radiation exposure, and requires no transport of the patient.

Dr. Joseph Esherick Monthly Blog – March 2012

Dr. Joseph Esherick Monthly Blog – November 2011

Numerous studies have shown that ultrasound guidance lowers the rate of complications and increases the success rate for virtually every hospital procedure compared with traditional landmark-based techniques.   This has proved to be the case for ultrasound-guided central lines, ultrasound-guided paracentesis, and ultrasound-guided lumbar punctures in obese patients.  This essay will focus on ultrasound-guided thoracentesis which has a decreased rate of pneumothorax and need for tube thoracostomy compared with the blind approach.

Pleural effusions affect nearly 1.5 million people each year in the United States.  Many of these people require thoracentesis for pleural fluid analysis to either determine the etiology of their pleural effusions or as a therapeutic procedure to relieve dyspnea and hypoxia.  Examination of the pleural space with sonography is best carried out using a convex array 3.5- to 5 MHz probe.[1]   Ideally, the patient is in the sitting position and sonography should identify the uppermost extent of the pleural effusion and the location of the diaphragm.  The depth of insertion can also be approximated by using the depth markers on the ultrasound screen.  At this point, a mark can be made on the posterior thorax just above the rib at the optimal site for thoracentesis.  The thoracentesis can then be carried out in standard fashion with the patient in the same sitting position.   Alternatively, the convex array probe can be placed in a sterile sheath and the thoracentesis can be performed using real-time ultrasound guidance.  The complication rate is identical with either technique for ultrasound-guided thoracentesis...

Dr. Joseph Esherick Monthly Blog – October 2011

Drotrecogin-alfa (DrotAA) has been an integral part of the care bundle for adult patients hospitalized with severe sepsis or septic shock and a high risk of death since 2002.  DrotAA is a synthetic activated Protein C (APC) which has good scientific evidence for why it may be beneficial in patients with severe sepsis and septic shock.  Patients with severe sepsis have abnormal activation of their coagulation pathways and inflammatory system and impaired fibrinolysis, which lead to a procoagulant state.  Normally, APC acts with Protein S to degrade clotting factors Va and VIIa to promote anticoagulation.  However, intrinsic levels of APC are diminished in patients with severe sepsis because of impaired APC synthesis and increased degradation by neutrophil elastases.  Therefore, the theory was that a synthetic APC could benefit patients by decreasing the abnormal clotting which occurs in the micro-circulation.

Dr. Joseph Esherick Monthly Blog – September 2011

National resident work hour restrictions were first implemented by the ACGME in 2003.   The debate started initially after the unfortunate death of Libby Zion in 1984 which prompted the state of New York to restrict resident duty hours.   The assumption was that resident fatigue caused the death of Libby Zion.  Among other restrictions, the 2003 regulations restricted resident shifts longer than 30 hours.  The regulations also stipulated that resident physicians must have at least one day in seven off and must have a 10 hour break between work shifts.

In 2008, the Institute of Medicine (IOM) declared that resident duty hour restrictions must be tighter to reduce medical errors and improve resident education.  The IOM proclaimed that resident shifts should not exceed 16 hours unless they are interrupted by a five-hour uninterrupted nap, no shift should exceed 30 hours, and moonlighting hours are counted as a part of the 80-hour weekly maximum.  Based on these recommendations, the ACGME has imposed new 2010 regulations that prohibit first-year residents from working shifts longer than 16 hours, senior residents must work shifts no longer than 24 hours, and shifts must be separated by a 10 hour break.  The assumption that has been made is that these duty hour restrictions will decrease resident fatigue and therefore lead to improved patient safety and improved resident education, which will eventually lead to better graduating physicians.

The reality, however, is these residency duty hour restrictions have led to neither improved patient outcomes nor improved resident education.  The data suggest that the IOMs assumptions are wrong... 

Dr. Joseph Esherick Monthly Blog – August 2011

There has been considerable interest in antibiotic stewardship programs over the past decade given the increase in drug-resistant bacteria.  The best way to combat the problem of drug-resistant bacteria is to develop systems which discourage the inappropriate initiation of antibiotics or the unnecessary prolongation of antibiotics.  The measurement of serum procalcitonin levels can aid sound clinical judgment for decisions regarding proper antibiotic use.

Procalcitonin, the precursor peptide of calcitonin, is released in response to a body’s exposure to bacterial antigens or toxins.  Furthermore, the procalcitonin levels are suppressed by exposure to cytokines activated during viral infections, namely interferon gamma.  We know that the level of procalcitonin elevation is directly correlated with the severity of the bacterial infection.^[1] In addition, procalcitonin levels rise within 6-12 hours after symptom onset of bacterial infections and decrease by about 50% per day once a bacterial infection is under control.^[2]

A number of randomized controlled trials have led to the development of procalcitonin guided clinical algorithms for various infections which have been used throughout Europe.  These protocols have led to a marked reduction in the use of antibiotics in adult patients treated in a variety of clinical settings with no increase in mortality or morbidity...

Dr. Joseph Esherick Monthly Blog – July 2011

The traditional landmark-guided needle lumbar puncture technique was first described by Heinrich Quincke in 1891^[1]This technique utilizes the iliac crest and the posterior lumbar spinous processes to determine the optimal sites for spinal needle introduction in either the L3-4 or the L2-3 interspinous spaces.  The landmark-guided technique of lumbar puncture is usually successful in experienced hands as long as the patient is not obese, pregnant, edematous, or have scoliosis, degenerative joint disease, or a history of lumbar spine surgery.  Patients who have any of these characteristics or conditions can lead to more difficult landmark-guided lumbar punctures.  It is in these cases when bedside ultrasound can increase the success rate of lumbar punctures.^[2,3,4,5]    

Ultrasound-guided regional neuraxial anesthesia has been described in the anesthesia literature since 1971.^[6]   The literature reports a reduction in the number of attempts, need for repositioning, and interspaces accessed compared with landmark-guided spinal or epidural anesthesia.^[7,8]  The use of bedside ultrasound to help guide difficult lumbar punctures has spread to the emergency room, ICU, and the hospital wards over the last 7 years.^[9]   Observational studies have demonstrated that lumbar landmarks can be correctly identified using ultrasound about 76% of the time when they are difficult to palpate.^[2,3,9]