52 in 52: Low Tidal Volumes in ARDS

ARDSnet

http://www.nejm.org/doi/full/10.1056/NEJM200005043421801

An idea from Dr. Emily Junck out of Univ of Washington EM, linked below is a list of 52 landmark studies which helped evolve the practice of EM. This week’s read is from the ARDSnet trial, which showed low tidal volumes decreased mortality in ARDS and acute lung injury patients.

http://academiclifeinem.com/52-articles-in-52-weeks-landmark-em-articles-2013/

Quick Fix:
Past mechanical ventilation tidal volumes (TV) were 10-12 cc/kg of ideal body weight. Mortality was observed to range from 40-50% in pts with Acute Lung Injury (ALI) and Acute Resp Distress Syndrome (ARDS). Compared to the physiological 7-8 cc/kg TVs, it was hypothesized that the excessive lung stretch cause an inflammatory surge, resulting subsequent organ injury. The study hypothesized that maybe less stretch = better (lower TV), even if at the expense of decreased oxygenation or increased acidosis.

The two compared groups observed were high TV (12 cc/kg, goal plateau pressure of less/equal to 50 cc of H2O) and low TV (6 cc/kg, goal plateau pressure of less/equal to 30 cc of H2O).

Amongst several other end points, the study saw in comparison that the low TV group had:
decreased mortality (P = 0.007), noting a 22% reduction.
– increased no. of vent-free days (P = 0.007).
– decreased no. of days of non-pulmonary organ failure (P = 0.006).
– decrease concentrations of Interleukin-6, a surrogate marker of inflammation (P = 0.002).
However, there was no statistical difference in the incidence of barotrauma, most commonly manifesting as pneumothorax (P = 0.43).

Plus ARDSnet introduced the “PEEP Ladder” used to sequentially improve oxygenation by incrementally augmenting FiO2 and PEEP.
PEEPladder
(image from: http://crashingpatient.com/ventilator-management/ventilator-management.htm/)

Bottom Line: Lower TV = Better for injured lungs.

Acute Pulmonary Edema (Summary)

Presented by Dr. Anand Swaminathan, NYU/Bellevue.

A 65 yo M pt with PMH of ESRD, HTN, CAD comes in c/o SOB x3 days after missing hemodialysis twice in the past week. A portable CXR is ordered, and it looks similar to this:
http://radiopaedia.org/cases/apo-arrowsjpg

Acute Pulmonary Edema.
Causes: MI, PE, dysrhythmia, infection, tox, therapy non-compliance

Managment:
– firstly, supportive – ABCs, IV, o2, monitor
– Airway? less and less patients need to be intubated

The pathophysiology helps us better understand/affects our management:
– LV can’t pump blood out as fast, resulting in blood backing up.
– fluids fills the alveoli, washes out surfactant
– results in sympathetic surge.
– RAAS is activated, leading to vasconstriction and water reabsorption
– ADH released, increasing the circulating volume

Treatment Options:
1.) Nitro
Effect of sublingual nitroglycerin in emergency treatment of severe pulmonary edema, Bussmann et al.
(http://www.ncbi.nlm.nih.gov/pubmed/417614)
– decreased in LV filling pressure, decrease in cardiac output
– nitrates are good for preload (and afterload) reduction

2.) Morphine
Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis, Peacock et al.
(http://www.ncbi.nlm.nih.gov/pubmed/18356349)
– increased risk of ICU admissions, mechanical ventilation, and mortality
– (study not randomized, and more correlational than causal)

3.) Loop Diuretics
Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema, Hoffman et al.
(http://www.ncbi.nlm.nih.gov/pubmed/3115687)
– pts who got morphine and furosemide did worse
– a lot of pts DON’T have fluid overload
– lots DON’T have functioning kidneys
– splanchinic circulation is clamped, so lasix won’t reach the kidney

4.) ACE Inhibitors
Rapid improvement of acute pulmonary edema with sublingual captopril, Hamilton et al.
(http://www.ncbi.nlm.nih.gov/pubmed/8673775)
– sublingual administration of captopril vs NG
– decreases afterload

5.) BiPAP
Randomized Trial of Bilevel versus Continuous Positive Airway Pressure for Acute Pulmonary Edema, Liesching et al.
(http://www.ncbi.nlm.nih.gov/pubmed/24071031)
although mechanism has not been proven:
-surfactant thought to be washed out of alveoli
– PEEP keeps alveoli open
– reduces afterload (especially versus CPAP)

**Takeaway point**
Initial APE Tx = Nitro + BiPAP

Shattering Urban Legends in Emergency Medicine.

Presented by Dr. Anand Swaminathan, NYU/Bellevue.

MEGACASE: 75 yo F with history of ESRD on HD presents to your E.D. after a looooong bus ride with unilateral leg swelling, shortness of breath, hemoptysis, and a recent history of hip surgery. Your thorough history further reveals that the patient has asthma, a severe shellfish allergy, and has had contrast reactions in the past. To make matters worse, the patient is writhing in pain on the stretcher complaining of right flank pain radiating to the groin and a history of renal calculus last year. And for some reason, this patient is still finding the time to tell you she has a “sore throat,” with fever, cough, tonsillar exudate and cervical lymphadenopathy. Oh yeah, and her throat snaps shut like a bear-trap if she has penicillin.

You just finished prepping the exam room, when…

image

1.) Do patients with ESRD need emergent dialysis after receiving IV contrast?

