1. Sepsis Update
Dr. Robert Rodriguez reviews the approach that we should all have for sepsis, the first of which is the rapid identification and stratification of sepsis (see sepsis classification). Elevated lactate levels >4 mg/dl denote a poor prognosis and a six fold mortality increase. ED lactate clearance (over 6h) has been shown to be a good predictor of adequate resuscitation and beneficial effects on mortality. Accurate assessment of the patient’s stage of sepsis is important in determining the patient’s prognosis and therapies. Patients usually do not die in the ED from sepsis (except in Crash syndrome-see below), but rather later in their course from MODS (Multiple Organ Dysfunction Syndrome). This is the final common pathway in the sepsis cascade and is the #1 cause of death in the ICU. Early and aggressive resuscitation can help circumvent the multi-organ damage seen from MODS. This is where Early Goal Directed Therapy comes into play. The goal for MAP is between 65-90. CVP should be maximized at 8-12 and SVO2 ≥ 70%. A simple central line, rather than special catheters can be used to measure these last two values. Broad spectrum antibiotics should be given early, ideally less than one hour. Norepinephrine remains the vasopressor of choice followed by Dopamine. Vasopressin can then be added at a low fixed dose (0.03 u/min) if MAP <65. Steroids remain controversial but should be considered in low doses (Hydrocortisone 50mg q6) in the patient that is persistently hypotensive after institution of pressors.
Source: Robert Rodriguez, MD
2. Crash Syndrome in Sepsis
Patients with sepsis do not usually die in the emergency department, but rather succumb to their disease after a prolonged ICU course. The exception to this is patients with certain diseases known as the Crash syndrome:
Asplenic pneumonia: At risk for life-threatening S. pneumoniae pneumonia
Liver failure and anything: At risk for Vibrio infections
Consider adding Vancomycin to any pneumonia patient that is ill appearing
WBC count may be useful in this disease process, rarely do these patients have a normal WBC
Source: Robert Rodriguez, MD
3. Can probiotics help prevent C. difficile colitis?
Any antibiotic that we give can cause antibiotic-associated diarrhea and clostridium difficile colitis. There is an increasing concern because C. difficile is now more common and has a more virulent toxin that can lead to toxic megacolon and death. Probiotics are becoming more common in the media and internet, some of the most popular being Saccharomyces, Lactobacillus and L. acidophilus. The theory of how probiotics function is that they introduce microorganisms into the GI tract that adhere to the intestinal mucosa and therefore decrease bacterial overgrowth. A recent meta-analysis of 25 randomized controlled trials for prophylaxis of diarrhea from antimicrobials using probiotics showed a 50% reduction in antibiotic associated diarrhea. Unfortunately, this benefit was not seen with C. difficile colitis and more studies are needed to examine their effect. Also, there was no standardized probiotic product or dosing across these studies, which makes specific recommendations difficult. As Dr. Sacchetti notes, probiotics are relatively safe and simple to administer with very little downside and therefore a reasonable adjunct to any patient that you are prescribing antibiotics.
Source: Chest. 2007; 132:286-294
4. New treatment recommendations for PID
Dr. Greg Moran reviews treatment for STDs including the new recommendations for PID. As clinicians, we should have a low threshold to diagnose and treat PID because of the high long term morbidity associated with this disease. Not only does PID increase infertility, but it can also increase the risk for ectopic pregnancy because of scarring of the fallopian tubes. Therefore, the CDC recommends “treatment for sexually active young women and other women at risk for STDs if they are experiencing pelvic or lower abdominal pain, if no cause for the illness other than PID can be identified, and if one or more of the following minimum criteria are present on pelvic examination: cervical motion tenderness OR uterine tenderness OR adnexal tenderness.” Simple outpatient therapy consists of Ceftriaxone 250mg IM plus Doxy 100 PO BID x14d +/- Metronidazole 500 po bid x 14d. Levofloxacin 500 mg daily can be substituted for Ceftriaxone in the case of a penicillin allergy. Because of the high morbidity associated with PID, prevalence of subclinical cases, and benignity of therapy, antibiotics may be indicated in high risk women even if minimal criteria not met.
Source: Greg Moran, MD; MMWR August 4, 2006 / 55(RR11);1-94
5. Why are you still getting ABGs?
Arterial blood gases are painful procedures that are time consuming for the physician. Venous blood gases on the other hand are safe, less painful and can be drawn with the patients regular blood draw. Multiple studies have shown that information obtained from VBGs correlates well with ABGs. The pH from ABGs and VBGs from studies done on patients in DKA shows a strong correlation with a mean difference of 0.3-0.4. HCO3 shows a similar correlation with mean differences of about 1.5 meq/L, which is minimal. pCO2 on the other hand, has shown only fair agreement with the pCO2, on average 5.8 mm Hg higher in venous samples. Although there is poor correlation, a venous pCO2 level of 45 mm Hg can be used as a potential screening cutoff (sensitivity for the detection of hypercarbia of 100%) in the patient that you are worried about CO2 retention. Dr Herbert concludes, the best way to reduce the pain from an ABG is to not do the ABG.
Source: Ann Emerg Med April 1998;31:459-465; J Emerg Med. 2002 Jan;22(1):15-9
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