NO

There may be a slightly increased risk of pulmonary edema with iodinated contrast secondary to higher molecular weights, but most hospitals use non-iodinated contrast now. Patients may continue their current dialysis schedule so long as they are dialysed within 24-72 hrs post-contrast administration, regardless of anuric/oliguric status. Check out wha t the American College of Radiology says:
“… Unless an unusually large volume of contrast medium is administered or there is substantial underlying cardiac dysfunction, there is no need for urgent dialysis after intravascular iodinated contrast medium administration.” ACR, version 9, pg 26. (http://www.acr.org/quality-safety/resources/contrast-manual)

2.) Is pretreatment necessary/effective in preventing adverse reactions to IV contrast?

NAH

“The efficacy of corticosteroid and/or antihistamine prophylaxis is unknown, though some have suggested this practice. However, given the likely differing mechanisms between acute and delayed reactions, as well as the extreme rarity or nonexistence of severe delayed reactions, premedication prior to future contrast-enhanced studies is not specifically advocated in patients with solely a prior history of mild delayed cutaneous reaction.” ACR, version 9, page 40. (http://www.acr.org/quality-safety/resources/contrast-manual)

3.) Ok, ok, how about flomax for renal stones? Everybody’s doing it.

Take it or leave it.

Most studies are equivocal showing no benefit. However, one recommendation that pervades the literature is that if you are going to use it, save it for distal stones. (http://www.ncbi.nlm.nih.gov/pubmed/21149761)

4.) I’ve heard pen allergic patient’s should never, ever get cephalosporins because the rate of cross-reactivity is 10%. This has to be true.

Listen, pal…

Well, when penicillins and cephalosporins were first produced, the were often made in the same factories – this 10% figure is more likely related to cross-contamination during the production process, not cross-reactivity. The actual rate is closer to 1-3%. There may be higher rates with 1st or 2nd generation cephalosporins, but 3rd generation or higher seem to be fine. Furthermore, the proportion of patients claiming to have a PCN allergy, that actually have a true PCN allergy, is 3%. Overall, the rate of anaphylaxis to cephalosporin in patient’s with a history of anaphylaxis to PCN in 0.001%.

Remember the rule of 3’s: 3% actually have it, 3% will have a reaction and 3rd gen cephalosporin or higher is best. (http://www.ncbi.nlm.nih.gov/pubmed/21742459)

Brian Hayes of UM puts it best on ALiEM:
http://academiclifeinem.com/busting-the-myth-the-10-cephalosporin-penicillin-cross-reactivity-risk/

5.) I know antibiotics can’t prevent PSGN. I get it, I know. But what about for Acute Rheumatic Fever (ARF)?

This one’s gotta be right.
As it turns out: not really. The rate of ARF is so low in industrialized nations, that the CDC does not track incidence of the disease any more. (In aboriginal populations, older thinking still holds strong; ARF remains problematic and necessitates antibiotic therapy). The risk of sequela from the disease is significantly and statistically low, and it is a self-limiting process. A Cochrane review demonstrated “resolution and improvement of pain in participants with sore throat” when comparing the efficacies of steroids and antibiotics. (http://www.ncbi.nlm.nih.gov/m/pubmed/23076943/)

GI Bleeding, an Evidence Based Approach.

presented by Dr. Mark Fenig, MD

With GI bleed patients, EM docs want to a.) differentiate between Upper and Lower sources and b.) stratify the severity of the bleed. Valuable buzzwords from the patient’s history include their age, hematemesis, melena, and/or cirrhosis. Objective measures include BUN:Cr…

“Great, but what did the Nasogastric (NG) Lavage show?”

Well… NG lavage has shown to have a sensitivity of 42%(1) and… amongst incision and drainage of abscesses, fracture reduction, urethral catheterization… NG Tube placement was scored to be THE most painful procedure patients experience in the ED (2).

In one study, NG Lavage did NOT improve mortality, did NOT lessen length of stay, did NOT prevent unnecessary surgeries, and did NOT lessen need for transfusions. The only thing it DID impact was time to endoscopy; but even this was institution-specific. (3)

So what other clinical measures can we use objectively to assess which patients are high risk versus low risk GI Bleeds? In comes the Glasgow Blatchford Bleeding Score (GBBS).  There has been good external validation of GBBS; scores of 0 had no complications, no high risk lesions, and were safe for discharge. In later examinations of the scoring system, everyone with a score of 0 (15% of patients) were discharged – there were no complications and no interventions after outpatient EGD (showing low risk lesions).(4)

GBBS proved successful in ruling in bleeding too: sensitivity of 99.6% and Negative Predictive Value of 96.4%. (5)

Next time you face a patient with a GI bleed, think about the Glasgow Blatchford Bleeding Score before reaching for that painful NG tube.

mdcalc.com/glasgow-blatchford-bleeding-score-gbs

Citations

1.) Usefulness and validity of diagnostic nasogastric aspiration in patients without hematemesis. Witting et al. 2004. PubMed Id 15039700

2.) Comparison of patient and practitioner assessments of pain from commonly performed emergency department procedures. Singer et al. 1999. PubMed ID 10339680

3.) Impact of nasogastric lavage on outcomes in acute GI bleeding. Huang et al. 2011. PubMed ID 21737077 

4.) Outpatient management of patients with low-risk upper-gastrointestinal haemorrhage: multicentre validation and prospective evaluation. Stanley et al. 2009. PubMed ID 19091393

5.) Risk scoring systems to predict need for clinical intervention for patients withnonvariceal upper gastrointestinal tract bleeding. Chen et al. 2007. PubMed ID 17870480

Emergency Medicine in the South Bronx